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A
SRB's Manual of Surgery
B
Figs. 6.28A and B: Ultrasound pictures of thyroid. It is often used to
see nodules, content—solid/fluid, size and extent.
Fig. 6.29: FNAC of thyroid (Courtesy: Dr Krishna Upadhya,
Pathologist,
Nandikoor Laboratory, Mangaluru).
Fig. 6.30: Patient earlier operated for nodular goitre. Note recurrent
nodule and scar of previous surgery.
is needed. Later suppressive dose of L thyroxine (0.2 to 0.3
mg daily) is given orally in morning time on empty stomach.
If FNAC report says follicular adenoma, then hemithyroidec-
tomy is done. If histology report says follicular carcinoma
(capsular and vascular invasion), then completion total
thyroidectomy is done. Completion thyroidectomy is done
usually within 7 days or after 3 weeks. If frozen section biopsy
proves carcinoma, then total thyroidectomy is done.
If FNAC report says medullary carcinoma of thyroid, then total
thyroidectomy with bilateral neck nodal dissection including
central compartment is done.
Indeterminate Nodule
If FNAC shows follicular neoplasm, then hemithyroidectomy,
paraffin section confirmation for capsular and vascular invasion; completion thyroidectomy in 7–14 days is done; later
radioactive iodine therapy is given.
If FNAC shows suspicious variety, then repeat FNAC is done.
If it is also suspicious then hemithyroidectomy is done;
frozen section biopsy is done to confirm if it is papillary
carcinoma; if so, total thyroidectomy with ipsilateral central
node neck dissection is carried out. (Frozen section is not
suitable for follicular neoplasm).
Solitary toxic nodule needs initial antithyroid drugs and then
radioactive iodine therapy (5 m curie); occasionally surgery
is done—hemithyroidectomy.
Colloid nodule can be observed or hemithyroidectomy is done
for cosmesis or just in pain or increase in size; thyroxine
therapy even though is commonly used, its benefit is not
proved.
Risk of malignancy in follicular lesion of undetermined signifi-
cance (FLUS) is 10%. Total thyroidectomy is indicated here.
If there is a nodule in the isthmus, isthmectomy is done with
excision of part of adjacent lateral lobes.
Malignant Nodule
If FNAC comes as papillary carcinoma of thyroid, then total
or near total thyroidectomy is done. If tumour is more than 2
cm, with extracapsular spread then radioactive iodine therapy
THYROID CYST
B
x It is thyroid swelling which is cystic in nature eliciting positive
fluctuation
x But tensely cystic swelling can be hard (thyroid paradox—with
cellular tumour of thyroid can be soft also)
x Common cause is colloid degeneration—50%. There will be
absence of epithelial lining
x Involution in follicular adenomas present like a cyst; 15% of such
cysts may be malignant
x 30% of solitary nodules are cystic
x 15% cystic swellings in thyroid are malignant
x Cyst formation is common in papillary carcinoma of thyroid
x A cyst if contains both solid and cystic areas, is called as complex
cyst which is more likely to be malignant
x FNAC may cause regression of simple cyst. Even after three
repeated aspirations if recurrence occurs, surgery is needed
x Surgery is indicated in complex cyst and if cyst is more than
4 cm in size.
x Percutaneous ethanol injection (PEI) may be useful in benign cyst.
Nondiagnostic Nodule
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Cyst that recurs and repeat FNAC also becomes nondiagnostic
then hemithyroidectomy and proceed is the better option
especially if nodule is more than 4 cm in size and or in highrisk group. Repeat FNAC becomes diagnostic in 50% of initial
nondiagnostic.
RETROSTERNAL GOITRE
Retrosternal goitre is defined as having >50% goitre below the
suprasternal notch, i.e. below the plane of thoracic inlet. Major
intrathoracic extension requiring mediastinal dissection, extension into the anterior mediastinum more than 2 cm in depth
or mass reaching the level of 4th thoracic vertebra are other
criterias considered.
Primary is rare—1%. Primary retrosternal goitre arises from
ectopic thyroid tissue from mediastinum. It gets its blood
supply from mediastinum itself, not from the neck. And also
it is not related to the existing thyroid in the neck.
Secondary is common. It is extension from the enlarged
thyroid from the neck. Usually arises from the lower pole
of a nodular goitre. Commonly seen in short neck or obese
individuals. Due to negative intrathoracic pressure, nodule
gets drawn into the superior mediastinum.
Types
1. Substernal type: Part of the nodule is palpable in the lower
neck.
2. Plunging goitre: An intrathoracic goitre is occa sionally forced
into the neck by increased intrathoracic pressure.
3. Intrathoracic goitre itself. Neck is normal. Common in men.
Features
Dyspnoea at night during lying down or neck extended.
Cough and stridor (stridor is harsh sound on inspiration).
Dysphagia.
Fig. 6.31: Superior vena cava obstruction due to thyroid extending
into the retrosternal area.
and arm.
Engorgement of neck veins and superficial veins on the
Note the dilated veins over neck, chest wall
chest wall.
Lower border is not seen on inspection and not felt on palpation.
Pemberton’s sign is positive. The patient is asked to raise the
arm above the shoulder level. Dilated veins are seen over neck
and upper part of chest wall. Stridor and rarely dysphagia may
occur. (When patient raises the arm above the shoulder level,
retrosternal goitre compresses over the easily compressible
structures like SVC and trachea causing dilated veins and
dyspnoea respectively).
