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Fig. 14.18: Lahey’s test.
https://t.me/med1917
Examination of Thyroid
Confirmation of Retrosternal Extension
Lower margin of the swelling/goitre is not visible—
even on deglutition. Lower margin is not palpable on
deglutition. Dilated veins over neck or chest wall may
be visible. Normal resonant note over the sternum
becomes dull on percussion.
Pemberton’s sign: Patient is asked to raise both the
arms above the shoulder so as to touch the ears and
asked to keep like that for 3 minutes. Patient will
develop dilated veins and cyanosis in the neck and
upper chest wall, puffiness in face, respiratory distress
and rarely dysphagia. It means sign is positive
signifying retrosternal extension of goitre (Figs 14.20
and 14.21). Dyspnoea can occur at night during lying
down or when neck is extended. Rarely recurrent
laryngeal nerve palsy can occur.
Retrosternal goitre is defined as having > 50%
goitre below the suprasternal notch. 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 it also is not related to the existing thyroid in
the neck. Secondary is common. It is extension from
331
Fig. 14.19: Kocher’s test.
rings occurs because of constant pressure which gets
narrowed/collapsed during compression. Trachea is
kept patent because of forward traction by goitre itself.
But after thyroidectomy lack of support to trachea
causes tracheomalacia—weakening of the tracheal
rings. Such patients need tracheostomy after
thyroidectomy . It is usually temporary tracheostomy
for 2-3 weeks, by then tracheal rings regain their
strength to maintain the patency of the trachea.
’Scabbard trachea’ is narrowing of trachea.
Fig. 14.20: Pemberton’s sign for retrosternal goitre.
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Fig. 14.21: Diagrammatic presentation of retrosternal
extension of thyroid.
SRB’s Clinical Surgery
the enlarged thyroid from the neck. Commonly retrosternal goitre arises from lower pole of a nodular goitre.
It is more observed in short necked people. Due to
negative intrathoracic pressure nodule gets drawn into
the superior mediastinum. Sometimes it may be also
ectopic thyroid tissue. Retrosternal goitre may be
substernal (part of the nodule is palpable in the neck)
or plunging goitre (intrathoracic goitre is forced into
the neck occasionally by increased intrathoracic
pressure) or intrathoracic goitre with normal neck.
It can be toxic/nontoxic nodules/malignant.
Retrosternal goitre is confirmed by CT scan and
radioiodine isotope study. It is treated by complete
surgical removal usually through neck approach,
occasionally through median sternotomy . Radioactive
iodine therapy is not used for retrosternal goitre.
Surgical removal should be complete because
recurrent retrosternal goitre is very difficult to reoperate. Stridor due to compression of tracheobronchial tree by r etrosternal goitre is very danger ous
because it is often not possible to clear the airway
either by intubation or by tracheostomy.
suprasternal space and index and ring fingers are placed
over sternal heads of the sternomastoid muscles on each
side. Middle finger is run from above downwards along
the trachea to feel the position—central or deviated. In
solitary nodule or disease of only one lateral lobe
trachea will be usually deviated towards opposite side.
In enlargement of both lobes trachea will be usually
central. Other features are absence of hollowness on
the side of the deviation (trail sign), on auscultation
breath sounds are heard well on the side of the deviation
(Figs 14.22 and 14.23A and B).
Superior border of the isthmus of the normal thyroid
gland is inferior to cricoid cartilage. Isthmus is felt
over the tracheal rings below . Bare tracheal rings are
observed in ectopic thyroid (which means thyroid tissue
is not present in normal location) and also in absence
of isthmus (rare).
Carotid pulsation should be checked. It is normally
felt at the level of the upper border of thyroid cartilage
over medial aspect of the sternomastoid muscle on
the Chaissagne tubercle (carotid tubercle) on the
transverse process of C6 vertebra. It may be deviated
posteriorly/laterally in a large goitre. It may be absent
in advanced carcinoma thyroid due to infiltration of
the carotid sheath by the tumour (Berry’s sign) (Fig.
