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The most common site of a nodule is at the junction of isthmus
with one lobe.
Manipal Manual of Surgery
Complications of Multinodular Goitre
1. Calcification in long-standing MNG.
2
. Sudden haemorrhage in one of the nodules causes
dyspnoea.
3. In 10–20% of cases, patients can develop secondary
thyrotoxicosis with CVS involvement. Palpitation is
the predominant symptom. Toxic multinodular
goitre is also called Plummer’s disease.
Tachycardia can be graded as follows—Crile’s grading
Grade I <90/min—mild
Grade II 90 to 100/min—moderate
Grade III >110/min—severe
4. Follicular carcinoma in a long-standing goitre 8 to
15%.
Management of Multinodular Goitre
Investigations
1. Complete blood picture (CBP), and a few investigations for fitness including baseline ECG and echo
cardiography more so in toxic goitres.
. X-ray of the neck: Anteroposterior and lateral view.
2
• To look for compression of trachea—to check feasi-
bility of intubation during anaesthesia (Fig. 37.15).
• To rule out retrosternal extension—soft tissue
shadow seen.
• Calcification in long-standing MNG.
. Flexible laryngoscopy is done to see vocal cord
3
mobility (this has replaced indirect laryngoscopy).
4. Ultrasonography: High frequency ultrasound (7–
15 MHz) is the first investigation in thyroid swellings.
(TIRADS—More details are given on page 417). In
multinodular goitres, ultrasound guided FNAC
can be done. It can also detect clinically impalpable
lymph nodes in the neck (suggest malignancy)
(Key Box 37.6). Like in the breast, ultrasound
examination of the thyroid gland has been categorised into TIRADS—Thyroid Imaging Reporting and
Data Systems. 5 categories have been identified. It is
applicable in all nodules more than 1 cm or more in
diameter.
• Ultrasound examination is inexpensive, easily done
and has more advantages than disadvantages.
Thus, it is often the first investigation in thyroid
swellings (Refer to clinical notes).
Key Box 37.6
Ultrasound
It can distinguish solid from cystic lesions.
It can measure the size of the nodule.
It can reveal multicentric nature of the goitre.
It can detect lymphadenopathy and can guide FNAC.
It can detect microcalcification—a feature of
malignancy-peripheral punctate calcification in the
cervical nodes.
↑ echogenicity means ↑ chances of tumour/malignancy.
↑ sonolucent means ↑ chances of cyst (benign).
5. Fine needle aspiration cytology (FNAC): It can be
done in suspected hard nodule of multinodular
goitre. It is a simple and useful investigation which
can detect malignancy. Since the treatment of MNG
is often total thyroidectomy and an ultrasonogram
can also help to rule out malignancy, FNAC is done
only in suspicious cases of MNG.
6. CT scan is done when you suspect retrosternal
extension, doubtful resectability in cases of carotid
pulses are not palpable or large lymph nodes in the
neck. They may also have intrathoracic lymph nodes
(Fig. 37.55).
Section II • General Surgery
Fig. 37.15: X-ray of the neck—lateral view
Classification of Investigations (Key Box 37.7)
Key Box 37.7
Investigations—Goitre
1. Simple goitres
Routine—blood tests, chest X-ray, flexible laryngo-
scopy, ultrasound
2. Toxic goitres
Routine and T
, T4, TSH
3
3. Malignant goitre
Routine and CT scan of the neck—optional
FNAC: Ultrasound guided is a must
Thyroid Gland
1. A 22-year-old lady was referred to us for a nodule in
the right side of neck in the thyroid region that was
moving with deglutition. She also had epigastric pain
since 6 months. Clinical diagnosis of solitary thyroid
nodule with hyperacidity was made. An ultrasound
examination of the neck was requested and the report
was a surprise. She was having a parathyroid adenoma
with calcific pancreatitis and nephrocalcinosis. You know
the diagnosis now—a case of hyperparathyroidism.
2. We sent a case of MNG to thyroid scan. The scan
detected jugular lymphadenopathy on both sides. The
diagnosis changed from MNG (benign) to malignancy
(papillary carcinoma because of lymph nodes). Lymph
nodes were not palpable on clinical examination in
this patient.
