Surgery thyroid

Topics discussed:
• Anatomy & Physiology
• Congenital Anomalies
• Examination of Thyroid
• Goiter
• Hyperthyroidism & Thyrotoxicosis
• Hypothyroidism
• Thyroiditis
• Neoplasm
• Thyroidectomy

THYROID
• Endocrine gland in midline of neck against
vertebra C5,6,7,T1.
• Weight 20-25 g.
• Lies infront of tracheal rings 2,3,4

DEVELOPMENT
• 1st endocrine gland to develop in body.
• Mainly develops from thyroglossal duct.

SURGICAL ANATOMY
• 2 lobes-right and left.
• Both lobes joined by
isthmus.
• In some pts remenant
of thyroglossal duct-
PYRAMIDAL LOBE
• Pyramidal lobe is
attached to hyoid by
fibres called LEVATOR
GLANDULAE
THYROIDAE

Ligaments & Fascia
• Suspensary ligament of Berry:- Condensed
connective tissue binds gland firmly to cricoid
cartilage and upper tracheal rings.
• Pretracheal fascia:-Part of deep cervical fascia
splits to invest gland.
• Note:-ligament of berry & pretracheal fascia
responsible for movement of gland with
deglutition.

Venous drainage of Thyroid
KOCHER’S VEIN:-Present between inferior & middle thyroid vein.
Very rare.

Lymphatic drainage
1.Level III & IV
nodes
2.Level VI nodes
3.Level VII nodes

Thyroid Function Test
• Serum T3
• Serum T4
• Serum TSH
• Thyroid Autoantibody levels
• Serum Protien Bound Iodine
• T3 resin uptake
• Serum Thyroglobulin
• Thyroid scintigraphy
• Thyroid imaging

INTERPRETATION
TSH(0.3-3.3mU/L) T3/FT3 (3.5-
7.5micromol/L)
T4/FT4 (10-
30nmol/L)
INTERPRETATION
HIGH NORMAL NORMAL •Subclinical
hypothyroidism
HIGH LOW LOW •Chronic thyroiditis
•Post thyroidectomy
LOW HIGH/NORMAL HIGH/NORMAL •Subclinical
hyperthyroidism
•Thyroxine ingestion
LOW HIGH HIGH •Primary
Hyperthyroidism
•DeQuervain’s
thyroiditis
LOW/NORMAL HIGH NORMAL •T3 Toxicosis

CONGENITAL
ANOMALIES
OF THYROID

 Ectopic thyroid
 Lingual thyroid
 Thyroglossal cyst
 Thyroglossal fistula
 Lateral aberrant thyroid
 Agenesis
 Dyshormonogenesis
Types of congenital anomalies of
THYROID

1.Ectopic thyroid
• It is RESIDUAL THYROID TISSUE,
along the course of thyroglossal tract.
• Thyroglossal duct is embryological anatomical structure
forming an open connection between the initial area of
development of thyroid gland and it’s final position.
• Located exactly midline between anterior 2/3rd and posterior
1/3rd of tongue.
 Thyroid gland start developing in the oropharynx in the fetus
and descend’s to it’s final position taking a path through
Beneath the tongue (foramen caecum)  HYOID bone  neck
muscle.

Residual thyroid lies in an abnormal position
either in the….
1. POSTERIOR PART OF THE TONGUE
OR
2. UPPER PART OF THE NECK IN MIDLINE
OR
3. INTRA THORACIC REGION
•Ectopic thyroid tissue may lie
anywhere along the line of descent.

DIAGNOSIS-
1.Radioisotope scan
2.CT-scan
for intrathoracic thyroid will confirm the
diagnosis.
•CARCINOMA develop’s more commonly in
Ectopic thyroid tissue then normal thyroid.

2.LINGUAL THYROID
• It is developmental anomaly which result when there is
incomplete migration of thyroid.
• It is a THYROID SWELLING.
• Its present in the POSTERIOR THIRD OF THE TONGUE at
the foramen coecum.
• It is presenting as ROUNDED SWELLING.
• It is common in FEMALE. [3:1]

Thyroid swelling of lingual thyroid may
cause’s-
1. DYSPHAGIA
2. PAIN
3. SPEECH IMPAIRMENT
4. RESPIRATORY OBSTRUCTION
5. HAEMORRHAGE

DIFFERENTIAL DIAGNOSIS FOR LINGUAL
THYROID
• Carcinoma of posterior third of tongue
• Angiofibroma
• Sarcoma
• Hypertrophid lingual tonsil

DIAGNOSIS
1. RADIOISOTOPE STUDY- shows uptake of
iodine by lingual thyroid and status of thyroid
in normal fossa.
2.USG-NECK - TO See the absence of thyroid
in normal location.

TREATMENT
1. L-THYROXINE is given daily orally.
2. Require surgical excision.
3. Radio isotope therapy for ablation

3. THYROGLOSSAL CYST
• It is a SWELLING which occur in the neck in any part
along the line of thyroglossal tract.
• Usually CONGENITAL wherein there will be
degeneration of the part of the tract causing CYSTIC
SWELLING.
• It’s TUBULODERMOID TYPE OF CYST. WHICH is lined
by PSEUDOSTRATIFIED, CILIATED COLUMNAR
EPITHILIUM.

Possible site for thyroglossal cyst
1.SUB HYOID-1ST Commonest site
2.THYROID CARTILAGE- 2ND Commonest site
3.supra hyoid
4.Beneath the FORAMEN COECUM
5.FLOOR OF MOUTH

4. SWELLING moves with DEGLUTITION as well as with
PROTRUDE of tongue.
5. MALIGNANCY can be developed in thyroglossal
cyst(PAPILLARY CARCINOMA-1%)
INVESTIGATION
1. Radioisotope study
2. Ultrasonography of neck
3. FNAC from the cyst

DIFFERENTIAL DIAGNOSIS FOR THYROGLOSSAL
CYST
1. SUBHYOID BURSA
2. PRETRACHEAL LYMPH NODE
3. DERMOID CYST
4. SOLITARY NODULE OF THYROID-ISTHMUS
5. SUBMENTAL LYMPH NODE

TREATMENT
SISTRUNK OPERATION-
Excision of cyst and also full tract upto the
foramen caecum is done along with removal of
central part of hyoid bone, as the tract passes
through it.
COMPLICATION-
1. RECURRENCE
2. THYROGLOSSAL FISTULA
3. HAEMORRHAGE / HEMATOMA
4. INFECTION

THYROGLOSSAL FISTULA
• It is not a congenital condition.
• It either follows infection of Thyroglossal cyst which
burst open or after in adequate removal of cyst.
• SITE- FISTULA is just lower the HYOID BONE
commonly. And in INFANT- much lower of hyoid
bone.
• Lined by columnar epithelium, discharge mucous and
is a seat of Recurrent inflammation.

•opening of fistula is indrown and been overlaid
By fold of skin as ‘hood’ is called Hood sign.
• PECULIER CRESCENTRIC APPERANCE is called
SEMILUNAR SIGN.
• It secrets mucous discharge.

