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Examination of Thyroid
https://t.me/med1917
Fig. 14.54: Anaplastic carcinoma of thyroid with infiltration
through the capsule. It commonly encases the carotid artery
causing positive Berry’s sign.
Fig. 14.55: Anaplastic carcinoma of thyroid.
derived from the ultimo bronchial body (neural crest).
They are part of APUD (Amine Precursor Uptake
Decarboxylation) cells. C cells are more in upper pole
of the thyroid. It contains characteristic ‘amyloid
stroma’ wherein malignant cells are dispersed. In these
patients blood levels of calcitonin both basal as well
as that following calcium or pentagastrin stimulation
is high, a very useful tumour marker. Tumour also
secretes 5-H.T (serotonin), prostaglandin and
vasoactive intestinal polypeptide (VIP). It spreads
mainly to lymph nodes (60% common). It may be
associated with MEN II syndrome and phaeochromocytoma with hypertension. There may be
351
mucosal neuromas in lips, oral cavity.
Clinical features: Thyroid swelling often with
enlargement of neck lymph node; diarrhoea, flushing;
hypertension, phaeochromocytoma and mucosal
neuromas when associated with MEN II syndrome.
Sporadic and familial types occur in adulthood
whereas cases associated with MEN syndrome II
occur in younger age groups.
Types: (1) Sporadic. Usually solitary—70%. (2) MCT
with MEN II syndrome. MCT with MEN II B
with Phaeochromocytoma is most aggressive type.
(3) Familial MCT—It is autosomal dominant with
proto-oncogene in chromosome number 10. It is
commonly multicentric.
Investigations: FNAC: shows amyloid deposition
with dispersed malignant cells and ‘C’ cell hyperplasia;
Tumour marker: Calcitonin level will be higher.
Normally it is less than 0.08 ng/L; U/S neck-thyroid
region; Urinary VMA, urinary catecholamines, urinary
metanephrine, serum calcium, serum parathormone
estimation; CT neck and chest to evaluate nodal
111
status is a must; Indium
in detecting medullary carcinoma thyroid (70%
sensitivity). It is also useful in postoperative follow
up to find out residual/metastatic disease.
If there is associated phaeochromocytoma it should
be treated first surgically by adrenalectomy and later
total thyroidectomy is done. All family members of
the patient should be evaluated for serum calcitonin
and if it is high they should undergo prophylactic
total thyroidectomy (Can also be assessed by genetic
evaluation.) If there is positive RET proto-oncogene
in MCT with MEN IIA and familial MCT types,
prophylactic total thyroidectomy is done at the age
of 5 years. In positive RET proto-oncogene in MCT
with MEN IIB prophylactic total thyroidectomy is done
at the age of one year. MCT when associated with
parathyroid hyperplasia (30%) in MEN IIA, total
thyroidectomy with central nodal dissection with total
parathyroidectomy is done followed by autotransplantation of half of gland in sternomastoid or nondominant forearm brachioradialis muscle.
Malignant lymphoma: It is NHL type. Occurs in a
octreotide scanning is useful
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https://t.me/med1917
SRB’s Clinical Surgery
pre-existing Hashimoto’s thyroiditis (Not proved well).
FNAC is useful to diagnose the condition.
positive, i.e. absence of carotid pulsation. Movement
with deglutition often may be difficult to elicit.
Hashimoto’s Thyroiditis (Struma Lymphomatosa)
It is also called as diffuse non-goitrous thyroiditis.
It is an autoimmune thyroiditis which is common in
women. Initially there is hyperplasia, then fibrosis,
eventually infiltration with plasma cells and lymphocytic cells. Askanazy cells are typical (like Hurthle
cells). The river Struma arises in Bulgaria and flows
into Aegean Sea. S truma means goitre. Banks of this
river are endemic area for goitre.
Clinical features: Painful, diffuse, enlargement of
usually both lobes of thyroid which is firm, tender
and smooth; initially they present with toxic features
but later, they manifest with features of hypothyroidism.
