about the thyroid

1. Thyroid

2. embryology
• The thyroglossal duct develops from the median bud of the
pharynx.
• The foramen caecum at the junction of the anterior two-
thirds and posterior one-third of the tongue is the vestigial
remnant of the duct. This initially hollow structure migrates
caudally and passes in close continuity with, and sometimes
through, the developing hyoid cartilage.
• The parathyroid glands develop from the third and fourth
pharyngeal pouches.
• The thymus also develops from the third pouch. As it
descends, the thymus takes the associated parathyroid
gland with it, which explains why the inferior parathyroid,
which arises from the third pharyngeal pouch, normally lies
inferior to the superior gland. However, the inferior
parathyroid may be found anywhere along this line of
descent (see also Chapter 51).
• The developing thyroid lobes amalgamate with the
structures that arise in the fourth pharyngeal pouch, i.e. the
superior parathyroid gland and the ultimobranchial body.
Parafollicular cells (C cells) from the neural crest reach the
thyroid via the ultimobranchial body.

3. Surgical anatomy
• Around 20 -25g
• Functioning unit is lobules. Lobules contain follicles (around 25-40) that have
colloid in which thyroglobulin is stored. Lined by cuboidal epithelium.
• Blood supply by right and left sup and inferior thyroid art.
Superior thyroid by ext carotid artery
Inferior thyroid is branch of the thyrocervical trunk of the subclavian artery.
Goes up, then medial portion of thyroid and then down to the lower lobes.
Thyroid ima – only some 3%. Comes from brachiocephalic or the aorta straight.
• Vein
• Superior middle and inferoir thyroid veins

5. Nerve supply
• Supplied by recurrent laryngeal nerve.
• From the vagus nerve. Left goes down and circles around the arch of the aorta before coming up and supplying.
Medial and posterior. Right circles around the subclavian and is shorter and obliquely running.
• Need to know how to access is. Runs posterior to the thyroid and enters larynx at the level of cricothyroid joint.
Enters thyroid at the level of berrys ligament. Most risk fo injury is here. supplies medially to the lobules.
• Also lies in close relatiogn with the tubercle of zuckerkandl which is posterolaterally and inferoir thyroid artery
• In terms of surgical anatomy, the nerve can be located in the tracheosophageal groove where it forms one side of
Beahrs’ triangle (the other two sides are the carotid artery and the inferior thyroid artery) or at the cricothyroid
joint
Lymph
• lymph channels pass directly to the deep cervical nodes, the subcapsular plexus drains principally to the central
compartment juxtathyroid – ‘Delphian’ and
• paratracheal nodes and nodes on the superior and inferior thyroid veins (level VI),
• and from there to the deep cervical (levels II, III, IV and V) and
• mediastinal groups of nodes (level VII)

6. Physiology - thyroxine
• The hormones tri-iodothyronine (T3) and l-thyroxine (T4) are bound to thyroglobulin within the colloid.
• Synthesis within the thyroglobulin complex is controlled by several enzymes, in distinct steps:
• ● trapping of inorganic iodide from the blood;
• ● oxidation of iodide to iodine;
• ● binding of iodine with tyrosine to form iodotyrosine;
• ● coupling of monoiodotyrosines and di-iodotyrosines to form T3 and T4.
• When hormones are required, the complex is resorbed into the cell and thyroglobulin is broken down.
• T3 and T4 are liberated and enter the blood, where they are bound to serum proteins: albumin, thyroxine-
binding globulin (TBG) and thyroxine-binding prealbumin (TBPA). The small amount of hormone that
remains free in the serum is biologically active.
• The metabolic effects of the thyroid hormones are due to unbound free T4 and T3 (0.03% and 0.3% of the
total circulating hormones, respectively). T3 is the more important physiological hormone and is also
produced in the periphery by conversion from T4.
• T3 is quick acting (within a few hours), whereas T4 acts more slowly (4–14 days).

7. TSH – thyroid stimulating hormone
In hyperthyroidism TSH production is suppressed,
whereas in hypothyroidism it is stimulated

8. • Parafollicular C cells produce calcitonin.
• Thyroid-stimulating antibodies
• A family of IgG immunoglobulins bind with TSH receptor sites (TRAbs) and
activate TSH receptors on the follicular cell membrane. They have a more
protracted action than TSH (16–24 versus 1.5–3 hours) and are responsible
for virtually all cases of thyrotoxicosis not due to autonomous toxic nodules.
Serum concentrations are very low but their measurement is not essential
to make the diagnosis.
• Serum thyroid hormones
• Serum TSH
TSH levels can be measured accurately down to very low serum concentrations
with an immunochemiluminometric assay. Interpretation of deranged TSH
levels depends on knowledge of the T3 and T4 values.
In the euthyroid state, T3, T4 and TSH levels will all be within the normal range.
Florid thyroid failure results in depressed T3 and T4 levels, with gross elevation
of TSH.
Incipient or developing thyroid failure is characterised by low normal values of
T3 and T4 and elevation of TSH.
In toxic states, the TSH level is suppressed and undetectable (Table 50.1).
T3 toxicity (with a normal T4) is a distinct entity and may only be diagnosed by
measuring T3, although a suppressed TSH in the presence of normal T4
suggests the diagnosis.