14.24).
Sympathetic chain in the neck may get involved
in locally advanced carcinoma thyroid causing
Position of Trachea
Position of trachea is checked by palpation using three
fingers from below . Middle finger is kept just above the
Fig. 14.22: Trachea in central position. It is central when
both lateral lobes are enlarged. It is deviated to opposite
side in solitary nodule thyroid.
Examination of Thyroid
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A
Fig. 14.24: Palpation of carotid artery (common carotid)
at the level of thyroid cartilage on the medial border of
sternomastoid muscle over Chaisagne tubercle in transverse
process of C
when the pulsation is absent. It signifies advanced carcinoma
of thyroid.
vertebra. Berry’s sign is said to be positive
6
333
B
Figs 14.23A and B: Method of examination of trachea
to find out deviation using three fingers.
Horner’s syndrome—enophthalmos due to Muller ’s
muscle weakness; drooping of upper eyelid (ptosis);
anhidrosis; miosis due to paralysis of dilator papillae;
absence of ciliospinal reflex; flushing of face and nasal
congestion. Causes for Horner’ s syndrome—It is due
to interruption of sympathetic nerve supply to head
and neck. Preganglionic fibres arise from 1st and 2nd
thoracic segments of the spinal cord which synapses
with three cervical sympathetic ganglia. Any disruption
of preganglionic fibres or cervical ganglia or their
fibres will cause Horner’s syndrome. Causes are—
Posterior inferior cerebellar artery thrombosis; often
cervical sympathectomy; Pancoast’s tumour; secon-
daries in the neck; carotid artery aneurysm; spinal
cord lesions; injuries to lower root of brachial plexus.
Examination of neck lymph nodes for secondaries
should be done. It is commonly palpable in papillary
carcinoma of thyroid. It is usually level III and IV
nodes. It could be firm, hard or cystic. It is usually
brownish black in colour often with papillary
projections. Lymph nodes often can get enlarged in
follicular carcinoma thyroid and lymphoma. Lateral
aberrant thyroid which was earlier thought as aberrant
thyroid in lateral part of the neck is actually not so
but it is secondary in lymph node with primary being
papillary carcinoma of thyroid.
Measurement of circumfer ence of the neck at regular
intervals is important if patient is not undergoing
surgery to assess the increase in size of the thyroid
(progress of the swelling) (Fig. 14.25).
Percussion over the manubrium sterni is important.
Dullness signifies retrosternal extension. T enderness
may signify secondaries in sternum from follicular
carcinoma of thyroid. Direct percussion method is the
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Fig. 14.25: Lymph node drainage of thyroid. Primary
and secondary nodes are drainage groups.
SRB’s Clinical Surgery
usual practice. But it is often painful. Indirect method
can also be used (Fig. 14.26).
Auscultation over the upper pole of the gland is
done to hear bruit—in patients with toxic thyroid and
in very vascular tumours (Figs 14.27A and B).
Cardiovascular system examination is important in
thyrotoxicosis—commonly secondary type. Tachycardia, ectopic beats, pulsus paradoxus, extrasystoles,
A
Fig. 14.26: Percussion over the sternum is important
to rule out retrosternal extension.
B
Figs 14.27A and B: Bruit over thyroid should be auscultated
to find out increased vascularity over upper pole.
atrial fibrillation are the cardiac presentations (Fig.
14.28).
Respiratory system examination: Secondaries and
pleural effusion can occur in follicular carcinoma of
thyroid.
Abdomen examination: Hepatomegaly is looked for
as secondaries in liver are known to occur in follicular
carcinoma of thyroid. Hepatosplenomegaly can occur
as part of Grave’s disease or Hashimoto’s disease
(Figs 14.29 and 14.30).
Examination of Thyroid
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Fig. 14.28: Cardiovascular system is examined and
auscultated for cardiac problems in secondary thyrotoxicosis.
