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Hyperthyroidism is an endocrine disorder characterized by a hyperactive thyroid gland, leading to elevated levels of free thyroxine (fT4) and free triiodothyronine (fT3) and decreased levels of thyroid-stimulating hormone (TSH). The condition can occur due to dysfunction within the thyroid gland itself, termed primary hyperthyroidism, or it can arise as secondary hyperthyroidism due to abnormal production of TSH by the anterior pituitary gland. Subclinical hyperthyroidism is a term used when TSH levels are low, but free T4 and free T3 levels remain within normal range.

Causes of Hyperthyroidism:

  1. Primary Hyperthyroidism – Graves’ disease, Toxic multinodular goitre, Toxic adenoma, Functioning thyroid carcinoma metastasis.
  2. Secondary Hyperthyroidism – TSH secreting pituitary adenoma, Exogenous intake of thyroid hormone (thyrotoxicosis factitia).
  3. Thyrotoxicosis without Hyperthyroidism – Thyroiditis, Ingestion of excess thyroid hormone.


  1. Nervousness, anxiety and irritability.
  2. Increased sweating and heat intolerance.
  3. Weight loss with increased appetite
  4. Fatigue and weakness especially in the upper arms and thighs.
  5. Sleep disturbances. Difficulty sleeping, insomnia, or frequent awakenings.
  6. Eye symptoms. In Graves’ disease – Lid retraction, exophthalmos, periorbital oedema, proptosis with lid lag (Von Graffe Sign), lid retraction (Dalrymple Sign), conjunctival injection (Goldzeiher’s Sign) and diplopia.
  7. Dermopathy. Pre-tibial myxoedema presents with waxy indurated skin that itches.
  8. Acropathy. Clubbing of the fingers with sub-periosteal new bone formation.


  1. Rapid or irregular heartbeat. Palpitations, tachycardia (rapid heart rate), and atrial fibrillation (irregular heartbeat) are common in the elderly.
  2. Fine trembling in the hands and fingers.
  3. Thin skin and hair.
  4. Muscle weakness especially in the upper arms and thighs.
  5. Gastrointestinal disturbances. Increased frequency of bowel movements or diarrhoea.
  6. Menstrual disturbances. Oligomenorrhoea.


  1. Blood investigations: Thyroid-stimulating hormone (TSH), T4, and T3. Low TSH levels with high T4 and T3 levels indicate hyperthyroidism.
  2. Radioactive iodine uptake (RAIU) test: It measures the amount of iodine, the thyroid gland absorbs from the bloodstream. It helps to determine the cause of hyperthyroidism.
  3. Thyroid scan imaging: It uses radioactive iodine or technetium to identify nodules or areas of increased activity.
  4. Antibody tests: Blood tests for specific antibodies, such as thyroid-stimulating immunoglobulins (TSI), can confirm autoimmune causes like Graves’ disease.

Treatment: The aim is to reduce thyroid hormone synthesis and manage symptoms:

  1. Antithyroid medications: thionamides (Carbimazole 10–20 mg every 8 or 12 hourly and Propylthiouracil 100–200 mg every 6–8 hourly for 4-6 weeks) inhibit thyroid hormone synthesis. They act by blocking the synthesis of T4 and T3 by inhibiting the thyroid peroxidase enzyme, reducing oxidation and organification of iodide. Additionally, Propylthiouracil (PTU) acts by inhibiting the conversion of T4 to T3. Propylthiouracil is reserved for use in pregnancy and thyroid storm.
  2. Radioactive iodine therapy: Radioactive iodine, sodium 131I is taken orally and it selectively destroys hyperactive thyroid cells, reducing hormone production. Oral sodium 131I  is used in Graves’ disease, toxic multinodular goitre and failed thionamides patients. It is contraindicated in pregnancy and breastfeeding. The treatment often leads to permanent hypothyroidism, which requires lifelong thyroid hormone replacement therapy.
  3. Beta-blockers: Medications like propranolol do not reduce thyroid hormone levels but help manage symptoms like palpitations, tachycardia (rapid heart rate), atrial fibrillation (irregular heartbeat), tremors, and anxiety.
  4. Thyroid surgery: Total or near-total thyroidectomy is indicated where medical and radioiodine treatment is not feasible or has large goitres causing compression symptoms. Post-surgery, patients typically require thyroid hormone replacement therapy. Surgery may lead to the rare, potentially life-threatening condition ‘thyroid storm’ due to the liberation of pre-formed thyroid hormone. It accounts for mortality of up to 50%.
  5. Ophthalmopathy: Usually no treatment is required. Artificial tears, paraffin-based eye ointment, and dark glasses can be used. Severe eye complaints, with optic nerve involvement or chemosis resulting in corneal damage, are an emergency ophthalmologist opinion.
  6. Thyroid dermopathy: Usually no treatment is required. Steroid ointment application can be used.
  7. Regular monitoring and follow-up with periodic thyroid function tests for changes in treatment strategy based on their response and any side effects. Lifestyle modifications, such as diet, exercise, and stress, can also support overall well-being and treatment outcomes.

