Tirotoxicosis por t3 pdf

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Serum thyroglobulin levels can be obtained to differentiate thyro- toxicosis from factitious thyroid disease. Autoantibodies can be obtained to determine the type of autoimmune disease that is present. Imaging studies can be performed to elucidate the specific cause of hyperthyroidism, but these tests are generally not prac- tical or warranted in the emergency department.

Ultrasonography with Doppler flow can be used when radiation exposure is con- traindicated, as in pregnancy and breastfeeding. In addition, the use of iodinated contrast studies should be avoided in thyrotoxicosis given that additional iodine sub- strate can increase serum thyroid levels. When the gland is hyperactive, more T3 than T4 is pro- duced.

Subacute and painless thyroiditis causes release of pre- formed hormone but does not generate new thyroid hormone, so the ratio of T3 to T4 is less than Therapy for thyrotoxicosis depends on the underlying cause. Treatment strategies include antithyroid drugs, radioactive iodine, thyroid surgery, and medications for symptom control Table 3. MMI dosage is 10 to 30 mg per day in once-daily dosing.

PTU dosage is to mg per day divided 2 to 3 times per day. Thyroid function tests are repeated every 4 weeks during initial medication management so dosages can be adjusted accordingly. More than one-third of patients go into remis- sion for 10 years or longer after starting antithyroid medication. Common adverse ef- fects of thionamides include abnormal taste, pruritus, urticaria, fever, and arthralgia. Less commonly, patients develop cholestatic jaundice, thrombocytopenia, lupuslike syndrome, hepatitis, and agranulocytosis.

It is the most common form of therapy for adults with Graves disease. Ther- apy is provided by a single oral dose of radioactive iodine that is absorbed by the thy- roid gland and causes organ-specific inflammation. Thyroid fibrosis and tissue destruction occur gradually over several months. The major drawback to radioactive iodine is hypothyroidism, which is an expected complication requiring lifelong L-thyroxine replacement therapy. Hypothyroidism occurs within 4 to 12 months of therapy.

Radioactive iodine therapy does not require hospitalization and is noninva- sive. The thyroid is the only tissue capable of absorbing the iodine so side effects are minimal. Iodine therapy is contraindicated in pregnancy, breastfeeding, and in pa- tients with severe ophthalmopathy. Thyroid surgery is rapid and effective but invasive and expensive. Patients need to be euthyroid before surgery. It can cause permanent hypothyroidism and transient hy- pocalcemia requiring calcium supplementation.

Surgical complications include recur- rent laryngeal nerve damage and permanent hypoparathyroidism. Because of the efficacy of antithyroid medication and radioactive iodine therapy, surgery is performed less frequently. It is generally reserved for pregnant women intolerant of thionamides, children with severe disease, severe ophthalmopathy, amiodarone-induced refractory disease, or unstable cardiac conditions.

Thyroid storm during surgery is exceedingly rare now with preoperative therapies including propranolol, antithyroid medication, and iodine. Symptom control can be achieved with a variety of medications. The American Thyroid Association with the American Association of Clinical Endocrinologists published guidelines for the management of hyperthyroid symptoms.

The use of propranolol, atenolol, and metoprolol has been shown to decrease heart rate, systolic blood pressure, muscle weakness, and tremor, and to improve irritability and emotional lability. The calcium channel blockers verapamil and diltiazem have been shown to decrease heart rate in patients for whom b-blockers were contraindi- cated, but can cause profound hypotension and should be used cautiously.

Treatment of subacute thyroiditis is initially aspirin or other nonsteroidal antiinflam- matory medication. Some patients require glucocorticoid therapy given as a once- daily burst for 1 week and then tapered over 4 weeks.

The thyrotoxicosis typically resolves spontaneously and no further treatment is needed. Subacute thyroiditis should not be treated with antithyroid medication from the emergency department. Antithyroid medications and b-blockers are the primary treatment of thyrotoxicosis during pregnancy. Surgery is reserved for women who are unable to tolerate antithyroid medication.

How- ever, MMI has been associated with scalp defects when used in the first trimester. Therefore, a woman with hyperthyroidism who desires pregnancy should be started on PTU and can be switched to MMI if desired after 12 weeks gestation. Children and adolescents with hyperthyroidism can be treated with antithyroid medication, radioactive iodine, or surgery as clinically indicated.

