Vous êtes sur la page 1sur 6
Toxicology Case Report Thyroid Storm During Pregnancy A Medical Emergency Patricia A. Waltman, RN, EdD,
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
Thyroid disease, which is actu-
ally several different diseases, affects
approximately 6% of the population.
It may result from either subnormal
or excessive levels of thyroid hor-
mones. 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 com-
mon form of hyperthyroidism 1 and is
characterized by 1 or more of the
signs and symptoms listed in Table 1.
Thyroid storm, a very rare complica-
tion of hyperthyroidism, can be fatal
if untreated. It is often precipitated
by a stressful event or trauma. Criti-
cal 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 recog-
nized 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.
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
the graduate nursing program and practices as a neonatal nurse
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
a family nurse practitioner.
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 physi-
cian 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 imme-
diately took her to the local hospital emer-
gency department for care, where she was
quickly seen. A physical examination indi-
cated that her body temperature, pulse, res-
pirations, 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 hor-
mone, 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 thy-
rotoxicosis in which production and secre-
tion of thyroid hormones into the blood
reach critically high levels. Wendy’s condi-
tion continued to worsen, and she was
admitted to the intensive care unit for fur-
ther evaluation and management.
Sharon Lobert
professor of nursing and
the assistant dean for the master of science
nursing program
at the University of Mississippi Medical Center
School of Nursing.
teaches advanced pathophysiology for nurse
addition to her role as a nurse researcher.
and nurse
educator students in
To purchase
reprints, contact The
InnoVision Group, 101
Columbia, Aliso Viejo,
CA 92656. Phone,
An example is hyperthyroidism,
which occurs in approximately 1 in
500 pregnancies and is one of the
most common endocrine disorders
(800) 809-2273 or (949) 362-2050 (ext 532); fax, (949) 362-2049;


Table 1 Common signs and symptoms of hyperthyroidism

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

of pregnancy, second only to diabetes. 3 Graves disease accounts for more than 85% of all cases of hyperthy- roidism. 4 Maternal and neonatal morbidity is significantly more com- mon 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 com- plications and adverse outcomes for both mother and infant.

Thyroid Function

Thyroid hormones, triiodothyro- nine (T 3 ) and thyroxine (T 4 ), are synthesized within the follicles of the thyroid gland, and their synthesis requires iodide. 5 Most T 4 is trans- formed to T 3 by the action of enzymes after T 4 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-

rotropin or TSH) produced in the anterior lobe of the pituitary gland and released as a result of the activ- ity of hypothalamic


releasing hormone (see Figure). Nega- tive feedback

mechanisms regu- late the release of TSH from the pituitary gland. Stress and temper- ature changes can induce the synthe- sis of thyroid hor-

mones, resulting in pronounced effects on the cardio- vascular system (Table 2). General- ized vasodilatation results in increased cardiac output. Heart rate and contractility are increased, as is

Hypothalamus Thyrotropin-releasing hormone (TRH) Anterior lobe of pituitary gland Thyrotropin (TSH) released
Thyrotropin-releasing hormone
Anterior lobe of
Increased cellular
Regulation of thyroid hormones.

blood pressure. The need for oxy- gen is increased, and as a result the respiratory rate increases. Under the influence of thyroid hormones, muscles react more readily, and the

Table 2 Effects of increased levels of thyroid hormones on physiological mechanisms

Carbohydrate metabolism Increased: Glucose uptake Glycolysis Gluconeogeneis Carbohydrate absorption rate in
Carbohydrate metabolism
Glucose uptake
Carbohydrate absorption rate in gastrointestinal tract
Insulin secretion
Fat metabolism
Lipid mobilization
Levels of free fatty acids in plasma
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
Loss of libido or impotence
Menorrhagia and polymenorrhea or amenorrhea



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

Thyroid Physiology During Pregnancy

The normal, but reversible hor- monal changes in pregnancy result in thyroid stimulation and increased levels of T 3 and T 4 , although TSH levels remain normal. During normal pregnancy, the thyroid gland may enlarge up to 50% because of hyper- plasia 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 hypothalamic- pituitary thyroid hormone system is relatively independent of the fetal sys- tem. The human placenta is imper- meable to the transfer of TSH and largely impermeable to the transfer of T 3 and T 4 . 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 preg- nancy can overlap with the signs and symptoms of thyroid disease. Clini- cians 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, thyroid dis ease and are not common in pregnancy, such as 76 C RITICAL C ARE


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 pro- duction of thyroid hormones and the clinical findings associated with hyperthyroidism. Because the thy- roid 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 dan- gerous levels. High TSI levels con-

firm the diagnosis of Graves disease.