Dull note over the sternum on percussion.
Retrosternal goitre can be either nodular, toxic or malignant.
Rarely recurrent nerve palsy can occur.
Retrosternal goitre has got similar chance of turning into
malignancy alike cervical goitre; but identifying by US or by
FNAC is difficult.
Differential diagnosis: Mediastinal tumours.
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CHAPTER 6 Thyroid
A B C
Figs. 6.32A to C: (A and B) X-rays (PA view and lateral view) showing retrosternal goitre.
(C) Diagrammatic representation of the retrosternal goitre.
Success consists of a series of little daily efforts.
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Investigations
Radioactive iodine study is diagnostic (I
CT/MRI is very useful investigation. CT neck and chest is
ideal.
T
, T4, TSH estimation.
3
Chest X-ray will show soft tissue shadow; barium swallow
X-ray will show oesophageal indentation.
Lung function tests are useful.
or technetium).
123
Treatment
SRB's Manual of Surgery
Surgical removal of retrosternal thyroid is done. Commonly,
it can be removed through an incision in neck (as blood
supply of retrosternal goitre is from neck), but in case of
large retrosternal extension or in malignant type median
sternotomy is required (rarely).
Even asymptomatic retrosternal goitre needs surgery; total
thyroidectomy with careful extirpation of the retrosternal extension through cervical incision is the choice.
Note:
• Radioiodine therapy is not accepted in retrosternal goitre.
• Stridor due to compression of tracheobronchial tree by retrosternal
goitre is very dangerous because it is often not possible to clear the
airway either by intubation or by tracheostomy.
• Surgical removal should be complete because recurrent retrosternal
goitre is very difficult to re-operate.
• In the case of retrosternal goitre, hemoptysis unmixed with sputum is
due to rupture of an engorged tracheal vein.—Peter Burgess
BREATHING DIFFICULTIES IN THYROID SWELLING
B
x Retrosternal goitre—positive Pemberton’s sign
x Multinodular goitre of long duration—positive Kocher’s test—
compressive stridor
x Secondary toxic goitre—congestive cardiac failure
x Carcinoma infiltrating the trachea—stridor on rest—without
compression with fingers
THYROTOXICOSIS AND HYPERTHYROIDISM
I have lately seen three cases of violent and long-continued palpitations
in females, in each of which the sample peculiarity presented itself—
viz., enlargement of the thyroid gland…. A lady, aged twenty, became
affected with some symptoms which were supposed to be hysterical….
It was now observed that the eyes assumed a singular appearance, for
the eyeballs were apparently enlarged, so that when she slept, or tried
to shut her eyes, the lids were incapable of closing.
—Robert James Graves, 1835 (Irish physician)
Thyrotoxicosis is symptom complex due to raised levels of
thyroid hormones.
Thyrotoxicosis refers to biochemical and physiological mani-
festations of excessive thyroid hormones. Hyperthyroidism is the
term used for overproduction of the hormones by thyroid gland.
In hyperthyroidism pathology is in thyroid gland itself. Hyperthyroidism is one of the causes of thyrotoxicosis. Thyrotoxicosis
can also occur due to other causes other than hyperthyroidism.
Other causes of thyrotoxicosis without hyperthyroidism
are—ectopic functioning thyroid, struma ovarii, functioning
metastatic follicular carcinoma, trophoblastic tumours, thyrotoxicosis factitia.
Types
1. Diffuse toxic goitre—(Graves’ disease, Basedow’s disease.
Primary thyrotoxicosis)–60%.
2. Toxic multinodular goitre (Secondary thyrotoxi cosis)
(Plummer disease)–20%.
3. Toxic nodule (Goetsch’s disease)–5%.
4. Thyrotoxicosis due to rarer causes:
a. Thyrotoxicosis factitia—drug induced. Due to intake of
L-thyroxine more than normal.
b. Jod-Basedow effect/phenomenon is hyperthyroidism
occurs in a goitre patient (not normal thyroid gland) after
administration of increased doses of iodides (in hyperplastic endemic goitre). It is also seen after administration of iodine contrast agents or amiodarone drug. Jod in
Germany means iodine.
c. Autoimmune thyroiditis or de Quervain’s thyroi ditis.
d. Neonatal thyrotoxicosis. It subsides in 3–4 weeks as TsAb
titres fall in the baby’s serum.
e.
Struma ovarii.
f. Drugs like amiodarone—an antiarrhythmic agent.
Amiodarone is rich in iodine having structural similarity
to T4 causing thyrotoxicosis.
g. Very rarely, well-differentiated carcinoma can cause
thyrotoxicosis-metastatic type.
h. Patients with hydatidiform mole or choriocarcinoma with
high levels of β HCG which can stimulate TSH receptor
and can cause thyrotoxicosis.
Graves Disease
Graves disease is an autoimmune disease with increased levels
of specific antibodies in the blood (TSH receptor antibodies).
Normal feedback mechanism is absent. It is often associated
with vitiligo. It is often familial. Thyroid stimulating immunoglobulins (TSI)/thyroid stimulating antibodies (Ts Ab) and longacting thyroid stimulator (LATS) cause pathological changes in
the thyroid. Histologically, there is acinar cell hypertrophy and
hyperplasia with absence of normal colloid in the tall columnar
epithelium (normal is flat epithelium with colloid). As cells
are empty, they look vacuolated. Tissues are highly vascular.
Exophthalmos producing substance (EPS) causes Graves
ophthalmopathy.
