Thyroid Case Presentation Viva — ENT Postgraduate Exam

ANATOMY

• Lies within the anterior leaves of the middle layer of deep cervical fascia (visceral space), anterior and lateral to the thyroid cartilage, cricoid cartilage, and upper tracheal rings
• Consists of two lateral lobes connected by an isthmus at the level of the 2nd–4th tracheal rings
• A pyramidal lobe is often present (remnant of thyroglossal duct), ascending from the isthmus, more often to the left
• Weight: 20–30 g in adults
• — Cummings Otolaryngology Head and Neck Surgery

• Superior thyroid artery (first branch of external carotid artery) — enters the superior pole
• Inferior thyroid artery (from thyrocervical trunk of subclavian artery) — enters posteriorly, closely related to the recurrent laryngeal nerve (RLN)
• Thyroid ima artery (present in ~3%) — from the aortic arch or brachiocephalic artery
• Venous drainage: superior and middle thyroid veins drain to the internal jugular vein; inferior thyroid veins drain to the brachiocephalic veins

• Recurrent laryngeal nerve (RLN): motor to all intrinsic laryngeal muscles except cricothyroid; sensory below vocal cords. Injury causes ipsilateral vocal cord palsy.
• External branch of superior laryngeal nerve (EBSLN): motor to cricothyroid muscle (pitch, voice projection). Injury causes a weak, low-pitched voice — the "Amelita Galli-Curci" nerve.
• On the right, the RLN loops under the subclavian artery; on the left, it loops under the aortic arch — making the left RLN longer and at greater risk.

PHYSIOLOGY

1. Iodide trapping (NIS pump, TSH-stimulated)
2. Oxidation of iodide to iodine (thyroid peroxidase)
3. Organification — iodination of tyrosine residues on thyroglobulin → monoiodotyrosine (MIT) and diiodotyrosine (DIT)
4. Coupling — MIT + DIT → T3; DIT + DIT → T4
5. Secretion — proteolysis of thyroglobulin releases T3 and T4 into circulation

• Thyroxine-binding globulin (TBG): accounts for ~75% of bound hormone, highest affinity for T4
• Transthyretin (prealbumin): ~10%
• Albumin: ~10–20% (low affinity, high abundance)
• Less than 1% circulates as free hormone — only the free fraction is biologically active (free T4: ~0.2%; free T3: ~0.3%)
• — Cummings Otolaryngology

• T4 must be deiodinated to T3 for most biological actions
• Type I deiodinase: primary source of circulating T3; found in liver, kidney, thyroid; activated by TSH; inhibited by PTU
• Type II: mainly in CNS, pituitary, placenta; produces local T3; negatively regulated by thyroid hormone; not inhibited by PTU
• Type III: inactivates T4 and T3 by inner-ring deiodination → reverse T3 (rT3); high in fetal tissues (protects against excess hormone)

CLINICAL ASSESSMENT

• Duration, rate of growth, pain
• Pressure symptoms: dysphagia, dyspnoea, voice change (hoarseness → RLN involvement = red flag for malignancy), stridor
• Symptoms of hyper/hypothyroidism
• Family history (MEN2, familial papillary thyroid cancer, FAP)
• History of radiation exposure (therapeutic or Chernobyl/Fukushima type)
• Occupation, residence in endemic goitre areas

• Inspection: swelling moving with deglutition (thyroid or thyroglossal cyst), visible pulsation, distended neck veins (retrosternal goitre)
• Palpation from behind: size, consistency, nodularity, tenderness, fixity, tracheal deviation
• Kocher's test: compress lateral lobes — stridor indicates tracheal narrowing
• Berry's sign: loss of carotid pulsation on palpation — indicates malignant invasion of the carotid artery
• Pemberton's sign: raise arms above head — facial congestion/stridor = retrosternal goitre causing SVC compression
• Percussion over sternum for retrosternal extension
• Auscultation: bruit over a hypervascular gland (Graves' disease)
• Examine lymph nodes (cervical, supraclavicular) and assess for vocal cord function (voice)

• Age < 14 or > 65 years; male sex
• Rapidly growing, hard, fixed mass
• Vocal cord paralysis (hoarseness)
• Cervical lymphadenopathy
• History of radiation exposure
• Family history of thyroid malignancy or MEN2
• Single "cold" nodule on scintigraphy
• Suspicious USG features: hypoechogenicity, microcalcifications, irregular margins, increased intranodular vascularity, size > 4 cm, subcapsular location, abnormal lymph nodes
• — Cummings Otolaryngology

INVESTIGATIONS

• Low TSH → hyperthyroidism → proceed to free T4, T3, uptake scan
• Normal/high TSH → proceed to USS and FNAC