3. A 21-year-old lady had a multinodular goitre with the
entire gland replaced by nodules. Case was posted for
a total/near total thyroidectomy. A senior experienced
Professor asked one question, ‘what is the duration of
this swelling?’ It was 10 years. He said postpone the
surgery, and do FNAC. As per his advice, FNAC was
done. FNAC report was lymphocytic thyroiditis.
Surgery was cancelled. She was put on T-Eltroxin
0.1 mg, 2 tablets/day. She is on follow-up now. Gland
size is reduced to 30% in the last 2 years.
Prevention of MNG
Prevention is mainly important in endemic area and is
done by supplementing iodine (Key Box 37.8).
Key Box 37.8
Prevention of MNG
Puberty goitre : 0.1 g to 0.2 mg of thyroxine.
Iodine deficiency goitre : Use iodised salt, sea food,
milk, egg, etc.
Goitrogens : Avoid cabbage, drugs.
Treatment
Three choices are given to patients.
1. Total thyroidectomy is the choice today provided
complications such as recurrent laryngeal nerve,
paralysis and hypocalcaemia due to removal of para-
thyroid glands can be avoided. Thus, it is desirable
to do a total thyroidectomy, if experience of the
surgeon is good and in a high volume centre. It gives
permanent quick cure to the patient (Fig. 37.16).
2. Subtotal thyroidectomy: In this operation, parts of
right and left lobes and entire isthmus are removed
in flush with tracheal surface leaving behind a small
amount of tissue in the tracheoesophageal groove to
protect recurrent laryngeal nerve and parathyroid
405
Fig. 37.16: Total thyroidectomy specimen
gland. Subtotal thyroidectomy is not done nowadays.
Students should study Fig. 37.17 first. Details of
management of MNG are given in Fig. 37.17.
3. Dunhill procedure: In a few cases, one lobe is
completely replaced with nodules and a few nodules
on the other side. In such cases total lobectomy on
one side and subtotal lobectomy on the other side
can be done.
• Some surgeons treat these patients with 0.1 mg of
thyroxine to suppress the TSH stimulation in the
postoperative period, for a period of 2–5 years.
• However, it should be remembered that risk of
osteoporosis, atrial fibrillation and increased
morbidity and mortality from cardiovascular
disease can occur. Hence, patients should be told
about these complications.
RETROSTERNAL GOITRE
Definition: When more than 50% of goitre is below
suprasternal notch, it is called retrosternal goitre. Very
often, it is a multinodular goitre that develops in the
neck and is slowly pulled down behind the sternum due
to the following reasons.
. Negative intrathoracic pressure
1
2. Pretracheal muscles are strong in men
3. Short neck, obesity
Rarely, it arises from an ectopic thyroid tissue.
Classification
. Primary: It arises from ectopic thyroid tissue in the
I
mediastinum. It also derives blood supply from
mediastinum. It is rare (1%).
II. Secondary: It is the common variety—it is MNG
which gets pulled down into thorax.
Clinical Types
• Substernal: The most common type where the lower
border of the gland is behind the sternum.
• Intrathoracic: No thyroid is seen in the neck, diag-
nosed by radio-iodine scan.
Section II • General Surgery
406
Manipal Manual of Surgery
Fig. 37.17: Management of multinodular goitre—for diagrams see operative surgery chapter on thyroid diseases
• Plunging goitre: When patient is asked to cough,
intrathoracic pressure increases. As the thyroid
plunges out, the lower border of gland is clearly seen
in the neck.
Clinical Features
• It can be suspected when the lower border of the
swelling is not seen.
• Most of the patients have difficulty in breathing or
even stridor.
• Dysphagia is more common.
• Engorgement of neck veins and superficial veins.
These become more prominent when the hands are
raised above the head, and the arms touch the ears
with congestion and cyanosis of the face—
Pemberton’s sign (Fig. 37.18).
Investigations
• They are similar to MNG. However, isotope scan is
very useful in the diagnosis of intrathoracic goitres.
• CT scan to localise and to know the size and extent.
