Deep tendon reflexes, magnesium, and calcium: assessments and implications.
ABSTRACT The perinatal nurse, in collaboration with physicians, can use deep tendon reflexes as a powerful tool in determining the need to start, adjust, or stop magnesium infusion. Toxicity can be detected using physical manifestations as a guide. Clinical signs may be a better indicator than serum levels of tissue levels of magnesium. Whether magnesium is given to prevent seizures or for tocolysis, patients in both situations are at risk for developing toxicity and must be assessed regularly to ensure patient safety.
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ABSTRACT: Magnesium enhances the effect of rocuronium. Sugammadex reverses rocuronium-induced neuromuscular block. The authors investigated whether magnesium decreased the efficacy of sugammadex for the reversal of rocuronium-induced neuromuscular block. Thirty-two male patients were randomized in a double-blinded manner to receive magnesium sulfate (MgSO4) 60 mg/kg or placebo intravenously before induction of anesthesia with propofol, sufentanil, and rocuronium 0.6 mg/kg. Neuromuscular transmission was monitored using TOF-Watch SX acceleromyography (Organon Ltd., Dublin, Ireland). In 16 patients, sugammadex 2 mg/kg was administered intravenously at reappearance of the second twitch of the train-of-four (moderate block). In 16 further patients, sugammadex 4 mg/kg was administered intravenously at posttetanic count 1 to 2 (deep block). Primary endpoint was recovery time from injection of sugammadex to normalized train-of-four ratio 0.9. Secondary endpoint was recovery time to final T1. Average time for reversal of moderate block was 1.69 min (SD, 0.81) in patients pretreated with MgSO4 and 1.76 min (1.13) in those pretreated with placebo (P = 0.897). Average time for reversal of deep block was 1.77 min (0.83) in patients pretreated with MgSO4 and 1.98 min (0.58) in those pretreated with placebo (P = 0.572). Times to final T1 were longer compared with times to normalized train-of-four ratio 0.9, without any difference between patients pretreated with MgSO4 or placebo. Pretreatment with a single intravenous dose of MgSO4 60 mg/kg does not decrease the efficacy of recommended doses of sugammadex for the reversal of a moderate and deep neuromuscular block induced by an intubation dose of rocuronium.Anesthesiology 03/2014; · 5.16 Impact Factor
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ABSTRACT: Background Irukandji Syndrome is caused by a potentially lethal jellyfish envenomation. Despite the low incidence, the condition is associated with possible life-threatening cardiovascular complications that make it difficult to manage in emergency departments. Managing Irukandji Syndrome is important for many emergency departments across Australia, particularly in North Queensland, the Northern Territory, and Western Australia. Methods The aim of this quality project was to identify current management, practices and nursing knowledge in the only emergency department in the regional city of Townsville, Queensland. This was undertaken via chart audit of all presentations over a 2-year period and a survey of nursing staff. Results Fifteen cases of Irukandji Syndrome were identified. Medical treatment options included use of opioids and magnesium for symptom control. Magnesium as a treatment option was used in 80% of cases. Chart audit indicated that in 20% of cases nursing management did not follow approved clinical guidelines for treatment and monitoring. The survey of nursing staff indicated a knowledge deficit with respect to the signs and symptoms of Irukandji Syndrome, standards of clinical monitoring, clinical assessment, and overall care provided. Conclusions To improve care of Irukandji Syndrome in the emergency department, in-service education, implementation of tendon reflex assessment for patients receiving magnesium therapy, and the development of a specific clinical documentation are recommended.Australasian Emergency Nursing Journal 08/2010; 13(3):78–88.
PRINCIPLES & PRACTICE
Deep Tendon Reflexes, Magnesium, and
Calcium: Assessments and Implications
Jan M. Nick
The perinatal nurse, in collaboration with physi-
cians, can use deep tendon reflexes as a powerful tool
in determining the need to start, adjust, or stop mag-
nesium infusion. Toxicity can be detected using physi-
cal manifestations as a guide. Clinical signs may be a
better indicator than serum levels of tissue levels of
magnesium. Whether magnesium is given to prevent
seizures or for tocolysis, patients in both situations are
at risk for developing toxicity and must be assessed
regularly to ensure patient safety. JOGNN, 33 221-
230; 2004. DOI: 10.1177/0884217504263145
Keywords: Calcium—CNS irritability—DTR—
sium toxicity—Pregnancy induced hypertension—
Accepted: February 2003
Perinatal nurses frequently manage patients
receiving magnesium sulfate (MgSO4) infusion for
treatment of preterm labor or preeclampsia. The
prescribed therapy requires nurses to monitor
patient progress and use judgment to adjust the infu-
sion. There is, however, a distinct lack of informa-
tion in the literature on the value of using deep ten-
don reflexes (DTRs) as a guide to titrate the
infusion. Research supports the relationship
between DTR findings and serum magnesium levels
but does not expound on titration methods. Nurses
need to understand how to titrate MgSO4by using
DTRs as a guide.
