74 CRITICALCARENURSE Vol 24, No. 2, APRIL 2004

Patricia A. Waltman is an associate professor of nursing and assistant dean for theundergraduate nursing program at the University of Mississippi Medical Center School ofNursing, Jackson, Miss. She coordinates and teaches the neonatal nurse practitioner trackin the graduate nursing program and practices as a neonatal nurse practitioner.

Joyce M. Brewer is an assistant professor of nursing at the University of MississippiMedical Center School of Nursing. She teaches in the undergraduate and graduate nursingprograms 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 sciencenursing program at the University of Mississippi Medical Center School of Nursing. Sheteaches advanced pathophysiology for nurse practitioner and nurse educator students inaddition to her role as a nurse researcher.

An example is hyperthyroidism,which occurs in approximately 1 in500 pregnancies and is one of themost common endocrine disorders

Patricia A. Waltman, RN, EdD, CNNPJoyce M. Brewer, RN, MSN, CS, CNM, CFNPSharon Lobert, RN, PhD

Thyroid disease, which is actu-ally several different diseases, affectsapproximately 6% of the population.It may result from either subnormalor excessive levels of thyroid hor-mones. In this article, we focus onthyroid storm during pregnancyand a condition that leads to excessamounts of thyroid hormone,Graves disease.

Graves disease is the most com-mon form of hyperthyroidism1 and ischaracterized by 1 or more of thesigns and symptoms listed in Table 1.Thyroid storm, a very rare complica-tion of hyperthyroidism, can be fatal

if untreated. It is often precipitatedby a stressful event or trauma. Criti-cal care nurses must recognize thesigns and symptoms of thyroid stormto properly manage this conditionand prevent further complications.2

Thyroid diseases are common inwomen of childbearing age. In manycases, these diseases are first recog-nized during pregnancy or in thepostpartum period. Some of thenormal changes of pregnancy can beconfused with signs and symptomsof various diseases, just as some signsand symptoms of a disease can beerroneously blamed on pregnancy.

Thyroid Storm During PregnancyA Medical Emergency

Toxicology

Authors

To purchase reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 809-2273 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints@aacn.org.

Case Report

Wendy is a 32-year-old woman currentlypregnant for the first time with no history ofmedical problems or complications. She hadher first prenatal visit at 14 weeks gestationbut has not had another visit because sheand her husband recently moved to a newcity. She is now 28 weeks pregnant and hasscheduled an appointment with a new physi-cian 2 weeks from now. She has been feelingvery nervous and jittery and has not beensleeping well, conditions that she and herhusband have attributed to the move, gettingsettled into a new home, getting ready forthe new baby, and just getting over the flu.Today, however, her husband noticed thatWendy was acting more nervous than usual.At dinner, it was obvious that she was veryconfused and disoriented. She complained ofshortness of breath and said that her heartwas racing. When her husband tried tolead her to the sofa to sit down, he noticedthat she was very hot and sweaty. He imme-diately took her to the local hospital emer-gency department for care, where she wasquickly seen. A physical examination indi-cated that her body temperature, pulse, res-pirations, and blood pressure were all muchhigher than the reference range. She also hada full goitrous thyroid gland, mild bilateralexophthalmos, and confusion. Because ofher recent symptoms and the findings on thephysical examination, laboratory tests forthyroid function were done. The testsrevealed an elevated level of free thyroxine, adecreased level of thyroid-stimulating hor-mone, and a high level of thyroid-stimulatingimmunoglobulin. Sonography of the fetusshowed a small-for-dates male fetus at 28weeks gestation; the fetus was tachycardicbut no goiter was noted. The diagnosis wasthyroid storm, a life-threatening state of thy-rotoxicosis in which production and secre-tion of thyroid hormones into the bloodreach critically high levels. Wendys condi-tion continued to worsen, and she wasadmitted to the intensive care unit for fur-ther evaluation and management.

of pregnancy, second only to diabetes.3

Graves disease accounts for morethan 85% of all cases of hyperthy-roidism.4 Maternal and neonatalmorbidity is significantly more com-mon in women whose hyperthyroidstate is not medically controlled.Thyroid storm is especially commonin women who receive limited or noprenatal care and have medical orobstetric complications.2 Pregnantwomen with hyperthyroidism requirecareful management to prevent com-plications and adverse outcomes forboth mother and infant.