INVESTIGATION
• RADIOISOTOPE STUDY
• FISTULOGRAM
TREATMENT
• SISTRUNK OPERATION

5. LATERAL ABERRANT THYROID
• It is at Present consider as a MISNOMER.
• It is metastasis into cervical lymph node from a
PAPILLARY CARCINOMA OF THYROID.
• FNAC has to be done and treated as PAPILLARY
CARCINOMA OF THYROID.

6. AGENESIS
• Total agenesis of one thyroid lobe may occur.
• This is rare but can be clinical important.
• Leads to confusion in Diagnosis is Specially in the
TOXIC GLAND , WHERE it could be diagnosis as a
SECRETING NODULE.

7.DYSHORMONOGENESIS
• It is AUTOSOMAL RECESSIVE condition .
it is caused by-
1. DEFICIENCY OF THYROID ENZYME(peroxidase or
dehalogenase)
2. INABILITY TO CONCENTRATE
3. INABILITY TO BIND
4. INABILITY TORETAIN IODINE.

May be familial and patient presents with LARGE
DIFFUSE VASCULAR GOITRE involving both LOBE.
• They respond very well to L-THYROXIN and may not
require surgery at any time.
• PENDRED’S SYNDROME – DYSHORMONOGENESIS
condition is associated with CONGENITAL
DEAFNESS.

INVESTIGATION
• CT-SCAN OF TEMPORAL BONE- shows
“abnormal bony labyrinth”
This condition shows “THYROID PEROXIDASE
DEFICIENCY”.

CLINICAL
EXAMINATION OF
THYROID
SWELLING

GOITRE
• Swelling of neck resulting from thyroid
enlargement is GOITRE.
• It can be euthyroid, hyperthyroid, or
hypothyroid.

CAUSES
• More common in women than men
• Physiological
• Iodine deficiency
• Autoimmune thyroid conditions

• Radiotherapy
• Radioactivity
• Unusual dietary habits
• Drugs

CLASSIFICATION OF GOITER
TOXIC
• DIFFUSE
• MULTINODULAR
• NODULE
• RECURRENT
NON TOXIC
• DIFFUSE
• MULTINODULAR
• NODULE
• RECURRENT
NEOPLASM
• PAPILLARY
• MEDULLARY
• FOLLICULAR
• ANAPLASTIC
INFLAMMATORY
• REIDEL’S
• HASHIMOTO
• DE QUERVAIN
RARE
• INFECTIONS
• AMYLOIDOSIS
• CYST
• ABSCESS

WHO GRADING
• GRADE 0: no visible or palpable goitre
• GRADE 1: palpable thyroid/goitre but not visible
in normal positioned neck
• GRADE 2: visible goitre.

• Swelling :
Long standing swelling: benign condition
Short duration with rapid growth:
malignant condition
Sudden increase in size with pain:
hemorrhage
• Rate of growth:
Slow growing
Rapid growing

• Dyspnoea:
Anaplastic ca
Retrosternal goiter
Long standing MNG
Secondary thyrotoxicosis
• Hoarseness of voice:
Malignancy

• Toxic features: of hyperthyroidism
CNS symptoms:- tremors
sweating
intolerance to heat
preference to cold
excitability
irritability
CVS symptoms:- palpitations
precordial chest pain
dyspnoea on exertion

• Swelling :
onset
duration
rate of growth
pain
• Local effects:
dyspnoea
dysphagia
hoarseness of voice
pain

• Toxicity:
CNS
CVS
GIT
Menstrual
• Hypothyroidism:
Lethargy
Deposition of fat
Deep, husky voice
Intolerance to cold

INSPECTION
• Location: in front of the neck extending
horizontally from one sternomastoid to another
sternomastoid vertically from suprasternal notch to
the thyroid cartilage.
• Size and shape
• Surface:
Smooth: adenoma, puberty goitre, Grave’s disease
Irregular: ca thyroid
Nodular: MNG

• Borders: usually round.
• With deglutition:
Swelling which move-
A. thyroid swelling
B. subhyoid bursitis
C. pretracheal and prelaryngeal LNs
D. thyroglossal cyst
E. Laryngocoele

Restricted in-
A. Malignancy
B. Retrosternal goiter
C. Large goiter
• Protrusion of tongue: thyroglossal cyst

PALPATION
• Local temperature
• Size, shape, surface, border
• Consistency:
1. Soft: grave’s ds. ,colloid goitre
2. Firm: adenoma, MNG
3. Hard: ca, calcification of MNG
• Confirm the movement
• Intrinsic mobility of the gland
“Very large nodular surface is bosselated surface”

• SCM contraction test
• Chin test (neck fixation test)
• Position of trachea
• Palpation of LNs
• Palpation of CCA
• Evidence of toxicity

• Special tests:
1. Crile’s method

PERCUSSION
• Normally- resonant note
• Retrosternal goiter – dull note
AUSCULTATION
• Should be done at the upper pole-
superior thyroid artery is more
superficial.
• Presence of thrills and bruits- toxic goiter.

Systemic examination
• CNS examination
• Eye examination
• Examination of Skeletal system
• CVS examination
• Deep tendon reflexes

DIFFERENTIAL DIAGNOSIS
• Thyroid masses;
nodules; cyst
• Thyroglossal cyst
• Dermoid cyst
• Swelling of skin
• Neural tumors of
vagus nerve
• Laryngocoele
• Lymph nodes
• SM Salivary gland
• Ranula
• Branchial cyst

DIAGNOSIS
• Based on its anatomical location and features.
ANATOMICAL FEATURES:
1. IN FRONT OF NECK
2. DEEP TO PRE TRACHEAL FASCIA
3. MOVES UP WITH DEGLUTITION
4. BUFFERFLY SHAPED WHEN ENLARGED

INVESTIGATIONS
• Blood tests
• X-rays
• Ultrasound scan
• Fine needle aspiration cytology (FNAC)
• Radioactive iodine scan

TREATMENT
This may involve one or several of the following:
• surgery
• radioactive iodine
• antithyroid medication
• levothyroxine tablets

GOITRE
Presented By:-
ANURADHA SAINI

Definition
Any enlargement of
thyroid gland
irrespective of its
pathology .