9. • Thyroid autoantibodies
• Serum levels of antibodies against thyroid peroxidase (TPO) and thyroglobulin are useful in determining the cause of thyroid
dysfunction and swellings.
• Autoimmune thyroiditis may be associated with thyroid toxicity, failure or euthyroid goitre. Levels above 25 units/mL for
TPO antibody and titres of greater than 1:100 for antithyroglobulin are considered significant, although a proportion of
patients with histological evidence of lymphocytic (autoimmune) thyroiditis are seronegative.
• The presence of antithyroglobulin antibody interferes with assays of serum thyroglobulin, with implications for follow-up of
thyroid cancers.
• TSH receptor antibodies (TSH-Rab or TRAB) are often present in Graves’ disease. They are largely produced within the
thyroid itself.
• Thyroid investigations
• Essential
• ● Serum: TSH (T3 and T4 if abnormal); thyroid autoantibodies
• ● FNAC of palpable discrete swellings; ultrasound guidance may reduce the ‘Thy1’ rate
• Optional
• ● Corrected serum calcium
• ● Serum calcitonin (carcinoembryonic antigen may be used as an alternative screening test for medullary cancer)
• ● Imaging: chest radiograph and thoracic inlet if tracheal deviation/retrosternal goitre; ultrasound, CT and MRI scan for known
cancer, some reoperations and some retrosternal goitres; isotope scan if discrete swelling and toxicity coexist

11. Thyroid imaging
• Ultrasound
• allows assessment of the gland and the regional lymphatics.
• characteristics of the gland substance be quantified, but critically the presence and features of thyroid nodules can be
described. Number, size, shape, margins, vascularity and specific features such as the presence of microcalcifications can be
used to predict the risk of malignancy within a specific nodule.
• Regional lymphatics, particularly in the lateral neck can be assessed accurately for the presence of metastatic deposits.
During ultrasound, fine needle aspiration (FNA) can be performed more accurately than free-hand techniques allow.
Ultrasound has the advantages that it is not associated with ionising radiation and is non-invasive and cheap (Figure 50.5).
Visualisation of the central neck nodes, in particular those behind the sternum, is however limited.
For most of these indications, the imaging modality of choice is computed tomography (CT). Rapid acquisition times minimise the
artifact secondary to breathing and the lung fields can be accurately assessed simultaneously.
In the setting of an invasive primary thyroid cancer, both CT and magnetic resonance imaging (MRI) may have a role
Contrast enhanced CT is useful for determining the extent of airway invasion (Figure 50.7) and MRI is superior at determining the
presence of prevertebral fascia invasion.
Positron emission tomography (PET) scans have limited application in thyroid disease. They may be considered in the setting of
recurrent thyroid cancer. This is particularly useful when the disease does not concentrate iodine, at which point
fluorodeoxyglucose (FDG) uptake increases and lesions become positive on PET scans.

12. • Isotope scanning
• The uptake by the thyroid of a low dose of either radiolabelled iodine (123I) or the cheaper technetium (99mTc).
• Routine isotope scanning is unnecessary and inappropriate for distinguishing benign from malignant lesions because the majority (80%)
of ‘cold’ swellings are benign and some (5%) functioning or ‘warm’ swellings will be malignant.
• Its principal value is in the toxic patient with a nodule or nodularity of the thyroid. Localisation of overactivity in
the gland will differentiate between a toxic nodule with suppression of the remainder of the gland, and toxic
multinodular goitre with several areas of increased uptake with important implications for therapy (Figure 50.8).
Whole-body scanning is used to demonstrate metastases. However, the patient must have all normally
functioning thyroid tissue ablated either by surgery or radioiodine before the scan is performed, because
metastatic thyroid cancer tissue cannot compete with normal thyroid tissue in the uptake of iodine.
• Fine-needle aspiration cytology
• Fine-needle aspiration cytology (FNAC) is the investigation of choice in discrete thyroid swellings. FNAC has
excellent patient compliance, is simple and quick to perform in the out-patient department
and is readily repeated. As stated above there is a trend
to use ultrasound to guide the needle to achieve more
accurate sampling and reduce the rate of unsatisfactory
aspirates.

13. Swelling
• Simple goitre Aetiology
Simple goitre may develop as a result of stimulation of the thyroid gland by TSH, either as a result of
inappropriate secretion from a microadenoma in the anterior pituitary (which is rare), or in response to a
chronically low level of circulating thyroid hormones.
The most important factor in endemic goitre is dietary deficiency of iodine (see below), but defective
hormone synthesis probably accounts for many sporadic goitres (see below).
TSH is not the only stimulus to thyroid follicular cell proliferation and other growth factors, including
immunoglobulins, exert an influence.
IODINE DEFICIENCY
The daily requirement of iodine is about 0.1–0.15mg
. Endemic areas are in the mountainous ranges, such as the Rocky Mountains, the Alps, the Andes and the
Himalayas.
Endemic goitre is also found in lowland areas where the soil lacks iodide or the water supply comes from far
away mountain ranges, e.g. the Great Lakes , the Struma valley, the Nile valley and the Congo.
Calcium is also goitrogenic and goitre is common in low-iodine areas on chalk or limestone, for example
Derbyshire and Southern Ireland.
, failure of intestinal absorption may produce iodine deficiency.
DYSHORMONOGENESIS
• Enzyme deficiencies). There is often a
• family history, suggesting a genetic defect
GOITROGENS
Well-known goitrogens are the vegetables of the brassica family (cabbage, kale and rape), which contain
thiocyanate, drugs such as para-aminosalicylic acid (PAS) and the antithyroid drugs.
Thiocyanates and perchlorates interfere with iodide trapping;
carbimazole and thiouracil compounds interfere with the oxidation of iodide and the binding of iodine to
tyrosine.
Surprisingly, iodides in large quantities are goitrogenic because they inhibit the organic binding of iodine and
produce an iodide goitre.