This article presents information on use of
MgSO4therapy in high-risk obstetrics, outlines titra-
tion techniques with the help of DTR assessments,
and emphasizes interventions for impending toxicity.
Because the body’s response to rising magnesium
levels is predictable, the perinatal nurse can closely
correlate physical manifestations with physiological,
therapeutic, and toxic ranges. Using DTRs as a
guide, the nurse can anticipate decisions regarding
the appropriateness of starting magnesium therapy
and provide recommendations on titration of the
A review of available literature on calcium as the
antidote to magnesium toxicity reveals practices that
vary and are not well supported by research. In this
era of evidence-based practice requirements, perina-
tal nurses must develop interventions based on sci-
ence and implement interventions based on good
judgment. Suggestions for collaborative research are
Rationale for Relying on DTRs
The ability to manage patients on MgSO4thera-
py requires nurses to develop expert nursing judg-
ment. Nurses use their judgment to determine who
needs DTR assessments, when to perform assess-
ments, and how often to assess. They can also pro-
vide recommendations about starting, increasing,
decreasing, or ceasing magnesium therapy. Cultivat-
ing expert technique in DTR assessment is possible.
The article “Deep Tendon Reflexes: The What, Why,
Where, and How of Tapping” (Nick, 2003) offers a
complete review of DTR assessments. The article
provides information on why the term deep tendon
reflex is a misnomer, why tendons move when
tapped, where to assess DTRs, and how to assess
them to obtain valid and reliable information.
The testing of DTRs, although common, can serve as a
powerful tool to estimate magnesium levels and indirect-
ly indicate changing magnesium levels in the patient. Con-
sistency in monitoring DTRs helps nurses develop judg-
ment regarding titration of MgSO4infusion. This method
is simple, quick, inexpensive, noninvasive, and reliable.
Perinatal nurses may perform DTR assessments inde-
pendently and will not need an order from a physician or
nurse midwife to do so. Such assessment is appropriate
and within the scope of nursing practice.
When a patient is treated with MgSO4intravenously,
the monitoring of DTRs is imperative. Surprisingly,
reliance on serum magnesium levels as an indicator poses
several problems. First, protocols for laboratory surveil-
lance of serum magnesium levels are not consistent. Not
all health care providers prescribe regular assessment of
serum magnesium levels in patients receiving MgSO4infu-
sion. Additionally, monitoring of serum levels can be pre-
scribed at intervals of every 8 hours, every 12 hours, or
less frequently. Consistency of practice does not exist. At
the least, nurses can be consistent in their assessments and
use the results to estimate magnesium levels in the tissue.
Research supports the relationship between reflex results
and tissue magnesium levels.
Second, serum magnesium levels have limited diagnos-
tic value. Only 0.3% of the body’s total magnesium con-
tent is located in serum (Matz, 1993). Researchers have
shown that the serum level is an insensitive indicator of
the tissue magnesium level (Carey, Lee, & Woeltje, 2001;
Frost, Danielsen, Dorup, Kjaer, & Pedersen, 1993;
Haigney et al., 1995; Romano, 1997; Shah, Santucci, &
Finberg, 1994). Because tissue magnesium content deter-
mines physical manifestations, clinical manifestations are
a better indicator of physiological response than serum
levels. The concept that serum levels may not be valid for
managing therapy may be new for those who rely heavily
on laboratory values for titration. In fact, the American
College of Obstetricians and Gynecologists (2001) sup-
ports using clinical symptoms as the indicator rather than
serum levels and states “In most situations, clinical assess-
ment of respirations, deep tendon reflexes, and urine out-
put is adequate to monitor for maternal toxicity without
the need to determine the actual maternal serum magne-
sium levels” (p. 174). Serum indicators can serve as a
crude estimate of what is happening in the tissues, but it
is the tissue response that is more important to determine.
DTR depression can exist even when serum magnesium
levels are in the therapeutic range. Therefore, although
serum levels do not indicate toxicity, if physical signs of
magnesium toxicity exist, interventions are required.
