Thyrotoxicosis

Thyrotoxicosis

1. Thyrotoxicosis Dr.Sundarprakash Sivalingam Associate Professor in surgery

2. Definition Thyrotoxicosis is the biochemical and clinical complex that results when the tissues are presented with excessive quantities of the thyroid hormones.

3. Classification Primary thyrotoxicosis Graves disease Diffuse toxic goiter 2. Secondary thyrotoxicosis Plummer’s disease 3. Toxic nodule 4. Other causes

4. Causes of hyperthyroidism Graves disease (Primary Thyrotoxicosis) Thyrotoxicosis in Multinodular goitre (Secondary Thyrotoxicosis) Toxic adenoma Thyroiditis Subacute Lymphocytic Drug induced Thyrotoxicosis factitia Jod Basedow thyrotoxicosis — Iodide induced Autoimmune thyroiditis or de Quervain’s thyroiditis . Neonatal thyrotoxicosis . Struma ovarii . Drugs like amiodarone

5. Primary thyrotoxicosis Graves' disease an autoimmune disorder caused by thyroid-stimulating antibodies directed at the TSH on follicular cells.

6. Pathogenesis The exact cause of Grave’s disease is unknown but several immunological phenomena have been observed. There is an increased frequency in HLA B8-DR3 in Caucasians with this disease. A circulating antibody, which stimulates the TSH receptors mimicking all effects of TSH is the patho­genetic event in Graves' disease. The thyroid gland is diffuse and smoothly enlarged with an increased vascularity. On microscopy, the epithelium is tall (columnar) with minimal colloid present. Prominent infoldings of hyperplastic epithelium. Lymphocytic infiltration may be seen in the thyroid.

7. Clinical Features Symptoms :- Hypermetabolism :- heat into­lerance excessive sweating hunger weight loss. Adrenergic discharge:- nervousness emotional lability insomnia tremors psychosis Cardiac:- Dyspnea palpitations enhancement of angina pectoris cardiac failure Gastrointestinal:- diarrhea Increased appetite Muscular:- Proximal muscle weakness Menstruation:- oligomenorrhea and amenorrhea and abortions or failure to conceive .

8. Examination Patient appears anxious, restless and fidgety. Warm skin Moist palm The hair is fine and silky. A fine tremor of the fingers and tongue is characteristic. Cardiovascular manifestations wide pulse pressure tachycardia atrial arrhythmias systolic murmurs cardiomegaly sometimes heart failure. Splenomegaly also may be present. A diffusely enlarged thyroid gland is seen. A bruit is generally present over the gland signifying that the patient is thyrotoxic . Skin Dermopathy is uncommon and usually occurs over the dorsum of the legs or feet and is termed pretibial myxedema. The affected area is raised, thickened and may be hyperpigmented .

9. Eye signs "DR Joffroy may validate symptoms" Dalrymple sign:- rim of sclera is seen all around the cornea, on looking straight forward. Rosenbach's sign:- fine tremor of the upper eyelids on slight closure of the eye. Joffroy's  sign:- lack of wrinkling of the forehead when a patient looks upward. Moebius sign:- lack of convergence on looking to near object. Von Graefe's sign (lid lag sign):- lagging of the upper eyelid on looking downward without movinh the head. Stellwag's sign:- staring look with infrequent blinking.

10. Toxic Multinodular Goiter (Plummer's Disease) Toxic multinodular goiter is a consequence of long­standing simple goiter. Commonly seen in endemic areas. The transition from nontoxic to toxic nodule involves the development of functional autonomy, i.e. some nodules become independent of TSH stimulation. In both endemic and sporadic goiters, administration of iodides may lead to the development of thyrotoxicosis. Toxic multinodular goiter is a disease of the aging or elderly and is less severe than Graves' disease ( Jod-Basedow phenomenon). An enlarged nodular thyroid is palpable sometimes with compressive symptoms-dysphagia or dyspnea. Cardiovascular involvement is more common and may manifest as arrhythmias (atrial fibrillation) or congestive cardiac failure precipitated by thyrotoxicosis. Weakness and wasting are predominant with loss of appetite. This listlessness of the patient is called apathetic thyrotoxicosis.

11. Toxic Adenoma Autonomously functioning thyroid nodules (AFTN) are nodules that function independently of the normal pituitary-thyroid negative feedback control mecha­nism. Autonomously functioning thyroid nodules usually produce hyperthyroidism and suppress TSH secretion by the pituitary.Hence , the extranodular tissue becomes functionally inactive. Most AFTN become clinically manifest when the diameter exceeds 3 to 4 cm in size.