GOITRE-
- Diffuse hyperplastic goitre
- Multinodular goitre
- Discrete thyroid nodule
- Solitary nodule
- Retrosternal goitre

DIFFUSE HYPERPLASTIC GOITRE
• Persistent increase in TSH level
Diffuse active lobules
• In late stage
• TSH stimulation decrease

Follicle become inactive
filled with colloid
colloid goitre
- Reversible stage
Treatment- L-thyroxine

• MULTINODULAR GOITRE
- End stage result of diffuse hyperplastic
goitre
- Due to excess metabolic demand
- common in female (10:1)
- Mostly in 20 to 40 years age group
Etiology
Puberty goiter,Pregnancy goitre

Iodine deficiency goitre
Goitrogens
Dyshormogenesis
Pathogenesis-
Discordant growth with functionally and
structurally
altered thyroid follicles
due to fluctuation in TSH level

Persistent TSH stimulation
Diffuse hyperplasia of gland
Later on fluctuation in TSH level
mixed areas of active and inactive lobules
Hemorrhages with necrosis in centre

Nodule formation
Centre of nodule inactive and only margine
active
formation of many nodules
Multinodular goitre

Stages of multinodular goitre formation-
1. Hyperplasia and hypertrophy
2. Fluctuation in TSH
3. formation of nodules
Clinical feature –
1.Patient present with nodular swelling over
neck
2.compressive symptoms such as cough,
dysphagia,
stridor may or may not be present

On examination-
- asymmetrical in shape
- nodular surface
- soft to hard consistency
- kocher’s test positive

Complications-
1. Secondary thyrotoxicosis
2. Follicular carcinoma of thyroid
3. haemorrhage in a nodule
4. Tracheal obstruction
5. Cosmetic problem

Investigation-
1. T3,T4,TSH
2. X-ray of neck
3. indirect laryngoscopy
4. USG
5. Radioisotope iodine scan
6. Routine blood investigations
7. CT scan and MRI
8. FNAC

Prevention –
1. Puberty goitre : 0.1mg of thyroxine
2. Iodine deficiency goitre : use iodised salt
,sea
food,milk,egg,etc.
3. Goitrogens : Avoid cabbage,drugs

DISCRETE THYROID NODULE
- Clearly palpable nodule
- Solitary (Isolated) OR Dominant nodule
- Common in females
- Solid or cystic

Risk factors for malignancy in discrete
thyroid nodule –
1. Solitary having 2 times more risk
2. Male having 4 times more risk than
female
3. Solid nodule 2 times more risk than
cystic

SOLITARY THYROID NODULE
Single palpable nodule in normal thyroid gland
Causes-
1. Thyroid adenomas
2. Papillary carcinoma of thyroid
3. May one nodule palpate in multinodular
goitre
4. Thyroid cyst

Types-
1. Toxic solitary nodule
2. Nontoxic solitary nodule
Based on radioisotope study-
1. Hot nodules –
* autonomous toxic nodule
* surrounding thyroid tissue inactive so not
take up isotop
*overactive nodule

2. Warm nodule-
* normally functioning nodule
* surrounding normal thyroid tissue take
up isotope
* active nodule
3. Cold nodule-
* non-functioning nodule
* not take up isotope
* underactive

Features-
- Tracheal deviation towards opposite side is
common confirmed by ,trail sign ,three-finger
test , auscultation and x-ray neck.
- Commonest site junction of isthmus with one
of the lateral lobes.
- It is most common thyroid surgical disease.

Investigations-
- USG of neck
- FNAC
- T3,T4,TSH
- Power Doppler done to know vascularity of
gland
resistive index-
normal RI is 0.65-0.7
>0.7 indicate melignancy

- Radioisotope study
- CT scan or MRI
- X-ray neck
Treatment-
- Nontoxic goitre do Hemithyroidectomy with
complete removal of lateral lobe and isthmus
- Papillary carcinoma of thyroid do near total
thyroidectomy
- Toxic nodule give radioiodine therapy

RETROSTERNAL GOITER
Defined as having >50% goiter below
suprasternal notch.
Classification-
1. Primary - rare
2. Secondary – common

Clinical types-
1. Substernal type
2. plunging goitre
3. Intrathoracic goitre
Clinical feature-
- Pressure symptoms
- Lower border not seen on inspection and not
felt on palpation
- Pemberton’s sign positive

- Dull note over sternum on percussion.
Differential diagnosis-
- Mediastinal tumors
Investigations-
- Chest X-ray
- Radioactive iodine study
- CT scan
Treatment –
Surgical removal of retrosternal goitre

Thyrotoxicosis/
hyperthyroidism

Hyperthyroidism :
State of excessive production of
thyroid hormone by thyroid gland.
Thyrotoxicosis :
State of excessive thyroid
hormone in the body due to any cause.

Hyperthyroidism is of two types:
(a) Primary hyperthyroidism: It is the term
used when the pathology is within the thyroid
gland.
(b) Secondary hyperthyroidism: It is the
term used when the thyroid gland is
stimulated by excessive TSH in circulation.

Types of thyrotoxicosis
1. Diffuse toxic goitre : Grave’s disease/
Basedow’s disease.
2. Toxic multinodular goitre : Plummer’s
disease.
3. Toxic nodule
4. Other cause :
(a) Thyrotoxicosis factitia
(b) Jod-Basedow thyrotoxicosis

(c) Autoimmune/ de Quervain’s thyroiditis
(d) Malignant goiter
(e) Neonatal thyrotoxicosis
(f) TSH secreting tumors of pituitary
(g) Struma ovarii
(h) Drugs- amidarone

Etiology
1. Autoimmune disorder :
- most common
- occurs due to increase level of TSH
receptor antibodies in the blood.
- Thyroid stimulating immunoglobulin(TSI)
and Long acting thyroid stimulator(LATS)
cause pathological changes in thyroid.
- Also associated with other autoimmune
disease like vitiligo.

2. Familial :
- This disease can run in a family.
- Familial/genetic Grave’s disease has
been documented in identical twins.
3. Exophthalmos producing substance (EPS) :
- Responsible for ophthalmopathy seen
in Grave’s disease.

Histopathology
• As a result of continuous stimulation, acinar
hypertrophy and hyperplasia take place.
• The acinar cell which are normally flat become
tall columnar. The normal colloid disappear
and the cells are empty.
• As cells are empty, they look vacuolated.
• Tissues are highly vascular.

Acini with flat cuboidal
epithelium filled with
homogenous colloid
Hyperplasic empty acini
lined by columnar
epithelium

Risk Factor
1. Postpartum state
2. Iodine excess
3. Lithium therapy
4. Infection- bacterial and viral
5. Smoking
6. Stress

Clinical features
• It is 8 times more common in females.
• Occurs at any age group.

PRIMARY vs SECONDARY
THYROTOXICOSIS
PRIMARY
THYROTOXICOSIS
SECONDARY
THYROTOXICOSIS
Age & signs Young;Appear
simultaneously for short
time
Older; long duration of
swelling & short duration
of signs
Consistency & surface Soft/firm ; smooth Firm/hard ; Nodular
Predominant symptoms CNS CVS
Eye signs Common rare
Pretibial myxoedema 1-2% patients Never seen
Proximal myopathy 5% patients Never seen
Malignant Exophthalmos Can be seen Never seen
Auscultation Bruit is common Bruit uncommon

Symptoms
1. Gastrointestinal sym. :
(a) weight loss in spite of
increase appetite.
(b) diarrhea
2. Cardiovascular sym. :
(a) palpitation
(b) shortness of breath
on min. exertion or rest.
(c) angina
(d) cardiac irregularity
(e) cardiac failure in elderly

5. Genitourinary symptom:
(a) oligo- or amenorrhea
(b) occasional urinary frequency
6. Integument:
(a) hair loss
(b) pruritis
(c) palmer erythema

3. CNS symptom:
(a) undue fatigue and muscle weakness
(b) tremor
(c) insomnia
(d) agitation
(e) exaggerated reflex
4. Skeletal system symptom:
(a) increase in linear growth in children

Signs
1. Eye signs :
(a) Stellwag’s sign – Absence of normal blinking.
(b) von Graefe’s sign – It is inability of the upper
eyelid to keep pace with the eyeball when it
looks downward to follow the examiner finger.
(c) Joffroy’s sign – Absence of wrinkling on
forehead when patient looks up.
(d) Moebius sign- Lack of convergence of
eyeball.