14. • Stages in goitre formation are:
• ● Persistent growth stimulation causes diffuse hyperplasia; all lobules are composed of active follicles and iodine uptake is uniform. This is
a diffuse hyperplastic goitre, which may persist for a long time but is reversible if stimulation ceases.
• ● Later, as a result of fluctuating stimulation, a mixed pattern develops with areas of active lobules and areas of inactive lobules.
• ● Active lobules become more vascular and hyperplastic until haemorrhage occurs, causing central necrosis and leaving only a
surrounding rind of active follicles.
• ● Necrotic lobules coalesce to form nodules filled either with iodine-free colloid or a mass of new but inactive follicles.
• ● Continual repetition of this process results in a nodular goitre.
Most nodules are inactive, and active follicles are present only in the internodular tissue.
DIFFUSE HYPERPLASTIC GOITRE
Diffuse hyperplasia corresponds to the first stages of the natural history.
The goitre appears in childhood in endemic areas but, in sporadic cases, it usually occurs at puberty when metabolic demands are high.
If TSH stimulation ceases the goitre may regress, but tends to recur later at times of stress such as pregnancy.
The goitre is soft, diffuse and may become large enough to cause discomfort.
A colloid goitre is a late stage of diffuse hyperplasia, when TSH stimulation has fallen off and when many follicles are inactive and full of
colloid (Figure 50.10).
NODULAR GOITRE Nodules are usually multiple, forming a multinodular goitre (Figure 50.11). Occasionally, only one macroscopic nodule is
found, but microscopic changes will be present throughout the gland; this is one form of a clinically solitary nodule. Nodules may be
colloid or cellular, and cystic degeneration and haemorrhage are common, as is subsequent calcification. Nodules appear early in
endemic goitre and later (between 20 and 30 years) in sporadic goitre,. All types of simple goitre are more common in the female than in
the male owing to the presence of oestrogen receptors in thyroid tissue.

15. Diagnosis
• The patient is euthyroid, the nodules are palpable and often visible; they are smooth, usually firm and not hard and the goitre is painless and
moves freely on swallowing. Hardness and irregularity, due to calcification, may simulate carcinoma. A painful nodule, sudden appearance or
rapid enlargement of a nodule raises suspicion of carcinoma but is usually due to haemorrhage into a simple nodule.
• Differential diagnosis from autoimmune thyroiditis may be difficult and the two conditions frequently coexist.
Investigations
• Thyroid function should be assessed to exclude mild hyperthyroidism, and the presence of circulating thyroid antibodies tested to
differentiate from autoimmune thyroiditis. Ultrasound is the gold standard assessment when undertaken by a suitably trained and
experienced operator. FNAC is only required for a nodule within the goitre that demonstrates ultrasonic features of concern.
• If there are swallowing or breathing symptoms then a CT scan of the thoracic inlet is the best modality to assess tracheal or oesophageal
compression.
Complications
• Tracheal obstruction
• Acute respiratory obstruction may follow haemorrhage
SECONDARY THYROTOXICOSIS
• Transient episodes of mild hyperthyroidism are common, occurring in up to 30% of patients.
CARCINOMA. Dominant or rapidly growing nodules in longstanding goitres should always be subjected to aspiration cytology. Prevention and
treatment of simple goitre In endemic areas the incidence of goitre has been strikingly reduced by the introduction of iodised salt.
In the early stages, a hyperplastic goitre may regress if thyroxine is given in a dose of 0.15–0.2mg daily for a few months. Although the nodular
stage of simple goitre is irreversible, more than half of benign nodules will regress in size over 10 years. Most patients with multinodular
goitre are asymptomatic and do not require operation.
.

16. . Surgery is indicated for nodular goitres with features of
• underlying malignancy,
• for swallowing symptoms if other causes have been excluded or
• for cosmetic reasons if the patient finds the goitre unsightly.
• tracheal compression then surgery should be considered There is a choice of surgical treatment in multinodular
goitre:
• total thyroidectomy with immediate and lifelong replacement of thyroxine or some form of partial resection to
conserve sufficient functioning thyroid tissue to subserve normal function while reducing the risk of
hypoparathyroidism that accompanies total thyroidectomy.
• Subtotal thyroidectomy involves partial resection of each lobe removing the bulk of the gland, leaving up to 8g of
relatively normal tissue in each remnant.
• Reoperation for recurrent nodular goitre is more difficult and hazardous and, for this reason, an increasing
number of thyroid surgeons favour total thyroidectomy in younger patients. However, when the first operation
comprised unilateral lobectomy alone for asymmetric goitre, reoperation and completion total thyroidectomy is
straightforward if required for progression of nodularity in the remaining lobe.
• Total lobectomy and total thyroidectomy have the additional advantage of being therapeutic for incidental
carcinomas (see below).
• After subtotal resection, it has been customary to give thyroxine to suppress TSH secretion, with the aim of
preventing recurrence.

