Thyrotoxicosis is an endocrine disorder characterized by elevated levels of either free thyroxine or triiodothyronine or both with sympathetic overstimulation and a constellation of symptoms involving various organ systems. The diagnosis is based on clinical features, laboratory evaluation of thyroid hormone levels and nuclear scintigraphy.
Thyrotoxicosis is a syndrome caused by either overproduction or excessive release of free thyroxine (T4) and/or triiodothyronine (T3) in the serum. The increased production of thyroid hormones is seen in toxic multinodular goiter, toxic adenoma, struma ovarii and Graves' disease while the excessive release of the hormone is secondary to inflammation or destruction of the thyroid glands e.g. autoimmune diseases, radiation, infection, chemical or mechanical injury. Increased intake of thyroid medication leads to factitious thyrotoxicosis.
Thyrotoxicosis occurs more frequently in women with Graves' disease presenting between the age of 20 and 40 years . Toxic nodular goiter is prevalent amongst older adults and in individuals with low levels of iodine in their diet while autoimmune thyrotoxicosis is seen more often in those who smoke .
Typical manifestations of overt thyrotoxicosis are anxiety, palpitations, intolerance to heat, myopathy, asthenia, menstrual irregularities in women, tremors , excessive sweating, exophthalmos, tachycardia  and diffuse thyromegaly. Orbital involvement with protrusion of the eyeballs, diplopia, and dryness is noted in one-third of the patients with Graves' disease . Sympathetic overstimulation and related symptoms like anxiety and tremors are found mostly in young thyrotoxic patients while the incidence of dyspnea, cardiac arrhythmias, atrial fibrillation (AF) and heart failure is higher in older patients .
Patients with subclinical thyrotoxicosis can present with non-specific symptoms although they have a higher risk of atrial fibrillation compared to patients with overt thyrotoxicosis.
Entire Body System
All study drug-related adverse events were mild and included headache and fatigue for sorafenib, and headache, increased alanine aminotransferase and glutamate dehydrogenase, fatigue, and nervousness for levothyroxine. [ncbi.nlm.nih.gov]
[…] recall: thyroid metabolism, so everything is revved up: Hyperactivity, Irritability, Dysphoria, Insomnia *Heat Intolerance, Sweating Palpitations Fatigue, Weakness Weight Loss, Hyperphagia, Frequent bowel movements Oligo- or amenorrhea Tremor, Insomnia [quizlet.com]
- Failure to Thrive in Infancy
BACKGROUND: Thyroid dysfunction can induce developmental delay and failure to thrive in infancy. Congenital hypothyroidism is one of the common causes of these symptoms in infancy. [ncbi.nlm.nih.gov]
Noncompliance with treatment was a major trigger in previously diagnosed patients, followed by infection. The mortality rate was 25% in this series. [ncbi.nlm.nih.gov]
Dermatological causes: primary, idiopathic hyperhidrosis Psychoautonomic causes: physical and emotional stress (e.g., hypoglycemia, agitation, anxiety ) Endocrinological causes Hyperthyroidism Menopause, pregnancy Pheochromocytoma Cushing's syndrome [amboss.com]
Beta-blockers : The indications include tachycardia and supraventricular arrhythmias, eyelid retraction, tremor, and hyperhidrosis. If antithyroid drugs alone are effective, beta-blockers are not required. [empendium.com]
- Flaccid Paralysis
We describe the development of acute hypokalemic paralysis in a middle-aged Caucasian man with recently diagnosed thyrotoxicosis and severe, active Graves' opthalmopathy who developed progressive flaccid paralysis 12 hours following intravenous administration [ncbi.nlm.nih.gov]
- Cerebellar Sign
The assessment demonstrated marked cerebellar signs on examination but no other neurological deficit. [ncbi.nlm.nih.gov]
On Day 10 of hospitalization, she developed ataxia, aphasia, and somnolence. Cranial magnetic resonance imaging showed increased bilateral thalamic signalization. [ncbi.nlm.nih.gov]
The workup in thyrotoxicosis comprises of a thorough history of the symptoms, their onset, duration, progress, whether residing in iodine deficient regions, dietary and medication intake, exposure to toxic radiation/chemicals, family and occupational history. Patients with Graves' disease may provide a family history of autoimmune disorders like rheumatoid arthritis or vitiligo. Physical examination is likely to show a single thyroid nodule or a multinodular goiter  with resting tachycardia, visible pulsations, myxedema and skin changes. On palpation there may be thyroid tenderness in patients with thyroiditis and auscultation may reveal a bruit. Ophthalmopathy features are rarely noticed in toxic nodular goiter but are a frequent finding in Graves' disease .
Laboratory tests include complete blood cell count, serum thyroid-stimulating hormone (TSH), free thyroxine (FT4), free triiodothyronine (FT3) levels and tests for specific autoantibodies if autoimmune etiology is suspected. TSH levels are diminished in overt as well as subclinical thyrotoxicosis while FT4 and/or FT3 levels are elevated only in case of overt thyrotoxicosis. Only T3 levels may be elevated in mild thyrotoxicosis.
A radioactive iodine uptake or scintigraphy scan is indicated if the cause of thyrotoxicosis is not revealed by either history or examination . It provides a differential diagnosis and helps in the subsequent treatment of the patient      . Increased uptake is seen in Graves' disease, toxic nodular goiter, and toxic multinodular goiter while low uptake is seen in thyroiditis.
If scintigraphy is contraindicated, then color doppler ultrasonography can be performed for diagnosing thyrotoxicosis  and will show increased vascularity in most cases. Ultrasonography, if performed shows a normal sized gland or moderate thyromegaly in Graves' disease.
An electrocardiogram is obtained to detect AF while more tests can be ordered if indicated by clinical findings and laboratory studies.
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- Rosario PW, Santos JB, Nunes NS, et al. Color flow Doppler sonography for the etiologic diagnosis of thyrotoxicosis. Horm Metab Res. 2014 Jun; 46 (7):505-9.