(d) Dalrymple’s sign : Upper eyelid retraction, so
visibility of upper sclera.
(e) Jellinek’s sign : Increased pigmentation of eyelid
margins.
(f) Enroth sign : Edema of eyelid and conjunctiva.
(g) Rosenbach’s sign : Tremors of closed eyelid.
(h) Cowen’s sign : Jerky pupillary contraction to
consensual light.
(i) Knie’s sign : Unequal pupillary dilatation.
(j) Loewi’s sign : Dilatation of pupil with weak
adrenaline solution.

Naffziger’s sign
Jellinek’s sign
Dalrymple’s sign
Enroth sign

(j) Kocher’s sign : When clinician places his hand on
patient’s eyes and lifts it higher, patient’s
upper eyelid springs up more quickly than
eyebrows.
(k) Naffziger’s sign : When patient in sitting position
and neck fully extended, protruded eyeball
can be visualized when observed from behind.
(l) Gifford’s sign : Difficulty in everting upper eyelid in
primary toxic thyroid.
Differentiate from other causes of
exophthalmos.

Exophthalmos
• It is the proptosis of the eye, caused by :
• Sclera can be seen clearly below the limbus of the eye.
Infiltration of
inflammatory
and round cells in
retrobulbar
tissue
Spasm of
LPS which
carry
sympathetic
fibers
Spasm of
Muller
muscle (
sympathetic
muscle)

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 edema,
raised intra-ocular pressure, diplopia
and ophthalmoplegia.
4. Progressive = In spite of proper
treatment, progression of eye
is seen with chemosis , corneal
ulceration and ophthalmoplegia.

Thyroid ophthalmopathy in Grave’s disease with
Werner’s abridged classification of ocular changes
with van Dyke’s modification
Class - grade Definition
0 No sign and symptom
1 Eye sign
2 Soft tissue involvement
3 Proptosis more than 22mm
4 Extraocular muscle involvement
5 Corneal involvement - ulceration
6 Loss of sight/vision due to optic nerve and
corneal involvement

Tachycardia is common
Pulsus paradoxous
Wide pulse pressure
Multiple extrasystoles
Paroxysmal atrial tachycardia
Paroxysmal atrial fibrillation
Persistent atrial fibrillation

Weakness of proximal muscles occurs.
Weakness is more when contracts isometrically
either while getting down steps,or lifting a full
bucket.
In severse forms,it resembles myasthenia gravis.

Usually bilateral,symmetrical,shiny,red thickned
dry skin with coarse hair in the feet and ankles.
It is due to deposition of myxomatous tissue
(mucin-like deposits).
It is associated with exopthalmos with high level
of thyroid stimulating antibodies.
Thyroid dermopathy occur.it includes pretibial
myxoedema,pruritus,palmar erythema,hair thinning,
dupuytren’s contracture

Thyroid acropachy is clubbing of finger and toes
in primary thyrotoxicosis.Hypertropic pulmonary
osteoarthropathy can develop.

Thrill is felt in the upper pole of the thyroid
and also bruit on auscultation.
Hepatoslenomegaly.

Thyroid Function Tests
• Serum T3 or T4 levels are very high. TSH is very
low or undetectable.
(Normal T3 – 3-9 pmol/L)
(Normal T4 – 8-26 nmol/L)

Radioisotope study
• An 123I or 131I uptake and scan should be
performed.
• An elevated uptake shows ‘hot areas or
nodules’.
• Grave’s disease shows diffuse uniform over-
activity.
• It also helps to differentiate it from other
causes of hyperthyroidism.

Antibodies
• Anti-Thyrogloblulin antibody and anti-TPO
antibodies are elevated in up to 75% of
patients.
• Elevated TSH-R or thyroid-stimulating
antibodies (TSAb) are diagnostic of Graves'
disease and are increased in about 90% of
patients

Other Investigations
• ECG to look for cardiac involvement.
• TRH estimation.
• Total count and neutrophil count are very
essential as anti-thyroid drugs may cause
agranulocytosis.

• Thyrotoxicosis may be treated by THE
FOLLOWING treatment modalities —
1. Antithyroid drugs
2. Radioiodine Therapy 131I
3. Surgery.

Antithyroid Drugs:-
Prevent release of hormone: Lugol’s iodine 10 drops-
3 times day.
Prevent production of thyroxine:
Methimazole:20-40 mg OD ,not used in pregnency.
Carbimazole:20mg three times a day up to 120mg.
Propyl thiouracil(PTU):100mg three times a day,used
in pregnency.

Radioiodine:-
• Destroys thyroid cells and reduces mass of
thyroid tissue below a critical level by
ablation.
• Indications
1. Primary Thyrotoxicosis
2. Autonomous toxic nodule
3. Recurrent Thyrotoxicosis

• Usual dosage is 160 microcurie/gm of thyroid
• Patient is first made euthyroid by anti-thyroid
drugs. Then discontinued for 5 days after 131I
is given orally.
• Then anti-thyroid drugs are started after 7
days and continued for 8 weeks.

• It normally takes about 3 months to get full
response.
• Often additional one or two doses of
radioiodine therapy are required to have
complete ablation.Eventually the patient may
go into a state of hypothyroidism. This can be
tackled by a maintenance dose of L-thyroixine
0.1mg daily.

HASHIMOTO’S
THYROIDITIS
• First described by hashimoto as struma
lymphomatosa i.e. transformation of thyroid
tissue to lymphoid tissue
• MC inflammatory disorder of the thyroid and
leading cause of hypothyroidism
Thyroid lymphoma is rare but well recognized
complication.
Papillary thyroid carcinoma may be occasionally
associated.

• Genetic association has been noted with ;HLA B8 DR3
DR5.
• More common in women(male:female,1:10),near
menopause(30-50).
ETIOPATHOGENESIS
• It is an AUTOIMMUNE DISEASE.
• THOUGHT TO BE INITIATED BY activation of CD4+
lymphocytes(helper) which further recruits cytotoxic
CD8+ T cells.
• Thyroid tissue is destroyed by cytotoxic t cells and
auto antibodies.

AUTO ANTIBODIES ARE DIRECTED AGAINST:
1.THYROGLOBULIN (60%)
2.THYROID PEROXIDASE (95%) TPO
3.TSH RECEPTOR (60%)

IT IS ALSO THOUGHT TO BE ASSOCIATED
WITH:
• Increased intake of iodine.
• Drugs such as; interferon alpha, lithium
,amiodarone.

pathology
• GROSS EXAMINATION:
Mildly enlarged thyroid with pale, grey tan cut surface.
• MICROSCOPIC EXAMINATION:
- Gland is diffusely infiltrated by small lymphocytes and
plasma cell and occasionally show well developed
germinal centre.
- Smaller thyroid follicle with reduced colloid and
increased interstitial connective tissue
- Follicles are lined by HURTHLE OR ASKANAZY CELLS (
characterized by abundant eosinophillic granular
cytoplasm).