Almost all children requiring antithyroid medication should be treated with MMI. Before initiating therapy, children should have baseline complete blood count and liver function tests.

Although MMI has better safety profile than PTU, it is associated with adverse risks including allergic reactions, rashes, myalgias, arthralgias, and rarely agranulocytosis. PTU is associated with hepatoxicity and subsequent liver failure.

Its use is contraindicated in children. There have been case reports of fatal fulminant hepatic necrosis. Neonatal thyrotoxicosis is almost uniformly a result of maternal Graves disease and the subse- quent transplacental passage of maternal thyroid-stimulating antibodies.

As a result, hyperthyroidism is usually self-limited because antibodies decline by 3 to 4 months of age. Treatment typically involves symptomatic care see Table 3.

Thyroid storm is a life-threatening hypermetabolic state with significant morbidity and mortality. Medication management is directed at controlling the overactive thyroid gland and blocking peripheral effects of thyroid hormones see Table 3. These patients are typically critical and should have rapid placement of large-bore intravenous access, supplemental oxygen, and cardiac monitoring.

Aggressive volume resuscitation should be started immediately with the exception of patients with concomitant heart failure, in which case use of fluids should be judicious. Because cardiovascular collapse is often the cause of decompensation, b-blockers should be initiated first. The initial b-blocker should be propranolol with esmolol infusion as an alternate choice. High- dose steroid should be given early to help augment vascular tone. PTU is the preferred medication for thyroid storm because it also decreases peripheral conversion of T4 to T3.

The initial loading dose for PTU is to mg, then mg every 4 hours. MMI can be given as 20 mg every 4 hours. Thionamides are effective at inhibiting synthesis of new thyroid hormone but are ineffective at decreasing preformed stored hormones.

Iodine and lithium are effective at blocking release of preformed hormones from the thyroid gland. Iodine should be given 1 hour after PTU or MMI to reduce the risk of increasing thyroid hormone pro- duction by providing more substrate. Salicylates should be avoided because they can increase free thyroid hormone levels by decreasing thyroid-binding protein in the serum.

If an underlying infectious cause is suspected early broad-spectrum antibiotics must not be forgotten and should be started as early as possible. Patients with refractory life- threatening symptoms can undergo hemodialysis if medical management is ineffective. Patients with thyroid storm require admission to the intensive care unit. Patients with symptomatic thyrotoxicosis may require inpatient admission if initial therapy in the emergency department fails to normalize vital signs, if symptoms are severe, or if the patient does not have adequate follow-up.

Patients requiring antithyroid medica- tion who are stable for discharge should be referred to the endocrinology clinic for further evaluation and medication management. Patients with subacute thyroiditis should not be started on antithyroid medication and can followed up with endocri- nology for further evaluation and management.

Thyroid storm has a broad differential. Keep the following in mind: a. Acute pulmonary edema b. Heat stroke c. Malignant hyperthermia d. Sympathomimetic overdose f. Serotonin syndrome g. Tachyarrhythmias 2. The classic triad of thyroid storm is high fever, exaggerated tachycardia out of proportion to fever, and central nervous system dysfunction or cerebral encephalopathy.

Wait at least 1 hour after antithyroid medication before giving iodide or serum thyroid hormone levels may inadvertently be increased, exacerbating the issue. Plasmapheresis, charcoal hemoperfusion, and plasma exchange can be used to rapidly decrease thyroid hormone levels in refractory cases. Do not use aspirin or other salicylates for fever control in thyroid storm because they can increase serum hormone levels. Be careful with b-blockers in patients with concomitant thyroid storm and heart failure.

Hyperthyroidism and thyrotoxicosis are hypermetabolic conditions that cause signif- icant morbidity and mortality. The diagnosis can be difficult because symptoms can mimic many other disease states leading to inaccurate or untimely diagnoses and management. Thyroid storm is the most severe form of thyrotoxicosis, hallmarked by altered sensorium, and, if untreated, is associated with significant mortality. Hyperthyroidism and other causes of thyrotox- icosis: management guidelines of the American Thyroid Association and Amer- ican Association of Clinical Endocrinologists.

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