Diffuse goitre, thyrotoxicosis and autoimmune manifestations
like infiltrative ophthalmopathy, dermopathy, myopathy are
essential components of Graves disease.
Thyroid stimulating immunoglobulins (TSIs) are produced
against thyroid antigen in Graves disease which is directed
to TSH receptor acting as TSH receptor antibody. This TSHR
Ab is observed only in Graves disease.
Puberty, pregnancy, emotion and infection are the precipi-
tating factors for primary thyrotoxicosis.
Familial/genetic cause is also attributed in Graves disease
(50%); both identical twins can develop Graves disease.
A B
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Figs. 6.33A and B: Graves disease in a female and male patient.
Note the exophthalmos with clearly visible lower sclera.
There is hyperplasia and hypertrophy of entire thyroid due to
prolonged continuous action by binding of abnormal thyroid
stimulating antibodies to TSH receptor sites. Scalloped
pattern of vacuolated colloid is typical.
Toxic Adenoma (Toxic Nodule)
It is benign functioning monoclonal thyroid tumour, usually
more than 3 cm in size.
It usually presents as functioning (toxic) solitary nodule of
thyroid.
It is autonomous functioning tumour; not TSH responding.
Toxic adenoma secretes large quantity of thyroid hormones
suppressing the function of the remaining normal thyroid
tissue.
There are no eye signs and other features of Graves disease.
It commonly shows higher T
TSH receptor or G protein genes show somatic mutation.
US neck, T
, T4, TSH and radioisotope scan (shows hot
3
levels than T4.
3
nodule)—are the relevant investigations.
Treatment:
¾
Initial control of toxicity with antithyroid drugs; later
hemithyroidectomy is done after 6 weeks. Once thyroidectomy is done, suppressed remaining normal thyroid
tissue starts functioning to secrete normal level of thyroid
hormones.
¾
Radioactive iodine therapy can be used which selectively
concentrates and ablates the thyroid adenoma; later
remaining normal thyroid starts functioning.
Note:
• Radioactive iodine therapy after initial control of toxicity using antithyroid
drugs, has become the standard mode of treatment after the age of 10
years. But RAI therapy should not be used in pregnancy, lactation as it
crosses placental barrier and get secreted in milk causing newborn or
infant hypothyroidism.
T3 Toxicosis
x Here T
x Free T
alone is raised; TSH is decreased; T4 is normal.
3
estimation is important.
3
Subclinical Hyperthyroidism
x Subclinical hyperthyroidism is defined as a state of decreased
TSH level but not undetectable with T
, T4, free T3 and free T4 are
3
within the normal range without any clinical symptoms.
x Its incidence is 1% of hyperthyroidism.
x It is one of the causes of infertility in females (both subclinical
hyper or hypothyroidism can cause infertility).
x It may present as cardiomyopathy or arrhythmias.
x Hormone assay, radioisotope scan and US neck, ECG are used
for evaluation.
Struma Ovarii
x Ovarian teratoma with thyroid differentiation will secrete T
and suppress TSH.
T
4
x Function of normal thyroid in neck is suppressed.
x Radioisotope scan shows uptake in pelvis with no or less uptake
and
3
in neck.
Note:
The River Struma arises in Bulgaria and flows into Aegean Sea.
Endemic goitre exists in area along its banks; ‘Struma’ means goitre.
Hashitoxicosis
x It is due to autoimmune Hashimoto’s thyroiditis.
x Mild toxic features develop during initial stage of hyperplasia.
x Already formed thyroid hormones are released by inflamed gland
causing toxicity. It eventually leads into euthyroid and later hypothyroidism in Hashimoto’s disease.
Thyrotoxicosis Factitia
Intake of L thyroxine without indications to lose weight or overdose
intake causes toxicity.
Postpartum Hyperthyroidism
x It is exacerbation of previously confirmed or undiagnosed hyper-
thyroidism during pregnancy or after delivery due to increased
autoimmune factors.
x It is associated with HLA DR3 and HLA DR5.
Neonatal Thyrotoxicosis
x It is seen in infants born to mother with Graves disease due to
crossing of the thyroid stimulating antibody (TSH RAb) across
placental barrier. Infant will be toxic for 3–4 weeks which subsides
gradually.
Trophoblastic Thyrotoxicosis
x HCG secreted from vesicular mole, choriocarcinoma or metastatic
embryonal carcinoma in females, acts like TSAb causing toxicity.
Amiodarone-induced thyrotoxicosis
x Amiodarone is antiarrhythmic drug. It can cause thyrotoxicosis.
Type I is treated with thionamide, potassium perchlorate, beta
blockers often with glucocorticoids. Type II is destructive and so
eventually patient recovers; glucocorticoids and beta blockers
are needed initially.
Apathetic Hyperthyroidism
x It lacks all usual clinical features of toxicity.
x It is commonly observed in old people.
x Thyroid gland is not enlarged.
Contd...
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CHAPTER 6 Thyroid
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Contd...
x Patient presents with behavioral problems; often considered as
psychiatry patient with decreased appetite.
x Such lethargic individual also often shows features of recent
angina and atrial fibrillation.
x Unless serum T
Subacute Thyroiditis (Toxic Phase)
x Other common cause of thyrotoxicosis is subacute thyroiditis
(15–20% of cases), a destructive release of preformed thyroid
hormone. Radioactive iodine scan does not show any radioactive iodine uptake in the thyrotoxic phase of the disease. Thyroid
hormone levels can be highly elevated. Low ESR, low T
are other features.
