Advances in Assessment, Diagnosis, and Treatment of Hyperthyroidism in Children Kim Siarkowski Amer, RN, PhD The thyroid gland is responsible for regulating multiple complex metabolic processes that affect most organs. Physical growth and cognitive development are dependent on proper levels of thyroid hormone. This article will review common challenges in the diagnosis of hyperthyroidism in children, the approaches to treatment, and the nursing interventions guided toward child and family responses to thyroid disease. A comparison of signs and symptoms of hypothyroidism and hyperthyroidism is also included. The nursing interventions addressed in the article integrate the biological, psychological, social, and environmental stresses and adaptations necessary to cope with hyperthyroid disease. n 2005 Published by Elsevier Inc. The word thyroid comes from the Greek word bto shield Q HE THYROID GLAND is responsible for regulating many metabolic processes including physical growth and cognitive development. The underfunction or overfunction of the thyroid gland can affect all organ systems, growth, development, and long-term functioning (Dallas & Foley, 1996). Nurses need to be aware of the multiple complex systems affected by thyroid status and use appropriate nursing assessments and interventions. For example, recent studies demonstrate that cognitive development is dependent on early and adequate thyroid hormone replacement in congenital hypothyroidism (Selva et al., 2002). Formerly, the most common cause of mental retardation, congenital hypothyroidism is now part of the newborn screening protocol in every state. Although infants are diagnosed early, their long-term health is dependent on normal thyroid status through thyroid hormone replacement. In contrast to hypothyroidism, hyperthyroidism is rare in young children or infants. However, hyperthyroidism in pregnancy can affect multiple systems in the infant. In children, 95% of the cases of hyperthyroidism are related to Graves’ disease (Dallas & Foley, 1996). Thyroid function is dependent on a feedback loop system, or the hypothalamic, pituitary, thyroidal axis. Thyroid hormone regulation is an excellent example of the delicate balance among the brain (hypothalamus), the pituitary gland, and the target gland (e.g., the thyroid gland). When too much thyroid hormone is produced, the hypothalamus T Journal of Pediatric Nursing, Vol 20, No 2 (April), 2005 attempts to slow down production and sends a signal, thyrotropin-releasing hormone (TRH), to the pituitary gland, which in turn slows down synthesis of thyroid-stimulating hormone (TSH), which should slow production of thyroid hormone. However, if the pathology is severe, the feedback regulation is ignored and overridden, and the thyroid may continue producing more hormone until a dangerous hyperthyroid state, or thyrotoxicosis, is at hand. EMBRYOLOGY OF THE THYROID The thyroid gland is a bow tie-shaped gland that originates in the palate in the first trimester of pregnancy. Because the fetus at this stage does not produce iodine, thyroid hormones T4 and T3 cannot be produced. Because there is no iodine produced, thyroid hormone cannot be produced and the fetus is dependent completely on maternal thyroid hormones. Therefore, maternal thyroid status is critical to the development of the fetus and child. If maternal iodine ingestion is inadequate, the fetus will not have adequate thyroid hormone. From the Department of Nursing, DePaul University, Chicago, IL. Address correspondence and reprint requests to Kim Siarkowski Amer, RN, PhD, Department of Nursing, DePaul University, Suite 3000, 990 W. Fullerton, Chicago, IL 60614. E-mail: [email protected] 0882-5963/$ - see front matter n 2005 Published by Elsevier Inc. doi:10.1016/j.pedn.2004.12.013 119 120 In the second trimester of pregnancy, the thyroid migrates to the neck area. Two etiologies for congenital hypothyroidism are athyrosis (absence of thyroid at birth) or lingual thyroid. Congenital hypothyroidism can be caused by the failure of the thyroid to migrate normally to the proper anatomical area, or in the case of athyrosis, by the absence of thyroid tissue at birth (DiGuiseppi, 1994). Thyroid hormone production begins in the fetus through the third trimester, and with normal function, an euthyroid state should be achieved. MATERNAL HYPERTHYROIDISM AND THE EFFECT ON NEWBORNS In a mother with a history of thyroid disease (Case 1), thyroid hormone levels and physical symptoms should be monitored closely during pregnancy (Haddow et al., 1999). Newborn thyroid levels and signs of overactive or underactive thyroid should also be monitored. Laboratory tests to assess function in both mother and infant evaluate