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imbalances are the mainstays of treatment to improve maternal and fetal outcomes, providers must remain vigi­lant for potentially more complicated obstetric manage­ment. Fetal considerations in the case of delivery include preterm birth, fetal hypoxia, fetal acidosis, fetal birth injury, and fetal loss; maternal considerations include concomitant preeclampsia, sepsis more likely to progress to septic shock, and peripartum hemorrhage from a vari­ety of causes.
CASE- BASED LEARNING DISCUSSION
1. Describe the pathophysiology and management goals intraoperatively for this diseasestate.
2. In the case described above, what tests should be done to evaluate the patient’s glucose tolerance?
3. How is the diagnosis of GDM established?
4. What would be the best treatment and follow- up strategy for this patient?
5. What are potential complications to the patient and her fetus if le untreated?
6. If the patient presented with ketones present in her urine, what additional testing should be performed to conrm a diagnosis ofDKA?
7. If DKA is conrmed, what are the primary goals of treatment?
REFERENCES
1. Committee of the Japan Diabetes Society on the Diagnostic Criteria
of Diabetes Mellitus, Seino Y, Nanjo K, Tajima N, etal. Report of the Committee on the Classication and Diagnostic Criteria of Diabetes Mellitus. Journal of Diabetes. 2010;1(5):212– 28.
2. American Diabetes Association. Gestational diabetes mellitus.
Diabetes Care. 2004;27(Suppl 1):S88– 90.
3. Powers AC. Chapter344:Diabetes mellitus. In:Longo DL, Fauci
AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds., Harrison’s Principles of Internal Medicine. 18th ed. 2012. Retrieved from http:// accessmedicine.mhmedical.com.ezp- prod1.hul.harvard. edu/ content.aspx?bookid=331§ionid=40727149. Accessed July 9,2015.
4. American Diabetes Association. Standards of medical care in
diabetes— 2009. Diabetes Care. 2009;32(Suppl 1):S13– 61.
5. Butler A, Cao- Minh L, Galasso R, etal. Adaptive changes in pancre-
atic beta- cell fractional area and beta- cell turnover in human preg­nancy. Diabetologia. 2010;53:2167– 76.
6. Catalano P, Drago N, Amini S. Longitudinal changes in pancreatic
beta- cell function and metabolic clearance rate of insulin in preg­nant women with normal and abnormal glucose tolerance. Diabetes Care. 1998;21:403– 8.
7. Buchanan T, Xiang A, Peters R, etal. Response of pancreatic beta­cells to improved insulin sensitivity in women at high risk for type 2 diabetes. Diabetes. 2000;49:782– 8.
8. Magon N, Chauhan M. Pregnancy in type 1 diabetes mellitus:how special are special issues? North American Journal of Medical Sciences. 2012;4:250– 6.
9. Rosenberg TJ, Garber S, Lipkind H, Chiasson MA. Maternal obe­sity and diabetes as risk factors for adverse pregnancy outcomes:dif­ferences among 4 racial/ ethnic groups. American Journal of Public Health. 2005;95:1545– 51.
10. Barbieri, R, Reece A. Obstetrics and Gynecology: e Essentials of Clinical Care. Stuggart, Germany: Georg ieme Verlag; 2010:253– 4.
11. Jameson, J, De Groot, L, Kretser D, etal. Endocrinology:Adult and Pediatric. 7th ed. Amsterdam, Netherlands:Elsevier; 2016:793– 5.
12. Nicholson WK, Wilson LM, Witkop CT, etal. erapeutic man­agement, delivery, and postpartum risk assessment and screen­ing in gestational diabetes. Evidence of Reproductive Technology Assessment (Full Report). 2008;162:1– 96.
13. Montoro MN, Myers VP, Mestman JH, Xu Y, Anderson BG, Golde SH. Outcome of pregnancy in diabetic ketoacidosis. Am J Perinatol. 1993;10:17– 20.
14. American College of Obstetricians and Gynecologists. Gestational diabetes mellitus. Practice Bulletin No. 137. Obstetrics and Gynecology. 2013;122:406– 16.