History of Magnesium as Therapy
The effectiveness of magnesium as therapy for the pre-
vention of seizures is well established. Before the late
1920s, traditional treatment for eclampsia included mor-
phine injections, quiet environment, colonic enemas,
venesection (bloodletting) of 500-1,000 ml of blood, and
operative delivery (Alton & Lincoln, 1925; Kane, 1926;
Wilson, 1925). Poor results from these treatments
prompted interest in a more conservative treatment
option. The first reports of magnesium as treatment for
eclampsia surfaced in 1925. Lazard (1925) reported
promising results with conservative management and
intravenous boluses of magnesium sulfate. Alton and Lin-
coln (1925) reportedly controlled eclamptic convulsions
by intraspinal injection of magnesium sulfate. Although
intraspinal injection fell out of favor in the mid-1900s,
intravenous MgSO4therapy continues as the frontline
treatment for preeclampsia and eclampsia today.
Use of magnesium as a tocolytic for preterm labor is
also well established. Beginning around 1980, literature
first appeared on the usefulness of magnesium as therapy
for preterm labor (Caritis, Edelstone, & Mueller-
Heubach, 1979; Guilliams & Held, 1979; Niebyl & John-
son, 1980). High efficacy, fewer maternal side effects, and
lower costs than existing therapies quickly made magne-
sium a favorite treatment method.
Unfortunately, literature on the neonatal benefits of
using magnesium as a tocolytic provides conflicting evi-
dence. Research has focused on in-utero exposure of mag-
nesium on reducing risks associated with prematurity.
Goldenberg and Rouse (1997) concluded magnesium
could provide a protective mechanism for the fetus/new-
born because they found an associated reduced incidence
of cerebral palsy. Yet Cantarino et al. (1999) found no dif-
ference in the incidence of intraventricular hemorrhage or
necrotizing enterocolitis in preterm infants when mothers
were treated with MgSO4therapy as a tocolytic therapy.
Other scientists studied the effect of magnesium as anti-
seizure therapy on the newborn infant. They concluded it
is not the medication that provides a protective effect as
much as the maternal hypertensive state that affects rates
of cerebral palsy (Gray, O’Callaghan, Mohay, Burns, &
The efficacy of magnesium as treatment for seizures
and as a tocolytic is well established for the pregnant
woman. The protective effect on the infant is unsettled at
this time. More interdisciplinary research is needed to
determine the effect of treatment on the outcome of the
Volume 33, Number 2
Pharmacology of Magnesium
As antiseizure therapy, elevated levels of magnesium
cause a threefold effect. First, elevated magnesium levels
depress the excited central nervous system (CNS) by
blocking/suppressing the receptor site N-methyl-D-aspar-
tate that produces the seizure (Lu & Nightingale, 2000).
Excitation of the CNS occurs as a result of hypoxic
changes in the brain, caused by cerebral vasospasm. To
counteract the cerebral hypoxia, magnesium also acts as a
cerebral vasodilator, increasing vascular blood flow to the
brain (Naidu, Payne, Moodley, Hoffmann, & Gouws,
1996). Third, magnesium affects the neuromuscular and
neurocellular signal transmission, which inhibits seizure
activity (“Magnesium Sulfate,” 2002). All three of these
effects collectively decrease an irritable/excitable CNS,
which then lowers the potential for seizures.
As treatment for preterm labor, elevated magnesium
levels decrease levels of the neurotransmitters acetyl-
choline and norepinephrine (Rude, 1996), two important
neurotransmitters that allow communication and trans-
mission of information among nerve cells. Acetylcholine
allows nerve cells to communicate with muscle cells,
whereas norepinephrine allows communication between
nerve cells and other nerve cells. Without acetylcholine,
communication from nerves to muscle does not occur and
muscle depression occurs (Hypermagnesemia, 2002).
Because magnesium decreases acetylcholine, it is an effec-
tive uterine tocolytic.
The heart, lungs, uterus, and intestines contain smooth
muscle that responds to an acetylcholine-enriched stimu-
lus. Each organ has a different threshold for acetylcholine
repression caused by magnesium. Depression and cessa-
tion of function occur at much higher magnesium levels in
heart and lung tissue than in the uterine muscle (see Table
1). This, fortunately, allows practitioners to use lower
magnesium levels effectively to treat preterm labor or
pregnancy-induced hypertension without causing high
rates of morbidity or mortality from respiratory and car-
Reaching Therapeutic Ranges
A therapeutic range of magnesium in the bloodstream
would need to be sufficient to improve a patient’s condi-
tion (Thomas, 1997). Therapeutic serum magnesium lev-
els are defined as a range from 4 to 7 mEq/L; this range
simultaneously decreases CNS irritability and relaxes
uterine smooth muscle (“Magnesium Sulfate,” 2002).