Complications: If left untreated or inadequately managed, hyperthyroidism can lead to several complications:

  1. Heart problems: Rapid heart rate, atrial fibrillation, and heart failure can occur due to prolonged hyperthyroidism.
  2. Osteoporosis: Excess thyroid hormones can lead to weakened bones and increased fracture risk.
  3. Thyroid storm: A rare but life-threatening condition characterized by a sudden and severe increase in thyroid hormone levels, leading to fever, rapid heart rate, delirium, and multi-organ failure.
  4. Eye problems: In Graves’ disease, untreated eye symptoms can progress to vision-threatening complications.

GRAVES’ DISEASE. It is an autoimmune disorder where the immune system produces antibodies that stimulate the thyroid gland to produce excess hormones. It is responsible for 60–80% of hyperthyroidism cases. It manifests with hyperthyroidism symptoms and goiter (enlarged thyroid gland), and predominantly affects women (5:1 to 10:1 ratio compared to men). Genetic and environmental factors influence its development. Graves’ disease arises from IgG antibodies targeting TSH receptors. These antibodies stimulate thyroid cells to overproduce thyroid hormones. Diagnosis involves clinical observation of hyperthyroidism symptoms and laboratory tests showing suppressed TSH levels and elevated T4 levels. Additionally, Graves’ disease can lead to extrathyroidal manifestations like ophthalmopathy (swelling of the extraocular muscles, proliferation of periorbital fat and late fibrosis leading to muscle tethering).

TOXIC MULTINODULAR GOITER (MNG). Occurring primarily in older individuals, toxic MNG arises when multiple thyroid nodules independently produce excess thyroid hormone. Cardiovascular symptoms such as palpitations, atrial fibrillation, and other tachyarrhythmias are common. Treatment options include radioiodine therapy or surgical intervention.

SOLITARY TOXIC ADENOMA. This benign tumour suppresses pituitary TSH secretion, resulting in elevated T3 and T4 levels. Radionuclide scanning helps differentiate it from toxic MNG and Graves’ disease. Treatment typically involves radioiodine therapy or surgical removal.

THYROIDITIS. The various types of thyroiditis share similarities primarily in their histological characteristics, while their etiologies vary significantly, spanning from infectious to autoimmune origins.

Causes of Thyroiditis:

  • Acute thyroiditis
    1. Bacterial infection: Staphylococcus, Streptococcus
    2. Fungal infection: Aspergillus, Candida, Coccidioides
    3. Radiation thyroiditis after 131I treatment
    4. Amiodarone (may also be subacute or chronic)
  • Subacute thyroiditis
    1. Viral (or granulomatous) thyroiditis
    2. Silent thyroiditis (including postpartum thyroiditis)
    3. Mycobacterial infection
    4. Drug-induced (interferon, amiodarone)
  • Chronic thyroiditis
    1. Autoimmunity: focal thyroiditis, Hashimoto’s thyroiditis
    2. Riedel’s thyroiditis
    3. Parasitic thyroiditis: echinococcosis, strongyloidiasis
    4. Traumatic: after palpation

(i) Acute thyroiditis – A suppurative infection of the thyroid gland characterizes acute thyroiditis. Patients present with thyroid pain, often radiating to the throat or ears, accompanied by a small, tender goitre that may appear asymmetric. Other common symptoms include fever, dysphagia, erythema over the thyroid, systemic symptoms of a febrile illness, and lymphadenopathy. Treatment usually involves appropriate antibiotics, drainage of abscess, antirheumatic drugs and local treatment with cooling.