Clinical features
• Most common presentation is minimally or moderately
enlarged firm gland.
• On examination an enlarged pyramidal lobe is often
palpable.
• Mild hyperthyroidism may be present initially (due to
destruction of thyroid tissue).
• Hypothyroidism is inevitable and usually permanent.

Laboratory findings
• Elevated TSH ,reduced T4 and T3 level.
• Elevated TSH and presence of thyroid auto
antibodies confirm the diagnosis.
• Presence to thyroid auto antibodies (particularly
TPO antibody).
• In case of doubt diagnosis is confirmed by FNA
biopsy.

management
• Thyroid hormone replacement therapy for overtly
hypothyroid patients or in euthyroid to shrink large
goiter.
• Treatment is advised especially for middle aged
patients with cardiovascular risk factors and in
pregnancy.
• Surgery may occasionally be indicated for suspicion
of malignancy or for goiter causing compressive
symptoms or cosmetic deformity.

DE QUERVAIN’S /GRANULOMATOUS OR VIRAL
THYROIDITIS
• PEAK INCIDENCE 30-50 YEARS,MORE COMMON IN
WOMEN THREE TIMES THAN MEN.
• USUALLY FOLLOWS UPPER RESPIRATORY TRACT
INFECTION.
• A VIRAL ETIOLOGY HAS BEEN PROPOSED.
• STRONG ASSOC. WITH HLA-B35 HALOTYPE.

THE DISEASE CLASSICALY PROGRESS THROUGH
FOUR STAGES:
1.INITIAL HYPERTHYROID PHASE ,DUE TO RELEASE OF THYROID HORMONE.
2.EUTHYROID PHASE
3.HYPOTHYROIDISM OCCUR IN 20-30%
4.RESOLUTION AND RETURN TO EUTHYROID STATES IN >90% OF PATIENTS

• In early stage of disease ,TSH is decreased and TG,T4 and
T3 levels are elevated due to release of preformed thyroid
hormone from destroyed follicles.
• ESR is typically >100mm/h.
• RAIU also is decreased <2%at 24hr,even in euthyroid
patient, due to release of thyroid hormone from
destruction of thyroid parenchyma.

Clinical features
• Painful and enlarged thyroid , accompanied by fever.
• Features of thyrotoxicosis or hypothyroidism
depending on phase of illness.
• Malaise and symptoms of upper respiratory infection
may preced the thyroid related features by several
weeks.
• The patients typically complains of sore throat and
small excusitively tender goitre.

• Pain is often reffered to jaw or ear.
• Complete resolution is the usual outcome.
• Permanent hypothroidism can occur particullary
with coincidental thyroid autoimmunity.

Lab findings
ESR is markedly elevated.
Antithyroid antibodies are low,with T3 ,T4,and
TSH l levels depend on the stage of disease.
*RAIU IS DECREASED DURING HYPERTHYROID
STATES(DISTINGUISHING FROM GRVES DISEASE)
*IN DOUBT;FNAC SHOW GIANT MULTINUCLEATED CELLS.

TREATMENT
• Treatment is primarily symptomatic,as disease is self limited.
• Aspirin or othr Nsaids are sufficient to control
symptom in most cases.
• Severe cases with marked local or systemic
symptoms are treated with glucocorticoids.
• Short term thyroid replacement may needed in
the hypothyroid phase.
• Thyroidectomy is reserved for the rare patients
who have a prolonged course not responsive to
medical measures.

Riedel’s thyroiditis
• A rare variant of thyroiditis, also known as riedel’s
struma or invasive fibrous thyroiditis.
• Characterized by replacement of all or part of the
thyroid parenchyma by fibrous tissue.
• Also invades into adjacent tissue.

etiology
• Primary autoimmune etiology
Riedel’s thyroiditis is associated with:
1.Mediastinal and retroperitoneal
fibrosis
2.Periorbital and retroorbital
fibrosis
3.Sclerosing cholangitis

Clinical features
• Occurs predominantly in women ,30-50yrs.
• Presents as painless,hard anterior neck
mass,which progress over week to years to
produce symptoms of compression ,including
dysphagia,dyspnea,choking and hoarseness.
• Patient may present with symptoms of
hypothyroidism and hypoparathyroidism as the
gland is replaced by fibrous tissue.
• Physical exmaination:hard woody thyroid gland
with fixation to surrounding tissue.

diagnosis
• Diagnosis is confirmed by OPEN THYROID
BIOPSY, as the firm and fibrous nature of the
gland renders FNAC INADEQUATE.

TREATMENT
• Surgery is the mainstay of treatment (decompress
the trachea by wedge excision of the thyroid
isthmus).
• Some patient show dramatic improvement with
tamoxifen and corticosteroids.

hypothyroidism
• Decrease in T3 And T4.
• Increase in TSH.
THREE TYPES;
PRIMARY:DISEASE OF THYROID GLAND
SECONDARY:DISEASE OF PITUITARY GLAND
TERTIARY:DISEASE OF HYPOTHALAMUS

CAUSES
• MOST COMMON CAUSE of primary hypothyroidism
is:HASHIMOTO’S THYROIDITIS
• 2ND MOST common cause is iodine deficiency.
OTHER CAUSES ARE:
• 1.Thyroid dysgenesis
• 2.Antithyroid drug
• 3.Post surgical (thyroidectomy)
• 4.Post radioiodine therapy

SIGN AND SYMPTOMS:
SYMPTOMS:
• COLD INTOLERANCE
• PREFERANCE TO HOT THINGS
• MENTAL LETHARGY
• DEC. APPETITE
• WEIGHT GAIN
• MENORRHAGIA
• CONSTIPATION

SIGNS:
• DECREASE SWEATING
• DRY SKIN
• BRADYCARDIA
• BRADIKINESIA
• DELAYED RELAXATION OF ANKLE REFLEX:MOST
IMPORTANT SIGN

CRETINISM:
• Also known as Congenital Hypothyroidism.
• Occur in 1/4000 live birth
• Causes thyroid dysgenesis, mother on anti thyroid
drug, dietary deficiency.
• CLINICAL FEATURES:
Hypotonia, prolonged jaundice, enlarged tongue,
umblical hernia, coarse or thick skin, hoarse cry.
• TREATMENT:
L thyroxine once a day morning orally.

Myxoedema:
• Severe form of hypothyroidism.
• Clinical feature: all sign and symptoms of
hypothyroidism
+
supraclavicular puffiness
+
malar flush(redness at cheek)
+
yellow tinge to skin

Myxedema coma:
• Myxedema neglecting patient go to myxedema
coma.
• All features of myxedema
+
hypothermia
+
mental detoriaration

Treatment:
 I.V levothyronine 10microgram 6th hourly
 I.V steroids
 Antibiotic
 Slow warming
 Electrolyte management.

