Toxicology

Case Report

Thyroid Storm
During Pregnancy
A Medical Emergency
Patricia A. Waltman, RN, EdD, CNNP
Joyce M. Brewer, RN, MSN, CS, CNM, CFNP
Sharon Lobert, RN, PhD

hyroid disease, which is actually several different diseases, affects

approximately 6% of the population.
It may result from either subnormal
or excessive levels of thyroid hormones. In this article, we focus on
thyroid storm during pregnancy
and a condition that leads to excess
amounts of thyroid hormone,
Graves disease.
Graves disease is the most common form of hyperthyroidism1 and is
characterized by 1 or more of the
signs and symptoms listed in Table 1.
Thyroid storm, a very rare complication of hyperthyroidism, can be fatal

if untreated. It is often precipitated

by a stressful event or trauma. Critical care nurses must recognize the
signs and symptoms of thyroid storm
to properly manage this condition
and prevent further complications.2
Thyroid diseases are common in
women of childbearing age. In many
cases, these diseases are first recognized during pregnancy or in the
postpartum period. Some of the
normal changes of pregnancy can be
confused with signs and symptoms
of various diseases, just as some signs
and symptoms of a disease can be
erroneously blamed on pregnancy.
Authors

Patricia A. Waltman is an associate professor of nursing and assistant dean for the
undergraduate nursing program at the University of Mississippi Medical Center School of
Nursing, Jackson, Miss. She coordinates and teaches the neonatal nurse practitioner track
in the graduate nursing program and practices as a neonatal nurse practitioner.
Joyce M. Brewer is an assistant professor of nursing at the University of Mississippi
Medical Center School of Nursing. She teaches in the undergraduate and graduate nursing
programs and practices as a nurse-midwife and a family nurse practitioner.
Sharon Lobert is a professor of nursing and the assistant dean for the master of science
nursing program at the University of Mississippi Medical Center School of Nursing. She
teaches advanced pathophysiology for nurse practitioner and nurse educator students in
addition to her role as a nurse researcher.
To purchase reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Phone,
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74 CRITICALCARENURSE Vol 24, No. 2, APRIL 2004

Wendy is a 32-year-old woman currently

pregnant for the first time with no history of
medical problems or complications. She had
her first prenatal visit at 14 weeks gestation
but has not had another visit because she
and her husband recently moved to a new
city. She is now 28 weeks pregnant and has
scheduled an appointment with a new physician 2 weeks from now. She has been feeling
very nervous and jittery and has not been
sleeping well, conditions that she and her
husband have attributed to the move, getting
settled into a new home, getting ready for
the new baby, and just getting over the flu.
Today, however, her husband noticed that
Wendy was acting more nervous than usual.
At dinner, it was obvious that she was very
confused and disoriented. She complained of
shortness of breath and said that her heart
was racing. When her husband tried to
lead her to the sofa to sit down, he noticed
that she was very hot and sweaty. He immediately took her to the local hospital emergency department for care, where she was
quickly seen. A physical examination indicated that her body temperature, pulse, respirations, and blood pressure were all much
higher than the reference range. She also had
a full goitrous thyroid gland, mild bilateral
exophthalmos, and confusion. Because of
her recent symptoms and the findings on the
physical examination, laboratory tests for
thyroid function were done. The tests
revealed an elevated level of free thyroxine, a
decreased level of thyroid-stimulating hormone, and a high level of thyroid-stimulating
immunoglobulin. Sonography of the fetus
showed a small-for-dates male fetus at 28
weeks gestation; the fetus was tachycardic
but no goiter was noted. The diagnosis was
thyroid storm, a life-threatening state of thyrotoxicosis in which production and secretion of thyroid hormones into the blood
reach critically high levels. Wendys condition continued to worsen, and she was
admitted to the intensive care unit for further evaluation and management.