the pituitary hormone TSH and the thyroid hormones for thyroxine (T4) and triiodothyronine (T3). Almost all thyroid hormones are bound to thyroid-binding globulin (TBG). Only 0.3% of thyroid hormone is bfreeQ or circulating. Thyrotoxicosis occurs with very high levels of unbound circulating thyroid hormone, which is caused by hyperfunction of thyroid follicular cells or increased synthesis and secretion of T3 or T4. Total thyroxine, or TT4, is elevated in hyperthyroidism; however, there are cases of T3 thyrotoxicosis that would not show an increase in TT4 (Williams & Brent, 1995). Case 1. C.J. is a newborn whose mother had active hyperthyroidism during pregnancy. The mother was treated with Tapazole, a thyroid suppressant; however, her symptoms persisted. A goiter was noted on C.J.’s initial exam, and at 7 days of life, C.J. is tachycardic at 220, sleeps 15 minutes at a time, and has had frequent runny stools since 2 days of life. Thyroid-stimulating antibodies were three times the normal level, and T4 levels were elevated with a suppressed TSH. The inability to self-regulate thyroid levels has many serious effects on the newborn such as those illustrated in Case 1. When the transplacental thyroid-stimulating immunoglobulin (TSIG) is passed to the infant, there may be fetal hyperthyroidism with goiter. Elevated maternal thyroid hormones may disrupt the fetal and newborn ability to regulate TSH and T4 levels. Newborns of mothers with hyperthyroidism can be affected in KIM SIARKOWSKI AMER many ways. In maternal Graves’ disease, there is a significant risk for low birth weight, prematurity, small for gestational age, and intrauterine death in infants (Seng, 2000). Congenital malformations are more common in mothers with a history of Graves’ disease that is not controlled during pregnancy (Momotani, Ito, & Noh, Oyanagi, Ishikawa, & Ito, 1986). Elevated maternal thyroid hormones may disrupt the fetal and newborn ability to regulate TSH and T4 levels. In Case 1, the baby has transient hyperthyroidism, which should be treated with hblockers and thyroid suppressants if needed. Physical signs and symptoms such as diarrhea, abnormal sleep patterns, and hyperreflexia should be monitored by nurses and documented. Neonatal Graves’ disease is relatively rare with cases occurring about 1 in 25,000 pregnancies (Russell, 1992). Infants with neonatal Graves’ disease are usually confined to offspring of mothers with Graves’ disease, as in Case 1. Maternal immunoglobulins that stimulate TSH receptors in utero result in a hyperthyroid state in the fetus (Seng, 2000). Additional effects of neonatal Graves’ disease is rare; the physiological effects can include growth retardation, irritability, restlessness, elevated temperature, flushed face, tachycardia, cardiomegaly, and heart failure. The infant has increased somatic growth, in contrast to infants of diabetic mothers; infants with neonatal Graves’ disease have decreased fat stores, tachycardia, and hyperalertness (Russell, 1992). Initial treatment for infants with thyrotoxicosis includes h-blockers and antithyroid drugs. Most infants have cleared the maternal immunoglobulins after 2 months and no longer need treatment. The initial symptoms of thyromegaly, thrombocytopenia, hepatomegaly, and cardiac arrhythmias can be significant, including mortality. Hence, although the condition is transient, it can be serious or fatal (Russell, 1992). After resolution of symptoms, the infant should retain normal function for life. GENETICS AND THYROID DISEASE Recent advances in elucidating the genetic mechanisms underlying thyroid metabolism include identifying the location of the gene for the thyrotropin h-subunit on chromosome 1 and advances in the genetics of autoimmune thyroid disease and the complex mechanisms of signal transduction. The regulation of synthesis of TSH involves a complex process of signaling receptors that sense whether thyroid hormone levels are 121 ADVANCES IN THYROID (T4-binding globulin), TTR (transthyretin), prealbumin, and albumin. Only 0.3% of thyroid hormone circulates unbound. However, this unbound hormone is metabolically active at the cellular level. Inherited or acquired deficiencies in the carrier proteins may change the serum thyroid levels significantly, which may be related to thyrotoxicosis. Such changes do not always result in clinical thyroid disease because the concentration of the free thyroid hormone does not change. If a patient has normal TSH, low thyroid hormone values, and proportionately low TBG, then thyroid function should be normal (Sarlis & Hirshberg, 2002). Figure 1. Thyroid activity: hypothalamic thyrotropinreleasing hormone. THYROID ANTIBODIES adequate. If thyroid hormone levels are