Classic studies on the pharmacokinetics of magnesium in
pregnant women have shown that therapeutic levels are
usually attained 6 to 8 hours after beginning infusion at a
rate of 2 g per hour (Cruikshank, Pitkin, Reynolds,
Williams, & Hargis, 1979; Pritchard, 1979). Because 6 to
8 hours is a long time to wait for therapeutic depression
of the CNS or uterus, the physician usually prescribes a
loading dose of 4 to 6 g of MgSO4intravenously. The
loading dose raises the magnesium level to the high range
of therapeutic levels almost immediately; the effect lasts
approximately 1 hour, and then the magnesium level
returns to the low end of the therapeutic range (Sibai,
Three different units of measurement for magnesium
are reported in the literature. Some authors report ranges
in milliequivalents per liter (Carey et al., 2001; “Magne-
sium Sulfate,” 2002; Metheny, 2000; Rude, 1996) or in
milligrams per deciliter (Sibai, 1996), whereas much of
the research has been reported using millimoles per liter
(Cao, Bideau, Valdes, & Elin, 1999; Haigney et al., 1995;
Lu & Nightingale, 2000; Matz, 1993). Because the ranges
for therapeutic in one unit of measurement look similar to
the toxic levels using another unit of measurement, con-
fusion exists as to cutoffs for normal, therapeutic, and
toxic ranges. Table 1 presents a summary of the normal,
therapeutic, and toxic ranges for magnesium in all three
units of measurement. Table 1 also shows physical mani-
festations that correlate with serum magnesium levels—
which are a better indicator of magnesium tissue content
than laboratory values—and nursing interventions for
titration and management of magnesium infusion.
Whether patients are receiving MgSO4infusion for
tocolysis or for seizures, they are at risk for developing
hypermagnesemia. For this reason, the perinatal nurse
should know the normal, therapeutic, and toxic ranges of
serum magnesium as well as her or his institution’s report-
ing unit of measurement. Professional nurses who under-
stand the pharmacodynamics of magnesium can use the
information to achieve the desired therapeutic effect for
Cardinal Reasons to Assess DTRs
in Obstetric Patients
When a patient receives MgSO4infusion, the obstetric
nurse must assess DTRs frequently. Information from
DTRs will help nurses develop judgment about titrating
the infusion. Three cardinal reasons to perform DTRs are
DTRs can be used to determine need for
magnesium therapy, evaluate efficacy of
magnesium therapy, and prevent toxicity from
to (a) determine the client’s need for MgSO4therapy, as
evidenced by hyperreflexia; (b) evaluate the efficacy of
MgSO4therapy in depressing the CNS, as evidenced by
normoreflexia; and (c) prevent the development of toxic-
ity, as evidenced by hyporeflexia or areflexia. Remember-
ing these three cardinal reasons enhances clinical practice
and benefits patients.
When caring for patients diagnosed with preeclampsia,
it is important to know the status of the CNS. In essence,
DTRs function as a window into the CNS. Therefore,
DTR assessment can be useful in providing information
on the patient’s need for magnesium sulfate. The Nation-
al Institute of Neurological Disorders and Stroke
(NINDS) of the National Institutes of Health developed a
DTR scale for practitioners (see Table 2) (Hallet, 1993).
For a full discussion on issues related to the different DTR
rating scales, refer to Nick (2003).
When hyperreflexia or brisk reflexes (3 or 4 on NINDS
scale) are present, the nurse should notify a health care
provider who can prescribe magnesium infusion. Hyper-
reflexia is a sign that the disease has affected the cortex,
and the patient should be managed with MgSO4therapy.
A second reason to conduct DTR assessments is to
determine magnesium efficacy. Once the nurse starts the
Volume 33, Number 2
Relationship Between Serum Magnesium Levels, Physical Manifestations, and Recommended Nursing
Levelsmmol/LmEq/Lmg/dL Physical ManifestationsNursing Action
Physiologic 0.65-1.1 1.3-2.1(1.6-2.7)c
Couples with adenosine triphosphate
(ATP) to increase ATP utilization.
Activates numerous enzyme systems,
facilitates nerve conduction and
potassium ion transport.
Peripheral vasodilation with facial
flushing, sense of warmth, nausea
and vomiting. These signs and
symptoms occur with overly rapid
Depression: CNS and uterine smooth
Arrest: Uterine smooth muscle
Dilute to at least a 20%
concentration and administer by
infusion pump over 20 minutes.