An example is hyperthyroidism,
which occurs in approximately 1 in
500 pregnancies and is one of the
most common endocrine disorders

Table 1 Common signs and

symptoms of hyperthyroidism

Thyroid Function
Thyroid hormones, triiodothyronine (T3) and thyroxine (T4), are
synthesized within the follicles of the
thyroid gland, and their synthesis
requires iodide.5 Most T4 is transformed to T3 by the action of enzymes
after T4 is released from the thyroid
gland. Thyroid hormones are carried
throughout the body by proteins,
primarily thyroxine-binding globulin
produced in the liver. Production of
thyroid hormones is regulated by
thyroid-stimulating hormone (thy-

of pregnancy, second only to diabetes.3

Graves disease accounts for more
than 85% of all cases of hyperthyroidism.4 Maternal and neonatal
morbidity is significantly more common in women whose hyperthyroid
state is not medically controlled.
Thyroid storm is especially common
in women who receive limited or no
prenatal care and have medical or
obstetric complications.2 Pregnant
women with hyperthyroidism require
careful management to prevent complications and adverse outcomes for
both mother and infant.

e
xin
yro ck
Th dba
fee

Increased appetite
Blurred vision
Irregular menses
Diplopia
Exertional dyspnea
Fatigue
Heat intolerance
Diarrhea
Increased perspiration
Irritability
Muscle weakness
Nervousness
Palpitations
Photophobia
Sleep disturbances
Goiter
Fine resting tremors
Weight loss

rotropin or TSH)
Hypothalamus
produced in the
Thyrotropin-releasing hormone
anterior lobe of
(TRH)
the pituitary gland
and released as a
Anterior lobe of pituitary gland
result of the activThyrotropin (TSH) released
ity of hypothalamic
thyrotropinThyroid gland
releasing hormone
(see Figure). NegaIodine
Thyroxine
tive feedback
released
mechanisms regulate the release of
TSH from the
pituitary gland.
Increased cellular
metabolism
Stress and temperature changes can
induce the syntheRegulation of thyroid hormones.
sis of thyroid hormones, resulting
blood pressure. The need for oxyin pronounced effects on the cardiogen is increased, and as a result the
vascular system (Table 2). Generalrespiratory rate increases. Under the
ized vasodilatation results in
influence of thyroid hormones,
increased cardiac output. Heart rate
muscles react more readily, and the
and contractility are increased, as is
Table 2 Effects of increased levels of thyroid hormones on physiological mechanisms
Carbohydrate metabolism
Increased:
Glucose uptake
Glycolysis
Gluconeogeneis
Carbohydrate absorption rate in gastrointestinal tract
Insulin secretion
Fat metabolism
Increased:
Lipid mobilization
Levels of free fatty acids in plasma
Decreased: Levels of cholesterol, phospholipids, and triglycerides in plasma
Increased need for vitamins
Increased basal metabolic rate
Increased blood flow and cardiac output
Increased respiratory rate and depth
Increased gastric motility
Increased cerebration resulting in decreased effective function of the central nervous system
Extreme nervousness
Psychoneurotic tendencies
Muscle tremor due to increased reactivity of neuronal synapses
Muscle weakness due to excess protein catabolism
Insomnia and fatigue due to constant effect on muscles
Increased secretion of other hormones and increased need at targets
Excess thyroid hormone in women: oligomenorrhea or amenorrhea
Deficient thyroid hormone
Men:
Loss of libido or impotence
Women:
Menorrhagia and polymenorrhea or amenorrhea

CRITICALCARENURSE Vol 24, No. 2, APRIL 2004 75

Toxicology
central nervous system is stimulated.
Because of this stimulation, sleep
disturbances can occur when excess
thyroid hormone is present. Endocrine
gland function is stimulated by thyroid hormones, and gastric motility
is increased.