• TSH is suppressed (to identify autonomously functioning "hot" nodules)
• Concern for ectopic thyroid tissue (lingual thyroid, thyroglossal duct remnant in known malignancy)
• A "hot" nodule is nearly always benign; a "cold" nodule has ~5–15% malignancy risk in adults (higher in children)
• — Cummings Otolaryngology

• Hypoechogenicity
• Microcalcifications (psammoma bodies in papillary carcinoma)
• Irregular or infiltrative margins
• Increased intranodular vascularity (on Doppler)
• Subcapsular location
• Size > 4 cm
• Abnormal lymph nodes (rounded, loss of fatty hilum, microcalcifications)

• Rapidly expanding tumour
• Retrosternal/mediastinal extension
• Bulky adenopathy
• Extrathyroidal disease
• Pre-op airway assessment
• Important: iodinated contrast CT should be avoided in suspected papillary or follicular carcinoma — it loads iodine and can delay radioactive iodine (RAI) therapy by months.

• Anti-thyroid peroxidase (anti-TPO): most sensitive for autoimmune thyroiditis (Hashimoto's); associated with hypothyroidism
• Anti-thyroglobulin (anti-Tg): less specific; can interfere with serum thyroglobulin assay used for cancer surveillance
• TSH-receptor antibodies (TRAb/TSHR Ab): in Graves' disease; stimulating antibodies drive hyperthyroidism
• Calcitonin: marker for medullary thyroid carcinoma (C-cell tumour)
• Thyroglobulin: tumour marker post-thyroidectomy for differentiated thyroid cancer; should be undetectable after ablation

THYROID DISORDERS

• Graves' disease (most common) — TSH receptor–stimulating antibodies
• Toxic multinodular goitre (Plummer's disease)
• Toxic adenoma (autonomously functioning "hot" nodule)
• Thyroiditis (early phase) — de Quervain's, Hashimoto's
• Iodine-induced (Jod-Basedow)
• TSH-secreting pituitary adenoma
• Exogenous thyroid hormone ingestion

1. Antithyroid drugs (ATD): Carbimazole (preferred) or PTU — blocks organification; PTU also blocks peripheral T4→T3 conversion. Treat for 12–18 months, ~50% relapse rate.
2. Radioactive iodine (RAI/I-131): Definitive; contraindicated in pregnancy and active moderate-severe GO. Note: RAI can worsen GO.
3. Surgery (thyroidectomy): Indicated for large goitre with pressure symptoms, malignancy suspicion, patient preference, failure of ATD. Patient must be rendered euthyroid before surgery.

• ATDs in large doses (PTU preferred — also blocks conversion)
• Propranolol IV/oral — controls tachycardia and neuromuscular symptoms (most immediately effective)
• Glucocorticoids — hydrocortisone 50 mg or dexamethasone 2 mg IV every 8 hours
• Inorganic iodine 50–100 mg QID (given after ATDs, to block hormone release — Wolff-Chaikoff effect)
• Supportive: anti-pyretics, IV fluids, treat precipitant
• Plasmapheresis: reserved for refractory cases prior to surgery

THYROID NODULE & GOITRE

• By aetiology: endemic (iodine deficiency), sporadic, physiological (puberty, pregnancy), inflammatory, neoplastic, Graves'
• By pathology: diffuse/nodular; toxic/non-toxic
• WHO grading (palpation):
  • Grade 0: No goitre
  • Grade 1: Palpable but not visible
  • Grade 2: Visible and palpable

1. TSH + USS
2. If USS suspicious → FNAC (Bethesda classification guides next step)
3. Benign (Bethesda II): serial USS every 6–18 months; repeat FNAC if growth
4. Bethesda IV (follicular neoplasm): lobectomy — cannot distinguish follicular adenoma from follicular carcinoma on cytology; diagnosis requires histopathological demonstration of capsular or vascular invasion
5. Bethesda V/VI: total thyroidectomy ± central neck dissection

THYROID MALIGNANCY

• PTC in adults: BRAF V600E mutation (most common ~60%)
• PTC in children: RET/PTC rearrangements (more common than BRAF in paediatric cases)
• MTC: RET proto-oncogene mutation (germline in MEN2A, MEN2B; somatic in sporadic)
• FTC: RAS mutations, PAX8-PPAR-γ translocation
• Anaplastic: TP53 mutations

• MEN2A: MTC + phaeochromocytoma + parathyroid hyperplasia (RET codon 634 mutation most common)
• MEN2B: MTC + phaeochromocytoma + mucosal neuromas + marfanoid habitus (RET codon 918 mutation)
• Genetic testing is mandatory in all MTC patients; prophylactic thyroidectomy is recommended in RET mutation carriers