low, TSH increases to try to increase production of thyroid hormone. If thyroid hormone levels are high, TSH decreases in an attempt to slow thyroid hormone production. TSH is a glycoprotein hormone that has common alpha and unique h-subunits. The TSHh is expressed uniquely in the anterior pituitary just as other regulatory hormones such as lutenizing hormone (LH) and follicle-stimulating hormone (FSH) (Williams & Brent, 1995). Regulatory factors in TSH transcription include TRH, somatostatin, dopamine, vasoactive intestinal peptide, and arginine vasopressin (Vacca, Moro, Caraccio, Guerrieri, Marra & Greco, 2003). The action is initiated by TRH, which binds to the plasma membrane receptors, which initiate a cascade of signal transduction events that activate phospholipase C kinases, which eventually cause regulation of thyroid hormone activity (Figure 1). In an animal model, thyroid hormone activity has been disrupted by exposure of fetal and suckling newborn rats to dioxin (2,3,7,8-tetrachlorodibenzop-dioxin), which is commonly found in the environment. Nishimura, Yonemoto, Miyabara, Sato, and Tohyama (2003) found that thyroid hormone homeostasis was disrupted by the exposure to dioxins due to sustained excessive secretion of TSH followed by hyperplasia of the follicular cells of the thyroid. Future research on humans may show a link between environmental toxins and thyroid function. THYROID-BINDING PROTEINS Thyroid hormones T4 and T3 are bound to the carrier proteins, most commonly identified as TBG The most common cause of acquired hypothyroidism is Hashimoto’s thyroiditis. The name came from the Japanese physician who first described the inflammation of the thyroid tissue that he examined through a microscope in 1912. The thyroid becomes enlarged because of the infiltration with lymphocytes (white blood cells) that cause an autoimmune reaction. The lymphocytes gradually destroy the thyroid tissues, and the result is underactive thyroid function with an enlarged thyroid gland. Eighty percent of people with Hashimoto’s thyroiditis have elevations in antimicrosomal and antithyroglobulin antibodies (Williams & Brent, 1995). In contrast to the hypothyroidism in Hashimoto’s thyroiditis, Grave’s disease, or hyperthyroidism, is caused by a different autoimmune antibody process. In this case, the thyroid works against itself because of the abundance of thyroid-stimulating antibodies that cause an excessive amount of thyroid hormone to be produced. TSIG and TSI were the antibodies tested to determine if Graves’ disease is present (Webster, Taback, Sellers, & Dean, 2003). The diagnosis of Graves’ disease is confirmed by additional laboratory data, including elevated T4, suppressed TSH, and elevated TSI. The clinical symptoms are similar to those for neonatal Graves’ disease and are listed in Table 1. The symptoms consistent with Graves’ disease are because of the hyperactivity of the sympathetic nervous system and hyperthyroidism (see Table 1). Additional symptoms include irritability, emotional lability, heat intolerance, and proximal muscle weakness (Webster et al., 2003). Physical findings on assessment include goiter, persistent tachycardia, systolic hypertension with widened pulse 122 KIM SIARKOWSKI AMER Table 1. Comparison of Thyroid Abnormalities, Hypothyroidism, Hyperthyroidism, Their Symptoms, Treatment, and Follow-Up Recommendation Thyroid Dysfunction Clinical Symptoms Laboratory Findings Treatment Follow-Up Congenital hypothyroidism Sleeping more than normal, hypotonia, poor feeding, dry skin, hoarse cry, in infants very few symptoms Elevated TSH (unless caused by pituitary dysfunction), low T4 10–15 Ag/kg/day of thyroid replacement (l-thyroxine) (Selva et al., 2002) Acquired hypothyroidism Dry skin, weight gain, constipation, sleeping more than normal Clinically euthyroid (normal without symptoms) Low T4 and high TSH Thyroid replacement Low T4, T3, low TBG, normal TSH No treatment Make sure patient understands that thyroid screening tests may be abnormal (if TBG is not measured) Malaise, weight gain, constipation, delayed relaxation phase in deep tendon reflexes, dry skin and hair Sweating, tachycardia, shakiness, a more hearty appetite than usual, mood changes/ feeling or acting more nervous, muscles aches, especially when climbing stairs, protruding eyes, difficulty in swallowing (because of a large thyroid), difficulty in concentration, diarrhea, weight loss Tachycardia, hyperkinesis, restlessness, diarrhea, poor weight gain, premature craniosynostenosis, and advanced bone age Elevated TSH, low T4 and T3, elevated antimicrosomal and antithyroglobulin antibodies Elevated T4 and T3, suppressed TSH (b1 Ag/L), elevated TSI Thyroid replacement Monitor