17. Clinically discrete swellings
• Discrete thyroid swellings (thyroid nodules) are common and are palpable in 3–4% of the adult population in the UK and USA.
They are three to four times more frequent in women than men.
• Diagnosis
• A discrete swelling in an otherwise impalpable gland is termed isolated or solitary, whereas the preferred term is dominant for
a similar swelling in a gland with clinical evidence of generalised abnormality in the form of a palpable contralateral lobe or
generalised mild nodularity. About 70% of discrete thyroid swellings are clinically isolated and about 30% are dominant.
. Demonstrating the presence of impalpable nodules does not change the management of palpable discrete swellings
The importance of discrete swellings lies in the risk of neoplasia compared with other thyroid swellings. Some 15% of isolated
swellings prove to be malignant and an additional 30–40% are follicular adenomas. The remainder are non-neoplastic, largely
consisting of areas of colloid degeneration, thyroiditis or cysts. Although the incidence of malignancy or follicular adenoma in
clinically dominant swellings is approximately half of that of truly isolated swellings, it is substantial and cannot be ignored
(Figure 50.13).
Investigation
THYROID FUNCTION Serum TSH and thyroid hormone levels should be measured. If hyperthyroidism associated with a discrete
swelling is confirmed biochemically, it indicates either a ‘toxic adenoma’ or a manifestation of toxic multinodular goitre. The
combination of toxicity and nodularity is important and is an indication for isotope scanning to localise the area(s) of
hyperfunction

18. • . AUTOANTIBODY TITRES
• The autoantibody status may determine whether a swelling is a manifestation of chronic
lymphocytic thyroiditis.
• The presence of circulating antibodies increases the risk of thyroid failure after lobectomy.
• ISOTOPE SCAN Isotope scanning used to be the mainstay of investigation of discrete thyroid swellings
but has been abandoned except when toxicity is associated with nodularity.
• ULTRASONOGRAPHY This is gold standard.
• FINE-NEEDLE ASPIRATION CYTOLOGY. FNAC should be used, ideally under ultrasound guidance, on all
nodules that do not fulfil a fully benign (U2) classification on ultrasound. FNAC is reliable in
identifying papillary thyroid cancer but cannot distinguish between a benign follicular adenoma
(Figure 50.14) and follicular carcinoma, as. FNAC is both highly specific and sensitive.
• RADIOLOGY Plain films have previously been used to assess tracheal compression and deviation,
• . CT scanning is also useful if ultrasound has identified metastatic disease in the neck as it can assist
surgical planning and also assess the superior mediastinum and lungs.
• LARYNGOSCOPY Flexible laryngoscopy has rendered indirect laryngoscopy obsolete and is widely
used preoperatively to determine the mobility of the vocal cords. The presence of a unilateral cord
palsy coexisting with an ipsilateral thyroid nodule of concern is usually diagnostic of malignant
disease.

19. CORE BIOPSY
• Core biopsy is rarely indicated in thyroid masses due to the vascularity of the thyroid gland and the risk of
postprocedure haemorrhage.
• It can be useful in the rapid diagnosis of widely invasive malignant disease, for example anaplastic carcinoma, or in
the diagnosis of lymphadenopathy. The main indication for operation is the risk of neoplasia, which includes
follicular adenoma as well as malignant swellings.
• The reason for advocating the removal of all follicular neoplasms is that it is seldom possible to distinguish between
a follicular adenoma and carcinoma cytologically.. Even when the cytology is negative, the age and sex of the
patient and the size of the swelling may be relative indications for surgery, especially when a large swelling is
responsible for symptoms
• . Hard texture alone is not reliable as tense cystic swellings may be suspiciously hard but a hard, irregular swelling
with any apparent fixity, which is unusual, is highly suspicious.
• Evidence of RLN paralysis, suggested by hoarseness and a non-occlusive cough and confirmed by laryngoscopy, is
almost pathognomonic.
• Deep cervical lymphadenopathy along the internal jugular vein in association with a clinically suspicious swelling is
almost diagnostic of papillary carcinoma.
• In most patients, however, such features are absent but there are risk factors associated with sex and age. The
incidence of thyroid carcinoma in women is about three times that in men, but a discrete swelling in a male is
much more likely to be malignant than in a female and it is seldom justifiable to avoid removing such a swelling in a
man. The risk increases as age advances beyond 50 years, more so in males.