1. Total thyroidectomy (as it allows RAI ablation and monitoring via thyroglobulin)
2. Central neck dissection (Level VI): if clinical/radiological lymph node involvement; routine bilateral central dissection is debated but performed in paediatric cases
3. Lateral neck dissection (modified radical/selective): for proven lateral nodal disease
4. Postoperative RAI ablation: indicated for distant metastases, T3/T4 tumours, or extensive nodal involvement
5. TSH suppression therapy: levothyroxine to suppress TSH below normal — reduces stimulation of any residual tumour cells
6. Surveillance: serum thyroglobulin (± anti-Tg antibodies) + neck USS; whole-body RAI scan if thyroglobulin rises

SURGERY

• Confirmed or suspected thyroid malignancy
• Follicular neoplasm (Bethesda IV)
• Pressure symptoms from goitre (dysphagia, dyspnoea, stridor)
• Retrosternal goitre
• Graves' disease refractory to or unsuitable for medical therapy or RAI
• Cosmetic indication
• Patient preference

• Hemithyroidectomy (lobectomy): removes one lobe + isthmus; for solitary nodule, follicular neoplasm
• Near-total thyroidectomy: leaves < 1 g of tissue at ligament of Berry to protect RLN
• Total thyroidectomy: removes all thyroid tissue; required for malignancy
• Subtotal thyroidectomy: leaves 5–7 g bilaterally; less popular now due to recurrence
• Completion thyroidectomy: removes residual lobe after prior lobectomy when malignancy confirmed on histology

• In the tracheoesophageal groove (most reliable landmark)
• At the level of Zuckerkandl's tubercle — the nerve lies medial to the tubercle
• Near Berry's ligament — the nerve may branch or pass through the ligament here
• Intraoperative nerve monitoring (IONM) is increasingly used — reduces risk but does not replace careful dissection

• Identifying all 4 parathyroids before ligating vessels
• Ligating branches of the inferior thyroid artery close to the thyroid capsule ("capsular dissection")
• Autotransplantation: if vascularity is compromised, the parathyroid is minced and implanted into the sternocleidomastoid or forearm muscle

COMPLICATIONS

• Haemorrhage → haematoma (life-threatening — can compress airway; requires immediate wound opening at bedside)
• Laryngospasm, tetany (early hypocalcaemia)

• Hypocalcaemia (most common complication) — due to hypoparathyroidism; transient or permanent; presents as perioral tingling, Chvostek's sign (facial twitch on tapping facial nerve), Trousseau's sign (carpopedal spasm on inflation of BP cuff)
• RLN palsy — hoarseness (unilateral); respiratory distress, stridor requiring re-intubation (bilateral)
• Wound infection, seroma
• Thyroid storm (if operated on unprepared hyperthyroid patient)

• Hypothyroidism (requires lifelong T4 replacement after total thyroidectomy)
• Permanent hypoparathyroidism
• Keloid/hypertrophic scar
• Voice change (EBSLN injury — loss of high pitch)
• Tracheomalacia (rare, in long-standing large goitre)

• Monitor serum calcium 12–24 hours post-op
• Symptomatic hypocalcaemia: IV calcium gluconate (10 mL of 10% solution) over 10 minutes, followed by infusion; oral calcium + calcitriol (active vitamin D) long term
• Intact PTH level at 24 hours predicts risk of permanent hypoparathyroidism — PTH < 10 pg/mL is a reliable predictor

1. Immediately open wound and evacuate clot at the bedside to relieve airway compression
2. Call for anaesthesia support
3. Return to theatre for formal haemostasis

SPECIAL TOPICS

• Primary (thyroid failure): High TSH, low free T4 — most common. Causes: Hashimoto's thyroiditis (iodine-sufficient areas), iodine deficiency (worldwide)
• Secondary (pituitary failure): Low TSH, low free T4 — e.g., pituitary adenoma, Sheehan syndrome
• Tertiary (hypothalamic failure): Low TRH → low TSH → low T4

• Amiodarone: can cause hypo or hyperthyroidism (contains large amounts of iodine; inhibits T4→T3 conversion)
• Lithium: inhibits thyroid hormone release → hypothyroidism/goitre
• Phenytoin, carbamazepine, phenobarbital, rifampin: increase T4 catabolism → increased dose requirement
• Oestrogens: increase TBG → increased total T4 (but free T4 unchanged)
• Ferrous sulfate, calcium carbonate, aluminum hydroxide, sucralfate, cholestyramine: impair T4 absorption from gut — separate dose by several hours

• Residual thyroid tissue
• Tumour recurrence It is monitored at regular follow-up intervals, with stimulation by TSH withdrawal or recombinant TSH (rhTSH/Thyrogen) to increase sensitivity. Anti-thyroglobulin antibodies (anti-Tg Ab) can interfere with the assay and must be measured simultaneously.