Section II • General Surgery
• CT scan classification of retrosternal goitre is
important because depending upon the extent of
intra-thoracic extension, treatment is planned.
Treatment
• No conservative line of treatment.
• It can be easily explored through the neck incision and
removed, with gentle dissection with the finger
specially when the intra-thoracic part has narrow apex.
• Very rarely, a sternal split may be necessary.
Fig. 37.18: Observe the engorged veins due to retrosternal
goitre. Such veins are also seen when mediastinal nodes are
enlarged as in papillary carcinoma thyroid
Thyroid Gland
407
Summary (Key Box 37.9)
Key Box 37.9
Retrosternal Goitre
Very often, it is an MNG with the lower border unseen
Rarely from ectopic thyroid tissue
Severe breathlessness even though small
Drugs should not be given, if it is toxic
Pressure effects diagnosed by Pemberton’s sign
Excision is the treatment
No radioiodine therapy
TOXIC GOITRE—THYROTOXICOSIS
It is a complex disorder which occurs due to increased
levels of thyroid hormones (hyperthyroidism) and
manifests clinically with various signs and symptoms
involving many body systems. Following are the causes
of thyrotoxicosis.
1. Primary thyrotoxicosis (Graves’ disease, exophthalmic
goitre, diffuse goitre).
2. Secondary thyrotoxicosis: Secondary to nodular
goitre (multinodular) (Plummer’s disease).
3. Solitary toxic nodule: Autonomous nodule which is
not under the influence of TSH but occurs due to
hypertrophy and hyperplasia of gland (tertiary thyrotoxicosis).
4. Other causes of thyrotoxicosis
• Thyrotoxicosis factitia: False thyrotoxicosis occurs
due to overdosage of thyroxine, given for puberty
goitre.
• Jod-Basedow’s thyrotoxicosis: Jod means iodine
in the German language, Basedow means toxic
goitre. Iodine-induced thyrotoxicosis (iodine given
for hyperplastic endemic goitres).
• Initial stage of thyroiditis: Hashimoto’s thyroiditis,
viral thyroiditis can produce temporary thyrotoxicosis features.
• Very rarely, malignant goitres can be toxic
(differentiated carcinoma).
• Neonatal thyrotoxicosis occurs in babies born to
thyrotoxic mothers.
• TSH-secreting tumours of pituitary
• Struma ovarii
• Drugs: Amiodarone is an iodine-containing
preparation given as antiarrhythmic drug.
GRAVES’ DISEASE
• Also called diffuse toxic goitre.
Aetiopathogenesis
The exact aetiological factors responsible for the disease
are not clear. Following are considered as possible
aetiological factors:
1. Autoimmune disorder is the first possible cause due
to the demonstration of autoantibodies in the
circulation. Example: TSH receptor antibodies. It can
be associated with other autoimmune disorders like
vitiligo, type 1 diabetes mellitus, Addison’s disease,
myasthenia gravis and pernicious anaemia.
2. Familial/genetic: The disease can run in families.
Familial/genetic Graves’ disease has been documented
in identical twins.
• Graves’ disease is associated with certain HLA
haplotypes, like HLA-B8, DR3, DQA1. Here a few
triggering factors can result in Graves’ disease.
(Key Box 37.10).
• HLA-DRB1*0701 is protective against Graves’
disease.
• Polymorphism of cytotoxic T lymphocyte antigen-4
(CTLA-4) is also associated with Graves’ disease.
3. Thyroid-stimulating immunoglobulins (TSI) and
long-acting thyroid stimulator (LATS) are responsible
for pathological changes in the thyroid gland in
Graves’ disease. They stimulate thyrocytes to grow
and synthesize excess thyroid hormones.
4. Exophthalmos producing substance (EPS) is
responsible for ‘ophthalmopathy’ seen in Graves’
disease.
5. Female sex, emotions, stress, young age also have
been considered as other factors responsible for the
disease.
Key Box 37.10
Triggering Factors for Graves’ Disease
Postpartum state
Iodine excess
Lithium therapy
Infection—bacterial and viral
Pathology
As a result of continuous stimulation, acinar hypertrophy and hyperplasia take place. The acinar cells
which are normally flat, become tall columnar. The
normal colloid disappears and the cells are empty.