Thyroid FunctionThyroid hormones, triiodothyro-

nine (T3) and thyroxine (T4), aresynthesized within the follicles of thethyroid gland, and their synthesisrequires iodide.5 Most T4 is trans-formed to T3 by the action of enzymesafter T4 is released from the thyroidgland. Thyroid hormones are carriedthroughout the body by proteins,primarily thyroxine-binding globulinproduced in the liver. Production ofthyroid hormones is regulated bythyroid-stimulating hormone (thy-

rotropin or TSH)produced in theanterior lobe ofthe pituitary glandand released as aresult of the activ-ity of hypothalamicthyrotropin-releasing hormone(see Figure). Nega-tive feedbackmechanisms regu-late the release ofTSH from thepituitary gland.Stress and temper-ature changes caninduce the synthe-sis of thyroid hor-mones, resultingin pronounced effects on the cardio-vascular system (Table 2). General-ized vasodilatation results inincreased cardiac output. Heart rateand contractility are increased, as is

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

CRITICALCARENURSE Vol 24, No. 2, APRIL 2004 75

Table 1 Common signs and symptoms of hyperthyroidism

Increased appetiteBlurred visionIrregular mensesDiplopiaExertional dyspneaFatigueHeat intoleranceDiarrheaIncreased perspirationIrritabilityMuscle weaknessNervousnessPalpitationsPhotophobiaSleep disturbancesGoiterFine resting tremorsWeight loss

Regulation of thyroid hormones.

HypothalamusThyrotropin-releasing hormone

(TRH)

Anterior lobe of pituitary glandThyrotropin (TSH) released

Increased cellularmetabolism

Thyroxinereleased

Thyroxine

feedback

Thyroid gland

Iodine

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

Carbohydrate metabolismIncreased: Glucose uptake

GlycolysisGluconeogeneisCarbohydrate absorption rate in gastrointestinal tractInsulin secretion

Fat metabolismIncreased: Lipid mobilization

Levels of free fatty acids in plasmaDecreased: Levels of cholesterol, phospholipids, and triglycerides in plasma

Increased need for vitaminsIncreased basal metabolic rateIncreased blood flow and cardiac outputIncreased respiratory rate and depthIncreased gastric motilityIncreased cerebration resulting in decreased effective function of the central nervous system

Extreme nervousnessPsychoneurotic tendencies

Muscle tremor due to increased reactivity of neuronal synapsesMuscle weakness due to excess protein catabolismInsomnia and fatigue due to constant effect on musclesIncreased secretion of other hormones and increased need at targetsExcess thyroid hormone in women: oligomenorrhea or amenorrheaDeficient thyroid hormone

Men: Loss of libido or impotenceWomen: Menorrhagia and polymenorrhea or amenorrhea

central nervous system is stimulated.Because of this stimulation, sleepdisturbances can occur when excessthyroid hormone is present. Endocrinegland function is stimulated by thy-roid hormones, and gastric motilityis increased.

Thyroid Physiology During Pregnancy

The normal, but reversible hor-monal changes in pregnancy resultin thyroid stimulation and increasedlevels of T3 and T4, although TSHlevels remain normal. During normalpregnancy, the thyroid gland mayenlarge up to 50% because of hyper-plasia of the glandular tissue andincreased vascularity. However,marked thyromegaly and goitershould be considered pathologicalchanges.6 The basal metabolic rateincreases by as much as 25%, resultingin increased cardiac output, increasedpulse rate and heat intolerance.3,7(p129),8

The maternal hypothalamic-pituitary thyroid hormone system isrelatively independent of the fetal sys-tem. The human placenta is imper-meable to the transfer of TSH andlargely impermeable to the transferof T3 and T4.

9 Thyroid-stimulatingimmunoglobulins (TSIs), found inmaternal hyperthyroidism, cross theplacenta and stimulate productionof thyroid hormones by the fetus andcan result in fetal and neonatalhyperthyroidism.10

Findings associated with thenormal hypermetabolic state of preg-nancy can overlap with the signs andsymptoms of thyroid disease. Clini-cians should be aware of other signsand symptoms of hyperthyroidismthat indicate thyroid disease and arenot common in pregnancy, such asweight loss, hyperemesis, diarrhea,

heart rate greater than 100/min thatdoes not decrease with the Valsalvamaneuver, and/or lymphadenopathy.