20. Thyroid cysts
• over 30% of clinically isolated swellings contain fluid and are cystic or partly cystic. Tense cysts may be hard and
mimic carcinoma.. About 50% of cystic swellings are the result of colloid degeneration, or of uncertain aetiology
because of an absence of epithelial cells in the lining.
• Papillary carcinoma is often associated with cyst formation (Figure 50.16).
• . Ultrasound is the most useful tool for assessing cysts. If there is no discernable solid element then the cyst is almost
certainly benign and does not need to be further investigated. If there is an associated solid element then
consideration should be given to targeting that area with an ultrasoundguided FNAC.
• Selection of thyroid procedure The choice of thyroid operation depends on: ● diagnosis (if known preoperatively); ●
risk of thyroid failure; ● risk of RLN injury; ● risk of recurrence; ● Graves’ disease; ● multinodular goitre; ●
differentiated thyroid cancer; ● risk of hypoparathyroidism. Total and near-total thyroidectomy do not conserve
sufficient thyroid tissue for normal thyroid function and thyroid replacement therapy is necessary. In most patients
with negative antithyroid antibodies, one thyroid lobe will maintain normal function. In subtotal thyroidectomy, the
volume of thyroid tissue preserved influences the risk of thyroid failure: larger remnants have a better chance of
normal function but a higher risk of recurrence in Graves’ disease.

21. • Subtotal resections for colloid goitre run the risk of later growth of the remnant and, if a second
operation is required years later, this greatly increases the risk to the RLN and parathyroid glands.
• In young patients, total thyroidectomy should be considered. It may be preferable to leave the least
affected lobe untouched to permit a straightforward lobectomy in the future if required, rather than
carry out subtotal resections.
• In Graves’ disease, preserving large remnants increases the risk of recurrence of the toxicity and, in
these cases, it is better to err on the side of removing too much thyroid tissue rather than too little
(Table 50.5).
Thyroid operations
• All thyroid operations can be assembled from three basic elements:
1 Total lobectomy
2 Isthmusectomy
3 Subtotal lobectomy
• Total thyroidectomy = 2 × total lobectomy + isthmusectomy
• Subtotal thyroidectomy = 2 subtotal lobectomy + isthmusectomy
• Near-total thyroidectomy = total lobectomy + isthmusectomy + subtotal lobectomy (Dunhill procedure)
• Lobectomy = total lobectomy + isthmusectomy

22. Retrosternal goitre
• Retrosternal goitre tends to arise from the slow growth of a multinodular gland down in to the mediastinum.
• As the gland enlarges within the thoracic inlet, pressure may lead to dysphagia, tracheal compression and eventually airway
symptoms.
• Patient should be considered for surgery if there is significant airway compression, if symptoms are present or in young
patients in whom symptoms are likely to develop
• . In elderly patients with incidentally discovered retrosternal goitres, most surgeons would observe rather than treat
prophylactically
• . The vast majority (>95%) of retrosternal goitres can be removed transcervically.
• All cases should have cross-sectional imaging. Ideally this is performed in the surgical position and when interpreting CT chest
scans, the surgeon should pay attention to the arm position. If the arms are up (as for standard CT chest) a great deal of
thyroid movement will be achieved when the arms are down and the neck extended.
• . A longer incision is required. The surgeon may mobilise the sternomastoid muscle from the strap muscles to improve access.
The ligamentous tissue between the sternal heads of the clavicles may be gently divided to increase the opening for gland
delivery. Blunt dissection on the capsule of the gland allows mobilisation. Gentle traction is applied to deliver the gland into the
neck. If the goitre has developed from a posteriorly positioned nodule there is a risk that the RLN may be displaced anteriorly,
so great care must be taken in dividing apparent fascial bands that overlie the gland. The blood supply is from the neck,
reducing the risk of catastrophic bleeding from the great vessels. Nonetheless, care should be taken in the region of the major
blood vessels in the neck and chest. If the gland is fixed and immobile or too large to deliver through a cervical approach, a
midline sternotomy is performed and the gland can be dissected from below to achieve a safe total thyroidectomy.

23. HYPERTHYROIDISM
• Thyrotoxicosis
• . Clinical types are:
• ● diffuse toxic goitre (Graves’ disease);
• ● toxic nodular goitre;
• ● toxic nodule;
• ● hyperthyroidism due to rarer causes.
Diffuse toxic goitre - Graves’ disease, a
• diffuse vascular goitre
• appearing at the same time as hyperthyroidism,
• usually occurs in younger women
• and is frequently associated with eye signs.
• The syndrome is that of primary thyrotoxicosis (Figure 50.17);
• 50% of patients have a family history of autoimmune endocrine diseases.
• The whole of the functioning thyroid tissue is involved, and the hypertrophy and hyperplasia are due to abnormal TSH-RAb that bind to TSH receptor sites and produce a
disproportionate and prolonged effect.
Toxic nodule
• A toxic nodule is a solitary overactive nodule, which may be part of a generalised nodularity or a true toxic adenoma
• . It is autonomous and its hypertrophy and hyperplasia are not due to TSH-RAb.
• TSH secretion is suppressed by the high level of circulating thyroid hormones and the normal thyroid tissue surrounding the nodule is itself suppressed and inactive.
HISTOLOGY The normal thyroid gland consists of acini lined with flattened cuboidal epithelium and filled with homogeneous colloid (Figure 50.2).
In hyperthyroidism (Figure 50.18), there is hyperplasia of acini, which are lined by high columnar epithelium. Many of them are empty, and others contain vacuolated colloid
with a characteristic ‘scalloped’ pattern adjacent to the thyrocytes.
Toxic nodular goitre
A simple nodular goitre is present for a long time before the hyperthyroidism,
usually in the middle-aged or elderly,
and very infrequently is associated with eye signs.
The syndrome is that of secondary thyrotoxicosis.
In many cases of toxic nodular goitre, the nodules are inactive, and it is the internodular thyroid tissue
that is overactive. However, in some toxic nodular goitres, one or more nodules are overactive and
here the hyperthyroidism is due to autonomous thyroid tissue as in a toxic adenoma