15. Wier LM, Witt E., Burgess J, Elixhauser A. Hospitalizations related to diabetes in pregnancy, 2008. HCUP Statistical Brief #102. Rockville (MD): Agency for Healthcare Research and uality;2010.
16. Parker JA, Conway DL. Diabetic ketoacidosis in preg­nancy. Obstetrics and Gynecology Clinics of North America. 2007;34:533– 43,xii.
17. Catalano PM, Tyzbir ED, Roman NM, Amini SB, Sims EA. Longitudinal changes in insulin release and insulin resistance in nonobese pregnant women. American Journal of Obstetrics and Gynecology. 1991;165:1667– 72.
18. Sibai BM. Management of Acute Obstetrics Emergencies: Female Pelvic Surgery. Video Atlas Series. 1st ed. Philadelphia, PA:Saunders Elsevier; 2011:137– 41.
19. Guo RX, Yang LZ, Li LX, Zhao XP. Diabetic ketoacidosis in preg­nancy tends to occur at lower blood glucose levels:case- control study and a case report of euglycemic diabetic ketoacidosis in pregnancy. Journal of Obstetric and Gynaecologic Research. 2008;34:324– 30.
20. Franke B, Carr D, Hatem MH. A case of euglycaemic diabetic keto­acidosis in pregnancy. Diabetic Medicine. 2001;18:858– 9.
21. Oliver R, Jagadeesan P, Howard RJ, Nikookam K. Euglycaemic dia­betic ketoacidosis in pregnancy:an unusual presentation. Journal of Obstetrics and Gynaecology. 2007;27:308.
22. Moore TR. Chapter 49: Diabetes in pregnancy. In Creasy RK, Resnick R, Iams JD, eds. Maternal- Fetal Medicine:Principles and Practice. 5th ed. Philadelphia, PA:Saunders; 2004:1031– 2.
23. Shimizu I, Makino H, Osawa H, etal. Association of fulminant type 1 diabetes with pregnancy. Diabetes Research and Clinical Practice. 2003;62:33– 8.
24. Cullen MT, Reece EA, Homko CJ, Civan E. e changing presenta­tions of diabetic ketoacidosis during pregnancy. American Journal of Perinatology. 1996;13:449– 51.
25. Schneider M, Umpierrez G, Ramsey R, Mabie W, Bennett K. Pregnancy complicated by diabetic ketoacidosis:maternal and fetal outcomes. Diabetes Care. 2003;26:958– 9.
26. Hawthorne G. Maternal complications in diabetic pregnancy. Best Practice in Research and Clinical Obstetrics and Gynaecology. 2011;25:77– 90.
27. Ditzel J, Standl E. e oxygen transport system of red blood cells during diabetic ketoacidosis and recovery. Diabetologia. 1975;11:255– 60.
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28. Philipps AF, Rosenkrantz TS, Raye J. Consequences of perturba­tions of fetal fuels in ovine pregnancy. Diabetes. 1985;34(Suppl
2):32– 5.
29. Kamalakannan D, Baskar V, Barton DM, Abdu TA. Diabetic ketoacidosis in pregnancy. Postgraduate Medicine Journal. 2003;79:454– 7.
30. Kitzmiller JL. Diabetic ketoacidosis and pregnancy. Contemporary Obstetrics and Gynecology. 1982;20:141– 7.
31. Hughes AB. Fetal heart rate changes during diabetic ketosis. Acta Obstetrics and Gynecology Scandanavia. 1987;66:71– 3.
32. Hagay ZJ, Weissman A, Laurie S, Insler V. Reversal of fetal distress following intensive treatment of maternal diabetic ketoacidosis. American Journal of Perinatology. 1994;11:430– 2.
33. Rizzo T, Metzger BE, Burns WJ, Burns K. Correlations between antepartum maternal metabolism and child intelligence. New England Journal of Medicine. 1991;325:911– 6.
34. Harding JE, Charlton VE. Eect of lactate and beta- hydroxybutyrate infusions on brain metabolism in the fetal sheep. Journal of Developmental Physiology. 1990;14:139– 46.
