Thyroid storm, also referred to as thyrotoxic crisis, is an acute lifethreatening endocrine emergency characterized by increased metabolism with excessive release of thyroid hormones. This could be the initial presentation in undiagnosed children, particularly in neonates.
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Diagnosis is primarily clinical with severe hyperthyroid symptoms. Because thyroid storm is almost invariably fatal if left untreated, rapid diagnosis and aggressive treatment are critical. This condition is rare in children. High index of suspicion for GD based on history and exam warrants laboratory investigation. The ratio of total T3 to total T4 can also be useful in assessing the etiology of thyrotoxicosis when scintigraphy is contraindicated. TSI is a functional assay which is measured by the production of cyclic AMP in cultured thyroid follicular cells.
This is in contrast to previous studies which pointed that TSI may not be present in all patients with GD . Although TSI is very useful for diagnosis of GD, they are not always used as the initial and confirmatory test. However, now there are increased recommendations for TSI use as an initial and diagnostic test for GD [41,42].
The Endocrine society guidelines for hyperthyroidism in pregnancy and postpartum recommended that measurement of TSHRAb in pregnant women may also help to distinguish GD from gestational thyrotoxicosis. They are also important to identify the neonates at risk due to maternal disease .
Scintigraphy: Besides those cases of GD that have negative TSHR-Ab and unclear etiology of hyperthyroidism, thyroid scan is not routinely done on every patient. As the thyroid gland actively concentrates iodine and radioactive iodine [RAI I ], radioiodine uptake scan RAIU is useful to aid in identifying the etiology of hyperthyroidism. Radiolabelled technetium 99 Tc can also be used as technetium is trapped by the thyroid gland but not organified. Even though these scans are reliable methods to diagnose GD, they are expensive and time consuming, moreover involve radiation exposure .
Thyroid ultrasound and color flow Doppler: Thyroid ultrasound is a very sensitive and reliable diagnostic tool, which is not necessary to conclude the etiology of hyperthyroidism as GD. Classically, the gland is hypoechoic due to lymphocytic infiltration, thyrocyte hyperplasia, decrease in colloid and increase in vascularity.
It provides an accurate estimation of the thyroid size, which is important in the therapeutic planning.
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It also allows the detection of non-palpable thyroid nodules . Color flow doppler CFD is useful for detection of blood flow, which is typically increased in patients with GD. Similar to iodine uptake scans, CFD is useful in the differential diagnosis between GD and other causes of thyrotoxicosis characterized by a low blood flow to the thyroid such as factitious thyrotoxicosis, subacute thyroiditis and type II amiodaroneinduced thyrotoxicosis, but with a lower sensitivity and specificity.
It is particularly useful in cases where uptake scans are not available or contraindicated for example, during pregnancy or lactation . After biochemical confirmation of disease, a choice between three main treatment options is required: antithyroid drugs ATD , radioiodine therapy or surgery. While the former may cause remission of disease, the latter two provide definitive treatment options. These drugs inhibit thyroid hormone synthesis by disturbing the thyroid peroxidase-mediated iodination of tyrosine residues in thyroglobulin .
These agents are actively concentrated by the thyroid gland against a concentration gradient . Although it is controversial, ATD may also have an immunosuppressive effect including apoptosis of intrathyroidal lymphocytes . ATD are used as the first line therapy in pediatric population with GD hoping for spontaneous remission.
MMI is superior to PTU due to longer half-life requiring once or twice daily dosing, thus improving treatment adherence.
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Also, PTU has a higher risk of liver failure 1 in including fulminant hepatic necrosis [47,50]. Hence, PTU is only used for a short course on patients with adverse reaction to MMI who are not candidates for radioiodine therapy or surgery . The MMI dose typically used is 0. Maximal clinical response to ATD occurs in approximately 4—6 weeks into treatment. However, because metaanalyses suggest a higher prevalence of adverse events using block and replace regimens than dose titration [47,51,52], ATA and AACE guidelines recommend avoiding this practice in general.