There may be hepatosplenomegaly; it is often associated with other autoimmune diseases; in 85% cases
significant rise in the thyroid antibodies (microsomal,
thyroglobulin, or colloid antibodies) is observed;
papillary carcinoma may develop in Hashimoto’s
thyroiditis; often condition may be associated with
or may predispose to malignant lymphoma. At present
it is not well proved.
de-Quervain’s Subacute Granulomatous
Thyroiditis
It is due to viral aetiology either mumps or Coxsackie
viruses causing inflammatory response with infiltration
of lymphocytes, neutrophils, multinucleated giant cells.
Clinical features: Pain is diffuse, swelling in thyroid
which is tender; commonly seen in females; initially
there will be transient hyperthyroidism with high T
and T4 but poor radioiodine uptake; it is usually a
self-limiting disease.
Riedel’s Thyroiditis (Woody Thyroiditis;
Ligneous Thyroiditis; 0.5% common)
A very rare benign entity wherein thyroid tissue is
replaced by fibrous tissue which interestingly infiltrates
the capsule, extends into muscles, paratracheal
tissues, and carotid sheath. It is often associated with
retroperitoneal and mediastinal fibrosis.
Clinical features: Stony hard, fixed, small swelling
in a male with stridor, often Berry’s sign may be
Differential diagnosis: Anaplastic carcinoma of
thyroid.
Investigations: T
, T4 may be low due to hypo-
3
thyroidism; radioisotope scan will not show any uptake;
FNAC to rule out carcinoma.
Thyroid Steal
Patient is taken to operation theatre for few days befor e
doing surgery so as to r educe the anxiety of the patient.
Eventually steal the patient for surgery.
Note: Condition resulting from total removal of thyroid
was called as Cachexia strumipriva by Kocher.
Thyrotoxic Crisis (Thyroid Storm)
It occurs in a thyrotoxic patient inadequately prepared
for thyroidectomy and rarely a thyrotoxic patient
presents in a crisis following an unrelated operation
or stress. They present in 12-24 hours with severe
dehydration due to circulatory collapse, hypotension,
hyperpyrexia and often cardiac failure. Treatment is
injection hydrocortisone, oral antithyroid drugs, tepid
sponging of whole body, beta blocker injection, oral
iodides, large amount of IV fluids for rehydration,
digitoxin, cardiac monitor, often ventilator support
and observation. It has got high mortality rate with
critical period of 72 hours. Fluid and electrolyte
management, cardiac management are important
aspects to be monitored and treated.
Thyroglossal Cyst
3
Thyroglossal cyst is a swelling occurring in the neck
in any part along the line of thyroglossal tract. It is
a tubulodermoid. It is accumulation of the cystic fluid
secreted by the portion of the unobliterated part of
the thyroglossal duct/tract.
Possible Sites for Thyroglossal Cyst
Beneath the foramen caecum; in the floor of mouth;
suprahyoid; subhyoid—commonest site; on the thyroid
cartilage; at cricoid cartilage level—here tug feel may
not be elicited and so difficult to differentiate from
adenoma of thyroid isthmus. It is usually congenital
wherein there will be degeneration of a part of the
Examination of Thyroid
https://t.me/med1917
tract causing cystic swelling. Normal thyroid may be
present in the normal location (fossa). Sometimes,
thyroid may not be present in the normal site but may
be present in the wall of the thyroglossal cyst. It contains
gel-like fluid. It is lined by columnar epithelium
surrounded by lymphoid tissues.
Clinical Features
Swelling in the midline, towards the left; moves with
deglutition as well as with the protrusion of tongue.
Patient is asked to open the mouth and keep the lower
jaw still. Examiner holds the cyst between the thumb
and forefinger. When patient is asked to protrude the
tongue, a ‘tugging sensation’ can be felt. Swelling
is smooth, soft, fluctuant (cystic), nontender, mobile,
often transilluminant. Thyroid fossa is empty , if there
is no thyroid in normal location. Thyroglossal cyst
can get infected and may form an abscess. Malignancy
can develop in thyroglossal cyst (papillary carcinoma).
353
Fig. 14.56: Thyroglossal duct anatomy.
Investigations
Radioisotope study; US neck; FNAC from the cyst;
, T4 and TSH estimation.
T
3
Differential Diagnosis for Thyroglossal Cyst
Subhyoid bursa; pretracheal lymph node; dermoid
cyst; solitary nodule thyroid. If tract is not completely
excised, it will result in thyroglossal fistula.