Graves DiseaseGraves disease is an autoimmune

disorder in which a group of TSIsattach to and activate TSH receptorson the thyroid follicular cells. Thisactivation leads to an increased pro-duction of thyroid hormones andthe clinical findings associated withhyperthyroidism. Because the thy-roid hormones control many bodilyfunctions, this increase in the levelof thyroid hormones causes thesebodily 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, hyperthyroidismduring pregnancy can lead to mater-nal complications, including pretermdelivery, perinatal morbidity, heartfailure, and thyroid storm. The fetusand newborn can also be affected.Maternal TSI titers are used to predictthe effect of maternal Graves diseaseon the fetus. The risk of thyrotoxicosisin the fetus and newborn is higher inwomen with high TSI titers.9 Carefulassessment and monitoring of thefetus are important for early detectionof effects, with particular attentiongiven to elevated resting heart rate andpoor fetal growth pattern.

Thyroid StormThyroid storm is a rare, life-

threatening endocrinologic emer-gency that can lead to cardiac arrestand death. A total of 20% to 30% ofall cases are fatal.11 Patients can havea wide range of signs and symptoms(Table 3). The tachycardia is oftenout of proportion to the hyperther-

mia. Blood pressure is commonlynormal, although a widened pulsepressure is common. Patients withthyroid storm usually appear con-fused and disoriented. Thyroid stormcan be precipitated by surgery,infection, trauma, or labor anddelivery.3,12 Patients with thyroidstorm require assessment and man-agement in an intensive care unitwhere they can be monitored forcardiac status, fluid and electrolytebalance, and control of hyperther-mia.6 The underlying cause of thyroidstorm must be identified and treated.

ManagementThyroid storm requires prompt

recognition, aggressive reversal ofthyroidotoxins with antithyroid drugs(ATDs), and supportive managementof signs and symptoms (Table 4).Antithyroid agents are propylth-iouracil and methimazole. Theseagents inhibit the synthesis of thy-roid hormones.13 Propylthiouracilhas been the drug of choice in preg-nancy because it was thought that itdid not cross the placenta as readilyas methimazole does and because itblocks conversion of peripheral T4to T3.

2,14 Recent studies suggest thatthis notion may be incorrect. In astudy15 in which the suppressive effect

76 CRITICALCARENURSE Vol 24, No. 2, APRIL 2004

Table 3 Signs and symptoms of thyroid storm

HyperthermiaNauseaAbdominal painVomitingSevere agitationDiaphoresisDehydrationTachycardiaCongestive heart failureArrhythmiaConfusionCardiovascular collapseMalignant exophthalmos

Toxicology

of maternal ingestion of propylth-iouracil on fetal thyroid status wascompared with that of methimazole,the occurrence of low T4 levels orhigh fetal TSH levels did not differsignificantly between the 2 groups.The standard practice is to give aninitial loading dose of 300 mg to600 mg propylthiouracil enterallyand then 150 mg to 300 mg every 6hours.14 If a patient cannot take thesolution by mouth, propylthiouracilcan be administered via the nasogas-tric tube or can be compounded bythe pharmacy and given as a rectalsuppository. Iodides are also com-monly given because they rapidlyinhibit the release of thyroid hor-mones. Iodides are administered sev-eral hours after propylthiouraciltherapy is initiated to avoid thebuildup of hormones stored in thethyroid gland. A saturated solutionof potassium iodide is given orally indosages of 2 to 5 drops every 8 hours,or sodium iodide is given intra-venously in dosages of 0.5 to 1 g every8 hours. -Blockers such as propra-nolol should also be given to help

decrease some ofthe thyrotoxiceffects on the car-diovascular system.Additional sup-portive measuresinclude administra-tion of intravenousfluids for dehydra-tion, antipyreticsfor control ofhyperthermia (acooling blanketmay be necessary),nutritional sup-port, correction ofpossible electrolyteimbalances, and

