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The Thyroid Gland
Tuberculous Adenitis

9


The Thyroid Gland

Dr.Barin Bose MS

Jabalpur Hospital and Research Centre

Jabalpur (M.P.)


Surgical Anatomy The normal gland weighs 20 to 25 Gms. The functional unit is the lobule which is supplied by a single arteriole and consists of 20 to 40 follicles which are lined by cuboidal epithelium. The resting follicle contains colloid in which thyroglobulin is stored.

Embryology The thyroid gland arise as a down growth of a column of cells from the pharyngeal floor between the first and second pharyngeal pouches (later on marked by foramen caecum of the tongue). The column of cell become canalized which becomes the thyroglossal duct which is displaced forward by the developing hyoid bone. Then below the hyoid bone lies slightly to the left side. The duct bifurcates to form the thyroid lobes.

Ectopic Thyroid and anomalies of the Thyroglossal Tract - Some residual thyroid tissue along the course of thyroglossal tract is not uncommon. So thyroid gland can be lingual, cervical, or intrathoracic. Very rarely the whole gland is ectopic.

Lingual thyroid This forms a round swelling at the back of the tongue at the foramen caecum and at times it may represents the only thyroid tissue present. It may cause dysphagia, impairment of speech, respiratory obstruction or haemorrhage. It is best treated by full replacement with thyroxin when it gets smaller, but excision or ablation with radioiodine is sometimes necessary.

Medial Ectopic Thyroid This forms a swelling in the upper part of the neck in Medline. It is often mistaken for a thyroglossal cyst. This may be the only normal thyroid tissue present.

Lateral Aberrant Thyroid There is no evidence that aberrant thyroid ever occurs in a lateral position. Normal thyroid tissue found laterally separate from the thyroid gland, must be considered and treated as a metastasis in a cervical lymph node from an occult thyroid carcinoma.

Thyroglossal Cyst This may be present in any part of thyroglossal tract. The common situations in order of frequency are beneath the hyoid in the region of thyroid cartilage and above the hyoid bone. Such a cyst occupies the midline, except in the region of the thyroid cartilage where the thyroglossal tract is pushed to one side, usually to the left. The swelling moves upwards on protrusion of the tongue as well as on swallowing because of the attachment of the tract to the foramen caecum. A thyroglossal cyst should be excised because infection occurs owing to the fact that the wall contains nodules of the lymphatic tissue which communicates by lymphatic with the lymph nodes of the neck. An infected thyroglossal cyst may often be mistaken for an abscess and incised, which is one way in which a thyroglossal fistula arises.

Treatment Because the thyroglossal tract is so closely related to the body of the thyroid bone, the central part of the hyoid bone must be excised together with the cyst of fistula, to prevent recurrence. Then the thyroglossal tract is traced upwards to the foramen caecum, where the thyroglossal tract is excised along with a core of lingual muscle.

Anatomy The thyroid gland occupies the centre of neck, lying in front and close to the trachea just above the thoracic inlet. The weight of the normal thyroid gland is 25 Gms. The gland has two lobes which are joined together across the midline by a thin isthmus. The gland lies hugging the antro lateral aspect of the trachea from the level of the thyroid cartilage to the 5th or 6th tracheal ring. The thyroid gland can be palpated from behind with the middle and index fingers lying just above the sterno clavicular joint across the trachea. Because of the fascial attachments the gland moves upwards with swallowing and therefore it slides under the examining fingers. The normal gland can be felt in thin necks. It is soft and the tracheal ring can be palpated through it.

Vascular supply Each thyroid lobe is supplied by a superior and an inferior thyroid artery and drained by three veins. The blood supply is very rich in the hyperthyroid state and there is an enormous increase in the volume of blood circulating through the gland.

Structures closely related to the Thyroid gland are

  1. The external laryngeal nerve.

  2. The recurrent laryngeal nerve.

  3. Parathyroid gland.

Physiology The hormones (T3) Tri iodo thyronine and (T4) Tetra

Iodo thyronine or thyroxin is bound to thyroglobulin within the colloid. Synthesis of T3 and T4 within the thyroglobulin complex is controlled by several enzymes in distinct steps

  1. Trapping of inorganic iodine from the blood.

  2. Oxidation of iodine to iodine.

  3. Binding of iodine with tyrosine to form iodo tyrosine.

  4. Coupling of mono iodo tyrosine and di iodo tyrosine to form T3 and T4.

  5. When hormone is required the complex is restored into the cell and thyroglobulin is broken down T3 and T4 are liberated and enters the blood where they are bound to serum proteins albumin, prealbumin and thyroxine binding globulin. A small amount of hormone remains free in the serum.