335
Fig. 14.31: Palpation of skull in thyroid enlargement to look
for secondaries when primary is follicular carcinoma of thyroid
(pulsatile, vascular, warm, and localised).
Fig. 14.29: Hepatomegaly can occur in Graves’ and
Hashimoto’s diseases as part of the autoimmune disease.
Fig. 14.30: Palpation of spleen in a patient with
thyroid enlargement.
Examination of skull and spine: Localised, warm,
vascular, pulsatile secondaries can occur in skull
commonly, rib and other bones occasionally as a spread
from follicular carcinoma of thyroid (Fig. 14.31).
In primary thyrotoxicosis exophthalmos and all eye
signs are looked for.
Both the eyelids cover the bulbar sclera partially
in normal individual. In lid retraction—due to spasm
of involuntary levator palpebrae superioris muscle,
upper eyelid is over or above the upper margin of
cornea, often with visible upper bulbar sclera. Here
lower eyelid is in normal position. It does not indicate
exophthalmos. In exophthalmos lower bulbar sclera
is clearly visible and lower eyelid is below and will
not cover the bulbar sclera. In severe exophthalmos
sclera will be visible all over both above and below
(Figs 14.32A and B). Exophthalmos is measured using
exophthalmometer (Figs 14.33A and B).
Other Eye Signs
Eye signs are common in primary thyr otoxicosis. Lid
lag, lid spasm can occur in secondary thyrotoxicosis
also.
1. Von Graefe’s sign: Lid lag sign is visible white
sclera above the corneal margin during lid lag as
upper eyelids cannot keep pace with the eyeball
when they look down. Place the examiner’s left
hand over the patient’s head. Place examiner’s
right index finger near the level of eye and slowly
bring it down and ask the patient to see the
downward moving finger. If upper sclera is visible
then it is positive lid lag sign. Test is repeated few
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A
SRB’s Clinical Surgery
A
B
Figs 14.32A and B: Lid lag check in primary
more times for confirmation. Normally upper eyelid
follows the finger downwards properly but in
primary thyrotoxicosis lid lag is observed.
2. Naffziger’s sign: Examiner stands behind the
patient, and patient’ s neck is extended and examiner looks from behind along the superior orbital
thyrotoxicosis.
B
Figs. 14.33A and B: Movements of the eyeball should be
checked in primary thyrotoxicosis with exophthalmos to rule
out involvement of eyeball muscle due to infiltration by
macrophages, inflammatory cells.
margin of the patient. Eyeball is seen beyond the
superior orbital margin in exophthalmos (Fig.
14.34).
3. Dalrymple’s sign: Upper eye lid retraction, so
visibility of upper sclera.
4. Stellwag’s sign: Absence of normal blinking —
so staring look. It is first sign to appear . It is due
to contraction of striated part of the levator
palpebrae superioris in toxic thyroid.
Examination of Thyroid
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Fig. 14.34: Naffziger’s sign.
5. Joffroy’ s sign: Absence of wrinkling on forehead
when patient looks up (frowns) with the neck
flexed as protruded eyeball obviates the necessity
for frowning.
6. Moebius sign: Lack of convergence of eyeball.
Defective convergence is due to lymphocytic
infiltration of inferior oblique and inferior rectus
muscles in case of primary thyrotoxicosis. There
will be diplopia. It may be an early sign of eventual
ophthalmoplegia. Examiner’s left hand is placed
over the patient’s head. Right index finger from
distance is brought towards root of the nose
between the eyes and patient is asked to follow
the approaching finger visually to look for
convergence. If positive patient will be unable to
converge and develops diplopia (Fig. 14.35).
7. Jellinek’s sign : Increased pigmentation of eyelid
margins.
8. Enroth sign: Oedema of eyelids (lower eyelid
specifically) and conjunctiva.
9. Rosenbach’s sign: Tremor of closed eyelids.
10. Gifford’ s sign : Difficulty in everting upper eyelid.
Differentiates from exophthalmos of other causes.