24. • An overactive thyroid can cause a wide range of symptoms, including:
• nervousness, anxiety and irritability
• mood swings
• difficulty sleeping
• persistent tiredness and weakness
• sensitivity to heat
• swelling in your neck from an enlarged thyroid gland (goitre)
• an irregular and/or unusually fast heart rate (palpitations)
• twitching or trembling
• weight loss

25. Principles of treatment of thyrotoxicosis
• rest and sedation and in
• established thyrotoxicosis. the use of antithyroid drugs, surgery and radioiodine.
ANTITHYROID DRUGS
Those in common use are carbimazole and propylthiouracil. Antithyroid drugs are used to restore the patient to a euthyroid state and to
maintain this for a prolonged period in the hope that a permanent remission will occur, i.e. that production of thyroid-stimulating antibodies
(TSH-RAb) will diminish or cease. Antithyroid drugs cannot cure a toxic nodule. The overactive thyroid tissue is autonomous and recurrence of
the hyperthyroidism is certain when the drug is discontinued.
● Advantages. No surgery and no use of radioactive materials.
● Disadvantages. Treatment is prolonged and the failure rate is at least 50%. The duration of treatment may be tailored to the severity of the
toxicity, with milder cases being treated for only 6 months and severe cases for 2 years before stopping therapy.
SURGERY
surgery cures by reducing the mass of overactive tissue by reducing the thyroid below a critical mass.
After subtotal thyroidectomy the patient should return to a euthyroid state, albeit after a variable period of hypothyroidism. There are however,
the long-term risks of recurrence and eventual thyroid failure.
In contrast total/ near total thyroidectomy accepts immediate thyroid failure and lifelong thyroxine replacement to eliminate the risk of
recurrence and simplify follow-up.
Operation may result in a reduction in TSH-RAb.
In the autonomous toxic nodule, and in toxic nodular goitre with overactive autonomous toxic nodules, surgery cures by removing all the
overactive thyroid tissue; this allows the suppressed normal tissue to function again. ● Advantages. The goitre is removed, the cure is rapid
and the cure rate is high if surgery has been adequate. ● Disadvantages. Recurrence of thyrotoxicosis occurs in at least 5% of cases when
subtotal thyroidectomy is carried out. There is a risk of permanent hypoparathyroidism and nerve injury. Young women tend to have a
poorer cosmetic result from the scar.

26. • . RADIOIODINE
• Radioiodine destroys thyroid cells and, as in thyroidectomy, reduces the mass of functioning thyroid tissue to
below a critical level.
• ● Advantages. No surgery and no prolonged drug therapy.
• ● Disadvantages. Isotope facilities must be available. The patient must be quarantined while radiation levels are
high and avoid pregnancy and close physical contact, particularly with children. Eye signs may be aggravated.
• Choice of therapy -age; facilities available,the personality and wishes of the individual patient, business or family
commitments and any other coexistent medical or surgical condition. Access to post-treatment care and
availability of replacement thyroxine.
DIFFUSE TOXIC GOITRE
Most patients have an initial course of antithyroid drugs with radioiodine for relapse. Exceptions are those who
refuse radiation, have large goitres, progressive eye signs or are pregnant.
TOXIC NODULAR GOITRE Toxic nodular goitre is often large and uncomfortable and enlarges still further with
antithyroid drugs. A large goitre should be treated surgically because it does not respond as well or as rapidly to
radioiodine or antithyroid drugs as does a diffuse toxic goitre.
TOXIC NODULE Surgery or radioiodine treatment is appropriate. Resection is easy, certain and with a low risk of
morbidity. Radioiodine is a good alternative for patients over the age of 45 years because the suppressed thyroid
tissue does not take up iodine and thus there is minimal risk of delayed thyroid insufficiency.
FAILURE OF PREVIOUS TREATMENT WITH ANTITHYROID DRUGS OR RADIOIODINE In this case, surgery or thyroid
ablation with 123I is appropriate.