, T4 and TSH are done, diagnosis is mas ked.
3
3 T4
ratio
SRB's Manual of Surgery
Clinical Features of Thyrotoxicosis
It is eight times more common in females.
It occurs in any age group. Primary type is seen commonly
in younger age group. Secondary type is common in older
age group.
Graves’s disease often presents without any obvious thyroid
swelling in the neck. Whenever, there is unexplained behav-
Fig. 6.34: Diffuse toxic goitre (primary) involves
both lobes with hyperfunctioning acini.
Fig. 6.35: Primary thyrotoxicosis. Note the exophthalmos.
A B
Figs. 6.36A and B: Note the dilated veins in an enlarged vascular
thyroid gland. Auscultation is important to hear a bruit.
ioural problem, insomnia, myopathy, unexplained diarrhoea
or loss of weight, tachycardia, Graves’s disease should be
suspected and evaluated.
The degree of thyrotoxicosis is determined by estimation of
thyroid hormone levels; the severity of clinical manifestations may not correlate with the degree of thyroid hormone
elevation.
Differentiating points between primary and secondary hyperthyroidism
Primary thyrotoxicosis Secondary thyrotoxicosis
1. Symptoms appear first, then thyroid swelling 1. Thyroid swelling appears first
2. Goitre is diffuse, smooth, firm or soft, both lobes are involved
with thrill and bruit
3. Features are much more severe compared to that of secondary
toxicosis of short duration
4. Eye signs and exophthalmos are common 4. Eye signs are not common
5. As it is an autoimmune disease, there may be hepatosplenomegaly
6. It occurs in younger age group 6. It occurs in adult and elderly individual
7. Entire gland is overactive 7. Internodular tissues are overactive
8. There is no preexisting goitre 8. Occurs in a long-standing pre-existing multinodular goitre
Histologically, there is hyperplasia of acini, lined by columnar
epithelium, often containing vacuolated colloid scalloping with
pseudopapillary formation
2. Swelling is large nodular, obvious
3. Symptoms appear after long time, which is less severe and slowly
progressive compared to primary toxicosis
5. Cardiac features are more common
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Symptoms of Hyperthyroidism/Toxicosis
A.
Gastrointestinal system: Weight loss in spite of increased appe-
tite; diarrhoea (due to increased activity at ganglionic level).
Cardiovascular system: Palpitations; shortness of breath at
rest or on minimal exertion; angina; irregularity in heart rate;
cardiac failure in the elderly (CCF).
Neuromuscular system: Undue fatigue and muscle weak-
ness; tremor.
Skeletal system: Increase in linear growth in children.
Genitourinary system: Oligo or amenorrhoea; occasional
urinary frequency.
Integument: Hair loss, gynaecomastia; pruritus; palmar
erythema.
Psychiatry: Irritability; nervousness; insomnia.
Sympathetic overactivity: It causes dyspnoea, palpitation,
tiredness, heat intolerance, sweating, hyperactivity, iriitability,
nervousness, increased appetite and decrease in weight.
Because of the increased catabolism, they have increased
appetite, decreased weight and so also increased creatinine
level which signifies myopathy (due to more muscle catabolism).
Fine tremor is due to diffuse irritability of grey matter.
B. Signs of Hyperthyroidism/Toxicosis
1. Eye signs in toxic goitre
Eye signs are common in primary thyrotoxicosis. Lid lag, lid
spasm can occur in secondary thyrotoxicosis also.
1. Lid retraction: Here upper eyelid is higher than normal;
lower eyelid is in normal position. It is due to sympa-
thetic overactivity causing spasm of involuntary smooth
muscle part of the levator palpebrae superioris (Muller’s
muscle). It is a sign of thyrotoxicosis, not a sign of
exophthalmos.
2. von Graefe’s sign (Lid Lag’s sign): It is inability of the
upper eyelid to keep pace with the eyeball when it looks
downwards to follow the examiner’s finger. It is contraction/
overactivity of the involuntary part of the levator palpebrae
superioris muscle—Muller’s muscle
3. Dalrymple’s sign: Upper eyelid retraction, so visibility of
upper sclera.
4. Stellwag’s sign: Absence of normal blinking—so staring
look. First sign to appear. It is due to widening of palpebral
fissure due to lid retraction and also due to contraction of
voluntary part of levator palpebrae superioris muscle.
5. Joffroy’s sign: Absence of wrinkling on forehead when
patient looks up (frowns) with head in bent down/flexed
position.
6. Moebius sign: It is lack of convergence of eyeball. Defective
convergence is due to lymphocytic infil tra tion of inferior
oblique and rectus muscles in case of primary thyrotoxicosis. There will be diplopia. It may be an early sign of
eventual ophthalmo plegia.
Wayne’s diagnostic indices (clinical) of thyrotoxicosis
Symptoms Present Absent
1. Dyspnoea on effort +1
2. Palpitation +2
3. Tiredness +2
4. Preference to heat
5. Preference to cold (Heat
intolerance)
6. Excessive sweating +3
7. Nervousness +2
8. Appetite increased +3
9. Weight decreased +3
Signs Present Absent
1. Bruit over thyroid +2
2. Exophthalmos +2
3. Lid retraction +2
4. Lid lag +1
5. Hyperkinetic movements +4 –2
6. Fine finger tremors +1
7. Hands hot +2 –2
Moist +1 –1
8. Atrial fibrillation +4 –3
9. Pulse rate 80/minute 0
80–90/minute +3
More than 90/minute +3
10. Palpable thyroid
<11 points—nontoxic goitre 11–19
+5
equivocal
–5
>19
points—
toxic
7. Naffziger’s sign: With patient in sitting position and neck
fully extended, protruded eyeball can be visualized when
observed from behind.