(ii) Subacute thyroiditis – Subacute thyroiditis primarily results from a viral infection of the thyroid gland. Initially, there is an elevation in T4 and T3 levels with a concurrent decrease in TSH levels (hyperthyroidism). However, as the disease progresses, the thyroid becomes depleted of stored thyroid hormone, leading to a phase of hypothyroidism characterized by decreased T4 and T3 levels and increased TSH levels. Patients typically present with symptoms of thyrotoxicosis or hypothyroidism along with a painful and enlarged thyroid gland accompanied by fever. Treatment options include aspirin (e.g., 600 mg every 4–6 hours) or NSAIDs for pain relief. In severe cases, steroid therapy tapered over 6–8 weeks may be necessary to alleviate symptoms.

(iii) Silent Thyroiditis: This form of thyroiditis is similar to subacute thyroiditis but lacks the severe pain and tenderness in the thyroid gland. It often starts with symptoms of hyperthyroidism and may progress to hypothyroidism before resolving on its own.

(iv) Chronic thyroiditis. – The most common cause of chronic thyroiditis is Hashimoto’s thyroiditis and Riedel’s thyroiditis, is characterized by persistent inflammation of the thyroid gland. Riedel’s thyroiditis typically affects middle-aged women and manifests as an insidious, painless goitre with compressive symptoms. The goitre is usually hard, non-tender, often asymmetric, and fixed, raising concerns for malignancy. Treatment may involve an open biopsy followed by surgical intervention to relieve compressive symptoms.

(v) Postpartum Thyroiditis: Occurring in some women after childbirth, postpartum thyroiditis involves inflammation of the thyroid gland. It can initially cause hyperthyroidism followed by hypothyroidism, typically within the first year after giving birth. Most women recover normal thyroid function within 12 to 18 months, but some may develop permanent hypothyroidism.

THYROTOXIC STORM also known as thyroid crisis is a rare condition. It is an exacerbation of hyperthyroidism, characterized by a spectrum of symptoms including fever, delirium, seizures, coma, vomiting, diarrhoea, and jaundice. The mortality rate associated with cardiac failure, arrhythmia, or hyperthermia escalates up to 50%, notwithstanding prompt treatment interventions. Typically, thyrotoxic crisis manifests following acute medical conditions (e.g., stroke, infection, trauma, diabetic ketoacidosis), surgical procedures (particularly those involving the thyroid gland), or radioiodine therapy administered to patients with inadequately managed hyperthyroidism.


  1. Identification and addressing of the precipitating factor.
  2. Loading dose of propylthiouracil (500–1000 mg) followed by 250 mg every 4 hours.
  3. Methimazole 20 mg every 6 hours (alternative of propylthiouracil)
  4. Propranolol orally 60–80 mg every 4 hours or intravenously at 2 mg every 4 hours for tachycardia and other adrenergic manifestations.
  5. I.V. esmolol to reduce heart rate.
  6. Additional therapeutic measures encompass the intravenous administration of hydrocortisone (300 mg bolus followed by 100 mg every 8 hours) and the initiation of antibiotics if concurrent infection is suspected.

———- End of the chapter ———–

Learning resources.

  • Scott-Brown. Textbook of Otorhinolaryngology Head and Neck Surgery.
  • Harrison’s principles of internal medicine.
  • David J. Terris. William S. Duke. Textbook of Thyroid and Parathyroid Diseases Medical and Surgical Management.
  • Stell and Maran’s. Textbook of Head and Neck Surgery and Oncology.
  • Hans Behrbohm. Textbook of Ear, Nose, and Throat Diseases With Head and Neck Surgery.
  • P L Dhingra. Textbook of Diseases of Ear, Nose and Throat.

Dr. Rahul Bagla ENT Textbook

Dr. Rahul Kumar Bagla

MS & Fellow Rhinoplasty & Facial Plastic Surgery.
Associate Professor
GIMS, Greater Noida, India

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