35. Arora S, Henderson SO, Long T, Menchine M. Diagnostic accu­racy of point of care testing for diabetic ketoacidosis at emergency department triage:{beta}- hydroxybutyrate versus dipstick. Diabetes Care. 2011;34:852– 4.
36. Wallace TM, Mathews DR. Recent advances in the monitoring and management of diabetic ketoacidosis. QJM:Monthly Journal of the Association of Physicians. 2004;97:773– 80.
37. Pasquel FJ, Umpierrez GE. Hyperosmolar hyperglycemic state:a historic review of the clinical presentation, diagnosis, and treatment. Diabetes Care. 2014;37:3124– 31.
38. Van Zyl DG, Rheeder P, Delport E. Fluid management in diabetic­acidosis— Ringer’s lactate versus normal saline: a randomized con­trolled trial. QJM:Monthly Journal of the Association of Physicians. 2012;105:337– 43.
39. Story DA, Morimatsu H, Bellomo R. Hyperchloremic acidosis in the critically ill: one of the strong- ion acidoses? Anesthesia & Analgesia. 2006;103:144– 8.
40. Sibai B, Viteri O. Diabetic ketoacidosis in pregnancy. Obstetrics and Gynecology Clinics. 2014;123:167– 78.
41. Kamana KC, Shakya S, Zhang H. Gestational diabetes mellitus and macrosomia: a literature review. Annals of Nutrition and Metabolism. 2015;66(Suppl 2):14– 20.
42. Langer O, Yogev Y, Most O, Xenakis EMJ. Gestational diabetes:the consequences of not treating. American Journal of Obstetrics and Gynecology. 2005;192:989– 97.
43. Knight M, Kenyon S, Brocklehurst P, Neilson J, Shakespeare J, Kurinczuk JJ, eds.; on behalf of MBRRACE- UK. Saving lives, improving mothers’ care— lessons learned to inform future mater­nity care from the UK and Ireland Condential Enquiries into Maternal Deaths and Morbidity 2009– 12. Oxford: National Perinatal Epidemiology Unit, University of Oxford;2014.
44. Acosta CD, Knight M, Lee HC, Kurinczuk JJ, Gould JB, Lyndon A. e continuum of maternal sepsis severity:incidence and risk fac­tors in a population- based cohort study. Public Library of Science One. 2013;8(7):e67175.
45. Bateman BT, Berman MF, Riley LE, Leert LR. e epidemiology of postpartum hemorrhage in a large, nationwide sample of deliver­ies. Anesthesia & Analgesia. 2010;110:1368– 73.
46. Fraser A, Nelson SM, Macdonald- Wallis C, et al. Association of pregnancy complications with calculated cardiovascular disease risk and cardiovascular risk factors in middle age:the Avon longitudinal study of parents and children. Circulation. 2012;125:1367– 80.
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SECTIONF
TOXINS
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59.
MAGNESIUM TOXICITY
Anthony T.Chau
CLINICALCASE
endplate to acetylcholine.7 Moreover, in the central nervous
system, magnesium blocks the inux of calcium through the A 33- year- old G1P0 at 36 weeks gestation was admitted for induction of labor for severe preeclampsia. Blood pressure on admission was 170/ 110mmHg. e patient complained of mild intermittent headache but denied other symptoms. Laboratory ndings were within normal ranges except for platelet count of 95,000/ mm3 and serum creatinine of 1.2 mg/ dL. She was otherwise healthy. Her blood pressure was controlled aer two doses of IV labetalol 20 mg. An intravenous magnesium infusion was started with a 4 gram loading dose over 20 minutes followed by 1 g/ hr. During this same time, the obstetrician ordered the oxytocin infu­sion to be doubled. Several hours later, the patient reported feeling ushed, blurry vision, and nauseated with shallow respirations and weakness in her extremities. Upon reenter­ing the room, the nurse quickly discovered the magnesium infusion was mistaken for the oxytocin and the patient had received a total of 10 g of magnesium in the last 3hours.