8. Jellinek’s sign: Increased pigmentation of eyelid margins.
9. Enroth sign: Oedema of eyelids and conjunctiva.
10. Rosenbach’s sign: Tremor of closed eyelids.
11. Gifford’s sign: Difficulty in everting upper eyelid in primary
toxic thyroid. Differentiates from exopht hal mos of other
causes.
12. Loewi’s sign: Dilatation of pupil with weak adrenaline solution.
13. Knie’s sign: Unequal pupillary dilatation.
14. Cowen’s sign: Jerky pupillary contraction to consensual
light.
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CHAPTER 6 Thyroid
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15. Kocher’s sign: When clinician places his hands on patient’s
eyes and lifts it higher, patient’s upper lid springs up more
quickly than eyebrows.
ORDER OF APPEARANCE OF SIGNS
B
x Stellwag’s sign—mild; first
sign to appear
x von Graefe’s sign—mild
x Joffroy’s sign—moderate
x Moebius sign—severe
EXOPHTHALMOS
It is proptosis of the eye, caused by infiltration of the retrob-
ulbar tissues with fluid and round cells, with lid spasm of
SRB's Manual of Surgery
upper eyelid (Lid spasm is spasm of levator palpebrae superioris muscle which is partly innervated by sympathetic fibres).
Exophthalmos is visible sclera first below (lower part) the
lower edge of the iris and later eventually upper part of sclera
will be visible. It is due to pushing of the eyeball forwards
due to fat, oedema fluid, cells like macrophages in retrobulbar
space
Proptosis can be measured by exophthalmometer.
Exophthalmos is of ten self-limiting, but not always. Sleeping
in propped up position and lateral tarsorrhaphy will help to
protect the eye.
Exophthalmos even though usually bilateral it can be unilat-
eral or frequently unequal in both eyes.
Fig. 6.37: Diagram showing normal relation of eyelid and pupil in lid
retraction and exophthalmos.
Severe Exophthalmos
Eyelid oedema, chemosis, conjunctival injection.
Diplopia, ophthalmoplegia (complete weakness of all extraoc-
ular muscles and so no movements possible).
Corneal ulceration.
Papilloedema soon develops.
Finally it may also cause loss of vision.
It is called as malignant exophthalmos (It is misnomer even
though it is not malignant nor related to any malignancy).
Treatment of severe exophthalmos—emergency
Steroids intravenously; IV antibiotics; Diuretics
Guanethidine, steroid, antibiotic drops
Lateral tarsorrhaphy; Orbital decompression by surgical
removal of lateral wall or roof of orbit
Dark spectacles, protective eye patches
Eyelid surgeries, extraocular muscle surgeries
Local radiation therapy to orbital space
1% methylcellulose eye drops to prevent corneal ulceration
Sleeping with head end elevation
Causes of Exophthalmos
Endocrinal: Thyrotoxicosis—common; Cushing’s syndrome,
acromegaly—rare
Congenital deformities of skull: Craniostenosis, oxycephaly,
hypertelorism
Primary tumours: Periorbital meningioma; Optic nerve
glioma; Orbital haemangioma; Lymphoma; Osteoma; Pseudotumour—granuloma
Secondary tumours: Antral carcinoma, neuroblastoma;
Inflammatory: Orbital cellulitis, frontal sinusitis;
Vascular causes: Cavernous sinus thrombosis/A-V fistula;
Ophthalmic artery aneurysm
Other eye causes: Severe myopia; Severe glaucoma—
buphthalmos
Note:
• Antithyroid drugs may worsen exophthalmos and the patient should be
observed once antithyroid drugs are started as steroid supplementation
may be required.
• Ophthalmopathy may worsen by thyroidectomy or radioiodine therapy
also.
• Visible lower sclera—sign of exophthalmos
• Moebius sign—most important—early sign of ophthalmoplegia
• Thyroid ophthalmopathy in Graves disease-Werner’s abridged classifica-
tion of ocular changes with van Dyke’s modification—here 0 –6 grades
with specified eye signs are used.
• Grading of exophthalmos: (1) Mild: Widening of palpebral fissure due
to lid retraction; (2) Moderate: Orbital deposition of fat causing bulging
with positive Joffroy’s sign; (3) Severe: Congestion with intraorbital
oedema, raised intraocular pressure, diplopia and ophthalmoplegia; (4)
Progressive: In spite of proper treatment progression of eye signs is
seen with chemosis, corneal ulceration and ophthalmoplegia
• Causes of pulsating exophthalmos: Carotid-cavernous sinus A-V
fistula; Cavernous sinus thrombosis; Orbital vascular neoplasm; Orbital
haemangioma; Ophthalmic artery aneurysm
2. Cardiac Manifestations
Tachycardia is common.
As per Crile’s grading; Sleeping pulse rate is usually checked
for three consecutive nights and average is taken as the
value.
Fig. 6.38: Malignant exophthalmos.