However, rich vascularity is seen. Thus, small follicles
with hyperplastic columnar epithelium is characteristic
(Flowchart 37.1).
Section II • General Surgery
408
Manipal Manual of Surgery
Flowchart 37.1: Aetiopathogenesis
Clinical Features
• Primary thyrotoxicosis is 8 times more common in
females than in males, especially in the age group of
15–25 years. Thyroid swelling, features of thyrotoxicosis and exophthalmos are considered as triad
of Graves’ disease. Symptoms, signs and swelling
appear simultaneously.
• Very often young women present with unexplained
loss of weight in spite of good appetite and insomnia
is brought with diarrhoea. Diarrhoea occurs due to
increased smooth muscle activity of small intestines.
Intolerance to heat, preference to cold, fine tremors,
excitability, hyperkinetic movements, excessive
sweating are the other features. Free steroid hormone
levels decrease Graves’ disease. This results in
decreased effective oestrogen at the cell level which
in turn causes oligomenorrhoea. Never forget to
examine pulse rate specially in young patients who
are losing weight unintentionally. Tachycardia is a
feature.
Sleeping pulse rate is counted after the patient is sedated with
30 mg of phenobarbitone. In a case of toxic goitre, the pulse
rate remains high even during sleep because of increased
metabolism. This is a simple bedside investigation in cases of
toxic goitre. In anxiety states, pulse rate may be high in the
waking hours and it comes back to normal during sleep.
etc. She was given unnecessary tonics. After nearly
6 months, when eye-signs started developing, it was
proved to be Graves’ disease.
2. A bank clerk’s only complaint was that he could not
sign the cheque because of excessive sweating.
Thyroid gland was not palpable. His pulse rate was
very high, investigations revealed that it was a case of
primary thyrotoxicosis. On careful questioning, he
admitted that he was a “nervous character”.
3. A 24-year-old lady was being asked by her friends
every day why her eyes were prominent. Her only
complaint was prominent eyes. On careful questioning,
she admitted having anxiety, tension, excitability.
Signs of Primary Thyrotoxicosis
I. Signs of Thyroid Gland in Graves’ Disease
• Uniformly enlarged (mild degree)
• Smooth surface—no nodules (treated cases may have
nodularity)
• Gland is soft or firm in consistency.
• It is warm—highly vascular and can be pulsatile
• Auscultation—a bruit can be heard.
II. Central Nervous System (CNS) Signs
• Tremors of the tongue when the tongue is within the
oral cavity and tremors of the outstretched hands are
characteristics. A piece of paper may be placed on
the fingers in doubtful cases for demonstrating the
tremors of the hand. Extensor surface of the hand is
used because extensors are weak when compared to
flexors.
• Hyperkinetic movements
• Always a moist, warm hand (shake hands with the
patient).
III. Cardiovascular System (CVS) Signs
• Pulse rate is always raised and rapid indicating
tachycardia. Depending upon the pulse rate,
thyrotoxicosis can be classified as follows: Mild—90–
100/min, moderate—100–110/min, severe—more
than 110/min.
• Palpitation and extrasystoles can also be found in
primary thyrotoxicosis even though other cardiac
features, such as fibrillation and cardiac failure, are
rare.
Following are three case reports which highlight the
clinical symptomatology of primary thyrotoxicosis.
1. An 18-year-old girl visited many doctors for her
complaint of loss of weight. She was investigated for
Section II • General Surgery
tuberculosis (common disease in India), malignancy,
IV. Eye Signs
• Prominent eyeballs and retraction of the eyelid result
in thyrotoxic exophthalmos. This is due to retrobulbar
deposition of inflammatory cells and round cells with
venous congestion resulting in oedema (Figs 37.19
and 37.20).
Thyroid Gland
Fig. 37.19: He was 31-year-old
with loss of weight of 12 kg in
3 months. There was diffuse
enlargement of the gland with
exophthalmos
Fig. 37.20: She was 48-year-
old lady who had multinodular
goitre of 10 years duration
also had lid-lag sign (rare in
toxic MNG)
. She
• Levator palpebrae superioris muscle is innervated
by oculomotor nerve which also carries sympathetic
fibres derived from cavernous plexus for the smooth
muscle part of the levator. Contraction of this muscle
produces lid spasm.