Note: Thyroid cartilage is shaped like a prow of a
ship and so thyroglossal tract during development
sweeps towards one side. So levator glandulae
thyroideae in normal people and thyroglossal cyst
when develops will be towards left side (Figs 14.56
to 14.58).
Thyroglossal Fistula
It is not a congenital condition. It either follows
infection of thyroglossal cyst which bursts open or
after inadequate removal of the cyst. It is lined by
columnar epithelium, discharges mucus and is a seat
of recurrent inflammation. ‘Hood sign’ is characteristic
(crescentic appearance is due to uneven rate of growth
of thyroglossal tract). It may be located in suprahyoid
position or on the side of the old scar (Fig. 14.59).
Investigations
Radioisotope study, study of discharge and
fistulogram. It may mimic tuberculous sinus.
Dyshormonogenesis
It is an autosomal recessive condition wherein there
is either deficiency of thyroid enzymes (either peroxidase or dehalogenase) or inability to concentrate or
to bind or to retain iodine. It may be familial and patient
presents with large diffuse vascular goitre involving
both lobes. They respond very well to L-thyroxine
and may not require surgery at any time. Condition
may be associated with congenital deafness which is
being called as Pendred’s syndrome.
Ectopic Thyroid
Ectopic thyroid tissue may lie anywhere along the line
of descent of thyroid during the developmental period.
Whole of the thyroid gland or residual thyroid lies
in an abnormal position either in the posterior part
of the tongue, or in the upper part of the neck in midline,
or intrathoracic region. Radioisotope scan, CT scan
for intrathoracic thyroid will confirm the diagnosis
(Fig. 14.60).
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SRB’s Clinical Surgery
A
Figs 14.57A to C: Thyroglossal cyst examination to feel the unmistakable upward ‘tug”.
Fig. 14.58: Thyroglossal cyst—suprahyoid position.
Lingual Thyroid
B
It is a thyroid swelling in the posterior third of tongue,
at the foramen caecum, presenting as rounded swelling.
It may be the only existing thyroid tissue which may
cause dysphagia, speech impairment, respiratory obstruction, haemorrhage. Any diseases which can occur
in normal thyroid can also occur in lingual thyroid,
i.e. nodularity, toxicity, malignancy.
C
Fig. 14.59: Thyroglossal fistula.
Diagnosis: Radioisotope study shows the uptake of
iodine by the lingual thyroid and also says the status
of the thyroid in normal fossa. US neck has to be
done to see the absence of thyroid in normal location.
Goitre in Infancy
It is seen in endemic area or in infants whose mother
was taking antithyroid drugs for thyrotoxicosis
Examination of Thyroid
https://t.me/med1917
Fig. 14.60: Thyroid ectopic sites. 1: Ectopic lingual thyroid,
2: Intralingual thyroid, 3: Sublingual thyroid, 4: Thyroglossal
cyst, 5: Retrosternal thyroid.
(excessive TRH secretion in mother crosses the
placenta). Untreated thyrotoxicosis in pregnancy also
can cause toxic goitre in infant.
Myxoedema (Word Meaning is
Mucous Swelling)
It is a clinical state of severe lack of thyroid hormone.
It is common in middle aged and elderly . It is common
in females. Tiredness, weakness, mental lethar gy, cold
intolerance, weight gain, poor appetite, dyspnoea,
ankle oedema, slow speech, decreased thinking,
menorrhagia are the symptoms. Signs: Previous scar
of thyroidectomy or nodular goitre or normal neck;
swollen heavy eyelids; loss of hairs on the lateral third
of eyebrows; smooth, pale yellow creamy skin; flushed
pink orange cheeks (peaches); thin ragged hairs; over
deposition of fat and connective tissues in supraclavicular fossa, back, neck and shoulders; dry, elastic,
nonsweating skin; nonpitting oedema; puffy spade
like hands; enlarged tongue; deep and hoarse voice;
bradycardia (40-60 beats/minute); low blood pressure;
cold hands; blue fingertips; sluggish reflex with
prolonged relaxation period. Myxoedema coma
develops eventually with hypothermia, hypotension,
hyponatraemia, hypoventilation, hypoglycaemia,
deadly cold skin like of a toad; rectal temperature
below 24°C.