27. Surgery for thyrotoxicosis
• Preoperative preparation
• Traditional preparation aims to make the patient biochemically euthyroid at operation. Preparation is as an out-patient and only
rarely is admission to hospital necessary on account of severe symptoms at presentation, failure to control the hyperthyroidism
or non-compliance with medication. Care should be coordinated with endocrinology input. Carbimazole 30–40mg per day is the
drug of choice for preparation. When euthyroid (after 8–12 weeks), the dose may be reduced to 5mg 8-hourly or a ‘block and
replace’ regime used. In this case, the high dose of carbimazole is continued to inhibit T3 and T4 production and a maintenance
dose of 0.1–0.15mg of thyroxine is given daily. The last dose of carbimazole may be given on the evening before surgery. Iodides
are not used alone because, if the patient needs preoperative treatment, a more effective drug should be given. An alternative
method of preparation is to abolish the clinical manifestations of the toxic state, using β-adrenergic blocking drugs. These act on
the target organs and not on the gland itself. Propranolol also inhibits the peripheral conversion of T4 to T3. The appropriate
dosages are propranolol 40mg t.d.s. or the longer acting nadolol 160mg once daily. Clinical response to β-blockade is rapid and
the patient may be rendered clinically euthyroid and operation arranged in a few days rather than weeks. The dose of β-
adrenergic blocking drug is increased to achieve the required clinical response and quite often larger doses (propranolol 80mg
t.d.s. or nadololol 320 mg once daily) are necessary. β-adrenergic blocking drugs do not interfere with synthesis of thyroid
hormones, and hormone levels remain high during treatment and for some days after thyroidectomy. It is, therefore, important
to continue treatment for 7 days postoperatively. Iodine may be given with carbimazole or a β-adrenergic blocking drug for 10
days before operation. Iodide alone produces a transient remission and may reduce vascularity, thereby marginally improving
safety. The use of iodine preparations is not universal because of more effective alternatives. Iodine gives an additional
measure of safety in case the early morning dose of β-adrenergic blocking drug is mistakenly omitted on the day of operation.
The extent of the resection depends on the size of the gland, the age of the patient, the experience of the surgeon, the need to
minimise the risk of recurrent toxicity and the wish to avoid postoperative thyroid replacement (Table 50.5

28. SURGICAL TECHNIQUE OF THYROIDECTOMY
• the first step is informed consent. Patients should understand the risk of scar, RLN damage, bleeding, hypocalcaemia and hypothyroidism.
Endotracheal intubation is performed, and if a nerve monitor is to be used its position should be confirmed once the patient is in the surgical
position (see New technology in thyroidectomy, below). The patient lies supine with the neck extended. Surgical preparation extends from the
mandible on to the chest. A skin crease incision is placed around the level of the cricoid cartilage. Classically those patients with ‘pendulous’
breasts should have an incision placed more superiorly as it will tend to migrate inferiorly over years and a sternal wound is less attractive.
Subplatysmal flaps are raised to an extent that allows access to the goitre, often from thyroid notch to sternal notch. The midline is identified
between the strap muscles. The plane is developed to dissect between the muscle layers, elevating sternohyoid laterally until ansa cervicalis is
visualised. The sternothyroid muscle is then mobilised from the gland, taking great care with the delicate vasculature. If required, the strap
muscles may be divided superiorly to afford greater exposure. Attention is turned first to the superior pole. A plane between the larynx and
superior pole is developed and the branching divisions of the superior vascular pedicle are dissected. As these insert onto the gland they are
dissected, controlled with ties or bipolar diathermy and divided individually. Not only does this mobilise the superior pole, but preserves the
blood supply to the superior parathyroid gland. In addition, this minimises risk to the superior laryngeal nerve, which can often be seen
passing medially towards the cricothyroid muscle. Gradually the superior pole is mobilised taking care not to dissect below the cricoid
cartilage, at which point the RLN is at risk. By now, the fascia around the thyroid has been clearly identified. This plane is followed over the
anterolateral aspect of the gland to the inferior pole. The tracheoesophageal groove should not be entered at this point as the RLN is yet to
be identified. Inferiorly the trachea should be dissected in order to confirm the anatomical landmark. At this point structures inferior and
superior to the RLN have been identified and careful dissection toward the lateral aspect of the gland allows the gland to be rotated medially,
displaying the tracheoesophageal groove. Careful dissection of this area proceeds being sure not to divide any structure that could be the
nerve. The fascia from the thyroid is mobilised, being vigilant throughout. The RLN is identified and confirmed by the anatomical location,
direction of travel and the nerve monitor, if in use. The nerve is then traced towards the larynx, allowing mobilisation of the lateral aspect of
the gland. During this part of the dissection the surgeon must prioritise identification of the nerve, preservation of the inferior parathyroid
and its blood supply, as well as control of branches of the inferior thyroid artery. Again, these should be divided in a controlled manner as
close as possible to gland in order to preserve parathyroid blood supply. At this stage the nerve should be traced towards the cricothyroid
joint as it enters the larynx. This point is the area where the nerve is most commonly damaged. The pretracheal fascia condenses into Berry’s
ligament at this stage. Small vessels within the ligament retract if not controlled with bipolar diathermy or ties, and the resulting bleeding can
disorientate the surgeon placing the nerve at risk (Figure 50.19). In order to avoid this, pre-emptive diathermy to the ligament and careful
layer by layer dissection allows final mobilisation of the thyroid lobe. Some surgeons prefer to isolate the ligament and apply a careful tie to
achieve haemostasis.

29. • Whichever method is preferred, great care must be taken at this point. The lobe is then mobilised
medially and the nerve falls laterally. If total thyroidectomy is indicated the procedure is repeated on
the contralateral side. If, however, lobectomy alone is indicated, the isthmus should be divided
between clamps and oversewn. The surgical bed is then inspected to confirm the integrity of the nerve
and the state of the parathyroid glands. Consideration may be given to reimplantation of parathyroids to
the sternomastoid muscle if they appear devascularised. Irrigation followed by meticulous haemostasis
should follow and no bleeding is acceptable. Ideally this is performed with a Valsalva manouvre with the
head down. Following complete haemostasis the strap muscles are loosely reapproximated in order to
avoid a water tight seal but to prevent adhesion between skin and trachea. The wound is then closed in
layers with absorbable suture to platysma and skin closure. This may be with clips, non-absorbable
sutures or subcuticular closure. It is important that those involved in postoperative care know how the
wound was closed and how to perform a bedside reopening in the event of a lifethreatening bleed. The
patient is then returned to the recovery room and the postoperative area for overnight monitoring. Not
only is the wound regularly reviewed, but for total thyroidectomy patients postoperative calcium should
be checked to identify hypocalcaemia.