• This is aided by spasm of Müller’s muscle, a
sympathetic muscle which lies adjoining the levator
palpebrae superioris muscle. This is responsible for
keeping the eyeball forwards. All these factors
together produce a classical stare.
1. Assessment of exophthalmos
• Upper sclera is seen above the limbus (upper margin
of the cornea and conjunctiva—Dalrymple’s sign.
• Naffziger’s method: Stand behind the patient and
look at the supraciliary arch, by tilting the patient’s
head backwards. In normal cases, eyeball is not
seen. In cases of exophthalmos, eyeball is protruded outside and hence it is seen.
2. Moebius’ sign: Loss of convergence of eyeball occurs
due to muscle paresis as a part of thyrotoxic
ophthalmoplegia. Diplopia is due to weakness of
extraocular muscles (inferior oblique-elevators).
409
3. Stellwag’s sign: Infrequent blinking and widening
of palpebral fissure is due to spasm of sympathetic
fibres in the levator palpebrae superioris.
4. Joffroy’s sign: Absence of wrinkling of the forehead
when the patient is asked to look upwards. This occurs
due to increase in the field of vision due to exophthalmos.
5. von Graefe’s sign (lid-lag sign): When the patient is
asked to look up and down, upper eyelid cannot cope
up with the speed of movement of the finger because
of the lid spasm. Hence, the lid lags behind.
6. Enroth sign: Oedema of eyelids and conjunctiva.
7. Gifford’s sign: Difficulty in everting the upper eyelid.
8. Kocher’s sign: When an attempt is made to lift the
eyes higher, upper eyelid springs up more quickly
than the eyebrows.
How to differentiate proptosis form exophthalmos? In thyrotoxicosis the upper eyelid cannot be everted or inverted easily
but in cases of proptosis due to intra-orbital mass upper eyelid
can be everted easily.
Summary (Table 37.4 and Key Boxes 37.11 to 37.13)
Key Box 37.11
Thyrotoxic Exophthalmos
Proptosis and lid retraction result in exophthalmos
Sclera is visible beyond limbus
Naffziger’s method to examine
Staring look
Typically seen in Graves’ disease
Rarely seen in secondary thyrotoxicosis
Key Box 37.12
Interesting 6 Ps of Graves’ Ophthalmopathy
Prominent eyes
Periorbital oedema
Papilloedema
Proptosis
Palpebral fissure widening
Progression to blindness
Table 37.4 Symptoms of thyrotoxicosis
Symptoms of Symptoms of increased In females In children
hyperthyroidism adrenergic stimulation
Heat intolerance Palpitations Amenorrhoea Rapid growth
Increased sweating, thirst Nervousness, fatigue Decreased fertility
Weight loss in spite of Emotional lability Miscarriages
good caloric intake Hyperkinesis, tremors
Prominent stare is due to catecholamine excess
Section II • General Surgery
410
Manipal Manual of Surgery
Key Box 37.13
Grading of Thyroid Eye Diseases
Grade 0 No signs or symptoms
Grade 1 Only signs, no symptoms
Grade 2 Both signs and symptoms
Grade 3 Proptosis
Grade 4 Extraocular muscle involvement
Grade 5 Corneal involvement
Grade 6 Loss of vision with optic nerve atrophy
Malignant Exophthalmos
• This occurs in untreated cases of Graves’ disease.
• If the disease continues, infrequent blinking secon-
dary to exophthalmos results in constant exposure
of the cornea to the atmosphere. This results in
keratitis, corneal ulcer, conjunctivitis, chemosis and
may even lead to blindness. This is called malignant
exophthalmos.
• Malignant exophthalmos is probably due to auto-
immune disease.
• In late stages, optic nerve damage and blindness can
occur.
Treatment of thyrotoxic ophthalmopathy
. Massive doses of steroids—methylprednisolone and
1
metronidazole
2. Lateral tarsorrhaphy
3. Orbital decompression may be necessary in late cases.
4. Guanethidine eyedrops are useful to decrease lid
spasm and lid retraction.