Therapeutic 2-3 4-64.9-7.3 Verify patient has reached
therapeutic range as evidenced by
uterine quiescence and normo-
reflexia. If uterine contractions or
hyperreflexia persist, dosage needs
to be increased.a
Dosage should be decreased.a
Administer diluted calcium
gluconate (not calcium chloride,
Monitor electrocardiograph changes
before and after calcium
administration. Have emergency
Depression: Deep reflexes
Arrest: Deep reflexes
bradycardia, heart block
Note. Serum magnesium levels that affect body systems are approximate. There is wide variation in reports of levels at which signs and symptoms
occur. Focus on generalizations and patterns in the data.
bMagnesium levels not reported in the literature but computed mathematically and rounded appropriately using the equation: y mmol/L = x(mEq/L)
cMagnesium levels not reported in the literature but computed mathematically and rounded appropriately using the equation: y mg/dL = x(mmol/L)
dMagnesium levels not reported in the literature but computed mathematically and rounded appropriately using the equation: y mg/dL = x(mEq/L)
prescribed MgSO4infusion, therapeutic levels can be val-
idated by observing for uterine relaxation or normore-
flexia. Reflex assessment cannot help evaluate efficacy of
treatment for preterm labor but can assist the nurse in
evaluating the effect on the CNS.
When the goal of treatment is to depress the CNS,
DTR assessments can assist nurses in evaluating the effi-
cacy of treatment. Hyperreflexia occurs as a result of CNS
irritability secondary to the vasospasms caused by
preeclampsia. Once CNS irritability decreases (as a result
of magnesium therapy), the cerebral cortex produces suf-
ficient dampening signals and sends them down the spinal
cord. Hence, normoreflexia (2 on NINDS scale) resumes.
If, however, the patient continues to have brisk reflexes,
the nurse should confer with the physician, because the
dosage is inadequate and should be increased. When
hyperreflexia (3 or 4 on NINDS scale) changes to nor-
moreflexia, proper dosing has been achieved and the
treatment is effective. The nurse should maintain the infu-
sion at the rate that achieves treatment goals while main-
taining normoreactive or slightly hyporeactive reflexes.
The third cardinal reason to perform DTR assessment
is to prevent magnesium toxicity from developing in the
patient. Toxicity develops from overdosing the patient
with the medication. DTR assessments are helpful for
developing clinical judgment and detecting impending
Use of DTR findings has been shown to be an inex-
pensive indicator of magnesium levels. In retrospective
studies, Chinayon (1998) and Raman and Rao (1995)
found that DTR response was a reliable indicator of tis-
sue magnesium levels when coupled with respiratory and
urine output indicators. Because the body excretes mag-
nesium via the kidneys, urine output must be sufficient to
process the continuous infusion (i.e., ≥ 30 mL/h). When
output drops below this level, the patient can rapidly
develop toxicity. But as long as DTR response, respirato-
ry rate, and urinary output are normal, practitioners are
reassured of attaining therapeutic levels.
Hypermagnesemia occurs primarily in two instances:
with impaired renal function or when a large magnesium
load is given to the patient (Agus & Lau, 1995). Because
the kidneys are the principal organ involved with magne-
sium excretion, patients diagnosed with preeclampsia
may have renal impairment as a result of the disease
process and are, therefore, at particular risk for develop-
ing hypermagnesemia (Rude, 1996). Magnesium toxicity
can develop rapidly in this instance if renal function
decreases suddenly. Thus, if a patient is receiving MgSO4
infusion and her urine output decreases, she should be
assessed for hyporeflexia or areflexia more frequently. If
depression of reflexes occurs, the nurse should notify the
physician and request new medication orders, because
decreasing the magnesium should be considered. For
patients with a compromised renal system, nurses should
develop judgment to determine how frequently to assess
DTR and urinary output to prevent hypermagnesemia.
Patients in preterm labor may not have impaired renal
function but often require high dosages to achieve uterine
quiescence. Additionally, such patients may be receiving
If a patient is receiving MgSO4infusion and
her urine output decreases, she should be
assessed for hyporeflexia or areflexia more
MgSO4intravenously for extended periods of time, which
places them at risk for developing hypermagnesemia. It is
helpful to employ diligence in assessing DTRs in patients
receiving MgSO4as a tocolytic.
Vigilant practitioners can, in many cases, prevent toxi-
city from developing by using information provided from
DTR assessment. When normoreflexia turns into hypore-
flexia or areflexia, the nurse should recognize these as
signs of developing toxicity and notify the physician in a
timely manner. A collaborative relationship between
physician and nurse is crucial to patient safety in this sit-
Physical Manifestations of Toxicity
The consequences of magnesium toxicity can be grave.
