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

Common Causes

• Graves disease
• Painless or transient (silent) thyroiditis
• Toxic adenoma (Plummer disease)
• Toxic multinodular goiter
• Postpartum thyroiditis
• Hyeremesis gravidarum
• Subacute granulomatous (de Quervain) thyroiditis
• Drug-induced thyroiditis

Diagnosis

Shown below is an algorithm summarizing the diagnosis of hyprthyroidism according to the American Thyroid Association guidelines. 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. The diagnosis of a thyrotoxic crisis is made entirely on the clinical findings. Most importantly, there is no difference in thyroid hormone levels between patients with "uncomplicated" thyrotoxicosis and those undergoing a thyroid storm.

Clinical assessment of signs & symptoms for hyperthyroidism: Tachycardia Palpitations Anxiety, insomnia Fine tremors in outstretched hands Heat intolerance Diaphoresis Weight loss irregular pulse (in atrial fibrillation) dyspnea orthopnea brisk deep tendon reflexes proximal muscle weakness pretibial myxedema (Graves’ disease) lid lag, lid retraction, decrease lacrimation (thyroid eye disease)

Measure serum Thyroid stimulating hormone levels

Low TSH

High TSH

Mild hyperthyroidism: Serum T4 and T3 values in normal range or only T3 levels are elevated.

Overt hyperthyroidism: Both serum T3 and T4 levels elevated

Elevated serum T4 and T 3 levels

Perform thorough physical examination of thyroid gland and look for signs for thyroid eye disease. Thyroid gland diffusely enlarged with symmetrical hypertrophy and new onset of ocular symptoms

Repeat TSH levels in serial dilution

Yes. Graves' disease

No

Positive

Negative

Measure serum assays of TRAb and radioactive iodine uptake thyroid scan

High TSH levels due to hetrophilic antibodies

Look out for pituitary lesion

Measurement of serum levels of human anti-mouse antibodies

* Perform MRI Brain High ratio of the serum level of alpha subunit of the pituitary glycoprotein hormone

Diffuse increase in iodine uptake

Localized increase in iodine uptake

Subnormal or absent uptake of iodine

Graves' disease

Toxic nodular goiter

Subacute thyroiditis/ Postpartum thyroiditis

Factitious ingestion of thyroid hormones

Excess intake of iodine recently

High levels of thyroglobulin in serum

Low thyroglobulin levels

Measure spot urine iodine or 24 hour urine iodine level

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. Patients who fail medical therapy should be treated with therapeutic plasma exchange or thyroidectomy. The mortality of thyroid storm is currently reported at 10%.

Drug List

Drug	Initial daily dose	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

Template:WikiDoc Sources