If left untreated, hyperthyroidism

during pregnancy can lead to mater- nal 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, life- threatening endocrinologic emer- gency 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
Abdominal pain
Severe agitation
Congestive heart failure
Cardiovascular collapse
Malignant exophthalmos

mia. Blood pressure is commonly normal, although a widened pulse pressure is common. Patients with thyroid storm usually appear con- fused and disoriented. Thyroid storm can be precipitated by surgery, infection, trauma, or labor and delivery. 3,12 Patients with thyroid storm require assessment and man- agement in an intensive care unit where they can be monitored for cardiac status, fluid and electrolyte balance, and control of hyperther- mia. 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 propylth- iouracil and methimazole. These agents inhibit the synthesis of thy- roid hormones. 13 Propylthiouracil has been the drug of choice in preg- nancy because it was thought that it did not cross the placenta as readily as methimazole does and because it blocks conversion of peripheral T 4 to T 3 . 2,14 Recent studies suggest that this notion may be incorrect. In a study 15 in which the suppressive effect

Table 4 Management of thyroid storm Recognition of signs and symptoms: hyperthermia, tachycardia, confusion, vomiting,
Table 4 Management of thyroid storm
Recognition of signs and symptoms: hyperthermia, tachycardia,
confusion, vomiting, hypotension, diaphoresis, irritability
Reversal of thyrotoxicosis with antithyroid drugs
1. Propylthiouracil 300-600 mg by mouth immediately,
followed by 150-300 mg by mouth every 6 hours; can be
administered by nasogastric tube or as a rectal suppository
if patient is unable to take by mouth.
2. Saturated solution of potassium iodide 2-5 drops every 8
hours or sodium iodide 0.5-1 g intravenously every 8 hours
3. β-Blockers to decrease effects on the cardiovascular system
Supportive therapy
1. Fluids
2. Nutritional support
3. Oxygen
4. Antipyretics (possibly cooling blanket)
5. Correction of electrolyte imbalance
6. Glucocorticoids such as dexamethasone 2 mg every 6 hours
for 4 doses.
7. Barbiturates if needed for sedation

of maternal ingestion of propylth- iouracil on fetal thyroid status was compared with that of methimazole, the occurrence of low T 4 levels or high fetal TSH levels did not differ significantly between the 2 groups. The standard practice is to give an initial loading dose of 300 mg to 600 mg propylthiouracil enterally and then 150 mg to 300 mg every 6 hours. 14 If a patient cannot take the solution by mouth, propylthiouracil can be administered via the nasogas- tric tube or can be compounded by the pharmacy and given as a rectal suppository. Iodides are also com- monly given because they rapidly inhibit the release of thyroid hor- mones. Iodides are administered sev- eral hours after propylthiouracil therapy is initiated to avoid the buildup of hormones stored in the thyroid gland. A saturated solution of potassium iodide is given orally in dosages of 2 to 5 drops every 8 hours, or sodium iodide is given intra- venously in dosages of 0.5 to 1 g every 8 hours. β-Blockers such as propra- nolol should also be given to help

decrease some of the thyrotoxic effects on the car- diovascular system. Additional sup- portive measures include administra- tion of intravenous fluids for dehydra- tion, antipyretics for control of hyperthermia (a cooling blanket may be necessary), nutritional sup- port, correction of possible electrolyte

imbalances, and use of glucocorticoids, which also inhibit conversion of T 4 to T 3 and prevent adrenal insufficiency. If sedation is required, barbiturates are most often used because they lower the levels of thyroid hormones by increasing the catabolism of the hor- mones. 14 Oxygen should be used as needed for possible increased oxy- gen demands. 14,16,17 Because of the hypermetabolic state of thyroid storm, medications are metabolized faster than normal. Therefore, higher and more frequent doses may be required to control the thyrotoxi- cosis. 18 Patients in thyroid crisis require close assessment and moni- toring of cardiovascular status, including continuous cardiac moni- toring and frequent monitoring of vital signs. Significant changes should be reported immediately. During this period, careful monitor- ing of the fetus is also a critical ele- ment of management. Current recommendations are to avoid deliv- ery during thyroid storm unless the condition of the fetus demands prompt delivery. 19



The gold standard of treatment


thyroid storm is primary preven-

tion. Prevention of thyroid storm requires careful control and man- agement of the hyperthyroidism. Standard treatment options for Graves disease include therapy with radioactive iodine, ATDs, and thy- roid 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 treat- ment during pregnancy is the use of ATDs to inhibit the biosynthesis of thyroid hormones. Because of the immunosuppressive effect of preg- nancy, ATDs can be given in lower doses in pregnant patients than in nonpregnant patients. Every attempt should be made to treat with the low- est possible effective dose of ATDs because these drugs can cross the pla-


centa, enter the fetal circulation, and affect the thyroid gland of the fetus. Even though propylthiouracil is the drug of choice during pregnancy,


is not given without careful observa-

tion, because it results in drug reac- tions in up to 5% of treated patients. These reactions include fever, rash,


urticaria, arthralgias, and leukopenia.