ALGORITHM FOR HYPOTHYROIDISM
MEASURE TSH
Increased TSH TSH Normal

TSH NORMAL
MRI
CONSIDER PATHOLOGY IN PITUITARY
YESNO
MEASURE FREE T4
NO TEST
NORMALLOW
NO TESTEVALUATE PITUITARY, SICK EUTHYROID, DRUGS EFFECT

INCREASED TSH
MEASURE FREE T4
NORMAL LOW
SUB-CLINICAL HYPOTHYROIDISM PRIMARY HYPOTHYROIDISM
MEASURE TPO

TPO
TPO +ve TPO -veTPO +veTPO -ve
OTHERS
HASHIMOTO
T4
REPLACEMENT
ANNUAL FU

CLASSIFICATION
BENIGN
Follicular adenoma
MALIGNANT PRIMARY
Follicular
epithelium-
Differentiated
Follicular Epi.
Undifferentiated
Para follicular cells
Lymphoid cells
Follicular papillary
Anoplastic
Medullary
Lymphoma
SECONDARY
Metastatic
Local infiltration

INCIDENCE ANDSPREAD
Annual incidence of thyroid cancers is 3.7 per
100000 population
Sex ratio= females : males
3:1
Thyroid is the only endocrine gland wherein
malignant tumors spread by all possible
routes- local, lymphatic & blood spread.
• Papillary carcinoma – lymphatic's
• Follicular carcinoma – Blood
• Anaplastic carcinoma – lymphatic's & blood

AETIOLOGY
• Irradiation to the neck during childhood
.Radiotherapy was given for given for conditions
such as tonsillitis those developed risk of
papillary ca thyroid. These are obsolete now.
• Complication of Hashimoto’s thyroiditis
• Papillary cancer of thyroid occurs with Cowden’s
synd. ,Gardner synd. Or Carney’s syndrome
• Associated syndromes : chromosomal
translocation involving RET proto-oncogene
chromosome 10q11

PAPILLARY CARCINOMA
THYROID
• It is 70-80% common
• common in females & younger age group
• Slowly progressive & less aggressive tumor
• Commonly multicentric
WOOLNER CLASSIFICATION:
i. Occult primary (>1.5 cm)
ii. Intrathyroidal
iii. Extra thyroidal

MICROSCOPY
• Made up of colloid-filled follicles with papillary
projections called as Psammoma bodies, these are
diagnostic features of papillary carcinoma of
thyroid.
• Characteristic pale, empty nuclei are present in a
few cases, described as Orphan Annie eye nuclei
• Follicular variant of papillary cancer
• Tall cell papillary cancer
GROSS FEATURES
o It can be soft, firm, hard, cystic
o Can be solitary or multinodular
o It contains brownish black fluid

CLINICAL FEATURES
• Soft or hard or firm, solid or cystic, solitary
or multinodular thyroid swelling
• Compression features are uncommon in
papillary carcinoma thyroid
• Often discrete lymph nodes in the
neck(40%) are palpable
• May present with secondaries in neck lymph
nodes with occult primary
• NOTE: Papillary carcinoma can be offered
as a clinical diagnosis only in the presence of
significant lymph nodes in the neck along
with a thyroid swelling.

DIAGNOSIS
• FNAC of thyroid nodule and lymph node
• Radioisotope scan shows cold nodule
• TSH level in the blood is higher
• Plain X-rays neck shows fine calcification where
as nodular goitre shows- ring/ rim calcification
• US neck to identify non-palpable nodes in neck
and also lymph node
• MRI may be useful

TNMSTAGING
TUMOUR
TX Primary cannot be assessed
T0 No evidence of primary
T1 Tumour <2 cm
T1a <1 cm
T1b >1 cm- <2 cm
T2 Limited to thyroid, >2 cm but < 4cm
T3 Limited to thyroid, >4 cm or any tumour with
minimal extra thyroid extension
T4 Any size with extensive extra thyroidal
extension
T4a moderately advanced
T4b very advanced

NODES
NX Cannot be assessed
N0 No regional node metastasis
N1 Regional node metastasis
N1a level VI
N1b any/all other levels
METASTASIS
MX Cannot be assessed
M0 No metastasis
M1 Metastasis present

STAGE UNDER 45 YEARS OVER 45 YEARS
I Any T, any N , M0 T1, N0 , M0
II Any T, any N , M1 T2 , N0 , M0
III T3 or T1, T2 & N1 a M0
IV A T4 or T1,T2,T3,T4a &N1b M0
IV B T4b Any N M0
IV C Any T Any N M1

TREATMENT
It can be discussed under three headings –
Treatment of the primary, treatment of the secondries
in the lymph nodes & suppression of lymph nodes
I. Treatment of the primary-
(a)Total thyroidectomy is the treatment of the choice
with central node compartment dissection.
(b) Lobectomy (HEMITHYROIDECTOMY) means
removal of one lobe & entire isthmus.
II. Treatment of secondries in the lymph nodes
Mostly central nodes are cleared .If nodes are
enlarged in the anterior triangle ,they are
dissected and removed with fat & fascia, called as
functional block dissection

Berry pricking means removal of enlarged
lymph nodes , it is no longer followed
III. Suppression of the TSH
suppressive dose of L-thyroxine 0.3 mg OD
life long ,TSH level should be <0.1 m U/L
PROGNOSIS
Prognosis is good and it is one of the curable
malignancies

FOLLICULAR CARCINOMA
THYROID
It is 10-15% of cases
Common in females
TYPES: a)Non invasive- blood spread not common
b)Invasive- blood spread common
Typical features: capsular invasion & angioinvasion
SPREAD: it is a more aggressive tumour, spreads
through mainly through blood into bones,lungs,liver
• Bone secondries are typically vascular, warm,
pulsatile, localized in skull, long bones, skull

CLINICAL FEATURES
• Swelling in the neck, firm or hard and nodular
• Tracheal compression/ infiltration and stridor
• Dyspnoea, hemoptysis, chest pain due to lung
secondaries
• Recurrent laryngeal nerve involvement causes
hoarseness of voice, +ve Berry’s sign signifies
advanced malignancy
• Well localized, non mobile, soft, fluctuant &
pulsatile

Follicular carcinoma appear to be macroscopically encapsulated, but
microscopically, there is a invasion of the capsule & of the vascular spaces in
the capsular region.

INVESTIGATION
• FNAC is inconclusive- capsular &
angioinvasion are not detected
• Frozen section biopsy- it may be inconclusive
or facility for frozen biopsy may not be in
many places, then initial hemithyroidectomy
is done
• USG abdomen, chest x-ray, x-rays bones are
the other investigations
• TRUCUT biopsy for tissue diagnosis, but
danger of hemorrhage and injury to vital
structures like trachea, recurrent laryngeal
nerve etc.