PULSE RATE (CRILE’S GRADING)
B
Grade I: < 90/min Grade II: 90-110/min Grade III: >110/min
Others: Ectopic; Pulsus paradoxus; Wide pulse pressure;
Multiple extrasystoles; Paroxysmal atrial tachycardia;
Paroxysmal atrial fibrillation.; Persistent atrial fibrillation (not
responsive to digoxin).
3. Myopathy
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Weakness of proximal muscles occurs, i.e. the front thigh
muscles, arm muscles.
Weakness is more when muscle contracts isomet rically either
while getting down steps, or lifting a full bucket.
Often when it is severe it resembles myasthenia gravis. Once
hyperthyroidism is controlled, recovery occurs.
4. Pretibial Myxoedema
It is a misnomer. Pretibial myxoedema is often a feature of
primary thyrotoxicosis:
Is usually bilateral, symmetrical, shiny, red thickened dry skin
with coarse hair in the feet and ankles.
In severe cases skin of entire leg below the knee with involve-
ment of foot and ankle can occur.
It is due to deposition of myxomatous tissues (mucin-like
deposits) in skin and subcutaneous plane. Glycosaminoglycans (hyaluronic acid) deposition occurs.
It might or might not regress completely after treatment for
toxicity.
It is associated with exophthalmos with high levels of thyroid
stimulating antibodies.
Skin becomes cyanotic when cold. Skin changes in toxicosis
are called as thyroid dermopathy. They include—pretibial
myxoedema, pruritus, palmar erythema, hair thinning,
Dupuytren’s contracture (fascial).
5. Thyroid Acropachy
Thyroid acropachy is clubbing of fingers and toes in primary thyro-
toxicosis. Hypertrophic pulmonary osteoarthropathy can develop.
6. Others
Thrill is felt in the upper pole of the thyroid and also bruit
on auscultation. It is because in upper pole, superior thyroid
artery enters the gland superficially and so thrill and bruit can
easily be felt. In lower pole inferior thyroid artery enters the
gland from deeper plane and so thrill cannot be felt.
Hepatosplenomegaly.
Investigations for Thyrotoxicosis
Thyroid function tests
Serum T3 and T4 levels are very high. TSH is very low or
undetectable. Sometimes, only T3 level is increased and is
called as T3 toxicosis. Here in T3 toxicosis, free T3 estimation
is important. Free T3, free T4 estimation is done as total T3 and
total T4 levels will vary depending on the amount of thyroid
binding globulin (TBG). TBG will be raised in pregnancy,
cirrhosis, hyperestrogenism. It decreases in conditions with
high androgen level, hypoproteinaemia, acromegaly. Free T
and free T4 are measured using radioimmunoassay. Normal
free T3 is 3.0–9.0 pmol/L; free T4 is 8–26 nmol/L.
Type of disease T
Conventional
hyperthyroidism
hyperthyroidism
T
3
Subclinical
hyperthyroidism
Radioisotope study
¾
Radioisotope study by I
4
Increased Increased Undetectable
→
→ →
T3 TSH
Increased Undetectable
Undetectable
131
(Diagnostic dose -5 microcurie
is used) shows more uptake, i.e. hot nodules or hot areas.
This is very useful in auto nomous solitary toxic nodule.
131
¾
I
causes more irradiation and its half-life is 8 days. So
intravenous
99m
Tc is used for diagnostic purpose. 99m
technetium has become isotope of choice for diagnosis
as it is cheap, less radiation, scanning is done 20 minutes
after IV injection of
99m
Tc (half-life is 6 hours). Drawback
of technetium is that it concentrates in carcinoma, so
forms hot nodule (means hot nodule need not be benign
in Tc scanning). Warm nodule in Tc scan may appear as
cold nodule in RAI scan and so is called as discordant
nodule which suggests malignancy. If radioactive iodine
is used for diagnosis, then I
123
is better as it has got short
half-life (13 hours).
¾
Autonomous toxic nodule is absolute indication for radioisotope scan in toxic thyroid showing hot nodule. Graves
disease shows diffuse overactivity (uniform); hypofunctioning cold nodule in Graves disease could be malignant.
In secondary thyrotoxicosis internodular tissues are
overactive (heterogeneous activity). Non-hyperthyroid
toxicosis shows increased uptake in non-thyroid areas
of toxicity like struma ovarii in pelvis.
TRH estimation.
ECG—to look for cardiac involvement; if required opinion
from cardiologists is taken and cardiac problems are
managed.
Total count and neutrophil count are very essential base-line
investigations before starting antithyroid drugs (as it may
cause agranulocytosis).
Thyroid antibodies estimation—antithyroglobulin antibody,
TSH receptor antibody, antithyroid peroxidase (anti-TPO)
antibody.
Treatment for Thyrotoxicosis
MEDICAL
B
x Relief of symptoms:
– Beta blockers-propranolol, nadolol, metoprolol—Control
cardiovascular and hyperadrenergic manifestations. Bronchial
Asthma, heart Block, Cardiac failure are contraindications.
– Calcium channel blockers (e.g. verapamil and diltiazem) can
3
be used
– Oral rehydration
463
CHAPTER 6 Thyroid
Contd...