Thyroid Physiology
During Pregnancy
The normal, but reversible hormonal changes in pregnancy result
in thyroid stimulation and increased
levels of T3 and T4, although TSH
levels remain normal. During normal
pregnancy, the thyroid gland may
enlarge up to 50% because of hyperplasia of the glandular tissue and
increased vascularity. However,
marked thyromegaly and goiter
should be considered pathological
changes.6 The basal metabolic rate
increases by as much as 25%, resulting
in increased cardiac output, increased
pulse rate and heat intolerance.3,7(p129),8
The maternal hypothalamicpituitary thyroid hormone system is
relatively independent of the fetal system. The human placenta is impermeable to the transfer of TSH and
largely impermeable to the transfer
of T3 and T4.9 Thyroid-stimulating
immunoglobulins (TSIs), found in
maternal hyperthyroidism, cross the
placenta and stimulate production
of thyroid hormones by the fetus and
can result in fetal and neonatal
hyperthyroidism.10
Findings associated with the
normal hypermetabolic state of pregnancy can overlap with the signs and
symptoms of thyroid disease. Clinicians should be aware of other signs
and symptoms of hyperthyroidism
that indicate thyroid disease and are
not common in pregnancy, such as
weight loss, hyperemesis, diarrhea,

76 CRITICALCARENURSE Vol 24, No. 2, APRIL 2004

heart rate greater than 100/min that

does not decrease with the Valsalva
maneuver, and/or lymphadenopathy.

Graves Disease
Graves disease is an autoimmune
disorder in which a group of TSIs
attach to and activate TSH receptors
on the thyroid follicular cells. This
activation leads to an increased production of thyroid hormones and
the clinical findings associated with
hyperthyroidism. Because the thyroid hormones control many bodily
functions, this increase in the level
of thyroid hormones causes these
bodily functions, such as heart rate,
or in some instances blood pressure,
to increase, sometimes to very dangerous levels. High TSI levels confirm the diagnosis of Graves disease.
If left untreated, hyperthyroidism
during pregnancy can lead to maternal complications, including preterm
delivery, perinatal morbidity, heart
failure, and thyroid storm. The fetus
and newborn can also be affected.
Maternal TSI titers are used to predict
the effect of maternal Graves disease
on the fetus. The risk of thyrotoxicosis
in the fetus and newborn is higher in
women with high TSI titers.9 Careful
assessment and monitoring of the
fetus are important for early detection
of effects, with particular attention
given to elevated resting heart rate and
poor fetal growth pattern.

Thyroid Storm
Thyroid storm is a rare, lifethreatening endocrinologic emergency that can lead to cardiac arrest
and death. A total of 20% to 30% of
all cases are fatal.11 Patients can have
a wide range of signs and symptoms
(Table 3). The tachycardia is often
out of proportion to the hyperther-

Table 3 Signs and symptoms of

thyroid storm
Hyperthermia
Nausea
Abdominal pain
Vomiting
Severe agitation
Diaphoresis
Dehydration
Tachycardia
Congestive heart failure
Arrhythmia
Confusion
Cardiovascular collapse
Malignant exophthalmos

mia. Blood pressure is commonly

normal, although a widened pulse
pressure is common. Patients with
thyroid storm usually appear confused and disoriented. Thyroid storm
can be precipitated by surgery,
infection, trauma, or labor and
delivery.3,12 Patients with thyroid
storm require assessment and management in an intensive care unit
where they can be monitored for
cardiac status, fluid and electrolyte
balance, and control of hyperthermia.6 The underlying cause of thyroid
storm must be identified and treated.
Management
Thyroid storm requires prompt
recognition, aggressive reversal of
thyroidotoxins with antithyroid drugs
(ATDs), and supportive management
of signs and symptoms (Table 4).
Antithyroid agents are propylthiouracil and methimazole. These
agents inhibit the synthesis of thyroid hormones.13 Propylthiouracil
has been the drug of choice in pregnancy because it was thought that it
did not cross the placenta as readily
as methimazole does and because it
blocks conversion of peripheral T4
to T3.2,14 Recent studies suggest that
this notion may be incorrect. In a
study15 in which the suppressive effect