11. Loewi’s sign: Dilatation of pupil with weak
adrenaline solution.
12. Knie’ s sign:Unequal pupillary dilatation.
13. Cowen’s sign: Jerky pupillary contraction to
consensual light.
337
Fig. 14.35: Moebius sign.
14. Kocher’s sign: When clinician places his hands
on patient eyes and lifts it higher, patients upper
lid springs up more quickly than eyebrows.
15. Grove’ s sign. Upper lid resistance to downward
traction.
16. Rochin’s sign: Reduced amplitude of blinking.
17. Boston’s sign: Uneven jerky movement of the
upper eyelid in inferior movement.
18. Mean’ s sign: Eye globe lags behind upper eyelid
on upward gaze.
19. Griffith’ s sign: Lower eyelid lags behind the eye
globe on upward gaze.
20. Sainton’s sign: Frontalis contraction after
cessation of levator activity.
21. Vigourox’s sign: Puffiness of lids.
22. Ballet’s sign: Ophthalmoplegia—paralysis of
more extraocular muscles.
23. Suker’ s sign: Difficulty in maintaining fixation in
extreme lateral gaze.
24. Wilder sign: Jerking of eyes on movement from
abduction to adduction.
25. Trousseau’ s/Payne’ s sign: Dislocation of the eye
globe.
26. Reisman’s sign: Bruit over eyelid.
27. Snellen/Donder’s sign: Bruit over the eye.
28. Goldzieher’ s sign: Deep infection of conjunctiva.
Exophthalmos
It is proptosis of the eye, caused by infiltration of
the retrobulbar tissues with fluid and round cells, with
visible lower bulbar sclera and with lid spasm of upper
eyelid (Lid spasm is spasm of levator palpebrae
superioris muscle which is partly innervated by
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Lid retraction is higher upper eyelid with normal lower
eyelid with visible sclera adjacent to upper eyelid.
Lid lag is inability of the upper eyelid to keep pace with
the eyeball when it looks downwards to follow the
examiner’s finger.
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 eyeball
forwards due to fat, oedema fluid, cells like macrophages
in retrobulbar space.
Order of appearance of signs
1. Stellwag’s sign - Mild. First sign to appear
2. Von Graefe’s sign - Mild
3. Joffroy’s sign - Moderate
4. Moebius sign - Severe
Important signs to be remembered
Visible lower sclera—sign of exophthalmos
Naffziger’s sign
VonGraefe’s sign-upper lid lag- contraction / overactivity
of the involuntary part of the levator palpebrae superioris
muscle – Muller’s muscle
Joffroy’s sign
Moebius sign—most important-early sign of ophthalmo-
plegia
SRB’s Clinical Surgery
the eye. Severe exophthalmos shows—eyelid oedema,
chemosis, conjunctival infection, diplopia, ophthalmoplegia (complete weakness of all extraocular 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
(even though it is neither malignant nor related to any
malignancy) (Figs 14.36 to 14.38).
Remember—Antithyroid drugs may worsen exophthalmos and so observe the patient once antithyroid
drugs are started as steroids are required to be
supplemented.
Grading of exophthalmos
Fig. 14.36: Malignant exophthalmos. Left side tarsorrhaphy
is done to prevent corneal ulcer formation.
Thyroid ophthalmopathy in Grave’s disease-Werner’
abridged classification of ocular changes with van
Dyke’s modification
Class- grade Definition
0 No signs and symptoms
1 Eye signs only—refer table below for eye
signs
2 Soft tissue involvement
3 Proptosis more than 22 mm
4 Extraocular muscle involvement
5 Corneal involvement- ulceration
6 Loss of sight / vision due to optic nerve
and corneal involvement
Eye signs only
Resistance to retro displacement of eye
Oedema of conjunctiva and caruncle
Lacrimal gland enlargement
Infection of conjunctiva
Oedema and fullness of lids
sympathetic fibres). Sclera can be seen clearly below
and often above the limbus of the eye. Proptosis can
be measured by exophthalmometer. Exophthalmos is
often self limiting, but not always. Sleeping in propped
up position and lateral tarsorrhaphy will help to protect
Fig. 14.37: Eyes in different conditions including
thyrotoxicosis.