5. Head end elevation and disease control.
6. Dark spectacles, 7% methylcellulose eye drops.
Important causes of exophthalmos
1. Thyrotoxicosis
2. Primary CNS tumours: Meningioma, optic nerve
glioma, haemangioma, lymphoma, etc.
3. Metastatic tumours: Neuroblastoma, central carcinoma.
4. Vascular: Cavernous sinus thrombosis—aneurysm of
ophthalmic artery.
Causes of pulsating exophthalmos
1. Cavernous sinus thrombosis
2. Carotid—cavernous sinus, A-V fistula
3. Orbital vascular tumour
4. Ophthalmic artery aneurysm
V. Thyrotoxic Myopathy
• Mild weakness of proximal limb muscles, ocular
Section II • General Surgery
and frontalis muscles is not uncommon. On careful
questioning, patient may admit difficulty in climbing
steps.
• Weakness of extraocular muscles results in double
vision (diplopia).
• Features suggestive of myasthenia gravis, periodic
paralysis can be found.
• Myopathy improves with treatment.
VI. Thyrotoxic Dermopathy (Key Box 37.14)
• Popularly called pretibial myxoedema—is seen in
thyrotoxicosis patients treated with surgery or
antithyroid drugs. It is always associated with
exophthalmos. It is seen in 1
–2% of patients.
• Bilateral symmetrical deposition of myxomatous
tissue (glycosaminoglycans) mainly in the pretibial
region, may also affect the foot and ankle, sometimes
the entire leg below knee. Skin is dry and coarse
(thickening of skin by mucin—like deposits).
Swelling is due to the obliteration of initial
lymphatics by mucin (see page 125).
• Pretibial myxoedema (misnomer) is nonpitting in
nature and may be associated with clubbing of
fingers and toes called thyroid acropachy. Responds
to topical steroids and thyroid disorder treatment
(Key Boxes 37.15 and 37.16).
Interestingly following 4 important features are seen
only in primary thyrotoxicosis, not in secondary
thyrotoxicosis (Key Box 37.17).
Key Box 37.14
Skin Changes
Pretibial myxoedema
Pruritis
Palmar erythema
Thinning of hair
Dupuytren’s contracture
Key Box 37.15
Pretibial Myxoedema—Misnomer
Acropachy—clubbing of fingers and toes
Coarse hair
Red shiny skin
Obliteration of initial lymphatics by mucin, oedema
non-pitting
Pretibial region, foot and ankle
After a few years of toxicosis, it develops
Cyanotic when cold
H • Hyaluronic acid deposition in dermis
Y • Bilateral and symmetrical
Remember as ACROPACHY
Thyroid Gland
411
Key Box 37.16
Some Misnomers
Pretibial myxoedema – Not seen in myxoedema
Mycosis fungoides – Not a fungal infection
White bile – Not white, not bile
Adenolymphoma – Not a lymphoma
Sternomastoid tumour – Not a tumour
Malignant hydatid – Not malignant
Key Box 37.17
Extrathyroidal Manifestations of Graves’ Disease
Pretibial myxoedema
Proximal myopathy
Pachy (acropachy)
Progressive ophthalmoplegia
At the end of clinical examination, commonly asked
question is, how will you differentiate primary thyrotoxicosis from secondary thyrotoxicosis (Table 37.5).
Management of Primary Thyrotoxicosis
Routine isotope scanning has been abandoned in toxic
goitres except when toxicity is associated with
nodularity.
Investigations
• Routine investigations such as complete blood
picture, flexible laryngoscopy and X rays are done.
• Serum T
, T4 and TSH are measured. T3 or T4 levels
3
are high and TSH levels are low in thyrotoxicosis.
The normal level of T
level of T
is 55–150 nmol/L.
4
is 1.3–3.5 nmol/L and normal
3
• Thyroid stimulating antibodies are elevated (TSHRAbs).
Measurement of IgG immunoglobulins (TSHRAbs)
is not essential to make the diagnosis of thyrotoxicosis.