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464
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Contd...
x Antithyroid pharmacotherapy. It prevents the:
– Release of hormones: Lugol’s iodine (potassium iodide and
iodine) 10 drops—3 times day
– Production of thyroxine : Methimazole: long-acting, 20–40
mg OD; more potent; but not used in pregnancy; Tapazole 5
or 10 mg tablets. Carbimazole 20 mg three times a day up to
120 mg. Propyl thiouracil (PTU) 100 mg three times a day,
used in pregnancy; 50 mg tablets
– Action of thyroxine on end organs: Propranolol—40 mg tid
up to 120–160 mg; PTU
– Production of antibodies: Steroids, methimazole, carbimazole;
Levels of TSH R Ab fall and permanent cure may occur in 50%
of patients in Grave’s
SRB's Manual of Surgery
Radioactive iodine therapy
Thyroidectomy
1. ANTITHYROID DRUGS
Indications for antithyroid drugs
Toxicity in pregnant women—Propylthiouracil is preferred.
Toxicity in children and young adults.
Before thyroidectomy, to make the patient euthyroid.
Soon after starting radioactive I131 therapy for 6 to 12 weeks
(Effects of radiotherapy start only in 6 to 12 weeks).
A. Thionamides
Thionamides are most commonly used antithyroid drugs. It
can be imidazole (carbimazole or methimazole) or thiouracil
(propylthiouracil) derivatives. They inhibit iodine organification,
iodide oxidation by peroxidase and iodotyrosine coupling. PTU
also blocks the type 1 deiodinase and so conversion of T4 to T3
peripherally (liver and other organs).
Carbimazole: It is the common drug used. Dose is 5–10 mg,
exactly 8th hourly (as T1/2 of carbimazole is 8 hours). Each
tablet is 5 mg; usually given for 12–18 months; peak plasma
level should be maintained in optimum concentration to have
a proper benefit; Often tri-iodothyronine 20 microgram 4 times
daily or Thyroxine 0.1 mg daily are given in combination with
antithyroid drugs, to prevent iatrogenic thyroid insufficiency or
to prevent the increase in size of goitre (Block and Replacement
therapy). Carbimazole also suppresses the autoimmune process
in thyroid in Grave’s disease. Carbimazole causes fever, rashes,
arthralgia, myalgia, neuritis, lymph node enlargement, liver cell
dysfunction, psychosis, agranulocytosis.
Methimazole: It is more potent and longer-acting than propylthiouracil. It is given as once a day dose; 20–40 mg. It is not used
in 1st trimester pregnancy as it may cause cloacal and scalp
abnormalities.
Propylthiouracil: It acts by blocking thyroid hormone synthesis
as well as by blocking peripheral conversion of T4 to T3. It also
decreases the thyroid autoantibody levels. It can be given for
hyperthyroidism in children and in pregnancy, lactation. Dose
is 200 mg 4th to 8th hourly. It is short acting. Propylthiouracil
is reserved for use in thyroid storm, first trimester of pregnancy
and methimazole allergy or intolerance. PTU causes dose unrelated hepatoxicity; agranulocytosis; antineutrophilic cytoplasmic
antibody in 20% of patients after long-term usage.
Note:
• Dose of antithyroid drug are titrated every 4 weeks until thyroid functions
(TSH and FT4) normalize.
• Toxic multinodular goitre and toxic adenoma will not go into remission.
• Reduction of thyroid hormones occurs in 2–8 weeks.
• In Graves, once patient is rendered euthyroid options include use of ATD
for 12–18 weeks or definitive treatment with RAI or surgery.
• After cessation of therapy, close follow up for 3–6 months is required
to detect relapse.
• 40% experience recurrence in 1 year in Grave’s; in such situation RAI
or surgery has to be considered.
• Antithyroid drugs are continued during and after surgery, for 7–10 days.
It has to be continued even after starting radioactive iodine therapy for
6 weeks to 12 weeks.
• Response to treatment and possibility of relapse in primary thyrotoxi-
cosis can be assessed by studying HLA status and TsAb level.
B. Beta adrenergic blocking drugs
Propranolol: Dose is 40 mg tid. It reduces the cardiac problems
and also blocks the peripheral conversion of T4 to T3, as it is
the T3 which is the principle active agent in periphery. Contraindications are bronchial asthma, heart block, cardiac failure. It
is very useful in toxicity induced due to thyroiditis which is self
limiting. 2 mg IV propranolol is used in thyroid storm. Long-
acting nadolol 160 mg OD can also be used.
C. Lugol’s iodine (5% iodine + 10% potassium iodide)
It decreases the vascularity of the gland and makes it more firm
and easier to handle during surgery. Dose is 10–30 drops/day
(minims) for 10 days prior to surgery. Potassium iodide tablets
60 mg tid also can be given instead of Lugol’s iodine. But its
use at present is disqualified. (One minim = one drop. One ml =
16 drops). Lugol’s iodine prevents the release of hormone from
the gland–thyroid constipation. After 2 weeks, effect of Lugol’s
iodine is lost causing thyroid escape from iodine control. Its
action is similar like Wolf Chaikoff effect.
Advantages of Antithyroid Drugs
It avoids surgery and its complications and also avoids radioiodine therapy its problems. Clinical improvement occurs in 2
weeks. Biochemical improvement occurs in 6 weeks. Remission
is confirmed by TsAb assessment, which will be low. But permanent remission rate is very less in adults and is 20% in children.
Disadvantages of antithyroid drugs
Prolonged course of treatment for 18 months, and in spite
of this, cannot predict the remission or relapse. Relapse rate
is 40%. Large gland/severe disease/abnormal TSH receptor
antibodies (TSH-RAbs) are likely to lead into high recurrence.
Size of swelling may not regress.