The metabolic effect of the thyroid hormone are due to unbound free T3 and T4. T3 is quick acting whereas T4 acts more slowly .T3 is more important physiological hormone and is also produced in the periphery by conversion from T4.

Test of Thyroid Function -

  1. Serum thyroid hormones In euthyroid state T3 ,T4 and TSH levels will be within the normal range. Thyroid failure results in depressed T3 and T4 levels with gross elevation of the TSH.

In toxic state the TSH level is suppressed while the thyroxin T4 and tri iodo thyronine T3 are transported in plasma bound to specific proteins ( Thyroxin binding globulin TBG) Only a small fraction of the total (0.03% of T4 and 0.3% of T3 ) is free and physiologically active. The values depend on the level of circulating proteins which are affected by the level of circulating estrogen. Thus pregnant women and those on the oral contraceptive pills have elevated total T3 and T4levels without evidence of toxicity. The free hormone levels are unaffected. Similarly some persons have low levels of TBG secondary to a reduction of serum protein levels due to liver disease the total levels of circulating hormone may be low. For these reasons the free levels are more meaningful. Highly accurate radio immuno assays free T3 and free T4 are now routine . T3 toxicity may be diagnosed by measuring the level of serum T3, although a suppressed TSH levels with normal T4 are suggestive.

  1. Isotope scanning Low dose radio labeled iodine uptake by the thyroid will demonstrate the activity in the whole gland. The test in inappropriate for distinguishing benign from malignant lesion, because majority of cold swelling is benign and some warm swelling will be malignant. The principal value is in the toxic patient with a nodule where a localization of over activity in the gland will differentiate between toxic nodules with suppression of the remainder of the gland and in toxic multi nodular giotre with several areas of increased uptake. Routine isotope scanning is not necessary. Whole body scanning is used to demonstrate metastasis but the patient must have all normally functioning thyroid tissue ablated either by surgery or by high dose of radioactive iodine ablation because thyroid cancer cannot compete with normal thyroid tissue in the uptake of iodine.

  2. Thyroid auto antibodies Serum titer of antibodies against thyroid tissue and thyroglobulin are useful in determining the cause of auto immune thyroid dysfunction and swellings. Auto immune thyroiditis may be associated with thyroid toxicity or thyroid failure. A titer greater than 1: 100 are considered significant but a proportion of patients with histological evidence of auto immune thyroiditis is sero negative.


Hypothyroidism - Thyroid failure of thyroid dysfunction.

(I) Fetal of infantile hypothyroidism causes cretinism Clinical features

  1. Patient is physically and mentally retarded.

  2. Patient has pot belly and umbilical hernia.

  3. Dry and wrinkled skin and Scapulo -Clavicular pad of fat.

(II) Adult Hypothyroidism Cause Myxoedema The term Myxoedema is reserved for severe thyroid failure and not applied to the much commoner mild thyroid dysfunction. The signs of thyroid deficiency are

  1. Bradycardia.

  2. Cold extremities.

  3. Dry skin and hairs.

  4. Periorbital puffiness.

  5. Hoarse voice.

  6. Slow movements.

  7. Delayed relaxation phase of ankle jerks.

Symptoms are

  1. Tiredness.

  2. Mental lethargy.

  3. Cold intolerance.

  4. Weight gain.

  5. Menstrual disturbance.

Treatment Oral thyroxine as a single dose is curative. If rapid response is required tri iodo thyronine may be used.


Auto immune thyroiditis- (1) Chronic lymphocytic thyroiditis.

(2) Hashimoto’s thyroiditis.


Thyroid Enlargement

The normal thyroid gland is impalpable. The term Goitre

(Latin, Guttur = the throat) is used to describe generalized enlargement of thyroid gland. A discrete swelling in (nodule) one lobe with no palpable abnormality else where is termed as solitary thyroid nodule.

Classification of Thyroid swellings

  1. Simple Goitre (Euthyroid)

    • Diffused Hyperplasic.

      1. Physiological.

      2. Pubertal.

      3. Pregnancy.

  • Multi nodular Goitre.