• As a first line investigation, ultrasound is done to rule
out nodularity (seconadry thyrotoxicosis).
Treatment of Primary Thyrotoxicosis
Aim of treatment
I. To restore patient to euthyroid state
To reduce the functioning thyroid mass to a very
II.
critical level (about 6–8 g of thyroid tissue)
III. To minimise complications
I. To Restore the Patient to Euthyroid State (Table 37.6)
• Other drugs such as potassium perchlorate are given
in the dose of 200 to 400 mg daily. Propylthiouracil
in the dose of 200 mg three times a day can also be
given in patients who develop neutropaenia due to
carbimazole.
• Propranolol inhibits peripheral conversion of T
to T3.
4
This results in rapid control of tachycardia and surgery
can be scheduled in a few days (within one week). It
should be continued for one week after surgery
because it does not interfere with synthesis of hormones.
Please note
• Iodine containing antiarrhythmic drug amiodarone may
worsen thyrotoxicosis.
• Propyl thiouracil is safe in pregnancy with Graves’ disease.
• Role of Lugol’s iodine is doubtful.
• Antithyroid drugs will not cure the disease. In selected
atients (30–40%), remission is possible with regular intake
p
of drugs. They may be continued for a maximum period of
2 years. If toxicity persists or recurs on stopping drugs,
surgery is recommended.+ However, majority of the patients
ultimately require surgery or radioiodine.
Table 37.5 Differences between primary and secondary thyrotoxicosis
Primary thyrotoxicosis (Graves) Secondary thyrotoxicosis (toxic MNG)
1. Age 20–40 years 35–50 years
2. Symptoms and signs Appear simultaneously, duration is short Long duration of a swelling and short duration of signs
3. Skin over thyroid Warm Not warm
4. Consistency Soft or firm Firm or hard
5. Surface Smooth Nodular
6. Auscultation Bruit is common Bruit uncommon
7. Eye signs Commonly found Rarely found (lid lag)
8. Predominant symptoms CNS CVS
9. Pretibial myxoedema Seen in 1–2% patients Never seen
10. Proximal myopathy Seen in 5% patients Never seen
11. Malignant exophthalmos Can be seen Never seen
Section II • General Surgery
412
Table 37.6 Antithyroid drugs: Routine preoperative preparation
Drugs and mode of action Dose Precautions/side effects
• Carbimazole: It blocks oxidation of 10 mg, 6th hourly and maintenance Takes 12 weeks for its action
iodide
to iodine and coupling dose of 10 mg two to three times a It should be given 6–8 hourly interval
reactions, thus reducing T
levels. It is metabolised to methimazole as sore throat. Skin rashes and toxic
after ingestion hepatitis are not uncommon. Aplasia cutis
and T
3
4
Manipal Manual of Surgery
day Dangerous agranulocytosis can manifest
is another side effect if carbimazole is given
in the first trimester.
• Propranolol is a nonselective β-blocker
reduces tachycardia. depending on the pulse rate Can precipitate bronchial asthma. T
Corticosteroids
• They can be used as reserve drugs in severe,
uncontrolled or resistant hyperthyroidism cases.
• They act by two ways—one by suppressing pituitary
thyroid axis and another by inhibiting peripheral
conversion of T
to T3.
4
• Action is rapid
• They are used along with other antithyroid drugs.
Block and replace treatment
• If a small dose of T
(20 mg up to 4 times/day) or T
3
(0.1 mg/day) is given along with antithyroid drugs,
there is less incidence of development of hypothyroidism and increase in the size of goitre.
, 20–40 mg, two or three times a day Congestive cardiac failure
levels are not decreased
T
4
operative care will reduce the complications of surgery.
Thus, antithyroid drugs, subtotal thyroidectomy and
radioiodine therapy are the three different modalities
available for the treatment of primary thyrotoxicosis.
The indications, merits and demerits of each treatment
are given in Fig. 37.21.