355
Hyperparathyroidism
Types
(1) Primary. (2) Secondary. (3) Tertiary. Primary is
unstimulated inappropriate high PTH secretion due
to hyperplasia or adenoma. Secondary is due to chronic
renal failure or due to malabsorption, i.e. due to chronic
hypocalcaemia. Tertiary is due to autonomous reactive
parathyroid hyperplasia seen after renal transplantation.
Primary Hyperparathyroidism
Adenoma—75%; Hyperplasia—20-24%; Carcinoma—rare—1%. Carcinoma of parathyroid is one
of the most aggressive tumour known but fortunately
rare. May present as a nodule and can have blood
born metastasis.
Clinical features: Clinical vignette of hyperparathyroidism— “Bones, stones, abdominal groans and
psychic moans.” (1) Hyperparathyroidism is common
in middle aged women. (2) Presentation may be
asymptomatic in 50% cases. (3) Nonspecific symptoms
and psychiatric symptom (They are most often named
as neurotics). (4) Behavioural problems. (5) In the
bone there will be osteitis fibrosa cystica (von
Recklinghausen disease of bone) which shows single
or multiple cysts or pseudotumour in the jaw, skull
or middle phalanges. (6) Lamina dura of tooth is the
first bone to show changes. (7) In the kidney there
may be bilateral multiple renal stones or nephrocal-
cinosis (may go for renal failure). (8) It may be
associated with the peptic ulcer, pancreatitis, MEN
I syndrome. (9) They are more prone for skin necrosis,
band keratopathy, pseudogout, myalgia, arthralgia,
polyuria, glycosuria and hypertension. Acute hyper-
parathyroidism crisis: It is rare but dangerous
presentation (crisis) wherein patient presents with
abdominal pain, vomiting, dehydration, oliguria and
death. Serum calcium is very high.
Investigations: High serum calcium - > 10 mg/100 ml;
Decreased serum phosphorus; Increased urinary
calcium - > 250 mg/24 hrs; Increased serum alkaline
phosphatase; Increased PTH level in the serum is
diagnostic - > 0.5pg/L; X-ray skull shows salt- pepper
appearance; X-ray phalanges and jaw is specific;
US abdomen to find out problems in kidney, pancreas;
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SRB’s Clinical Surgery
US neck or CT scan neck and mediastinum may show
the parathyroid adenoma; Selective venous sampling
for PTH is also very useful; Thallium—Technetium
scan shows hot spots which is diagnostic of parathyroid
adenoma;
99m
Technetium labeled Sestamibi isotope
scan is more sensitive.
Differential diagnosis: Sarcoidosis; over intake of
vitamin D; secondaries in bone; multiple myeloma;
functioning carcinomas.
MEN Syndrome (MEA Syndrome)
It is multiple endocrine neoplasia syndrome. It is
commonly inherited as autosomal dominant; Cells
involved has got common features of apud cells
(Apudomas).
Types: Type I: Parathyroid hyperplasia or adenomas;
pituitary tumour; pancreatic tumour [Endocrine- (Insulinoma , gastrinoma, glucoganoma, vipoma)]. It is also
called as Wermer ’s syndrome. Type II: Also called
as Sipple’ s disease; II A includes medullary carcinoma
of thyroid + phaeochromocytoma + parathyroid
hyperplasia (50%); IIB. includes medullary carcinoma
of thyroid + phaeochromocytoma + mucosal neuromas
in lips and eyelids with bumpy-lumpy lesions, with
marfanoid face, megacolon.
Tetany
It is decreased level of calcium in blood causing its
effects.
Causes: After thyroidectomy (it is decreased level
of paratharmone in the blood causing hypocalcaemia).
It is usually temporary lasts for 4-6 weeks. It is the
commonest cause of hypoparathyroidism. Other causes
of hypoparathyroidism are neck dissection, haemochromatosis, Wilson’ s disease, di-George’ s syndrome
(absence of parathyroids; thymic aplasia; cardiac
Fig. 14.61: Carpal spasm due to tetany in post-thyroidectomy
patient. Note the thyroidectomy scar.
defects); severe vomiting, hyperventilation associated with respiratory alkalosis; metabolic alkalosis;
rickets, osteomalacia; chronic renal failure; acute
pancreatitis.