PHYSIOLOGY AND PHARMACOLOGY OFMAGNESIUM
N- methyl- D- aspartate (NMDA) receptor to exert antinoci-
ceptive eects demonstrated in both animal and human pain
models.
8– 10
Magnesium can exert hemodynamic eects by increas­ing the production of endothelial prostacyclin, leading to vasodilation.
11,12
It also decreases catecholamine release from the adrenal medulla and adrenergic nerve endings.13 Compared with those without pretreatment, patients who had pretreatment with magnesium sulfate 60 mg/ kg prior to tracheal intubation experienced a lower increase of heart rate and systolic blood pressure postintubation with sig­nicantly lower serum concentrations of epinephrine and norepinephrine.14 Although there is a theoretical risk of exaggerated hypotension when magnesium is combined with calcium channel blockers, the combination appears well tolerated in practice.
15
Magnesium is not metabolized and is solely eliminated
by renal excretion with a half- life of 4 hours.
11,16
In patients with normal renal function, an increase in serum magnesium concentration increases the fractional magnesium clearance and decreases reabsorption. is serves as a method for the kidneys to maintain magnesium homeostasis and also a pro-
Magnesium is the second most abundant intracellular cat­ion in the human body aer potassium.1 Serum magnesium represents only 0.3% of the total body magnesium and exists as ionized (62%), protein bounded (33%) or com­plexed with anions such as citrate or phosphate(5%).
2
Physiologically, magnesium acts as a calcium antagonist. On smooth muscle membranes, magnesium competes with calcium for surface binding sites to regulate muscle contrac­tions.2 In the myocardium, magnesium mediates the activation
2 +
of Ca excitability and suppress cardiac arrhythmias.
ATPase and Na +- K + ATPase to reduce myocardial
5,6
At the neu­romuscular junction, magnesium competes with calcium for binding sites on the acetylcholine vesicle, thereby decreasing the release of acetylcholine and lowering the sensitivity of the
tective mechanism against toxicity.17 Patients with impaired renal function cannot compensate for the increased magne­sium load and are thus at risk of toxicity.
In a pregnant patient, magnesium readily crosses the
placenta. Following intravenous administration, there is an
3,4
average delay of 2 hours before equilibrium between fetal and maternal serum magnesium concentration is estab-
11,18
lished.
Ameta- analysis found that maternal administra­tion of magnesium sulphate can result in decreased baseline fetal heart rate (FHR) up to 15 beats per minute, decreased short- and long- term heart rate variability, and decreased number and frequency of accelerations on FHR monitor­ing. ese changes, however do not appear to be associated with adverse outcomes.
19
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CLINICAL USE OFMAGNESIUM
use, drug errors still occur; thus when administering mag­nesium, providers must maintain a high vigilance to ensur-
Magnesium sulfate is currently recommended as the drug
ing patient safety. of choice for prophylaxis against eclampsia in women with preeclampsia and rst- line treatment for eclampsia. However, there is currently no consensus on the optimal time of initiation, duration of therapy, dosing, and route of administration.
23,24
Magnesium sulfate is also used for fetal neuroprotection when imminent birth is anticipated at <32 weeks gestation.25 Other common clinical uses of mag­nesium that perioperative crisis management providers may encounter include treatment of torsades de pointes, status asthmaticus,26 and postoperative pain control.
e most commonly used magnesium sulfate dose for seizure prophylaxis in a preeclamptic parturient is an intravenous loading dose of 4– 6 g over 15 to 20 minutes, followed by a maintenance infusion of 1 to 2 g/ hr. Based on retrospective data, a therapeutic range of 4.8 to
8.4 mg/ dL has been suggested.29 Following the intravenous loading dose of 4 to 6 g, there is an immediate but tran­sient increase in serum concentrations to 5.1 to 9.2 mg/ dL, which typically declines to 3.2 to 4.1 mg/ dL within 60 minutes.11 With simply starting an infusion of 1 g/ h, serum magnesium concentrations reach a plateau aer 24 hours at approximately 4.1 mg/ dL.