several times a year to ensure adequate replacement Treatment for hypothyroidism may cause hyperthyroidism Treatment may cause hypothyroidism High free T4 and suppressed TSH, elevated TSI will persist for 3–5 months Lasts weeks to 6 months; if symptomatic, treat with medications TBG deficiency (can be inherited, such as X-linked deficiency or carbohydrate-deficient glycoprotein syndrome, which is autosomal recessive, or acquired, such as hyperthyroidism, nephrotic syndrome, renal failure, or malnutrition Hashimoto’s thyroiditis (acquired hypothyroidism) (autoimmune process) Graves’ disease hypertyroidism (autoimmune process) Neonatal thyrotoxicosis (neonatal Graves’ disease) pressure, brisk reflexes, exophthalmus (protruding eyes), eyelid retraction, hand tremor, hyperreactive deep tendon reflexes, and smooth, moist, and warm skin (Siarkowski Amer, 1993). At the time of diagnosis of Graves’ disease, there may be a history of declining school performance over several months. The reported average duration of symptoms in the pediatric population prior to diagnosis is 1 year (Cooper, 1983; Safa, Schumacher, & Rodriguez-Antunez, 1975; Webster Thyroid suppressant drugs such as propylthiouracil or Tapazole, ablation therapy, or surgery also may need h -blocker for elevated heart rate Frequent blood tests to ensure adequate replacement (higher thyroid hormone values show better cognitive development in the first 2 years of life) Follow-up at least twice a year Presence of maternal antibodies (TSI) may occur even after mother is euthyroid; can cause hyper- or hypothyroidism in infant et al., 2003) A thorough history, physical assessment, and thyroid function testing usually makes the diagnosis straightforward. Unfortunately, there is no cure for the autoimmune process that occurs during Graves’ disease. Future research may use TSI for treatment as well as diagnosis. The goal is to find a physiological way to block the production of immunoglobulins. The direct effect of this immune component on the hyperthyroidism is not fully understood; however, 123 ADVANCES IN THYROID current research suggests that there is a defect in immune surveillance. The exact prevalence of Graves’ disease is not known; however, it is estimated to be approximately 0.4% of the population of the United States (Williams & Brent, 1995). It is much less common in children than in adults and is five to six times more common in girls than in boys. Graves’ disease may appear at any time; however, it is rare in infancy, unless the mother has hyperthyroidism, and shows a peak incidence during preadolescence and adolescence (Dallas & Foley, 1996). Case 2. Lucy is a 15-year-old who was diagnosed with Graves’ disease at 11. She was initially treated with thyroid-suppressive drugs and then received radioactive iodine (RAI). Her thyroid replacement has been adequate for the past 3 years; however, lately, she has been very tired, sleeping 12 hours a day. She also has had some weeks where she only has two to three stools. Her constipation is making her bloated and she is frustrated. Lucy’s deep tendon reflexes are slow to react. Is this adolescent malaise or hypothryoidism caused by the treatment of her Graves’ disease? As in Case 2, after initial diagnosis and initiation of treatment for Graves’ disease, thyroid function tests should be followed regularly every month for the first 2 months, then at least three times a year until they normalize with treatment. If thyroid values are borderline, more specific tests can be done. These include T3 resin uptake, free T4, thyroid antibody titer, or RAI uptake (Williams & Brent, 1995). If there is an elevation in T4 without suppression of TSH, it is unlikely the patient will require treatment. After treatment for Graves’ disease or a remission, the patient may need to be treated for hypothyroidism, as in Case 2. During active Graves’ disease, the state of such extreme hyperfunctioning can sometimes lead to bburnout Graves’ disease,Q which is a state of hypothyroidism. In addition, suppressant drugs and other treatments may leave the thyroid underfunctioning or with very minimal function. Such is the case of Lucy (Case 2), who needs thyroid replacement after treatment of Graves’ disease. Nurses must be aware of the divergent symptoms of hypothyroidism and hyperthyroidism and the potential for shifts between diagnosis. For example, if a patient has a diagnosis of Graves’ disease, they have hyperfunction initially, but may become hypothyroid from treatment. MEDICAL MANAGEMENT Treatment of Grave’s disease consists of three options: medical therapy with thioamides (antithyroid drugs), surgical resection of all or a major portion of the thyroid gland, or ablation of the