use of glucocorticoids, which alsoinhibit conversion of T4 to T3 andprevent adrenal insufficiency. Ifsedation is required, barbiturates aremost often used because they lowerthe levels of thyroid hormones byincreasing the catabolism of the hor-mones.14 Oxygen should be used asneeded for possible increased oxy-gen demands.14,16,17 Because of thehypermetabolic state of thyroidstorm, medications are metabolizedfaster than normal. Therefore,higher and more frequent doses maybe required to control the thyrotoxi-cosis.18 Patients in thyroid crisisrequire close assessment and moni-toring of cardiovascular status,including continuous cardiac moni-toring and frequent monitoring ofvital signs. Significant changesshould be reported immediately.During this period, careful monitor-ing of the fetus is also a critical ele-ment of management. Currentrecommendations are to avoid deliv-ery during thyroid storm unless thecondition of the fetus demandsprompt delivery.19

PreventionThe gold standard of treatment

of thyroid storm is primary preven-tion. Prevention of thyroid stormrequires careful control and man-agement of the hyperthyroidism.Standard treatment options forGraves disease include therapy withradioactive iodine, ATDs, and thy-roid surgery.20 However, pregnancylimits these treatment options.Because of possible destruction ofthe thyroid gland in the fetus,radioactive iodine cannot be given,and surgery is avoided because ofthe increased risk for miscarriage orpreterm delivery.

As a result, the standard treat-ment during pregnancy is the use ofATDs to inhibit the biosynthesis ofthyroid hormones. Because of theimmunosuppressive effect of preg-nancy, ATDs can be given in lowerdoses in pregnant patients than innonpregnant patients. Every attemptshould be made to treat with the low-est possible effective dose of ATDsbecause these drugs can cross the pla-centa, enter the fetal circulation, andaffect the thyroid gland of the fetus.

Even though propylthiouracil isthe drug of choice during pregnancy,it 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.A rare adverse effect, agranulocyto-sis, an acute condition distinguishedby a deficit or absolute lack of granu-locytes, usually is manifested byfever and sore throat. If fever andsore throat occur, a complete bloodcell count should be done, and ifagranulocytosis is diagnosed, treat-ment with thiopropyluracil shouldbe stopped.19

CRITICALCARENURSE Vol 24, No. 2, APRIL 2004 77

Table 4 Management of thyroid storm

Recognition of signs and symptoms: hyperthermia, tachycardia,confusion, vomiting, hypotension, diaphoresis, irritability

Reversal of thyrotoxicosis with antithyroid drugs1. 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. -Blockers to decrease effects on the cardiovascular system

Supportive therapy1. Fluids2. Nutritional support3. Oxygen4. Antipyretics (possibly cooling blanket)5. Correction of electrolyte imbalance6. Glucocorticoids such as dexamethasone 2 mg every 6 hours

for 4 doses.7. Barbiturates if needed for sedation

of medication, to avoid suppressingthe thyroid gland in the fetus.23

Fetal and NeonatalThyrotoxicosis

Transplacental passage of TSIscan result in fetal and neonatal thy-rotoxicosis, although this complica-tion is rare. It occurs in only 1% ofbabies born to women with a historyof Graves disease, but it may haveserious consequences if not recog-nized.24 Potential fetal and neonatalcomplications are listed in Table 5.

The level of TSIs should be meas-ured in the third trimester in allpregnant women with active or inac-tive Graves disease. High TSI levels,more than 5 times the referencerange, are common in the mothersof babies with neonatal hyperthy-roidism.24 The activity of the mothersdisease, however, does not necessar-ily correlate with fetal or neonataldisease. In cases of quiescent Gravesdisease, the prediction of neonatalGraves disease on the basis of thematernal clinical status is not alwayspossible because the mother maynot manifest signs or symptoms. Insome infants, both stimulating andblocking antibodies are acquiredfrom the mother, and the blockingantibodies block the effect of thestimulating antibodies for 4 to 6weeks such that late-onset neonatal

