Hyperthyroidism resident survival guide

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Pervaiz Laghari, MD[2]

Overview

Hyperthyroidism and thyroid storm are disease states that result from thyroid hormone-induced hypermetabolism. The excess thyroid hormone is released from the thyroid gland as a result of excess thyroid hormone production, or by processes that disrupt the follicular structure of the gland with subsequent release of stored hormone . Most patients with severe hyperthyroidism present with a dramatic symptom constellation. Hyperthyroidism's typical symptoms include palpitations,heat intolerance, increased bowel movement frequency tremor, anxiety, weight loss despite normal or increased appetite and shortness of breath.Goiter is commonly found on physical examination.

Specific organ systems

Cardiovascular	Heart rate is increased,Systolic hypertension ,pulse pressure is widened, congestive heart failure, Atrial fibrillation
Neuropsychiatric	Anxiety, tremor, restlessness, irritability,insomnia,psychosis, agitation,depression, seizures
Respiratory	Dyspnea, tracheal obstruction, exacerbate underlying asthma,Pulmonary arterial systolic pressure is increased
Gastrointestinal	Weight loss,hyperphagia,hyperdefecation and malabsorption
Skin	Sweating,Onycholysis,Hyperpigmentation,Thinning of the hair
Eyes	Stare and lid lag, ophthalmopathy.
Genitourinary	Urinary frequency and nocturia
Hematologic	normochromic, normocytic anemia
Neck	Thymic enlargement
Bone	osteoporosis and an increased fracture risk

Causes

Life Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

• Thyroid storm 1
• Life threatening cause 2
• Life threatening cause 3

Common Causes

• Amiodarone
• Graves’ disease
• Thyroiditis
• Toxic multinodular goiter
• Toxic nodular goiter
• Iatrogenic

Diagnosis

Serum TSH measurement has the highest sensitivity and specificity of any single blood test used in the evaluation of suspected thyrotoxicosis and should be used as an ini-tial screening test . However, when thyrotoxicosis is strongly suspected, diagnostic accuracy improves when aserum TSH, free T4, and total T3 are assessed at the initial evaluation. Serum TSH levels are considerably more sensitive than direct thyroid hormone measurements for assessing thyroid hormone excess. In overt hyperthyroidism, serum free T4,T3,or both are elevated, and serum TSH is subnormal (usually<0.01mU/L ina third-generation assay). In mild hyperthyroidism, serum T4 and free T4 can be normal, only serum T3 may be elevated, and serum TSH will be low or undetectable

Check TSH level

High TSH

Low TSH

High Free T4

High Free T4

Normal Free T4

Secondary hyperthyroidism

Primary hyperthyroidism

Subclinical hyperthyroidism

Pituitary imaging

Treatment

Thyroid storm may lead to irreversible cardiovascular collapse and death if proper treatment is not initiated in the Emergency Department. For patients with clinical features of thyroid storm,we start immediate treatment with a beta blocker And then either 200 mg of propylthiouracil (PTU) every four hours or methimazole (orally 20 mg every four to six hours). PTU is preferred over methimazole due to the effect of PTU to decrease the conversion from T4 to T3. Iodine administration should be postponed for at least one hour after administration of thionamide to prevent the iodine from being used as a substrate for new hormone synthesis. We also administer glucocorticoids (hydrocortisone, 100 mg intravenously every eight hours) in patients with thyroid storm clinical features.Supporting therapy and the detection and treatment of any precipitating factors ( e.g. infection) in addition to specific thyroid therapy can be vital to the eventual outcome.The infection needs to be detected and treated, and the aggressive correction of hyperpyrexia is required. Acetaminophen should be used instead of aspirin, as the latter will increase concentrations of serum-free T4 and T3 by interfering with protein binding.

Once clinical improvement is shown, iodine therapy may be discontinued and glucocorticoids may be tapered and discontinued.Beta blockers can be stopped but only after the tests on thyroid function have returned to normal.To maintain the euthyroidism, the dosage of thionamides should be titrated. PTU should be changed to methimazole due to the improved safety profile of methimazole and higher compliance rates.

Drug List

Drug	Initial daily dose, target dose (mg)	Mechanisim of action
Beta blocker	Propranolol 60 to 80 mg orally every four to six hours,	Control the symptoms and signs
Thionamide	PTU 200 mg every four hours or methimazole,20 mg orally every four to six hours	Block new hormone synthesis
Iodine	(Lugol's) solution, 10 drops (6.25 mg iodide/iodine per drop [0.05 mL]) three times daily	Block the release of thyroid hormone
Glucocorticoids	Hydrocortisone, 100 mg intravenously every eight hours	Reduce T4-to-T3 conversion, promote vasomotor stability, possibly reduce the autoimmune process in Graves' disease, and possibly treat an associated relative adrenal insufficiency
An iodinated radiocontrast agent	0.5 to 1 g once daily.	inhibit the peripheral conversion of T4 to T3
Bile acid sequestrants	Cholestyramine,4 g orally four times daily	Decrease enterohepatic recycling of thyroid hormones

Do's

• start immediate treatment with a beta blocker

• Acetaminophen should be used instead of aspirin

• Iodine administration should be postponed for at least one hour after administration of thionamide

• Propranolol, PTU, and methimazole can be administered through a nasogastric tube

Don'ts

• The content in this section is in bullet points.

References

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