thyroid with RAI. Because the specific cause of the gland hyperactivity is not known, these are the most effective therapies at this time. The two most commonly used thioamides are propylthiouracil and methimazole (Tapazole). Both block the formation of T4 and T3. Agranulocytosis is a very serious side effect of both drugs (Cooper, 1983). Families should be educated about the importance of reporting any fever and/or sore throat to the physician immediately, as these symptoms may signify the onset of agranulocytosis. Scheduled periodic white blood cell counts have not been useful to monitor patients because the agranulocytosis can occur over a short period, over 2 weeks (Siarkowski Amer, 1993). Mild leukopenia can be a result of the hyperthyroidism itself, and if it remains mild, it poses no threat. Other side effects of the medications include rash, fever, nausea, and arthralgia. Side effects occur in less than 5% of patients on thioamides. Medical management with thioamides is the least invasive approach, and many patients achieve a remission of the disease with thioamide treatment. About 20–25% of patients achieve remission in 2 years and up to 50% by 5 years of therapy. Compliance is an concern with thioamides, especially with adolescents who self-administer, since an every-6-hour or an every-8-hour schedule can be difficult in some patients. Patients may skip their afternoon dose while at work or at school, which is against the advice of health-care providers. Reminders, such as watches with alarms, cell phones, or personal digital assistants (PDAs), can be invaluable for busy teens. If achievement of remission fails, the other options are surgery or RAI. Both have potential side effects and possible morbidity. The hesitancy to use radioiodine in children because of the oncogenic potential has not been validated in the small number of studies reported (Moll & Paatel, 1997). Moll and Paatel (1997) compared outcomes from three different treatment groups: one used radioiodine as the second choice after antithyroid medication failure, one had thyroidectomy after medication failed, and the third group received initial radioiodine treatment. Of the three groups, the group receiving immediate radioiodine had the highest first year remission (88%). The other two groups had a remission rate of 65% within 5 years. 124 KIM SIARKOWSKI AMER Hence, from this pilot study, it appears that RAI may be the first choice for a timely remission with minimal medical therapy or surgical intervention. This approach was also confirmed by Webster et al. (2003), who state that in many Canadian centers, radioiodine is used as a first course treatment with adolescents who may have trouble with compliance. Surgical removal of most of the thyroid gland is an acceptable treatment especially if there is an experienced pediatric thyroid surgeon in the institution. The risks associated with surgery include thyroid storm if the child is hyperthyroid before surgery or if thyroid hormone is released during surgery (Ball & Bindler, 2003). Other risks include potential loss of part or all of the parathyroid glands, vocal cord paralysis, and bleeding, in addition to all the risks associated with any surgery and anesthesia (Siarkowski Amer, 1993). Calcium and phosphorous should be monitored closely after thyroidectomy (Maier et al., 1984). In the United States, the trend is to attempt medical management, and if this is unsuccessful, then either surgery or RAI is used. RAI is considered a safe and effective means of treating pediatric Graves’ disease (Chapman, 1983). Many clinicians remain cautious with its use because of the possible, although not proven, risk of infertility or cancer. The RAI treatment dose of radiation to the gonads is equal to an upper gastrointestinal series or intravenous pyelography. Both thyroidectomy and RAI treatments may leave patients hypothyroid because of the removal or ablation of the thyroid gland (Siarkowski Amer, 1993). This may occur some time after treatment. Thus, these therapies can commit the patient to lifelong thyroid replacement. Patients who achieve a remission within the first year of treatment have a much better long-term prognosis (Siarkowski Amer, 1993). If medical therapy fails, ablation or thyroidectomy should be discussed (Ball & Bindler, 2003). THYROID STORM The most emergent risk for a patient with Graves’ disease is thyroid storm in uncontrolled hyperthyroidism or during times of stress or infection. Thyroid storm is not common in neonatal Graves’ disease. Thyroid storm can be caused by noncompliance with medication or overdosage of l-thyroxine replacement. The symptoms include more pronounced symptoms of hyperthyroidism. The patient may