decrease some of
the thyrotoxic
Recognition of signs and symptoms: hyperthermia, tachycardia,
effects on the carconfusion, vomiting, hypotension, diaphoresis, irritability
diovascular system.
Reversal of thyrotoxicosis with antithyroid drugs
Additional sup1. Propylthiouracil 300-600 mg by mouth immediately,
portive measures
followed by 150-300 mg by mouth every 6 hours; can be
administered by nasogastric tube or as a rectal suppository
include administraif patient is unable to take by mouth.
tion of intravenous
2. Saturated solution of potassium iodide 2-5 drops every 8
hours or sodium iodide 0.5-1 g intravenously every 8 hours
fluids for dehydra3. -Blockers to decrease effects on the cardiovascular system
tion, antipyretics
Supportive therapy
for control of
1. Fluids
hyperthermia (a
2. Nutritional support
3. Oxygen
cooling blanket
4. Antipyretics (possibly cooling blanket)
may be necessary),
5. Correction of electrolyte imbalance
6. Glucocorticoids such as dexamethasone 2 mg every 6 hours
nutritional supfor 4 doses.
port, correction of
7. Barbiturates if needed for sedation
possible electrolyte
imbalances, and
of maternal ingestion of propylthuse of glucocorticoids, which also
iouracil on fetal thyroid status was
inhibit conversion of T4 to T3 and
compared with that of methimazole,
prevent adrenal insufficiency. If
the occurrence of low T4 levels or
sedation is required, barbiturates are
high fetal TSH levels did not differ
most often used because they lower
significantly between the 2 groups.
the levels of thyroid hormones by
The standard practice is to give an
increasing the catabolism of the horinitial loading dose of 300 mg to
mones.14 Oxygen should be used as
600 mg propylthiouracil enterally
needed for possible increased oxyand then 150 mg to 300 mg every 6
gen demands.14,16,17 Because of the
14
hours. If a patient cannot take the
hypermetabolic state of thyroid
solution by mouth, propylthiouracil
storm, medications are metabolized
can be administered via the nasogasfaster than normal. Therefore,
tric tube or can be compounded by
higher and more frequent doses may
the pharmacy and given as a rectal
be required to control the thyrotoxisuppository. Iodides are also comcosis.18 Patients in thyroid crisis
monly given because they rapidly
require close assessment and moniinhibit the release of thyroid hortoring of cardiovascular status,
mones. Iodides are administered sevincluding continuous cardiac monieral hours after propylthiouracil
toring and frequent monitoring of
therapy is initiated to avoid the
vital signs. Significant changes
buildup of hormones stored in the
should be reported immediately.
thyroid gland. A saturated solution
During this period, careful monitorof potassium iodide is given orally in
ing of the fetus is also a critical eledosages of 2 to 5 drops every 8 hours,
ment of management. Current
or sodium iodide is given intrarecommendations are to avoid delivvenously in dosages of 0.5 to 1 g every
ery during thyroid storm unless the
8 hours. -Blockers such as propracondition of the fetus demands
nolol should also be given to help
prompt delivery.19
Table 4 Management of thyroid storm

Prevention
The gold standard of treatment
of thyroid storm is primary prevention. Prevention of thyroid storm
requires careful control and management of the hyperthyroidism.
Standard treatment options for
Graves disease include therapy with
radioactive iodine, ATDs, and thyroid surgery.20 However, pregnancy
limits these treatment options.
Because of possible destruction of
the thyroid gland in the fetus,
radioactive iodine cannot be given,
and surgery is avoided because of
the increased risk for miscarriage or
preterm delivery.
As a result, the standard treatment during pregnancy is the use of
ATDs to inhibit the biosynthesis of
thyroid hormones. Because of the
immunosuppressive effect of pregnancy, ATDs can be given in lower
doses in pregnant patients than in
nonpregnant patients. Every attempt
should be made to treat with the lowest possible effective dose of ATDs
because these drugs can cross the placenta, enter the fetal circulation, and
affect the thyroid gland of the fetus.
Even though propylthiouracil is
the drug of choice during pregnancy,
it is not given without careful observation, because it results in drug reactions in up to 5% of treated patients.
These reactions include fever, rash,
urticaria, arthralgias, and leukopenia.
A rare adverse effect, agranulocytosis, an acute condition distinguished
by a deficit or absolute lack of granulocytes, usually is manifested by
fever and sore throat. If fever and
sore throat occur, a complete blood
cell count should be done, and if
agranulocytosis is diagnosed, treatment with thiopropyluracil should
be stopped.19