12. Primary thyrotoxicosis Secondary thyrotoxicosis Etiology—Autoimmune Not autoimmune Enlargement of goiter is diffuse, firm or soft Bosselated or nodular not uniform Onset is abrupt Insidious Hyperthyroidism is usually severe Hyperthyroidism usually mild Cardiac failure is rare Cardiac failure or multiple extrasystole , paroxysmal atrial tachycardia, paroxysmal atrial fibrillation, or persistent atrial fibrillation Eye signs common Except lid lag and retraction other eye signs are not seen No pre-existing goiter Pre-existing nodular goiter for a long duration Usually younger women Usually middle aged or elderly The entire gland is overactive Internodular thyroid tissue is overactive, rarely one or more nodules also may be overactive Presence of bruit Bruit need not be present . It is due to abnormal thyroid stimulating antibodies (TSAb) No such antibodies (it is due to over activity of nodules)   Can be managed by, drugs, radioiodine, and surgery Surgery is the treatment of choice after control of the toxicity Manifestations not due to hyperthyroidism pretibial myxedema may occur Not seen

13. Other Varieties of Thyrotoxicosis Thyrotoxicosis factitia :- It results from ingestion of large amounts of thyroid hormone. The syndrome is usually seen in women with underlying psychiatric disorder and in hospital personnel. Trophoblastic Tumor :- Patients with choriocarcinoma or hydatidiform mole frequently display eleva­tions of serum total and free T. and T 3 concen­trations. A circulating thyroid stimulator of tropho­blastic origin, possibly hCG , causes thyroid hyperfunction . Ectopic thyroid tissue with widespread functioning metastasis of thyroid carcinoma or struma oveaii may occasionally give rise to thyrotoxicosis.

14. Investigations Thyroid function tests Ultrasound of thyroid Radio-iodine uptake study Thyroid antibodies

15. Treatment Medical therapy Radioiodine ablation Surgery

16. Medical Therapy Antithyroid drugs Carbimazole (CBZ) Methimazole propyl­thiouracil (PTU) belonging to the thioureas group also blocks the conversion of T 4 to T 3 in the peripheral tissues. PTU is started at a dose of 100 mg CBZ at a dose of 10 to 20 mg thrice daily. Most patients become euthyroid within 4 to 8 weeks of therapy. The dose is then reduced to a maintenance dose.

17. Iodides It is the fastest acting thyroid inhibitor. It reduces iodide transport, oxidation and organification and to block the release of T 4 and T 3 from the thyroid gland. The preparations used include Lugol's iodine (3 to 5 drops thrice daily). 5% sol has 5% iodine and 10% pot iodide. The major use of iodide is in preoperative preparation and in the management of thyrotoxic storm. Beta-blockers block beta-adrenergic receptors and provide relief from symptoms like tremors, palpitations, anxiety and heat intolerance. decrease the heart rate, cardiac output and oxygen consumption in thyrotoxicosis. The drugs used are propranolol (40 to 180 mg/day) or atenolol (25 to 100 mg/day). contraindicated in patients with congestive cardiac failure, asthma and diabetes.

18. Radioiodine Therapy Radioiodine is simple and economical therapy. Indicated in patients above 40 years, especially those who fail to respond to antithyroid drugs and failures of surgery. Contraindicated during pregnancy and lactation and in severe thyrotoxicosis or in patients with large or malignant thyroids. A dose that will deliver about 5,000 to 8000 rads to the thyroid will be effective in ameliorating the hyperthyroidism in Graves' disease. The patients should be euthyroid prior to radioiodine therapy to prevent thyroid storm. Thyroid function gradually declines beginning in 2 to 3 weeks. The main draw­backs are hypothyroidism, risk of carcinogenesis, and teratogenicity after the use of radioiodine, though the precise likelihood of the latter two remain contentious.

19. Surgical Therapy The objective of thyroidectomy is complete and per­manent control of thyrotoxicosis. The patients should be euthyroid before operation, with antithyroid drugs that should be continued up to the day of surgery. Lugol's iodine, in the preoperative preparation, will reduce the vascularity of the gland. The preparation is necessary to reduce the risk of thyroid storm. Subtotal thyroidectomy is commonly performed leaving 4 to 8 gm of residual thyroid tissue. Total thyroidectomy should be considered in patients with infertility and Graves' disease with coexisting eye disease.

20. Complications of surgery Postoperative hemorrhage leading to the develop­ment of tension hematoma and respiratory distress. Respiratory obstruction caused by laryngeal edema, Recurrent laryngeal nerve injury. Hypoparathyroidism that may be temporary or permanent. Thyrotoxic storm. Hypothyroidism. Wound problems-infection and keloid.

21. Thyrotoxic Crisis (or Thyroid Storm) A thyroid storm is a life-threatening situation rarely encountered nowadays owing to the good preope­rative preparation for thyrotoxicosis. It may be noticed after operation when the patient has tachycardia, fever, and mental confusion. Dehydration from vomiting and fever be present and may progress on to coma. It may also occur in medical conditions like infection, trauma or radiation thyroiditis. Treatment The patient is treated in the acute phase with a fluid replacement, anti-thyroid drugs, beta blockers and Lugol's iodine through a nasogastric (NG) tube. They should also receive steroids. Sedation and correction of hyperpyrexia are important.