30. POSTOPERATIVE COMPLICATIONS
• Haemorrhage is the most frequent life-threatening complication of thyroidectomy. If an arterial bleed occurs, the tension in the central compartment pressure can rise
until it exceeds venous pressure. Venous oedema of the larynx can then develop and cause airway obstruction leading to death.
• When closing the wound, avoiding a watertight closure of the strap muscles may allow a haematoma to escape into the subcutaneous tissues. Wound drains have not
been shown to have a protective effect. Close monitoring of the wound is advised postoperatively.
• If a haematoma develops, clinical staff should know to remove skin sutures in order to release some pressure and seek senior advice immediately. Endotracheal
intubation should be used to secure the airway while the haematoma is evacuated and the bleeding point controlled.
• Recurrent laryngeal nerve paralysis and voice change RLN injury may be unilateral or bilateral, transient or permanent. Early routine postoperative laryngoscopy reveals
a much higher incidence of transient cord paralysis than is detectable by simple assessment of the integrity of the voice and cough. If a RLN is injured during surgery and
the transected ends are identified, they should be reanastomosed. In the event that a length of nerve is excised (due to invasion by malignancy for example),
anastomosis of the ansa cervicalis may be considered. This does not return mobility of the vocal cord but maintains neurological input to the muscles of the larynx. By
avoiding denervation and related muscle atrophy, the vocal quality is improved.
• Permanent vocal cord paralysis should be treated conservatively with speech therapy. If voice quality is unacceptable, medialisation procedures can be performed.
Nerve grafting has shown promise but experience is limited.
• Injury to the external branch of the superior laryngeal nerve is more common because of its proximity to the superior thyroid artery. This leads to loss of tension in the
vocal cord with diminished power and range in the voice.
• . Thyroid insufficiency Following total thyroidectomy, clearly thyroxine replacement will be required. Around one in three patients who has a lobectomy will require
supplementation; rates are higher in those with thyroid autoantibodies. Subtotal thyroidectomy was at one time performed with the aim of leaving sufficient tissue to
maintain thyroid function
• Parathyroid insufficiency This is due to removal of the parathyroid glands or infarction through damage to the parathyroid end arteries; marked hypocalcaemia may be
asymptomatic. The complication is limited to total thyroidectomy, as when lobectomy is performed the contralateral parathyroid glands are sufficient to maintain
calcium levels
• Thyrotoxic crisis (storm) This is an acute exacerbation of hyperthyroidism. It occurs if a thyrotoxic patient has been inadequately prepared for thyroidectomy and is now
extremely rare. Very rarely, a thyrotoxic patient presents in a crisis and this may follow an unrelated operation. Symptomatic and supportive treatment is for
dehydration, hyperpyrexia and restlessness. This requires the administration of intravenous fluids, cooling the patient with ice packs, administration of oxygen, diuretics
for cardiac failure, digoxin for uncontrolled atrial fibrillation, sedation and intravenous hydrocortisone. Specific treatment is by carbimazole 10–20mg 6-hourly, Lugol’s
iodine 10 drops 8-hourly by mouth or sodium iodide 1g i.v. Propranolol intravenously (1–2mg) or orally (40mg 6-hourly) will block β-adrenergic effects.

31. • Wound infection
• Cellulitis requiring prescription of antibiotics, often by the general practitioner, is more common than
most surgeons appreciate. A significant subcutaneous or deep cervical abscess is exceptionally rare and
should be drained.
• Hypertrophic or keloid scar This is more likely to form if the incision overlies the sternum and in dark
skinned individuals. Intradermal injections of corticosteroid should be given at once and repeated
monthly if necessary. Scar revision rarely results in significant long-term improvement.
• Stitch granuloma This may occur with or without sinus formation and is seen after the use of non-
absorbable, particularly silk, suture material. Absorbable ligatures and sutures should be used
throughout thyroid surgery. Some surgeons use a subcuticular absorbable skin suture rather than the
traditional skin clips or staples.
• POSTOPERATIVE CARE Following surgery, the patient should be returned to the recovery room and
nursed overnight on the ward. Wound care should include vigilance for signs of a haematoma. Following
total thyroidectomy, calcium levels should be checked postoperatively. Not all patients develop
immediate hypocalcaemia and they should be educated about the signs (parasthesia of the fingers and
toes or round the mouth). Serial calcium monitoring should be recommended for those at highest risk.
Those patients who had a total thyroidectomy require thyroxine replacement, which should start day 1
postoperatively. On clinic review, in addition to checking the histology report, the wound should be
inspected and the larynx examined for vocal cord function. Biochemical assessment of thyroid function
and calcium, if required, should be arranged.