Once started on ATD, patients are initially monitored via history of symptomatic relief and TFT every month and then every months . Medication dose is titrated based on TFT and once biochemical euthyroidism is reached, patient can be followed up at every three to four month intervals. Side effects from ATD can be divided as minor and major depending on the severity.
Minor side effects are dermatitis, including rash, urticaria; gastrointestinal upset, arthralgia, pruritus and fever . It is generally recommended to discontinue the drug for a few days until the symptom subsides. Major side effects include agranulocytosis, even life-threatening pancytopenia, vasculitis lupus-like syndrome , hepatitis and liver failure. Side effects of MMI usually occur within the first 6 months of starting therapy . Because patients with hyperthyroidism can have slightly low white blood cell counts WBC and slightly high serum aminotransferase and gamma glutamyl transpeptidase concentrations due to the disease itself or side effect of treatment, it is recommended to measure these at baseline before beginning antithyroid drug therapy .
While routine monitoring of WBC may occasionally detect early agranulocytosis, it is not recommended because of the rarity of the condition and its sudden onset, which is generally associated with symptoms . The ATA and AACE guidelines recommend informing patients and guardians about the medication side effects, necessity to discontinue the medication immediately and informing their physician if they develop pruritic rash, jaundice, acolic stools or dark urine, arthralgias, abdominal pain, nausea, fatigue, fever or pharyngitis. Some endocrinologists recommend written instructions and re-emphasis at clinical follow up visits.
If the granulocyte count is normal, antithyroid drug treatment may be restarted. If the granulocyte count is low but not meeting criteria for agranulocytosis, neutrophil counts usually recover spontaneously within one to two weeks . ATD treatment can cross the placenta and have an increased risk of birth defects if continued during pregnancy. Hence, this prospect should be discussed with adolescent females of reproductive age.
PTU leads to malformations of the face and neck. Both drugs are associated with urinary tract malformations . Because MMI does not result in teratogenic effects after first trimester compared to PTU and theoretically reduced risk of placental transport, which causes severe hepatotoxicity, it is consensus to use PTU to treat maternal hyperthyroidism during the first trimester of pregnancy, and to switch to MMI for the remainder of the pregnancy .
Role of beta blockers: Until the signs and symptoms of hyperthyroidism are controlled and euthyroidism is achieved with ATD, beta-blockers such as atenolol or propranolol can be used to counteract symptoms of adrenergic over activity, such as palpitations, tremors or neuropsychological symptoms . Atenolol is preferred for its cardioselective nature.
Therefore, risk of bronchospasm in patients with asthma is reduced as compared with other beta blockers . In addition, it is administered once daily, resulting in better compliance. If remission euthyroid after 1 year of cessation of therapy is not achieved, consider definitive treatment options with radioiodine therapy or surgery . One prospective study suggested that the likelihood of remission could be best predicted by the initial response to antithyroid medication, with achievement of euthyroid state within 3 months.
Younger children and those with high initial thyroid hormone levels were also found to be less likely to achieve remission within 2 years in the prospective study . Radioiodine therapy provides definite treatment for GD. Following oral administration of the radioiodine I, it is actively taken up by the hyperactive gland and leads to an intense radiation thyroiditis, progressive interstitial fibrosis and glandular atrophy and hence, results in hypothyroidism.
It could result in transient increase in thyroid hormone levels with possible worsening of thyrotoxic symptoms including thyroid storm due to the release of the preformed hormone due to the acute gland destruction.
Also, can worsen GO if present prior to the treatment with radioiodine . Pediatric patients, who are not candidates for ATD, should be offered Radioiodine therapy or surgery. These include patients who failed to undergo remission or had major side effects with ATD. As mentioned above, as per ATA and AACE guidelines, radioiodine treatment is an acceptable therapeutic regimen in children between 5 years of age and older if the appropriate dose of I is administered .
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