TREATMENT
I .Treatment of the primary
• Situation 1: patient has enlarged thyroid gland and
scalp swelling, total thyroidectomy is the of choice.
Secondries do not take up the radioisotope in the
presence of primary tumour so, hemithyroidectomy
should not be done.
• Situation 2: patient undergoes subtotal
thyroidectomy for MNG & final report is follicular
carcinoma thyroid. So in such case completion
thyroidectomy within 7 days or after 4 weeks.
• Situation 3: patient with solitary nodule reported as
follicular cells, so in such case total thyroidectomy
should be done

II. Treatment of the metastasis
• A single secondary can be treated by oral
radioiodine therapy, followed if necessary by
external radiotherapy depending upon the
tumour.
• Multiple secondries are treated by oral
radioiodine therapy
III. Postoperative thyroxine
In postoperative period, patients should receive
thyroxine 0.3 mg/day to suppress TSH and to
supplement thyroxine.
PROGNOSIS:15% mortality in 10 years

HURTLE CELL CARCINOMA
• Hurtle cell ca is a variant of follicular
carcinoma
• >75% of follicular cells having oncocytic
features
• Contains sheets of eosinophilic cells packed
with mitochondria
• They secrete thyroglobulin
• 99mTc sestamibi scan is very useful for
hurtle cell carcinoma
• Treatment – Total thyroidectomy is the
treatment of the choice, others like MRND &
TSH suppression can also be done.

MEDULLARY CARCINOMA OF
THYROID
• Uncommon type of thyroid malignancy(5%)
• Arises from parafollicular ‘C’ cells which are derived
from ultimobranchial bodies (neural crest) and not
from thyroid follicle
• Contains characteristic ‘amyloid stroma’ wherein
malignant cells are dispersed
• In these patients, blood levels of calcitonin stimulation
is high, is a very useful tumour marker
• When it is associated with mucocutaneous neuromas
involving lips, tongue, eyelids, called as SIPPLE
SYNDROME

MEN TYPE I MEN TYPE II a
• Pituitary Adenoma Parathyroid
adenoma
• Parathyroid Adenoma
Pheochromocytoma
• Pancreatic Adenoma Medullary
carcinoma

CLINICAL FEATURES
• Thyroid swelling with enlargement of neck
lymph node
• Diarrhea, flushing (30%)
• Hypertension, Pheochromocytoma and
mucosal neuromas associated with MEN II
syndrome
• Sporadic and familial types occur in
adulthood whereas cases associated with
MEN II syndrome occur in younger age
groups

Investigation
• USG neck- mass, nodal status. US abdomen to rule out
Pheochromocytoma
• FNAC- amyloid stroma with dispersed malignant cells &
c- cell hyperplasia
• S.calcitonin level- >100 pg/ml , suggestive of MCT
• S.CEA level will be raised in 50% of patients
• CT neck, chest, abdomen should be needed for
metastasis
• 111-Indium octreotide scanning is useful in detecting
Medullary carcinoma of thyroid (70% sensitivity)

TREATMENT
Surgery is the main therapeutic modality
• Total thyroidectomy with b/L central node dissection
• Thyroid Replacement / maintenance therapy 100
microgram
• Somatostatin/ octreotide for diarrhea
• Adriamycin is used as chemotherapy
• All family members should be evaluated for S. calcitonin
& if it is high they should undergo prophylactic total
thyroidectomy
PROGNOSIS: Sporadic MCT are aggressive
familial MCT not with MEN II has got good prognosis
presence of nodal disease carries poor prognosis

ANAPLASTIC CARCINOMA
• It is an undifferentiated, very aggressive carcinoma
occurs commonly in elderly females
• It is a tumour of short duration, presents with a
swelling in thyroid region which is rapidly progressive
causing:
-stridor & hoarseness of voice
-Dysphasia
-Fixity to the skin
-Positive berry’ sign
• Swelling is hard with involvement of isthmus and
lateral lobes

TREATMENT
• FNAC is diagnostic
• All Anaplastic carcinoma are T4,
T4a –surgically resectable: T4b- unresectable
• Shows p53 & p21 positive, causes multiorgan
spread
• Tracheotomy and isthmectomy relieve
respiratory obstruction temporarily
• Treatment is external radiotherapy and
Adriamycin as chemotherapy
• However prognosis is poor, death occurs within
6 to 8 months

MALIGNANT LYMPHOMA
• It is NHL type. Occurs in a pre-existing Hashimoto`s
thyroiditis
• FNAC is useful to diagnose the condition
• Chemotherapy & Radiotherapy is the main treatment
• Rarely total thyroidectomy is done to enhance the
results

Investigations of thyroid
 THYROID FUNCTION TEST
 FINE NEEDLE ASPIRATION CYTOLOGY (FNAC):
• It is investigation of choice in all Thyroid Malignancies ,
Lymphoma, thyroiditis.
• Minimum 6 aspirations should be done for diagnosis.
• Following patterns are observed:
Thy 1: Non Diagnostic
Thy 2: Non-Neoplastic
Thy 3: Follicular
Thy 4 : Suspicious of Malignancy
Thy 5 : Malignancy
 RADIO ACTIVE IODINE
 USG NECK

INDICATIONS
• As therapy for patients with thyrotoxicosis
• To treat benign and malignant thyroid tumors
• To relieve pressure symptoms such as respiratory
distress (dyspnoea, dysphagia).
• Cosmetic purpose
• To establish a definitive diagnosis of a mass in
thyroid gland, especially when cytological results
are indeterminate.

TYPES
• Hemi Thyroidectomy
• Subtotal Thyroidectomy
• Partial Thyroidectomy
• Near Total Thyroidectomy
• Total Thyroidectomy
• Hartley Dunhill operation

• It involves removal of one
entire lobe plus entire
isthmus is removed.
• It is performed in benign
diseases involving only one
lobe
• Also done in Follicular
Carcinoma involving only one
lobe
• Other Indications-
• 1) Solitary toxic or nontoxic
Nodule
• 2)Thyroid cyst

• Here, about 8gm ,or
tissue, size of pulp of
finger, is retained on lower
pole of thyroid on both
sides and rest of thyroid
gland is removed
• Indications –
• 1)Toxic Thyroid(Primary or
Secondary)
• 2)Non-toxic Multinodular
Goitre

• Here, both the lobes,
except less than 2 gm of
thyroid tissue on the
lower pole, near to the
recurrent laryngeal nerve
and parathyroid, are
removed (to retain blood
supply to parathyroid
gland)
• Mostly done in Papillary
Carcinoma of thyroid

• Tissue in the tracheo-
oesophageal groove is
retained, isthmus and
gland in front is removed.
• It is done in non-toxic
multinodular goiter
• It is not commonly done
now.

• Here, entire gland is
removed.
• Indications-
1)Follicular Carcinoma
2)Medullary Carcinoma

• It involves removal of one
entire lateral lobe along
with isthmus and
partial/subtotal removal
of opposite lateral lobe
• It is done in non-toxic
multinoduar Goiter (4 gm
of thyroid tissue is left
behind only on one side)

PRE-OPERATIVE PREPRATION
• Blood grouping and cross matching. Keep the required
blood ready.
• Indirect laryngoscope. Patient is asked to tell “E” to
check the abduction of vocal cords
• Serum calcium estimation is done
• T3,T4,TSH estimation done
• Thyroid Antibodies
• ECG and cardiac fitness, especially in case of toxic goiter
• Lugol’s Iodine is given 10 days prior to surgery to
make the gland firm and less vascular

PRE OPERATIVE CONSENT
• Scar
• Airway obstruction
• Voice changes
• Hypothyroidism
• Hypo parathyroidism

PROCEDURE
POSITION
Under general anesthesia, patient is put in supine
position, with neck hyper extended by placing a
sand bag under the shoulder– table tilt of 15
degree head up to reduce venous congestion (ROSE
POSITION).

