An unusual presentation of large colloid goiter – A case report

INTRODUCTION

Benign nodular goiter is one of the most common endocrine disorders, especially in countries like India, where iodine deficiency is endemic.^[1] Goiter is an enlargement of the thyroid gland irrespective of its pathology caused by compensatory hyperplasia and hypertrophy of follicular epithelium. Nodular goiter is rarely seen before middle age and is more common in females.^[2] We are presenting a case of large colloid goiter. Nowadays with the advent of daily use of iodized salt and increased awareness about the deficiency of iodine, the occurrence of large colloid goiters has become a rarity. Hence, when in clinical practice, such a huge thyroid nodule is encountered that too which is unilateral that it becomes an interesting case mandating reporting.

CASE DESCRIPTION

A 55-year-old male presented to our outpatient Department of Otolaryngology and Head and Neck Surgery, Adesh University, Bathinda with large swelling over the anterior part of neck for past 2 years. Clinical examination revealed smooth lobulated solid mass approximately 10 × 10 × 10 cm³ in size extending from below the chin to the suprasternal notch [Figure 1].

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Figure 1:

Pre-operative lesion from the left lateral position.

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Swelling moved with deglutition, and there were no dilated vessels over the swelling. No enlarged lymph nodes in the neck were palpated.

Thyroid function test (TFT), ultrasonography (USG), fine-needle aspiration cytology (FNAC), and computerized tomography (CT) were advised. Although TFT was normal, USG showed features of colloid goiter, FNAC showed many colloidophages and few groups of benign follicular epithelial cells with background showing abundant thin colloid and hemorrhage. CT scan showed a large cystic lesion with heterogeneously enhancing soft tissue in it in the right lobe of thyroid along with conglomerate lymph nodal mass along the right external jugular vein [Figure 2].

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Figure 2:

Pre-operative lesion from the right lateral position.

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All other hematological and biochemical tests were within normal limits. On the basis of above findings, surgery, namely, hemithyroidectomy was planned under general anesthesia. Horizontal skin incision was given extending from one anterior border of sternocleidomastoid (SCM) to other anterior borders of SCM about two finger breath above suprasternal notch. Subplatysmal flaps were raised superiorly (upper) up to thyroid notch and inferiorly (lower) to clavicle. Midline vertical incision was made in fascia separating the two sternohyoid muscles and separated from the thyroid gland. Gentle finger dissection was used to free the swelling from the surrounding soft tissues. Thyroid capsule identified, dissected, and subcapsular dissection of swelling started. Inferior thyroid veins which formed venous plexus in front of trachea were identified and ligated. Branches of inferior thyroid artery were ligated medially preserving blood supply to parathyroids then dissection of superior thyroid pedicle and the upper pole was done and vessels ligated, preserving the parathyroids, isthmus was separated from trachea and clamped, wound irrigation was done, drain kept and closure of wound done in layers [Figure 3].

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Figure 3:

Specimen after thyroidectomy.

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The patient was observed in ward after keeping the patient in post-operative recovery room for 2 h. There were no features of hypocalcemia and hoarseness of voice postopertaively. The patient was kept in ward for 5 days during which period daily dressings were done in minor operation theater (OT). Sutures were removed on 10^th post-operative day. The specimen was sent for histopathological examination that revealed colloid goiter [Figure 4].

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Figure 4:

Contrast-enhanced computed tomography neck.

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DISCUSSION

When diffuse enlargement of the thyroid occurs in the absence of nodules and hyperthyroidism, it is referred to as a diffuse non-toxic goiter also called “simple goiter” due to the absence of nodules, or “colloid goiter” due to the presence of uniform follicles that are filled with colloid. Diffuse goiter is most commonly caused by iodine deficiency and is termed “endemic goiter” when it affects >5% of the population in a given geographic area.^[1]

The prevalence of goiter, diffuse, and nodular is dependent on the status of iodine intake of the population. In countries with a previous deficiency corrected by universal salt iodination, elderly subjects may have a prevalence of approximately 10%. This can be attributed to lack of nutritional iodine in early adult life, as longstanding endemic goiters usually do not regress with iodine supplementation.^[2]

Etiology of Multinodular goiter, also called nodular hyperplasia, involves irregular enlargement of thyroid gland due to repeated episodes of hyperplasia and involution (degeneration) of simple goiter. Thyroid gland often weighs 100 g or more and may resemble a neoplasm, particularly if a single firm dominant nodule is present. Nodules are clonal or polyclonal and are due to heterogeneous responses of follicular epithelium to TSH. Exophthalmos of Graves’ disease is not present.

Indications for treatment of non-toxic multinodular goiter are compression of the trachea or esophagus, venous-outflow obstruction, growth of the goiter, neck discomfort, and cosmetic issues.^[3]

CONCLUSION

The majority of thyroid nodules are benign, as in this case. However, if the thyroid nodule is very big, it produces compressive symptoms such as dysphagia or stridor. Surgery is the effective treatment.