With mild magnesium toxicity (serum levels between 6
NINDS Scale for Tendon Reflex Assessment
Reflex small, less than normal; includes a trace
response, or a response brought out only by
Reflex in lower half of normal range
Reflex in upper half of normal range
Reflex enhanced, more than normal; includes
clonus if present, which can be noted in an
added description of the reflex
Note. From “NINDS Myotatic Reflex Scale,” by M. Hallett, Neurol-
ogy, 43, p. 2723. Copyright 1993 by the National Institutes of
Health. Reprinted with permission.
and 8 mEq/L), magnesium functions as a neuromuscular
blockade. Physical manifestations of neuromuscular
blockade include muscle dysfunction such as lethargy,
muscle weakness, slurred speech, and decreased DTRs. At
higher levels of toxicity, magnesium secondarily functions
as an effective calcium channel blocker (Agus & Lau,
1995). Signs of calcium channel blockade include
hypotension and arrhythmia, such as bradycardia, pro-
longed P-R interval, widened QRS interval, and heart
block (serum levels estimated at 15–20 mEq/L).
If the patient receives too much elemental magnesium,
or the kidneys cannot handle the excretion load, the
serum magnesium level will rise past the therapeutic range
and vital systems will be affected. Fortunately, the signs of
magnesium toxicity are easily detected. There is a pre-
dictable progression from alteration (i.e., depression) of
the CNS to alteration then arrest of the deep reflexes, fol-
lowed by alteration then arrest of the respiratory system,
followed by alteration then arrest of the cardiac system.
Because of this linear progression, tissue magnesium lev-
els can be estimated using tendon reflexes as the guide.
Management Techniques With Magnesium
With hyporeflexia (0 or 1 on NINDS scale), the mag-
nesium infusion should be decreased or discontinued,
which requires an updated medication order from the
physician. However, if respiratory alteration occurs, the
nurse should not hesitate to turn off the infusion before
notifying the physician. A delay could cause respiratory
alteration to progress to respiratory arrest. Quick action
with the magnesium infusion may prevent further prob-
lems. With normoreflexia (2 on NINDS scale), the infu-
sion should remain constant. With hyperreflexia (3 or 4
on NINDS scale), the infusion should be increased, which
again necessitates collaboration with the physician.
Because nurses are at the bedside providing continuous
care, the nurse’s frequent monitoring can detect signs of
toxicity and help the physician fine-tune the dosing
requirements for each patient (see Table 1). Interventions
for overdosing include decreasing or stopping the infusion
and administering calcium to reverse the effects of mag-
For mild magnesium toxicity (hyporeflexia or areflex-
ia), slowing the rate of or discontinuing the intravenous
magnesium should be a first priority. Working closely
with the physician, the nurse can titrate the magnesium
infusion and enhance patient well-being.
After achieving distribution into the extracellular-
extravascular space, moving magnesium out of this space
is more difficult. Unfortunately, the elimination half-life
for magnesium is rather slow—about 4 hours (Chen, Li,
& Guo, 1991, as cited in Lu & Nightingale, 2000; Hall,
1957). That is, in patients with normal renal function, if
the therapy were discontinued, in about 4 hours the
serum level would be about half what it was initially.
Twenty-four hours after magnesium infusion is discontin-
ued, 90% of the extra magnesium is excreted from the
body (Cruikshank, Pitkin, Donnelly, & Reynolds, 1981).
For patients with abnormal renal function, such as those
with preeclampsia, the elimination half-life is even greater
(Belfort & Moise, 1992). Therefore, because of the slow
elimination, if signs of moderate toxicity are apparent,
discontinuing the magnesium may not be sufficient. Cal-
cium reversal is required. Signs of moderate toxicity
include respiratory depression and cardiac arrhythmia.
Intravenous calcium, which quickly reverses the effects of
magnesium toxicity, may be required when moderate to
severe toxicity occurs (Agus & Lau, 1995; Metheny,
Calcium as Antidote
Since the beginning of the last century, scientists have
known about the effect of calcium on hypermagnesemia
(Meltzer & Auer, 1907). However, only sporadic infor-
mation can be found on calcium antidosing (Bryant,
Lehman, & Knoefel, 1939; Mordes, Swartz, & Arky,
Calcium counteracts the effects of magnesium intoxi-
cation by simply undoing what magnesium has done. It
increases acetylcholine and norepinephrine release during
each depolarization (Rubin, 1970). Early on, authors
demonstrated that calcium antidosage directly relates to
magnesium dosage, and the magnesium-to-calcium ratio
is important (Bryant et al., 1939). The higher the magne-
sium overload, the more calcium will be required to coun-
teract the effect.