11
20– 22
24,27,28
CLINICAL DIAGNOSIS OFMAGNESIUM TOXICITY
Similar to local anesthetics, the clinical eect and tox­icity of magnesium are directly related to its concentra­tion in serum. However, the initial signs and symptoms experienced by each patient may vary, so a low thresh­old for suspecting toxicity should be maintained.31 e interpretation of serum magnesium concentration can be confusing because it may be reported in milligrams per deciliter (mg/ dL), milliequivalents per liter (mEq/ L) or millimoles per liter (mmol/ L)30 (see Box 59.1). e nor­mal serum concentration of magnesium ranges from 1.6 to 2.7 mg/ dL.1 Hypermagnesemia is dened as a serum magnesium concentration greater 2.7 mg/ dL.1 Signs and symptoms of hypermagnesemia are not usually apparent until the serum magnesium is >4.8 mg/ dL.33 In general, symptoms of toxicity can be grouped into four major categories:early nonspecic, neurologic, neuromuscular, and cardiovascular.
Rapid infusion of magnesium can lead to a transient
ETIOLOGY OFHYPERMAGNESEMIA
spike in serum level, precipitating diaphoresis, ushing, and warmth, likely related to peripheral vasodilation.
Deep tendon reexes are diminished when serum con­A common cause of hypermagnesemia is renal insu­ciency.1 As such, in patients with normal renal function magnesium toxicity is rarely seen. Unfortunately, in the population most likely to receive magnesium on labor and delivery, patients with preeclampsia, renal dysfunction is not uncommon.30 Because most women do not have severe enough renal failure to cause signicant toxicity, medica­tion administration error is more frequently the cause of magnesium toxicity, again particularly in parturients who receive magnesium sulfate for preeclampsia. Simpson and Knox31 reported seven lethal cases of accidental magnesium overdose in obstetrics related to the use of 1- L intravenous bags containing 40 g of magnesium sulfate following tem­porary removal of intravenous line from the infusion pump. McDonnell et al.30 described an intraoperative program-
centration is greater than 6.1 mg/ dL17 and become absent
as concentration reaches beyond 8.5 mg/ dL.11 Between
9 and 12 mg/ dL, nonspecic symptoms including nau-
sea, vomiting, and headache may be seen, although these
symptoms are not diagnostically helpful, as they may
present at much lower concentrations and in many cases
exist in healthy parturients in labor who are not receiving
magnesium. e category of early nonspecic symptoms
also includes nervous system eects such as somnolence,
ataxia, confusion, lethargy, and visual disturbances,
reecting magnesium’s ability to readily cross the blood-
brain barrier.
1,11
As the serum concentration of magne­sium escalates further to 12– 15 mg/ dL, severe muscle weakness including uterine atony and respiratory paralysis can occur. Levels exceeding 18 mg/ dL may produce loss
ming error, where magnesium was mistakenly administered through an electronic infusion device in place of oxyto­cin. Feng etal.32 reported a case where a patient developed magnesium toxicity following an inadvertent free- owing
BOX 59.1 CONVERSION TABLE FORMAGNESIUM SERUM
CONCENTRATIONS
bolus administration of the medication without an infu­sion device.17 Even with systems improvement and protocol
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of consciousness, along with severe cardiovascular symp-
TREATMENT OFMAGNESIUM TOXICITY
toms including bradycardia, cardiac arrhythmias, and cardiorespiratory arrest (Table 59.1). Finally, acute hyper­kalemia has also been reported during the management of magnesium therapy in an obstetric patient.30 At high concentrations, magnesium can inhibit sodium potassium ATPase, resulting in buildup of potassium in the extracel­lular space, leading to development of hyperkalemia, with peaked T- waves becoming evident on ECG at a serum magnesium of 2.5– 5mmol/ L.