Mild: Widening of palpebral fissure due to lid retraction
Moderate: Orbital deposition of fat causing bulging with
positive Joffroy’s sign
Severe: Congestion with intraorbital oedema, raised
intra-ocular pressure, diplopia and ophthalmoplegia
Progressive: In spite of proper treatment progression
of eye signs occurs with chemosis, corneal ulceration
and ophthalmoplegia.
Examination of Thyroid
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Causes of exophthalmos Causes of pulsating exophthalmos
Endocrinal Carotid-cavernous sinus A-V fistula
Thyrotoxicosis—common Cavernous sinus thrombosis
Cushing’s syndrome, acromegaly—rare Orbital vascular neoplasm
Orbital haemangioma
Congenital deformities of skull Ophthalmic artery aneurysm.
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
339
Fig. 14.38: Unilateral exophthalmos. Causes other than toxic
thyroid have to be thought of-aneurysm of ophthalmic artery,
AV malformation, orbital tumours, paranasal sinus tumours,
tumours of nasopharynx extending above.
Causes of dyspnoea/stridor in thyroid diseases
Carcinoma thyroid infiltrating recurrent laryngeal nerve/
trachea
Large, long standing goitre causing tracheomalacia
Retrosternal goitre
Congestive cardiac failure in thyrotoxicosis
Recent rapid increase in thyroid swelling is due to
Malignant transformation in previous MNG
Haemorrhage into a nodule
Anaplastic carcinoma of thyroid.
In a case of thyroid diase following things should be
made very clear
Functional status-hyperthyroid/euthyroid/hypothyroid
Compression to trachea/recurrent nerve
Neck lymph nodal status
Tracheal deviation
Carotid infiltration
Retrosternal extension
Systemic features like toxicity or malignant spread to different
organs like bone/liver/lungs.
Remember
Goitre is enlargement of the thyroid gland
Solitary nodule is single palpable nodule on clinical examination
with rest of the gland not palpable
Dominant nodule is single nodule in a palpable enlarged thyroid
gland.
Thyroid swelling is confirmed by its movement with deglutition
due to attachment of enclosed pretracheal fascia to inferior
constrictor muscle which is attached to trachea and cricoid
cartilage and so moves with deglutition. Berry’s ligament is
condensed vascularised pretracheal fascia postero-superomedially. It is important as it is close to recurrent laryngeal
nerve.
Any thyroid swelling can be malignant unless proved otherwise
U/S neck, FNAC, T
CT scan neck is needed in large goitre and fixed or malignant
thyroid
Radioisotope study I
borderline toxicity, ectopic thyroid, retrosternal goitre and
during follow up period after thyroidectomy in follicular
carcinoma thyroid to look for secondaries.
Normal thyroid gland is usually not palpable.
, T4, TSH are essential investigations
3
123
is done only in selected cases like
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SRB’s Clinical Surgery
Investigations for Thyroid Diseases
Thyroid Function Tests
•T3, T4, TSH, Free T3, Free T4. T4 is transported in
plasma, binding to thyroxin binding globulin and
thyroxin binding prealbumin. Free T
Normal T4 is 55-150 nmol/litre. T3 is still lesser than
T4. It is 1.2- 3.1 nmol/litre. Normal TSH is 0-5 IU/
ml of plasma. In hyperthyroidism, T
increased; TSH is decreased/undetectable. T3, T4 is
decreased; TSH in increased in hypothyroidism. T
is more reliable than T4. Free T3 and Free T4 are
much more reliable indicators. If one investigation
is to be asked, it is better to do TSH estimation. TSH
increase is also seen in papillary carcinoma of
thyroid. Free T
is 0.3% (3-9 pmol/litre). Free T4 is
3
0.03% (8-26 pmol/litre).