complain of palpitations, eyelid lag, fever, muscle weakness, excessive sweating, voracious appetite, diarrhea, or tremor, mostly due to sympathetic nervous system hyperactivity (Ball & Bindler, 2003). In late stages, there may be stupor or coma, cardiac failure, or circulatory collapse (Dallas & Foley, 1996). Thyroid storm is a medical emergency, and treatment is the same as the treatment for hyperthyroidism but with higher dosages of thioamides and possibly a h-blocker such as propranolol (Inderal) to control the cardiovascular hyperactivity and to decrease the risk of heart failure (Ball & Bindler, 2003). The patient must be hospitalized for management and stabilization. In some cases, it is necessary to do monitoring in the intensive care unit (Dallas & Foley, 1996). NURSING ASSESSMENT, INTERVENTION, AND ONGOING EVALUATION The family aspects of managing the care of a child with thyroid disease are related to the health perception and health management of the patient and family. Common concerns include difficulties adhering to the medical regime, the child being perceived as fragile or different from other children, missing school, or poor school performance due to illness. Before the diagnosis and during treatment, the child may be irritable and hyperactive, and such hyperthyroid child may be misdiagnosed as having attention deficit/hyperactivity disorder, or a child who is lethargic and always sleeping when hypothyroid can strain even the strongest family relationships (Ball & Bindler, 2003). Some families become overly concerned about the disease because of the language that is used. Words such as grave represent an ominous or dismal outcome, and when remission is mentioned, people often associate it with cancer. Because of this, it is important to state clearly to parents and patients that this is not a life-threatening disease if well managed (Siarkowski Amer, 1993). Families learning about thyroid disease may have a great deal of anxiety related to managing a chronic illness. There may be concerns about cognitive and perceptual functioning and sleep and rest patterns with this disease. Nurses should be actively involved in the patient and family by teaching things related to thyroid disease (Ball & Bindler, 2003). The alterations in cognitive, perceptual, and sleep and rest patterns should be temporary, lasting only until the patient is euthyroid. The patient and family need to be supported during the difficult time of adjusting dosage or 125 ADVANCES IN THYROID evaluating other treatment modalities (Wong, Wilson, Hockenberry-Eaton, Winklestein, & Schwartz, 2003). The goal of the family should be normalization, which includes acknowledging the disease, integrating the management into the family routine, and getting back to normal routines (Deatrick, Knafl, & Murphy-Moore, 1999). Self-perception and self-concept may be altered in patients with thyroid disease if they have outward signs such as exophthalmos or tremor (Ball & Bindler, 2003). Nursing interventions should be aimed at identification of positive aspects of the child. It should also be stressed that with a variety of treatment options, the likelihood of controlling the disease is good. Siarkowski Amer (1993) emphasizes that anticipatory dietary counseling is essential as treatment of the hyperthyroidism is initiated. As the metabolic rate normalizes with treatment, parents, children, and adolescents must learn to reregulate food intake to avoid extreme weight fluctuations (Siarkowski Amer, 1993). Nurses may need to communicate with the child’s teacher or principal to explain the difficulties the child may be experiencing because of the disease. It is important to stress the fact that these problems are temporary and should abate after the thyroid levels normalize. Several weeks to months may elapse before the child is back to normal. Potential side effects of antithyroid medications should be taught to patients and their caregivers. The most important of these is monitoring the patient for fever during illness. The potential agranulocytosis coupled with a fever can constitute a great risk (Ball & Bindler, 2003). The nurse should assess the family to evaluate if compliance with medication will be a problem. Frequently, when patients are not well controlled on antithyroid drugs, it can be traced back to a misunderstanding of dosage or noncompliance. For this reason, the medical regime should be reviewed in detail at each visit. The patient and caregiver should repeat the medication name, dosage, and times administered and the nurse should document the interchange. The family should also verbalize knowledge that the medication takes many days to weeks to correct the hyperthyroidism (Wong et al., 