30
Deep tendon reexes, respiratory rate, and at times, serum concentrations, are the most commonly moni­tored parameters in patients receiving magnesium infu­sions on labor and delivery. Electrocardiography (ECG) may also help reveal some evidence of hypermagnesemia (Box 59.2), however continuous telemetry is rarely used in laboring patients. If deep tendon reexes are intact, providers can take comfort that magnesium concentra­tions will rarely be in the toxic range. In otherwise healthy parturients on magnesium for prevention or treatment of eclampsia, routine monitoring of serum magnesium lev­els is not recommended.34 Monitoring of serum concen­tration should be considered when magnesium toxicity is suspected (e.g., absent deep tendon reexes, respiratory rate less than 12)or in the presence of renal insuciency (i.e., serum creatinine > 1.0 mg/ dL or urine output < 100 cc for 4 hours).
7
e rst step in the management of a patient with magne­sium toxicity is to discontinue further administration of exogenous magnesium. Help should be summoned imme­diately, with mobilization of resuscitation teams and equip­ment depending on the patient status. Airway should be quickly assessed and managed if necessary and 100% oxy­gen delivered, and the patient should be placed in lateral uterine displacement position. Cardiorespiratory support may be required until magnesium levels are reduced.
Calcium is the mainstay of treatment and should be administered as soon as magnesium toxicity is diagnosed. Calcium can directly reverse the signs and symptoms of mag­nesium toxicity and increase magnesium excretion by dis­rupting the electrochemical gradient at the thick ascending limb (TAL) of the loop of Henle that regulates magnesium reabsorption.35 Calcium is available as calcium gluconate or calcium chloride salt solutions.36 Calcium chloride con­tains threefold greater elemental calcium per gram but has a greater potential for infusion site reactions (e.g., necro­sis from extravasation) compared to calcium gluconate, so administration via central venous access or a large bore peripheral venous catheter is usually recommended.
37,38
e most appropriate dose and formulation of calcium in cases of magnesium toxicity remain elusive. However, the usual recommended initial dose for calcium gluconate is 1,000 to 2,000 mg (10 to 20 mL of 10% solution) intravenously at a
TABLE59.1 SERUM CONCENTRATION OFMAGNESIUM AND OBSERVED CLINICAL SIGNS AND SYMPTOMS
mg/ dL
<1.2 <1 <0.5 Tetany, seizures, arrhythmias
1.2- 1.8 1- 1.5 0.5- 0.8 Neuromuscular irritability, hypocalcemia,hypokalemia
1.8- 2.4 1.5- 2.1 0.8- 1.0 Normal Range
2.5- 5.0 2.1- 4.2 1.1- 2.1 Typically asymptomatic
4.9- 8.5 4- 7 2- 3.5 Therapeutic range for seizure prophylaxis for preeclampsia
>6.1 >5 >2.5 Diminished DTR
6.1- 9.7 5- 8 2.5- 4.0 Target level for treatment for eclampsia
8.5- 12.2 7- 10 3.5- 5 Absent DTR
9.2- 12.2 7.6- 10 3.8- 5 Flushing, increased warmth, headaches, nausea, vomiting,
12.2- 15.8 10- 13 5- 6.5 Respiratory paralysis
>18.2 >15 >7.5 Altered cardiac conduction
>30 >25 >12.5 Cardiac Arrest
mEq/ L mmol/ L
Clinical Signs and Symptoms
35
35
35
17
11
confusion, ataxia, blurry vision, lethargy
11
11
11
17
11
35
11
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toxicity should be maintained in parturients with decreased
BOX 59.2 ECG MANIFESTATIONS OFMAGNESIUM
TOXICITY
• Increased PR and QT intervals
• Increased QRS duration
• Variable decrease in P- wave voltage
40
deep tendon reexes or impaired respiratory status. Intravenous calcium is the treatment of choice for patients with suspected magnesium toxicity.
CASE- BASED LEARNING DISCUSSION
• Variable degree of T- wave peaking
• Complete AV block, asystole
1. What are your dierential diagnoses?
2. What are your initial steps in managing this patient? Would you consider transferring this patient to
rate no exceeding 0.5 to 2 mL/ min.38 Calcium chloride may be used if this formulation is more readily available.
In severe hypermagnesemia or in patients with com­promised renal function, dialysis may be required, because elimination of magnesium ultimately requires renal excre-
1,39
tion.
However, preparation for hemodialysis or peri­toneal dialysis oen takes an hour or longer, so other supportive measures including advanced cardiac life sup­port and calcium should be repeated until the patient is acutely stabilized and/ or those therapies are available.