INCISION :
Horizontal crease incision is given, two finger breadth above
the sternal notch, from one sternomastoid to other
(KOCHER’S thyroid incision)

SUBPLATYSMAL FLAPS :
Subcutaneous tissue and platysma are incised
(subplatysmal plane) remaining superficial to Anterior
Juglar Vein -
Upper Flap is raised up to the Thyroid Cartilage
Lower Flap is upto the Sterno-Clavicular joint.
 Deep fascia is opened vertically in the midline.

Separating the Strap Muscles and Exposing the
Anterior Surface of the Thyroid :
Strap muscles retracted laterally, fascia white tissue between them.
•The fascia between strap muscles (sternohyoid, sternothyroid and
omohyoid) , is divided along the midline and muscles are retracted
laterally.
•In case of a large goiter or any neoplasm, strap muscles are
divided in upper part
•Often, the Anterior Juglar Vein needs to be ligated.

Pretracheal Fascia:
• It covers the thyroid gland.
• It is opened Vertically to expose the thyroid gland.

Identify the Middle Thyroid Vein.
•The thyroid gland is rotated medially (using the surgeons fingers).
• The middle thyroid vein is identified
(it will be tightly stretched by the medial rotation of the gland), which
is then ligated.
•This permits further mobilization of the gland.
Medial rotation of the right thyroid lobe to expose
the middle thyroid vein
Identifying the middle thyroid vein(above the tip of
the forces)

Superior Pole of Thyroid
• Superior pole is dissected
• Identify the superior thyroid artery, close to the superior pole of the
thyroid parenchyma , and ligate it.
• Dissection is done in an avascular plane between upper pole of gland
and cricothyroid muscle to avoid trauma external branch of superior
laryngeal nerve , entering cricothyroid.

Identifying Superior Parathyroid Gland.
•Location: In a posterior position, at the level of the upper 2/3 of the
thyroid and approximately 1 cm above and behind the crossing point of
the recurrent laryngeal nerve and the inferior thyroid artery.
• It is orange- yellow in color.
•They are identified and dissected.
•The gland must remain in situ with blood supply intact.

Identifying The Inferior Parathyroid Gland
• Location : Between the lower pole of the thyroid and the isthmus ,
below and in front of the crossing
• Care must be taken to preserve it in situ and to avoid damaging its
inferior thyroid artery(supplying both glands)

Capsular Ligation of Inferior Thyroid
Artery:
• It is a branch of thyrocervical trunk.
• Its ligation is done at the capsular level at the lower pole of
thyroid gland where it turns toward midline ,behind the
carotid artery.
• It retains the blood supply of PARATHYROID GLANDS, which
is very important.

Identifying The Recurrent Laryngeal Nerve.
•RLN should be identified with dissection through its entire
course
• Recurrent laryngeal nerve is located in Riddle’s Triangle
•If nerve is not found along its course, anomalous (non-
recurrent) nerve should be suspected.
•Lateral: Common Carotid
Artery
•Medial : Trachea
•Superior: Inferior Thyroid
Artery

Dissection of Thyroid Gland
•Berry’s ligament defines the poster lateral attachment of the thyroid
gland.
• Blunt dissection can be used to further expose this fascia ,and then
with a scalpel, transect the ligament.
•Often, a minimal amount of thyroid tissue is left adjacent to the
entrance of the recurrent laryngeal nerve into the larynx, to reduce the
risk of injuring the nerve.

Removing The Thyroid Gland
•If the patient is undergoing a Total Thyroidectomy, attention should first
be turned to the opposite thyroid lobe and RLN.
• Once the entire specimen has been dissected it can be removed.
• The removed specimen should be inspected.

Post-Thyroidectomy Scar
Thyroidectomy scar after 6 months.

complications
1) HAEMORRHAGE :
 It occurs due to slipping of ligature either of
superior thyroid artery or small veins.
 It causes tachycardia ,hypotension, breathlessness ,
severe stridor and Respiratory obstruction.
 T/t: Ligation of Bleeders under General Anasthesia.

2)RESPIRATORY OBSTRUCTION
It may occur due to
 Hematoma
 laryngeal Edema (Commonest Cause)
 Bilateral Recurrent Nerve palsy.
 T/t: Evacuation of haematoma

3)RECURRENT LARYNGEAL NERVE PARALYSIS
UNILATERAL:
Mostly asymptomatic
Some changes in voice , which gradually becomes normal with
speech therapy.
T/t: No specific treatment
Prednisolone 20 mg tid
BILATERAL:
Change in voice
Severe Dyspnoea and Stridor leading to respiratory arrest.
T/t : Emergency Tracheostomy
Excision of vocal cord through an endoscope or laser
cordectomy

4) HYPOPARATHYROIDISM
• It is a rare complication
• Mostly it is temporary due to vascular spasm of
parathyroid gland
• Occurs on 2nd -5th post-operative day
• It presents with muscle weakness, convulsions.
• T/t:
Calcium gluconate is given IV 8th hourly.
Later supplemented by oral calcium carbonate 500
mg 8th hrly.

5) THYROTIXIC CRISIS (THYROID STORM):
Causes
• Occurs in thyrotoxic patient inadequately prepared for
surgery .
• Other causes- infection, trauma, diabetes, pre-
eclampsia
Features:
• Presents 12-24 hrs after surgery with
• Severe dehydration, Circulatory collapse, Hypotension,
Hyperpyrexia,
• Tachypnoea, Palpitations ,Cardiac failure, later Coma.
• GIT Symptoms: Diarrhea, vomiting,

• Investigations :
 Raised T3,T4 , Raised Serum Calcium
 Changes in ECG and Echocardiography , ABG.
• T/t: It has a critical period of 72 hrs.
Fluid therapy, cold sponging, IV paracetamol
IV hydrocortisone 500mg
Propanolol 80mg orally.
Propylthiouracil 200mg or Methimazole 20mg followed
by Lugols iodine or KI after 1 hour.
Cholestyramine 4gm
Digitoxin along with cardiac monitoring
Other like- haemodialysis , Plasmaphresis, Exchange
Transfusion, etc.

INJURY TO EXTERNAL LARYNGEAL NERVE
HYPOTHYROIDISM
• Revealed clinically after 6 months.
RECURRENT THYROTOXICOSIS
• It is due to retaining of more thyroid tissue during
thyroidectomy for toxic thyroid.
WOUND INFECTION AND STITCH GRANULOMA
FORMATION
KELOID FORMATION

BIBLIOGRAPHY
• Love and Bailey
• SRB Mannual of Surgery
• S. Das Clinical Surgery.
• https://www.google.co.in/#q=thyroid
• https://www.google.co.in/#q=thyroidectomy
• https://www.google.co.in/#aThyroiditis

Thank you and have a great day!

Surgery thyroid

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