  1. Toxic Goitre

  • Diffused toxic (Graves Disease)

  • Multi nodular toxic Goitre.

  • Toxic adenoma.

  1. Neoplastic (a) Benign.

(b) Malignant.

(4) Inflammatory

  1. Auto immune thyroiditis.

  • Chronic lymphatic Thyroiditis.

  • Hushimoto’s Thyroiditis.

  1. Granulomatous thyroiditis.

    • De quervain’s thyroiditis.

  2. Fibrosing thyroiditis.

  • Riedel’s thyroiditis.

  1. Infective thyroiditis.

  • Bacterial Thyroiditis.

  • Viral Thyroiditis.

  • Sub acute Thyroiditis.

  1. Chronic Thyroiditis Tuberculosis, Syphilis.


Simple Goitre

Causes of Simple nontoxic goitre (1) May develop due to stimulation of thyroid gland by increased secretion of TSH by pituitary adenoma which is rare or in response to a chronically low level of circulating thyroid hormones.(2) The most important factor in endemic goitre is dietary deficiency of iodine.

(3)Genetically determined deficiencies in the enzymes controlling the synthesis of thyroid hormones. (a) if severe result in goiter formation with hypothyroidism , (b) if moderate degree a simple eythyroid goiter results.

When thyroglobulin is broken down by the enzyme dehalogenase into free iodine which is retained within the thyroid gland. If dehalogenase is deficient iodo tyrosine pass into the blood and is excreted in the urine and this result in iodine deficiency and goitre formation.

Goitrogens Are substances that cause enlargement of thyroid gland. These are vegetables of brassica family e.g. Cabbage which contains thiocyanate, drugs such as Para amino salicylic acid (PAS) and of course the anti thyroid drugs, thiocyanate and per chlorates interfere with iodine trapping. Carbimazole and thiouracil compound interfere with the oxidation of iodine and binding of iodine to tyrosine.

Natural History of Simple Goitre Stages of goitre formation are

    1. Persistent growth stimulation causes diffuse hyperplasia , all lobes are composed of active follicles and iodine uptake is uniform . This is a diffused hyper plastic Goitre , which may persists for a long time but is reversible if stimulation ceases

    2. Later as a result of fluctuating stimulation a mixed pattern develops with area of active lobules and area of inactive lobules.

    3. Active lobules become more vascular and hyperplasic, haemorrhage occur causing central necrosis and leaving only a surrounding ring of active follicles.

    4. Necrotic lobules coalesce to form nodules filled with iodine free colloid.

    5. Repetition of this process results in nodular goitre. Most nodules are inactive and active follicles are present only in internodular tissue.

Diagnosis All types of goitre are more common in the female than in the male . Simple goitre is commonly seen in girls approaching puberty. Both multi nodular and solitary nodular Goitre well as colloid goitre are found in women of 20 to 40 years. The patient is euthyroid, the nodules are palpable and often visible, they are smooth firm and not hard. The goitre is painless and moves freely on swallowing. Hardness and irregularity due to calcification may simulate carcinoma. A sudden appearance of painful nodule or rapid enlargement of a nodule raises suspicion of carcinoma but is usually due to haemorrhage into nodule.

Investigation Test of thyroid function may be necessary to exclude mild hyper thyroidism.Estimation of of thyroid antibodies to differentiate from Hashimoto’s goitre.

Plain X Ray neck may show calcification and tracheal deviation or compression.

Complication (1) Tracheal obstruction due to compression of trachea in a lateral or anterior posterior plane. Acute respiratory obstruction may follow haemorrhage into a nodule impacted in thoracic inlet.

(2) Secondary Thyrotoxicosis Many patients with nodular goitre develop hyperthyroidism sooner or later. Figures as high as 30% has been suggested.

(3) Carcinoma Malignant conversion is uncommon, an incidence of

5 to 8% has been suggested.

Preventions and treatment of Simple Goitre All table salts should be iodised (Potassium iodide 1 part in 10,000 parts). In endemic areas the incidence of goitre the incidence of goitre has been strikingly reduced with this prophylactic measure. In the early stage hyper plastic Goitre is reversible if thyroxin is given. If regression does not occur thyroidectomy may be indicated.