In patients with normal renal function, further options may be considered to hasten renal excretion of magnesium. In contrasts with other cations that are reabsorbed in the proximal tubules, 60%– 70% of ltered magnesium is reab­sorbed in the TAL due to relative the impermeability of the proximal tubular epithelium to magnesium.39 e reabsorp­tion of magnesium in the TAL is passive and inversely related to ow. erefore, an increase in tubular ow (e.g., crystal­loid infusion for volume expansion, diuretics) would help reduce magnesium reabsorption. For this reason, intrave­nous normal saline bolus and furosemide 1 mg/ kg have been recommended to enhance renal excretion by promoting diuresis.
30,38
is technique is not without risks— resultant hypocalcemia may worsen the signs and symptoms of hyper­magnesemia and the large uid load may increase the risk of pulmonary edema in patients with severe preeclampsia.
30
the operating room? What would determine your resuscitation location?
3. What are other therapeutic uses of magnesium in obstetric patients? What are your doses used in these scenarios?
4. How does maternal administration of magnesium inuence the fetal heart tracing?
5. What is the therapeutic level for magnesium when administered for seizure prophylaxis? At what serum concentration of magnesium does the patient rst develop signs of systemic toxicity?
6. Physical examination revealed absent deep tendon reexes. Are you concerned? How does this nding help speculate what the magnesium level wouldbe?
7. ASTAT magnesium level sent to the lab revealed a serum magnesium concentration of 15.5 mg/ dL. What do you think about this level? How would you proceed in managing this patient? What medication should you consider? What dose would you use? How frequently would you repeat the dose? What other consultants would you consider to involve in this care of this patient? Do you think this patient would be at a higher risk for postpartum hemorrhage? Why or whynot?
8. What could help prevent magnesium toxicity in this patient?
CONCLUSION
REFERENCES
Anesthesia providers on labor and delivery will frequently care for patients receiving intravenous magnesium therapy for either preeclampsia/ eclampsia or fetal neuroprotection. Because the therapeutic serum concentration far exceeds normal “goal” physiologic levels, patients are subjected to high- dose magnesium infusions that carry a risk of toxicity, especially in cases of renal insuciency or when medica­tion errors occur. Ahigh level of suspicion for magnesium
1. ECC Committee, Task Forces of the American Heart Association.
2005 American Heart Association guidelines for cardiopulmo­nary resuscitation and emergency cardiovascular care. Circulation. 2005;112(24 Suppl):IV1– 203.
2. Fawcett WJ, Haxby EJ, Male DA. Magnesium:physiology and phar-
macology. Br Journal of Anaesthesia. 1999;83(2):302– 20.
3. Altura BM. Introduction:importance of Mg in physiolog y and med-
icine and the need for ion selective electrodes. Scandanavian Journal of Clinical Laboratory Investigation, Supplement. 1994;217:5– 9.
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4. Iseri LT, French JH. Magnesium: nature’s physiologic calcium blocker. American Heart Journal. 1984;108(1):188– 93.
5. Hall SK, Fry CH. Magnesium aects excitation, conduction, and contraction of isolated mammalian cardiac muscle. American Journal of Physiology. 1992;263(2 Pt 2):H622– 33.
6. Reinhart RA. Clinical correlates of the molecular and cellular actions of magnesium on the cardiovascular system. American Heart Journal. 1991;121(5):1513– 21.
7. James MF. Magnesium in obstetrics. Best Practice and Research in Clinical Obstetrics and Gynaecology. 2010;24(3):327– 37.
8. Bardgett ME, Schultheis PJ, McGill DL, Richmond RE, Wagge JR. Magnesium deciency impairs fear conditioning in mice. Brain Research. 2005;1038(1):100– 6.
9. De Oliveira GS Jr, Castro- Alves LJ, Khan JH, McCarthy RJ. Perioperative systemic magnesium to minimize postoperative pain:a meta- analysis of randomized controlled trials. Anesthesiology. 2013;119(1):178– 90.
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