Clinical features: Decreased PTH causes decrease
in calcium level in the blood leading to-circumoral
paraesthesia, paraesthesia of neck, fingers and toes,
Twitching and weakness of tongue muscles, muscles
of forearm, hand, foot and digits—carpopedal spasm;
Chvostek-Weiss’s sign —tapping above the angle of
the jaw stimulates branches of facial nerve causing
the twitching of the angle of mouth and eyelids;
Applying the sphygmomanometer to the arm and
inflating the pressure more than systolic pressure of
the patient for three minutes can demonstrate carpal
spasm (Trouseau’s sign); Stridor and difficulty in
breathing due to paralysis of respiratory muscles;
Generalized weakness and twitching all over the body
in severe cases mimicking convulsions (Fig. 14.61).
Examinations of Face and Head
https://t.me/med1917
Examinations of
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15
Introduction
Many specific and peculiar conditions pertaining to
face and head occurs. Because of their individuality,
they are being discussed as a separate chapter. Relevant
history, examination methods are same as in chapters—
ulcer, swelling, neck and oral cavity. Student should
refer specific chapters for method of examination (Figs
15.1 to 15.4).
Hippocratic facies: It is seen in patients with acute
sunken bright eyes, pinched nose, dry, shriveled
tongue, crusted lips, cold clammy forehead, distended
abdomen with features of peritonitis.
Adenoid facies: High vaulted palate, narrow dental
arch, protruding incisor teeth, earlier was considered
as feature of enlarged adenoid is now not accepted.
In fact these features are familial anomaly . Enlarged
adenoids are a coincidental.
Face and Head
Fig. 15.2: Underdeveloped ear—anomaly.
Fig. 15.1: Conjunctival haemorrhage.
Fig. 15.3: Developmental anomaly of
face with underdeveloped mandible.
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Fig. 15.4: Accessory ear. An accessory auricle is a protruded
posterolateral part of the face with cartilage, fibrous tissue
and skin covering. It is commonly cylindrical erect in front
of the tragus. It is sequestration of an island of cartilage
from the mandibular arch during closure of first branchial
cleft.
SRB’s Clinical Surgery
Facies of cretinism—seen in infancy; pale, puffy,
wrinkled face; dry cold skin; protruded tongue; open
anterior fontanelle; palpable (in endemic type) or
impalpable ( in sporadic type gland is atrophic) thyroid
gland.
Facies of congenital syphilis: Bossing of frontal
bones; interstitial keratitis; Hutchinson’s teeth; saddle
nose.
Facies of hepatic cirrhosis: Sunken eyes; jaundiced
sclera; watery conjunctiva.
Virile facies in a women suffering from adrenocortical
hyperplasia or tumour is typical (face looks like that
of men).
Moon face of Cushing’s syndrome: Rubicund round
face like of full moon; pursed lips.
Face of myasthenia gravis: Unilateral or bilateral
intermittent ptosis; drooping jaw; sneering smile face
due to reduced action of risorius and zygomatic
muscles.
Carcinoid facies: Typical facial flushing seen in
metastatic carcinoid tumour.
Rhesus sardonicus face of tetanus with trismus—
painful smiling.
Cleft Lip and Cleft Palate
Development of Face
Face develops from median nasal process, lateral nasal
process, maxillary process, mandibular arch, globular
arch, olfactory pit and eye. Any change in the
development or fusion of these arches leads to
formation of different types of cleft lip or cleft palate.
Aetiology
Familial—More common in cleft lip or combined cleft
lip and palate (Risk is 1:25 live births); protein and
vitamin deficiency; Rubella infection; radiation;
chromosomal abnormalities; maternal epilepsy and
drug intake during pregnancy (steroids/eptoin/
diazepam).
Classification
I. Cleft lip alone: Unilateral; Bilateral; Median.
II. Cleft of primary palate (in front of incisive foramen)
only: (a) Complete—means absence of pre-maxilla.
(b) Incomplete—means rudimentary pre-maxilla:
Unilateral; Bilateral; Median. III. Cleft of secondary
palate (behind the incisive foramen) only: a) Complete
– nasal septum and vomer are separated from palatine
process. b) Incomplete. c) Submucous. It can be - Cleft
with soft palate involvement. Cleft without soft palate
involvement. IV . Cleft of both primary and secondary
palates. V. Cleft lip and cleft palate together.