It may lead to agranulocytosis and thrombocytopenia, liver
damage, hair loss (except propranolol). Sore throat is the
earliest presentation of agranulocytosis. If it is so, drug is
stopped, total count is done. If it is less, agranulocytosis is
confirmed. High doses of injection benzyl penicillin 10–20
lac, 6th hourly, IV is started to prevent infection. If required,
blood transfusion is done. Patient usually recovers by this. To
control toxicity, Tab. Propranolol 40 mg tid is started. Rarely,
they need bone marrow transplantation.
Complications of antithyroid drugs
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Allergic reactions; agranulocytosis (0.2 to 0.5%); severe hepatitis
(0.2%) more often with PTU; polyarthritis; Lupus vasculitis;
abnormal taste.
Note:
• They are dose-related in methimazole but not so in PTU.
• Patients with agranulocytosis usually present with fever and pharyngitis.
• After the drug is stopped, granulocyte counts usually start to rise within
several days but may not normalize for 10–14 days.
• Granulocyte colony-stimulating factor (G-CSF) appears to accelerate
recovery in patients with a bone marrow aspiration showing a granulocyte-to-erythrocyte ratio of 1:2 or greater than 0.5.
OTHER DRUGS WHICH ARE EFFECTIVE (BUT NOT
B
COMMONLY USED)
x Potassium perchlorate inhibits iodide transport by direct inhibi-
tion of the sodium iodine symporter. It can be combined with
thionamides. Dose is 500 mg bd. It is used in amiodarone induced
type I thyrotoxicosis.
x Iopanoic acid 1 g/day is used in severe unresponsive cases. It
inhibits peripheral conversion of T4 to T3.
x Lithium carbonate 300 mg 6th hourly. It inhibits the coupling
of the iodotyrosines and prevents thyroid hormone release. It is
useful in when thionamide is contraindicated. Lithium level should
be maintained below 1 mEq/L.
x Guanethidine 40 mg orally 6th hourly. Reserpine 5 mg IM.
x Dexamethasone 2 mg orally 6th hourly. It inhibits peripheral
conversion of T4 to T3. It is used in thyroid storm.
x Cholestyramine—decreases reabsorption of thyroid hormones
from the enterohepatic circulation; used orally at the rate of 4 g
four times daily, in combination with methimazole or PTU.
x High dose of glucocorticoids: It impairs peripheral conversion of
T4 to T3 and also lowers serum TSH level; hence can be used in
severe resistant/refractory cases.
2. SURGERY
INDICATIONS
B
x Failure of drug treatment in primary thyrotoxicosis in young
patients
x Autonomous toxic nodule; Nodular toxic goitre
x When malignancy cannot be ruled out
x Graves disease in children, Graves with nodules
x Need for antithyroid drugs for more than 2 years
x Large goitre, substernal/intrathoracic goitre
x Pressure symptoms, Graves ophthalmopathy
x Amiodarone-induced thyrotoxicosis.
It is now observed that total thyroidectomy may be a better
option in Graves disease to achieve lowest relapse rate and
successful stabilisation of thyroid ophthalmopathy as it
clears the antigenic focus in thyroid completely.
Surgery done is subtotal thyroidectomy—Both lobes with
isthmus are removed and a tissue equivalent to pulp of
finger is retained at lower pole of the gland on both sides
(5–8 grams).
In autonomous nodule, hemithyroidectomy is done. Here
entire lateral lobe with whole of isthmus is removed.
Advantages
Rapid and high cure rate.
Problems of radioiodine therapy are avoided.
Surgery provides tissue for biopsy, removes the occult
malignant foci.
Surgery is better option for ophthalmopathy due to thyro-
toxicosis.
It is the option for women planning for child.
Coexisting parathyroid carcinoma can be removed.
For intrathoracic retrosternal toxic thyroid, surgery is the
choice. Antithyroid drugs and also radioactive iodine may
increase the goitre size.
Patient should be made euthyroid before doing sur
should be confirmed by repeated estima
tion of serum T3, T4
gery. (It
and TSH levels).
Disadvantages
Recurrent thyrotoxicosis (5%).
Thyroid insufficiency (20–45%). It is revealed in 6 months to
2 years and is confirmed by estimating T3, T4 and TSH levels.
Hypothyroidism is better than recurrent thyrotoxicosis. It is
treated by tab. L-thyroxine 0.1 mg daily (OD) for life-long—
usually given in morning.
Complications of thyroid surgery itself.
3. RADIOIODINE THERAPY
INDICATIONS
B
x Primary thyrotoxicosis
x In recurrent thyrotoxicosis
Radioiodine destroys the cells and causes the complete abla-
tion of thyroid gland.
Usual dose is 5 to 10 millicurie, or 160 microcurie/gm of
thyroid.
Patient is made euthyroid using antithyroid drugs; drug is
discontinued for 5 days; I
antithyroid drugs are started after 7 days and are continued
for 8 weeks. In 30% of patients, additional 2 or 3 doses may
be required.
It takes 3 months to get full response and so until then, the
patient has to take antithyroid drugs. Often additional one or
two doses of radioiodine are required to have complete ablation. Eventually they go for hypothyroidism and so require
main tenance dose of L-thyroxine 0.1 mg daily.
To give therapeutic dose, patient should be admitted and
isolated for 7 days (Half-life) to prevent irradiation. It is given
orally soon after getting from the manufacturer without much
delay to have optimal efficacy.
x In autonomous toxic nodule
131
300–600 MBq is given orally;
465
CHAPTER 6 Thyroid
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