Unfortunately the literature does not specify how often
to give calcium to reverse magnesium toxicity or how
many doses are required to reverse hypermagnesemia.
Authors state that reversal is transient and repeated doses
may be required (Carey et al., 2001; Metheny, 2000;
Mordes & Wacker, 1978; Rude, 1996). Tissue response
such as normal cardiac rhythms (determined via electro-
cardiography) and normal reflexes will need to serve as
Volume 33, Number 2
Many obstetric personnel see the importance
of assessing DTRs in preeclamptic patients
but fail to assess DTRs regularly in
preterm labor patients treated with
intravenous magnesium therapy.
the guide for repeated doses until further research estab-
lishes quantitative guidelines.
Calcium administration warrants careful attention,
because injecting the medication intravenously as a bolus
dose can cause tissue necrosis, hypotension, bradycardia
(Hypermagnesemia, 2002), or, worse, ventricular fibrilla-
tion (Auerbach & Langenberg, 1985; Chin, Garmel, &
Harter, 1995). For this reason, it would be prudent to
attach an electrocardiograph to the patient for monitor-
ing purposes before, during, and after administration.
Calcium Dosing Information
There is wide variation in the literature regarding cal-
cium antidosing and rate of administration required for
magnesium reversal. Agus and Lau (1995) and Rude
(1996) recommended 100 to 200 mg of elemental calcium
over 5 to 10 minutes. Interestingly, those authors used
Mordes and Wacker (1978) as their supporting reference,
but that reference only stated, “Immediate but transient
reversal of toxicity may be effected with calcium,” and no
dosing recommendations were given.
Sibai (1996), a leading expert on pregnancy-induced
hypertensive disorders, recommends 1 g of 10% solution
of calcium gluconate administered over 3 minutes. Sisson
and Sauer (1995) recommend 1 g of calcium gluconate
given over 1 to 2 minutes. Metheny (2000) recommends
10 to 20 mL of 10% calcium gluconate (equal to 1–2 g of
calcium) but cautions to give the antidote over 10 min-
utes. Nursing textbooks specify 1 g of intravenous calci-
um gluconate to be given over 3 minutes as a bolus dose
(Dickason, Silverman, & Kaplan, 1998; Olds, London,
Ladewig, & Davidson, 2004). The American College of
Obstetricians and Gynecologists (1996) recommended 1 g
of calcium gluconate intravenously over 2 minutes. In
more recent publications by ACOG, there is either no
mention of calcium as antidote (2001) or there are no
dosing recommendations given, and it is stated only that
“if toxic serum levels or side effects are encountered, mag-
nesium sulfate infusion must be discontinued, and calci-
um gluconate may be administered to reverse these
effects” (American Academy of Pediatrics and American
College of Obstetricians and Gynecologists, 2002, p.
The well-known electronic pharmacologic database
MICROMEDEX recommends either calcium chloride,
350 to 700 mg intravenously over 10 minutes or calcium
gluconate, 500 to 800 mg over 2 minutes (Hypermagne-
semia, 2002). Although calcium chloride is an acceptable
antagonist for magnesium, it tends to be more caustic and
will extravasate into tissues, thus causing tissue damage.
Therefore, calcium chloride must be given over a longer
period of time than calcium gluconate.
Many believe that the causticity of calcium chloride is
related to the chloride ion forming hydrochloric acid.
Heckler and McCraw (1979) found this to be erroneous,
however. They demonstrated that the causticity and
necrosis were not caused by pH changes but, rather, were
caused from the concentration of free calcium once disas-
sociation occurs in the bloodstream. Whereas calcium
chloride immediately disassociates, calcium gluconate dis-
associates over a period of time and is thus not as caustic
to vessels. After their own experience with calcium chlo-
ride causing severe tissue damage, Semple and Booth
(1996) recommended administering calcium solutions
into central veins (i.e., subclavian, internal jugular, or
femoral), increasing the dilution before infusion, and
using gluconate instead of chloride, which is less irritating
Areas for Future Research
Although magnesium therapy and calcium coun-
tertherapy have historical precedence, knowledge gaps
still exist in perinatal nursing. Independent nursing stud-
ies and interdependent research between disciplines can
be accomplished in this area of research. A well-thought-
out research project has the potential to impact the pro-
fession of nursing positively, increase the validity of inter-
ventions, and improve patient health.