rare adverse effect, agranulocyto-

sis, an acute condition distinguished by a deficit or absolute lack of granu- locytes, 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, treat- ment with thiopropyluracil should be stopped. 19

be done, and if agranulocytosis is diagnosed, treat- ment with thiopropyluracil should be stopped. 1 9



The starting dose is typically 300 to 450 mg per day divided into 3 doses. If methimazole is used, the starting 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

patient’s signs and symptoms and laboratory values. 4,8 Biochemically, the aim is to keep the serum level of total T 4 between 154 and 193 nmol/L (12-15 µg/dL) and the serum level of free T 4 within the ref- erence range for the laboratory test used. (These values will vary from one laboratory to another. 8 ) Fetal and neonatal hypothyroid- ism, as well as the occurrence of goi- ters, 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 local- ized 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 mother’s hyperthyroidism by

using the smallest possible amountgoal is to control the mother’s hyperthyroidism by 78 C RITICAL C ARE N URSE Vol


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 thy- rotoxicosis, although this complica- tion 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 recog- nized. 24 Potential fetal and neonatal complications are listed in Table 5. The level of TSIs should be meas- ured in the third trimester in all pregnant women with active or inac- tive Graves disease. High TSI levels, more than 5 times the reference range, are common in the mothers of babies with neonatal hyperthy- roidism. 24 The activity of the mother’s disease, however, does not necessar- ily 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 thyrotoxicosis 2,24

Hyperthyroidism Tachycardia Intrauterine growth retardation Size small for gestational age Prematurity Stillbirth
Intrauterine growth retardation
Size small for gestational age
Advanced bone age
Feedback suppression of the fetal
hypothalamic-pituitary-thyroid axis

Graves disease develops in an infant in whom the disease was not previ- ously 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 thyro- toxicosis 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 fail- ure 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, tachy- cardia, hypertension, poor weight gain, thrombocytopenia, and jaun- dice. Arrhythmias, cardiac failure, and death may occur if the thyro- toxicosis is severe and treatment is

Table 6 Clinical manifestations of neonatal thyrotoxicosis 2,24

Marked irritability Hyperthyroidism Hyperthermia Tachycardia Hypertension Goiter Respiratory distress Exophthalmos
Marked irritability
Respiratory distress
Poor feeding
Failure to gain weight
Severe diarrhea
Heart failure

inadequate. High levels of total T 4 , free T 4 , and T 3 in postnatal blood confirm the diagnosis. Treatment of neonatal thyrotoxi- cosis is similar to the methods used in treating the mother. Thionamides, β-blockers, and iodine are most commonly used. In the most severe cases, digitalis, glucocorticoids, and sedatives many be necessary to pre- vent cardiovascular collapse. 24 Hyperthyroidism results in increased metabolic demands, and infants with hyperthyroidism require careful attention to nutri- tional needs and a high caloric intake to maintain growth. Fatigue and exhaustion can also result from the hypermetabolic state, and meas- ures to conserve energy stores are essential to the well-being of these infants. The half-life of immuno- globulins 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 hyperthy- roidism occurs within 3 to 12 weeks. 24 Breast-feeding in women with hyperthyroidism remains controver- sial, 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 sources 2,26 suggest that breast- feeding should not be routinely con- traindicated in women taking these medications if the women are care- fully monitored.


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

precipitating factor such as labor and delivery, surgical delivery, infec- tion, or trauma. Thyroid storm most often occurs in patients with under- treated or undiagnosed hyperthy- roidism. 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 mon- itoring was performed continuously to assess fetal well-being. Both an endocri- nologist and a maternal-fetal specialist were consulted. After 48 hours in the intensive care unit, Wendy’s 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 propylth- iouracil 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.


1. Manifold CA. Hyperthyroidism, thyroid storm, and Graves’ disease. eMed J. 2001;2(6). Updated July 25, 2002. Available at: http://www.emedicine.com/emerg /topic269.htm. Accessed January 19, 2004.

2. Mestman JH. Hyperthyroidism in preg- nancy. Clin Obstet Gynecol. 1997;40:45-64.

3. Sherwen LN, Scoloveno MA, Weingarten CT. Maternity Nursing: Care of the Childbear- ing Family. 3rd ed. Stamford, Conn: Apple- ton & Lange; 1999.