Nodular stage of simple goitre is irreversible. A multi nodular goitre is uncomfortable, unsightly and in a view of complication subtotal thyroidectomy and leaving 8 gms of normal thyroid tissue in each lobe. If causative factors persist, recurrence is likely, unless further TSH stimulation is prevented. 0.1 mg to 0.2 mgs of l thyroxine a day should be given post operatively to all patients.


Toxic Goitre

The term Thyrotoxicosis is retained because hyperthyroidism i.e. symptoms due to raised levels of circulating thyroid hormones is not responsible for all manifestations of the disease.

Clinical Types

    1. Diffused toxic goitre.

    2. Toxic nodular goitre (Graves disease).

    3. Toxic solitary thyroid nodule.

    4. Hyper thyroidism due to rare cause.

Symptoms -

Thyrotoxicosis is 8 times more common in female than in males.

It may occur at any age. The most significant symptoms are loss of weight inspite of good appetite, preference for cold and palpation.

The most significant signs are the excitability of the patient, presence of goitre, exopthalmos, tachycardia or cardiac arrhythmia.

Primary Thyrotoxicosis the Goitre is diffused and vascular, it may be larger or small, firm or soft and a thrill and bruit may be present usually at the upper poles over the superior thyroid arteries onset is abrupt remission and exacerbation is frequent.

Hyperthyroidism is more severe than in secondary Thyrotoxicosis but cardiac failure is rare.

Secondary Thyrotoxicosis The goitre is multi nodular. Onset is insidious and may present with cardiac failure or atrial fibrillation. Hyperthyroidism is not severe.

Treatment of Thyrotoxicosis

Non specific measures are rest and sedation.

While specific measures are the use of ant thyroid drugs, surgery and radio-iodine.

  1. Anti thyroid drugs those commonly used drug are Carbimazole and Propyl Thiouracil. Iodine which reduces the vascularity of thyroid should be given as preoperative preparation, ten days before surgery. Ant thyroid drugs cannot cure a toxic nodular goitre and recurrence of hyperthyroidism is certain when drugs is discontinued.

  2. Surgery— In diffuse toxic goiter and toxic nodular goitre, surgery cures by reducing the mass of overactive tissue.

  3. Radio-iodine destroys thyroid cells and as in thyroidectomy the mass of overactive tissue is reduced.


POST OPERATIVE COMPLICATIONS OF THYROIDECTOMY

  1. Haemorrhage—A tension hematoma deep to the cervical fascia is usually due to slipping of ligature on the superior thyroid artery occasionally haemorrhage is from thyroid remnant or thyroid veins. It may be necessary to open the wound in the ward in order to relieve tension.

  2. Respiratory obstruction—it is due to laryngeal edema caused by tension haematoma.

  3. Recurrent laryngeal nerve paralysis—Can be unilateral or bilateral transient or permanent causing hoarseness to the voice.

  4. Thyroid insufficiency This usually occurs within 2 years and is due to change in the autoimmune response from stimulation to destruction of thyroid cells and rarely due to operative removal of too much of thyroid tissue.

  5. Parathyroid insufficiency—Most cases present within 2 to 5 days after operation

  6. Thyrotoxic crises It is an acute exacerbation of acute hyperthyroidism. It occurs when thyrotoxic patient is inadequately prepared for thyroidectomy.

  7. Wound infection

  8. Keloid scar


Choice of Therapeutic Agents

    1. Diffuse toxic goitre

      • Over 45 years- Radio iodine.

    • Under 45 years Surgery for large goiter and anti thyroid drugs for small goitre.

  1. Toxic nodular goitre Surgery.

  2. Toxic nodule—Surgery or Radio iodine.

  3. Recurrent Thyrotoxicosis after surgery Over 45 years Radio iodine, Under 45years ant thyroid drugs.

  4. Failure of previous treatment with ant thyroid drugs or radioiodine Surgery.





Classification of Thyroid Neoplasm

  1. Benign

    1. Papillary adenoma

    2. Follicular adenoma

It is doubtful if there is such an entity as a papillary adenoma and all papillary tumours should be considered as malignant even if encapsulated.

  1. Malignant

    • Primary-

      1. Carcinoma-

        1. Papillary carcinoma

        2. Follicular carcinoma

        3. Undifferentiated carcinoma

      2. Malignant lymphoma

      3. Medullary Carcinoma

    • Secondary-

  1. Local infiltration

  2. Metastatic (blood borne).