•T
resin uptake study: It is the most common
3
indirect method available for the measurement of
the proportion of T4 which is unbound. Patient’s
serum added with radio labeled T
ion exchange resin/thyropac. It competes for
unoccupied free protein binding sites of T
hyperthyroidism unoccupied free binding sites are
low and so resin uptake is low; so resin uptake ratio
is less than 85% or low. In hypothyroidism free
binding sites are more; so resin uptake is high >
120%. Normal range of resin uptake is 0.9-1.2 µg.
100 × total serum T
percentage is called as free T
divided by T3 resin uptake
4
index. Normal range
4
is 55-145. Free T4 index is commonly used; it is
single best test available. It is helpful in diagnosing
T
thyrotoxicosis. Free T3 index also can be
3
calculated. It is 1.4-3.5.
• TRH stimulation test for hypothalamic-pituitary
axis: Intravenous TRH (200 µg) shows rise in serum
TSH level in 20 minutes (from basal 1 µ unit/ml to
10 µ unit/ml) and reaches to normal in 2 hours.
Patients with pituitary insufficiency patients develop a subnormal response; patient with hypothyroidism will show enhanced TSH response; in
hyperthyroidism there will be no response. This test
is useful in doubtful hyperthyroidism, hypothyroidism, T
thyrotoxicosis, ophthalmic Graves’
3
disease. Drugs like L thyroxine, steroids,
oestrogens, levodopa interfere with the response.
is very less.
4
, T4 are
3
is incubated with
3
. In
4
• Protein bound iodide (PBI): It is cheaper but
nonspecific and unreliable test as it also measures
nonhormonal forms of iodide. Normal value is 4 8 µg/100 ml. False positivity is seen in pregnancy,
use of iodide containing cough syrups, iodide
containing X-ray contrast, and oral contraceptives.
False negativity is found with use of salicylates,
androgens, hydantoins.
• Radioisotope studies: Uptake study - Thyroid traps
iodine and rate reflects hormone secretion. Uptake
3
is measured in 10-120 minutes. Later protein bound
131
is measured. Dose of I
I
131
of I
is 8 days; I
132
131
is 5µ curie. Half life
is 2.3 hours; I
123
is 13 hours.
Now Technetium 99 is also used as it has short half
life with very less radiation dose. It gets
concentrated similar to iodine isotopes and does not
bind to tyrosine and so precise iodine trap can be
assessed. Uptake study cannot be done after contrast
X-rays like IVU. It takes 2 weeks to excrete contrast
after IVU; 4 weeks after cholecystogram; many
years after bronchography and myelography.
Thyroid scan—It is done using I
123/I131
or
is not done in every patient with thyroid disease. It
is indicated in solitary nodule; borderline toxicity;
retrosternal goitre; ectopic thyroid; to study the
metastases in entire body in functioning thyroid
carcinomas after total thyroidectomy.
injected intravenously. I
99m
When
Tc is used scan is done in half an hour.
123/I131
is given orally.
When iodine radioisotopes are used, scan is done
in 24 hours. Cold nodule is non-functioning nodule;
hot nodule is hyperfunctioning nodule; warm nodule
is normal functioning gland. In autonomous nodule,
nodule is hot and rest of gland will not show any
activity. In functioning nodule which is not
autonomous, nodule as well as remaining gland will
show the activity.
• Werner’ s T
suppression test: Initial isotope uptake
3
study is done. 40 µg of T3 is given to the patient orally
8th hourly for 5 days. Uptake study is repeated. In
normal uptake suppression upto 80% is noted. In
toxic goitre suppression is 10 - 20%. It is used in
patients with antithyroid drugs for primary
thyrotoxicosis to assess the remission status.
• Other tests: BMR (increased in toxicity); Serum
cholesterol (decreases in toxicity); serum creatinine
(increases in toxicity).
99m
99m
T c. It
Tc is
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