CRITICALCARENURSE Vol 24, No. 2, APRIL 2004 77

Toxicology
The starting dose is typically 300
to 450 mg per day divided into 3
doses. If methimazole is used, the
starting dose is 20 mg twice a day.
Results of laboratory tests should be
monitored carefully, and once a
patient becomes euthyroid, the dose
can be tapered gradually. Many
patients need only 50 mg per day,
and some patients may not need any
medication by the third trimester;
however, the dosage may vary from
50 to 200 mg of propylthiouracil
every 8 hours, or methimazole 10 to
60 mg a day, depending on the
patients signs and symptoms and
laboratory values.4,8 Biochemically,
the aim is to keep the serum level of
total T4 between 154 and 193
nmol/L (12-15 g/dL) and the
serum level of free T4 within the reference range for the laboratory test
used. (These values will vary from
one laboratory to another.8)
Fetal and neonatal hypothyroidism, as well as the occurrence of goiters, may occur from passage of
thionamides across the placenta.2
During the first trimester, transfer
of ATDs transplacentally can affect
thyroid development in the fetus.
Fetal exposure to ATDs can produce
hypothyroidism and fetal growth
restriction.21
Methimazole therapy may be
associated with aplasia cutis (a localized lesion in the parietal area of the
scalp, characterized by congenital
absence of the skin, punched-out
ulcer lesions, that usually heal
spontaneously) in the offspring of
treated women and is another reason
that propylthiouracil has become the
drug of choice during pregnancy.22
The therapeutic goal is to control
the mothers hyperthyroidism by
using the smallest possible amount

78 CRITICALCARENURSE Vol 24, No. 2, APRIL 2004

of medication, to avoid suppressing

the thyroid gland in the fetus.23

Fetal and Neonatal

Thyrotoxicosis
Transplacental passage of TSIs
can result in fetal and neonatal thyrotoxicosis, although this complication is rare. It occurs in only 1% of
babies born to women with a history
of Graves disease, but it may have
serious consequences if not recognized.24 Potential fetal and neonatal
complications are listed in Table 5.
The level of TSIs should be measured in the third trimester in all
pregnant women with active or inactive Graves disease. High TSI levels,
more than 5 times the reference
range, are common in the mothers
of babies with neonatal hyperthyroidism.24 The activity of the mothers
disease, however, does not necessarily correlate with fetal or neonatal
disease. In cases of quiescent Graves
disease, the prediction of neonatal
Graves disease on the basis of the
maternal clinical status is not always
possible because the mother may
not manifest signs or symptoms. In
some infants, both stimulating and
blocking antibodies are acquired
from the mother, and the blocking
antibodies block the effect of the
stimulating antibodies for 4 to 6
weeks such that late-onset neonatal
Table 5 Potential fetal and neonatal
complications of thyrotoxicosis2,24
Hyperthyroidism
Tachycardia
Intrauterine growth retardation
Size small for gestational age
Prematurity
Stillbirth
Advanced bone age
Craniosynostosis
Feedback suppression of the fetal
hypothalamic-pituitary-thyroid axis