The starting dose is typically 300to 450 mg per day divided into 3doses. If methimazole is used, thestarting dose is 20 mg twice a day.Results of laboratory tests should bemonitored carefully, and once apatient becomes euthyroid, the dosecan be tapered gradually. Manypatients need only 50 mg per day,and some patients may not need anymedication by the third trimester;however, the dosage may vary from50 to 200 mg of propylthiouracilevery 8 hours, or methimazole 10 to60 mg a day, depending on thepatients signs and symptoms andlaboratory values.4,8 Biochemically,the aim is to keep the serum level oftotal T4 between 154 and 193nmol/L (12-15 g/dL) and theserum level of free T4 within the ref-erence range for the laboratory testused. (These values will vary fromone laboratory to another.8)

Fetal and neonatal hypothyroid-ism, as well as the occurrence of goi-ters, may occur from passage ofthionamides across the placenta.2

During the first trimester, transferof ATDs transplacentally can affectthyroid development in the fetus.Fetal exposure to ATDs can producehypothyroidism and fetal growthrestriction.21

Methimazole therapy may beassociated with aplasia cutis (a local-ized lesion in the parietal area of thescalp, characterized by congenitalabsence of the skin, punched-outulcer lesions, that usually healspontaneously) in the offspring oftreated women and is another reasonthat propylthiouracil has become thedrug of choice during pregnancy.22

The therapeutic goal is to controlthe mothers hyperthyroidism byusing the smallest possible amount

78 CRITICALCARENURSE Vol 24, No. 2, APRIL 2004

Graves disease develops in an infantin whom the disease was not previ-ously diagnosed.9 In all pregnanciesconsidered to be high risk, the fetusshould be closely monitored. Fetalthyrotoxicosis is suggested by aresting heart rate that is elevated(>160/min) and poor fetal growth.10,25

In many cases, neonatal thyro-toxicosis is not evident at birth whenthe mother has been treated withthionamides. As thionamide levelsdecrease in the neonate, clinicalsigns of thyrotoxicosis occur, usually5 to 10 days after birth (Table 6).Common signs are irritability,tachycardia, poor feeding, and fail-ure to gain weight. The disease isusually self-limiting over 1 to 3months as the circulating levels ofmaternal immunoglobulinsdecrease. In severe cases, clinicalmanifestations may include goiterwith resultant respiratory distress,hyperthermia, exophthalmos, tachy-cardia, hypertension, poor weightgain, thrombocytopenia, and jaun-dice. Arrhythmias, cardiac failure,and death may occur if the thyro-toxicosis is severe and treatment is

Table 5 Potential fetal and neonatalcomplications of thyrotoxicosis2,24

HyperthyroidismTachycardiaIntrauterine growth retardationSize small for gestational agePrematurityStillbirthAdvanced bone ageCraniosynostosisFeedback suppression of the fetal

hypothalamic-pituitary-thyroid axis

Table 6 Clinical manifestations ofneonatal thyrotoxicosis2,24

Marked irritabilityHyperthyroidismHyperthermiaTachycardiaHypertensionGoiter Respiratory distressExophthalmosPoor feedingFailure to gain weightVomitingSevere diarrheaArrhythmiasHeart failure JaundiceThrombocytopeniaHepatosplenomegalyHypoprothrombinemia

Toxicology

inadequate. High levels of total T4,free T4, and T3 in postnatal bloodconfirm the diagnosis.

Treatment of neonatal thyrotoxi-cosis is similar to the methods usedin treating the mother. Thionamides,-blockers, and iodine are mostcommonly used. In the most severecases, digitalis, glucocorticoids, andsedatives many be necessary to pre-vent cardiovascular collapse.24

Hyperthyroidism results inincreased metabolic demands, andinfants with hyperthyroidismrequire careful attention to nutri-tional needs and a high caloricintake to maintain growth. Fatigueand exhaustion can also result fromthe hypermetabolic state, and meas-ures to conserve energy stores areessential to the well-being of theseinfants. The half-life of immuno-globulins received from the motheris 8 to 20 days, and as the circulatinglevel of the antibodies decreases in theinfant, the disease wanes and theinfant shows signs of improvement.Complete resolution of the hyperthy-roidism occurs within 3 to 12 weeks.24

Breast-feeding in women withhyperthyroidism remains controver-sial, primarily because of passage ofATDs in breast milk. Propylthiouracilis excreted in breast milk in relativelysmall amounts, whereas methimazoleis excreted in slightly larger amounts.Most sources2,26 suggest that breast-feeding should not be routinely con-traindicated in women taking thesemedications if the women are care-fully monitored.