Potential Research for Magnesium
Perinatal patients may receive MgSO4therapy for long
periods of time. Studies need to answer questions regard-
ing appropriate length of treatment and elucidate short-
term and long-term effects on maternal and fetal health.
After the patient has been on MgSO4infusion for weeks,
are physical manifestations still a reliable indicator? Do
tissues build up a tolerance to MgSO4over time? Or, pos-
sibly, are tissues more sensitive to MgSO4over time?
Could tolerance or sensitivity account for the wide varia-
tion in reports of levels at which signs and symptoms first
occur? With the increased autonomy of the nurse, devel-
oping titration protocols would seem appropriate. Nurs-
es titrate other medications on the basis of patient param-
eters, yet protocols do not exist for titrating magnesium
first then notifying the physician after altering the dosage.
Has nursing judgment developed enough to work toward
developing protocols for magnesium titration? Can this
action be changed from a dependent nursing action to an
interdependent action? Research would need to demon-
strate the safety and effectiveness of such a service.
Because serum levels are not a reliable indicator of
intracellular content, there may be other indicators or
parameters that nurses can use. Do all deep reflexes
respond similarly to beginning toxicity, or is one more
sensitive than another? How do superficial reflexes
respond to magnesium overload? Do they become
depressed at similar levels as the deep reflexes? Does sali-
va contain magnesium? Could saliva become another
indicator? Because magnesium causes peripheral vasodi-
lation, would peripheral skin temperature monitoring
prove useful in estimating magnesium load? These are
questions that can be answered by nurse researchers.
Potential Research for Calcium
Although it is known that a ratio between magnesium
and calcium exists, and a certain magnesium level
requires a certain calcium level to counteract the effects,
specific guidelines for calcium dosing do not exist. For
example, how many calcium dosages are required when
the serum magnesium level is 12 mEq/L? How many
dosages are required to reverse the effects when the mag-
nesium level is 15 mEq/L? Is tissue response the best indi-
cator, or would guidelines help practitioners manage
patients with hypermagnesemia?
There are several options recommended for calcium as
antidote, which makes developing protocols difficult. The
dosage ranges from 100 mg to 2 g of elemental calcium,
the counter-ions can be either chloride or gluconate, and
the rate of administration ranges from 1 to 10 minutes.
Why do these variations exist? How many doses are
required to effectively reverse hypermagnesemia? After an
exhaustive search of databases including the Cochrane
Library, MICROMEDEX, CINAHL, and MEDLINE
(using both Silver Platter and PubMed) for the years 1966
to 2002, this author found no research-based articles
relating to dosage and rate of administration of calcium
for magnesium toxicity reversal. Although magnesium
therapy as treatment for eclampsia has been used since the
mid-1920s (Alton & Lincoln, 1925; Kane, 1926; Lazard,
1925), treatment for hypermagnesemia did not appear
until 15 years later (Bryant et al., 1939). The Cochrane
Library has future plans for a meta-analysis of treatment
options for pregnancy-induced hypertension and preterm
labor, but the compiled information is not available yet.
How can nurses evaluate practice if the supporting refer-
ences are not research based? This topic clearly is an area
for interdisciplinary research among nurses, physicians,
Regardless of the purpose of MgSO4therapy (anticon-
vulsant or tocolytic), the goal of treatment is to achieve a
therapeutic situation without creating toxicity. Too much
or too little magnesium compromises the maternal/fetal
condition. Magnesium underdosing results in continued
brisk reflexes or an irritable uterus. Overdosing results in
diminished or absent reflexes. Because of the linear pro-
gression of magnesium toxicity, DTR assessment can be
used as a tool to indicate or estimate the serum magne-
sium level and to decide on titration needs. Necessary
interventions for hypermagnesemia include slowing the
infusion, turning off the intravenous magnesium, and, if
patient condition warrants, administering calcium.
Although the literature provides instruction for calcium
reversal, there is wide variation of protocols and they do
not seem to be research based. Magnesium sulfate and
calcium use would benefit from further research, allowing
nurses to practice in a more evidence-based manner.
The author thanks Elizabeth Johnston-Taylor, PhD,
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Jan M. Nick is an associate professor in the School of Nursing
at Loma Linda University, Loma Linda, CA. She is lead teacher
of the Nursing of the Childbearing Family course in the under-
graduate nursing program.
Address for correspondence: Jan M. Nick, PhD, RNC, Loma
Linda University, School of Nursing, Loma Linda, CA 92350.
Volume 33, Number 2