4. Mestman JH. Hyperthyroidism in preg- nancy. Endocrinol Metab Clin North Am.


5. Guyton AC, Hall JE. The thyroid metabolic hormones. In: Textbook of Medical Physiology. 10th ed. Philadelphia, Pa: WB Saunders Co;


6. Cunningham FG, Leveno KJ, Gilstrap LC, Hauth JC, Wenstrom KD. Williams Obstetrics. 21st ed. New York, NY: McGraw-Hill; 2000.

7. Murray SS, McKinney ES, Gorrie TM. Physiologic adaptations to pregnancy. Foundations of Maternal-Newborn Nursing. 3rd ed. Philadelphia, Pa: WB Saunders Co;

Physiologic adaptations to pregnancy. Foundations of Maternal-Newborn Nursing. 3rd ed. Philadelphia, Pa: WB Saunders Co;



8. Levin RM. Thyroid disease in pregnancy [on-line course]. January 15, 2001. Available at: http://www.bumc.bu.edu/www/busm/



Accessed July 2, 2002.

9. Polk D, Fisher D. Disorders of the thyroid

gland. In: Tauesch AW, Ballard R, eds. Avery’s Diseases of the Newborn. Philadelphia, Pa:

WB Saunders Co; 1998:1224-1234.


10. Fisher D. Fetal thyroid function: diagnosis and management of fetal thyroid disorders. Clin Obstet Gynecol. 1997;40:16-21.

11. Tietgens ST, Leinung MC. Thyroid storm. Med Clin North Am. 1995;79:169-184.

12. Gabbe SG, Niebyl JR, Simpson JL. Obstetrics:

Normal and Problem Pregnancies. 3rd ed. New York, NY: Churchill Livingstone; 1996.

13. Wynne AL, Woo TM, Millard M. Drugs affecting the endocrine system. In: Pharma- cotherapeutics for Nurse Practitioner Pre- scribers. Philadelphia, Pa: FA Davis;



14. Barron WM, Lindheimer MD. Pituitary, thyroid, adrenal, and parathyroid disorders. In: Medical Disorders During Pregnancy. 3rd ed. St Louis, Mo: Mosby; 2000:101-146.

15. Momotani N. Effects of propylthiouracil and methimazole on fetal thyroid status in mothers with Graves’ hyperthyroidism.


Clin Endocrinol. 1997;82:3633-3636.

16. Offutt CA. Endocrine problems. In: Logan

P, ed. Principles of Practice for the Acute Care Nurse Practitioner. Stamford, Conn: Apple- ton & Lange; 1999:899-943.

17. Kuhn MA. Emergency situations, hypoten- sion, and shock. In: Kuhn MA, ed. Pharma- cotherapeutics: A Nursing Process Approach. 3rd ed. Philadelphia, Pa: FA Davis;



18. Malchiodi L. Thyroid storm: recognizing the signs and symptoms of this life-threat- ening complication. Am J Nurs. May



19. American College of Obstetrics and Gynecol- ogy. ACOG practice bulletin: thyroid disease in pregnancy. No. 37, August 2002. Ameri- can College of Obstetrics and Gynecology. Int


Gynaecol Obstet. 2002;79:171-180.

20. Singer PA, Cooper DS, Levy EG, et al. Treat- ment guidelines for patients with hyperthy- roidism and hypothyroidism. Standards of Care Committee, American Thyroid Associ- ation. JAMA. 1995;273:808-812.

21. Mestman JH. Diagnosis and management of maternal and fetal thyroid disorders. Curr Opin Obstet Gynaecol. 1999;11:167-175.

22. Mazzaferri EL. Evaluation and management of common thyroid disorders in women. Am


Obstet Gynecol. 1997;176:507-514.

23. Ecker JL, Musci TJ. Treatment of thyroid disease in pregnancy. Obstet Gynecol Clin North Am. 1997;24:575-589.

24. Seely LB, Burrow GN. Thyroid disease and pregnancy. In: Resnik R, ed. Maternal-Fetal Medicine. 4th ed. Philadelphia, Pa: WB Saunders Co; 1999:996-1014.

25. Moore TR. Endocrine disorders in preg- nancy. In: Ballard RA, ed. Avery’s Diseases of the Newborn. Philadelphia, Pa: WB Saun- ders Co; 1998:65-77.

26. Momotani N, Yamashita R, Makino F, Noh JY, Ishikawa N, Ito K. Thyroid function in wholly breast-feeding infants whose moth-

ers take high doses of propylthiouracil. Clin Endocrinol (Oxf ). 2000;53:177-181.

ers take high doses of propylthiouracil. Clin Endocrinol (Oxf ). 2000;53:177-181.