Defect is often associated with other congenital
anomalies of cardiac, gastrointestinal, neurological
system, Pierre-Robin syndrome (most commonly
associated syndrome with features of isolated cleft
palate, retrognathia, posteriorly displaced tongue),
Klippel-Feil syndrome, Stickler’s syndrome (eye,
skeletal, muscular, cleft), Shprintzen’s syndrome
(cardiac and cleft disorder), Down’s syndrome,
Treacher-Collin’s syndrome, Apert’s syndrome and
trisomy.
Incidence
Common in Caucasians; in 75% of cases it is unilateral.
Commonly occurs on the left side (60%); in 50% of
Examinations of Face and Head
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cases it is combined cleft lip and palate. Incidence
is 1:600 live births; common in boys; in 15-25% of
cases it is cleft lip alone; in 25-40% of cases it is
cleft palate alone. Incidence is 1:1000 live births; more
common in girls.
Problems in Cleft Disorders
Difficulty in sucking and swallowing. This is commonly
observed in cleft palate than in cleft lip; speech is
defective especially in cleft palate, mainly to phonate
B, D, K, P , T and G . Altered dentition or supernumerary
teeth; recurrent upper respiratory tract infection;
respiratory obstruction (in Pierre-Robin syndrome);
chronic otitis media, middle ear problems; cosmetic
problems; hypoplasia of the maxilla; problems due
to other associated disorders (Figs 15.5 to 15.9).
359
Fig. 15.6: Lateral type of cleft lip (Type II variety—it is
commonest). It is due to imperfect fusion of maxillary process
and median nasal process. It can be unilateral or bilateral.
Fig. 15.5: Central cleft lip (Hare lip,
Type I cleft lip—It is rare).
• Central—Rare. In upper lip. Between two median nasal
processes. (Hare lip)
• Lateral —Maxillary and median nasal process,
commonest; can be unilateral or bilateral
• Incomplete cleft lip does not extend into nose
• Complete cleft lip extends into nasal floor
• Simple cleft lip is only cleft in the lip
• Compound cleft lip is cleft lip with cleft of alveolus
LAHS classification of cleft disorders
• ‘L’ for lip, ‘A’ for alveolus, ‘H’ for hard palate, ‘S’ for
soft palate
• Capital ‘LAHS’ for ‘complete’ type
• Small letters ‘lahs’ for ‘incomplete type’
• Asterisks ‘lahs’ for microclefts
• ‘LAHSHAL’ for bilateral clefts
Fig. 15.7: Bilateral cleft lip.
Cleft lip
Fig. 15.8: Unilateral cleft lip, lateral type
which is commonest.
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Fig. 15.9: Bilateral cleft lip involving palate.
SRB’s Clinical Surgery
Cleft Palate
It is due to failure of fusion of the two palatine
processes; defect in fusion of lines between premaxilla
(developed from median nasal process) and palatine
processes of maxilla one on each side; when premaxilla
and both palatine processes do not fuse, it leads into
complete cleft palate (Type I cleft palate). Incomplete
fusion of these three components can cause incomplete
cleft palate beginning from uvula towards posteriorly
at various lengths. So it could be T ype IIa—Bifid uvula,
Type IIb—bifid soft palate (entire length) or T ype IIc
–bifid soft palate and posterior part of hard palate
(but anterior part of hard palate is normal). Small
maxilla with crowded teeth, absent/poorly developed
upper lateral incisors. Bacterial contamination of upper
respiratory tract with recurrent infection is common.
Chronic otitis media with deafness may occur.
Swallowing difficulties to certain extent and speech
problems can occur; cosmetic problems can occur (Figs
15.10 to 15.14).
Bifid Nose
One-half of the frontonasal process remains isolated
from rest.
Facial Cleft
Lateral nasal process fails to unite with maxillary
process causing a fissure from upper lip to the inner
canthus of the eye alongside of the nose.
Fig. 15.10: Cleft palate only. Lip is normal.
Premaxilla is not involved.
Fig. 15.11: Complete cleft palate Type I.
Macrostoma
Size of the mouth is more than the normal due to
imperfect union of maxillary process with mandibular
arch.
Mandibular Cleft
Mandibular arch of one side fails to unite with
mandibular arch of opposite side.
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