Treatment of Secondary Thyrotoxicosis
(Plummer Disease)
• Patients with severe cardiac damage entirely or partly
due to hyperthyroidism are middle-aged or elderly
4
with secondary thyrotoxicosis and the hyperthyroidism is not very severe. These patients develop
atrial fibrillation and cardiac failure, if left untreated
(Key Box 37.19). In elderly patients, when the opera-
II. To Reduce the Functioning Thyroid Mass
1. Total thyroidectomy can be offered to young patients
with a small-sized gland. This is the choice of treatment today. It controls the toxicity very faster. Hypothyroidism occurs but it is easy to treat. However, it
should be done by an experienced surgeon.
2. Radioiodine therapy: This is a suitable alternative to
surgery in cases of primary thyrotoxicosis in patients
above the age of 30 (Key Box 37.18).
tive risk is unacceptable, radioiodine is given.
Treatment with antithyroid drugs is started 48 hours
later and continued until radioiodine has had its effect
(6 weeks).
• If the cardiac symptoms are controlled well and
anaesthesia risk is acceptable, subtotal thyroidectomy/total thyroidectomy is done. However, the
gland that is left behind should be equal to the distal
phalanx of the thumb of the patient.
and
3
III. To Minimise Complications
Good preoperative preparation of the patient, good
anaesthetic and surgical techniques, and good post-
Key Box 37.18
Radioiodine Therapy
Today there is ‘no restriction of age and gender’.
(However, this is preferred in children only after
completion of growth and in adults only after family is
complete.)
Absolute contraindication is pregnancy.
Conception must be avoided for a period of 4 months
Section II • General Surgery
after radioiodine therapy.
Secondary Thyrotoxicosis Effects on CVS (Key Box 37.19)
Key Box 37.19
Secondary Thyrotoxicosis Effects on CVS
Tachycardia
Wide pulse pressure
Systolic scratch (Means-Lerman scratch)*
Extrasystoles
Atrial fibrillation
Cardiac failure
*Means-Lerman scratch is occasionally heard in left 2nd ICS during
expiration due to hyperdynamic circulation in thyrotoxicosis (Described
by J. Lerman and J. H. Means of Massachusetts’ General Hospital)
Thyroid Gland
413
Fig. 37.21: Indications, merits and demerits of different modalities of treatments for primary thyrotoxicosis
SOLITARY TOXIC NODULE
Treatment
• This is not under control of TSH. It is an autonomous
nodule.
• The control of toxicity is in the usual manner—
carbimazole and propranolol.
• This is an indication to do I
131
scan or preferably 99mTc
scan. Hot nodule takes up isotope (also in carcinoma).
Rest of the gland does not.
• Treatment is either by hemithyroidectomy or radio-
131
active iodine therapy—I
(details will be given later).
• More details about solitary thyroid nodule and how
to evaluate has been given later.
A Few Specific Thyroid Conditions
Causing Thyrotoxicosis
1. Thyrotoxicosis in children: Initially antithyroid drugs
are given for 10–15 years followed by surgery.
• Radioiodine is absolutely contraindicated as there
is a fear of carcinoma and growth retardation
(Key Box 37.21).
2. Thyrocardiac: It refers to a condition wherein cardiac
damage has resulted due to hyperthyroidism.
Classically, it happens in secondary thyrotoxicosis.
It is usually seen in middle-aged or old-aged patients.
Propranolol controls the disease very well. Radioiodine therapy is the treatment of choice.
3. Hyperthyroidism in pregnancy: Invariably, it occurs
in Graves’ disease. In the first trimester, surgery and
radioiodine are contraindicated. Carbimazole and
propylthiouracil cross the placenta. Surgery, if
necessary, can be done in 2nd trimester.
4. Apathetic thyrotoxicosis: Thyrotoxicosis in elderly
wherein pulse rate is low, they appear to be hypothyroid rather than hyperthyroid. Thyroid gland is
rarely palpable. Lethargy and behaviour changes.
5. Graves’ disease in postpartum period: Postpartum
thyroiditis with transient thyrotoxicosis due to
thyroid cell dysfunction may occur in 5 to 10%
patients during the first 4 to 12 months after delivery.
6. Struma ovarii: Thyroid tissue is present in 5 to 10%
of teratomas and occasionally such foci are hyper-
Section II • General Surgery