2003). Nursing management of thyroid storm includes educating patients about the phenomenon at initial diagnosis of Graves’ disease and monitoring the patient’s vital signs, laboratory data, and response to treatment in the hospital. If propranolol (Inderal) is ordered immediately for thyroid storm, it can be given intravenously (Ball & Bindler, 2003). The nurse needs to monitor heart rate and blood pressure every 30 minutes for 2 hours after administration. Although thyroid storm is rare in the pediatric population, it is important to recognize it because of the risk of significant mortality if not treated properly. In the past, it was a common problem postsurgically in both elective and unplanned surgeries and was the main cause of morbidity and mortality in thyrotoxicosis (Webster et al., 2003). Now that good treatment options are available, there is less concern about this phenomenon. With educated counseling from well-educated and prepared nurses, patients and parents managing thyroid disease should feel confident that their lives will be normal. Long-term health of patients with thyroid disease can be ensured with excellent comprehensive care managed by nursing. REFERENCES Ball, J. W., & Bindler, R. C. (2003). Pediatric nursing caring for children. New Jersey: Prentice-Hall. Chapman, E. M. (1983). History of the discovery and early use of radioactive iodine. Journal of the American Medical Association, 250, 2042 - 2044. Cooper, D. S. (1983). Antithyroid drugs. The New England Journal of Medicine, 31, 1353 - 1362. Dallas, J., & Foley, T. (1996). Hyperthyroidism. In F. Lifshitz (Ed.) Pediatric endocrinology. 3rd ed. New York, NY: Marcel Dekker. Deatrick, J., Knafl, K., & Murphy-Moore, C. (1999). Clarifying the concept of normalization. Image: The Journal of Nursing Scholarship, 31, 209 - 214. DiGuiseppi, C. (1994). Screening for thyroid disease. US Preventive Service Task Force. Retrieved from www.angelfire. com/md/danil/thyroidpysiology6/04. Haddow, J. E., Palomaki, G. E., Allan, W. C., Williams, J. R., Knight, G. J., Gagnon, J., et al. (1999). Maternal thyroid deficiency during pregnancy and subsequent neuropsychological development of the child. The New England Journal of Medicine, 341, 549 - 555. Maier, W. P., Derrick, B. M., Marks, A. D., Channick, B. J., Au, F. C., & Caswell, H. T. (1984). Long-term follow-up of patients with Graves’ disease treated by subtotal thyroidectomy. American Journal of Surgery, 147, 266 - 268. Moll, G. W., & Paatel, B. R. (1997). Pediatric Graves’ disease: Therapeutic options and experience with radioiodine at the University of Mississippi Medical Center. Southern Medical Journal, 90, 1017 - 1022. Nishimura, N., Yonemoto, J., Miyabara, Y., Sato, M., & Tohyama, C. (2003). Rat thyroid hyperplasia induced by gestational and lactational exposure to 2,3,7,8,-tetrachlorodibenzo-p-dioxin. Endocrinology, 144, 2075 - 2081. Russell, W. E. (1992). Endocrine and other factors affecting growth. In R. A. Polin, W. W. Fox (Eds.) Fetal and neonatal physiology (pp. 295 - 305). Philadelphia: WB Saunders. 126 Safa, A. M., Schumacher, O. P., & Rodriguez-Antunez, A. (1975). Long-term follow-up results in children and adolescents treated with radioactive iodine (I131) for hyperthyroidism. The New England Journal of Medicine, 292, 167 - 171. Sarlis, N. J., & Hirshberg, B. (2002). Thyroxine binding globulin deficiency. Retrieved from www.emedicine.com5/04. Selva, K. A., Mandel, S. H., Rien, L., Sesser, D., Miyahira, R., Skeels, M., et al. (2002). Initial treatment dose of l-thyroxine in congenital hypothyroidism. The Journal of Pediatrics, 141, 786 - 792. Seng, L. Y. (2000). Maternal graves’ disease: Effects on the newborn. Retrieved from www.med.nus.edu.sg/paed/medical_ education/postgraduate/endocrine_metabolism/maternal_ graves.htm5/04. Siarkowski Amer, K. (1993). Nursing care of children with Graves’ disease. Pediatric Endocrinology Nursing Society KIM SIARKOWSKI AMER resource manual. Pediatric Endocrinology Nursing Society, Gaithersburg, MD. Vacca, R., Moro, L., Caraccio, G., Guerrieri, F., Marra, E., & Greco, M. (2003). Thyroid hormone administration to hypothyroid rats restores the mitochondrial membrane permeability properties. Endocrinology, 144, 3783 - 3788. Webster, J., Taback, S. P., Sellers, E., & Dean, H. (2003). Graves disease in children. Canadian Medical Association Journal, 169, 104 - 105. Williams, G. R., & Brent, G. A. (1995). Thyroid hormone response elements. In B. D. Weintraub (Ed.) Molecular endocrinology: Basic concepts and clinical correlations. Raven Press. Wong, D., Wilson, D., Hockenberry-Eaton, M., Winkelstein, M., & Schwartz, P. (2003). Nursing care of infants and children. St Louis, MO: Mosby.
© Copyright 2019