SummaryThyroid storm is the major risk

to pregnant women with thyrotoxi-cosis. This life-threatening conditionis more likely to occur with another

precipitating factor such as laborand delivery, surgical delivery, infec-tion, or trauma. Thyroid storm mostoften occurs in patients with under-treated or undiagnosed hyperthy-roidism. As many as 20% to 30% ofcases can end in maternal and fetalmortality.11 Therefore, critical carenurses must be able to recognizeand initiate proper medical andnursing interventions promptly.

References1. Manifold CA. Hyperthyroidism, thyroid

storm, and Graves disease. eMed J.2001;2(6). Updated July 25, 2002. Availableat: 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, WeingartenCT. 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.1998;27:127-149.

5. Guyton AC, Hall JE. The thyroid metabolichormones. In: Textbook of Medical Physiology.10th ed. Philadelphia, Pa: WB Saunders Co;2000:858-868.

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;2002:119-161.

8. Levin RM. Thyroid disease in pregnancy[on-line course]. January 15, 2001. Availableat: http://www.bumc.bu.edu/www/busm/cme/modules/thyroid_10-99/bcs.htm.Accessed July 2, 2002.

9. Polk D, Fisher D. Disorders of the thyroidgland. In: Tauesch AW, Ballard R, eds. AverysDiseases of the Newborn. Philadelphia, Pa:WB Saunders Co; 1998:1224-1234.

10. Fisher D. Fetal thyroid function: diagnosisand 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. Drugsaffecting the endocrine system. In: Pharma-cotherapeutics for Nurse Practitioner Pre-scribers. Philadelphia, Pa: FA Davis;2002:538-542.

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

15. Momotani N. Effects of propylthiouraciland methimazole on fetal thyroid status inmothers with Graves hyperthyroidism. J Clin Endocrinol. 1997;82:3633-3636.

16. Offutt CA. Endocrine problems. In: LoganP, ed. Principles of Practice for the Acute CareNurse 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;1994:1568-1599.

18. Malchiodi L. Thyroid storm: recognizingthe signs and symptoms of this life-threat-ening complication. Am J Nurs. May2002;102:33-35.

19. American College of Obstetrics and Gynecol-ogy. ACOG practice bulletin: thyroid diseasein pregnancy. No. 37, August 2002. Ameri-can College of Obstetrics and Gynecology. IntJ 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 ofCare Committee, American Thyroid Associ-ation. JAMA. 1995;273:808-812.

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

22. Mazzaferri EL. Evaluation and managementof common thyroid disorders in women. AmJ Obstet Gynecol. 1997;176:507-514.

23. Ecker JL, Musci TJ. Treatment of thyroiddisease in pregnancy. Obstet Gynecol ClinNorth Am. 1997;24:575-589.

24. Seely LB, Burrow GN. Thyroid disease andpregnancy. In: Resnik R, ed. Maternal-FetalMedicine. 4th ed. Philadelphia, Pa: WBSaunders Co; 1999:996-1014.

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

26. Momotani N, Yamashita R, Makino F, NohJY, Ishikawa N, Ito K. Thyroid function inwholly breast-feeding infants whose moth-ers take high doses of propylthiouracil. ClinEndocrinol (Oxf ). 2000;53:177-181.

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Outcome of Case Study

Wendy remained in the intensivecare unit for several days, where she wasclosely monitored as her thyrotoxicosiswas brought under control. Electrolytelevels and results of thyroid functiontests were checked daily, and fetal mon-itoring was performed continuously toassess fetal well-being. Both an endocri-nologist and a maternal-fetal specialistwere consulted. After 48 hours in theintensive care unit, Wendys levels ofthyroid hormones had decreased andwere no longer life-threatening. She wastransferred to a high-risk perinatal unitfor further monitoring while her vitalsigns and thyroid hormone levelsreturned to normal. Wendy continuedtaking maintenance doses of propylth-iouracil until delivery. After continuedcareful monitoring of her thyroid levelthroughout her pregnancy, Wendydelivered a 2.74 kg (6 lb 2 oz) healthyboy at 39 weeks gestation.