Graves disease develops in an infant

in whom the disease was not previously diagnosed.9 In all pregnancies
considered to be high risk, the fetus
should be closely monitored. Fetal
thyrotoxicosis is suggested by a
resting heart rate that is elevated
(>160/min) and poor fetal growth.10,25
In many cases, neonatal thyrotoxicosis is not evident at birth when
the mother has been treated with
thionamides. As thionamide levels
decrease in the neonate, clinical
signs of thyrotoxicosis occur, usually
5 to 10 days after birth (Table 6).
Common signs are irritability,
tachycardia, poor feeding, and failure to gain weight. The disease is
usually self-limiting over 1 to 3
months as the circulating levels of
maternal immunoglobulins
decrease. In severe cases, clinical
manifestations may include goiter
with resultant respiratory distress,
hyperthermia, exophthalmos, tachycardia, hypertension, poor weight
gain, thrombocytopenia, and jaundice. Arrhythmias, cardiac failure,
and death may occur if the thyrotoxicosis is severe and treatment is
Table 6 Clinical manifestations of
neonatal thyrotoxicosis2,24
Marked irritability
Hyperthyroidism
Hyperthermia
Tachycardia
Hypertension
Goiter
Respiratory distress
Exophthalmos
Poor feeding
Failure to gain weight
Vomiting
Severe diarrhea
Arrhythmias
Heart failure
Jaundice
Thrombocytopenia
Hepatosplenomegaly
Hypoprothrombinemia

inadequate. High levels of total T4,

free T4, and T3 in postnatal blood
confirm the diagnosis.
Treatment of neonatal thyrotoxicosis is similar to the methods used
in treating the mother. Thionamides,
-blockers, and iodine are most
commonly used. In the most severe
cases, digitalis, glucocorticoids, and
sedatives many be necessary to prevent cardiovascular collapse.24
Hyperthyroidism results in
increased metabolic demands, and
infants with hyperthyroidism
require careful attention to nutritional needs and a high caloric
intake to maintain growth. Fatigue
and exhaustion can also result from
the hypermetabolic state, and measures to conserve energy stores are
essential to the well-being of these
infants. The half-life of immunoglobulins received from the mother
is 8 to 20 days, and as the circulating
level of the antibodies decreases in the
infant, the disease wanes and the
infant shows signs of improvement.
Complete resolution of the hyperthyroidism occurs within 3 to 12 weeks.24
Breast-feeding in women with
hyperthyroidism remains controversial, primarily because of passage of
ATDs in breast milk. Propylthiouracil
is excreted in breast milk in relatively
small amounts, whereas methimazole
is excreted in slightly larger amounts.
Most sources2,26 suggest that breastfeeding should not be routinely contraindicated in women taking these
medications if the women are carefully monitored.

Summary
Thyroid storm is the major risk
to pregnant women with thyrotoxicosis. This life-threatening condition
is more likely to occur with another

precipitating factor such as labor

and delivery, surgical delivery, infection, or trauma. Thyroid storm most
often occurs in patients with undertreated or undiagnosed hyperthyroidism. As many as 20% to 30% of
cases can end in maternal and fetal
mortality.11 Therefore, critical care
nurses must be able to recognize
and initiate proper medical and
nursing interventions promptly.

Outcome of Case Study

Wendy remained in the intensive
care unit for several days, where she was
closely monitored as her thyrotoxicosis
was brought under control. Electrolyte
levels and results of thyroid function
tests were checked daily, and fetal monitoring was performed continuously to
assess fetal well-being. Both an endocrinologist and a maternal-fetal specialist
were consulted. After 48 hours in the
intensive care unit, Wendys levels of
thyroid hormones had decreased and
were no longer life-threatening. She was
transferred to a high-risk perinatal unit
for further monitoring while her vital
signs and thyroid hormone levels
returned to normal. Wendy continued
taking maintenance doses of propylthiouracil until delivery. After continued
careful monitoring of her thyroid level
throughout her pregnancy, Wendy
delivered a 2.74 kg (6 lb 2 oz) healthy
boy at 39 weeks gestation.
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