Surgery thyroid

THYROID GLAND

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

ANATOMY &

PHYSIOLOGY

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

Capsules of Thyroid

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.

Arterial Supply Of Thyroid

Venous drainage of Thyroid

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

Nerves IN RELATION TO THYROID

Riddle’s Triangle

Lymphatic drainage

1.Level III & IV nodes

2.Level VI nodes3.Level VII nodes

Histology

Physiology

Feed back mechanism

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

INTERPRETATIONTSH(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.

ECTOPIC THYROID

DIAGNOSIS-

1.Radioisotope scan2.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]

position of lingual thyroid

Thyroid swelling of lingual thyroid may cause’s-

1. DYSPHAGIA2. PAIN3. SPEECH IMPAIRMENT4. RESPIRATORY OBSTRUCTION5. 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.

TREATMENT1. 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 site2.THYROID CARTILAGE- 2ND Commonest site3.supra hyoid4.Beneath the FORAMEN COECUM5.FLOOR OF MOUTH

THYROGLOSSAL CYST

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 study2. Ultrasonography of neck 3. FNAC from the cyst

DIFFERENTIAL DIAGNOSIS FOR THYROGLOSSAL CYST

1. SUBHYOID BURSA2. PRETRACHEAL LYMPH NODE3. DERMOID CYST4. SOLITARY NODULE OF THYROID-ISTHMUS5. 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 / HEMATOMA4. 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.

THYROGLOSSAL FISTULA

• 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.

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 study2. Ultrasonography of neck 3. FNAC from the cyst

DIFFERENTIAL DIAGNOSIS FOR THYROGLOSSAL CYST

1. SUBHYOID BURSA2. PRETRACHEAL LYMPH NODE3. DERMOID CYST4. SOLITARY NODULE OF THYROID-ISTHMUS5. 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 / HEMATOMA4. 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.

THYROGLOSSAL FISTULA

• 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.

LATERAL ABERRANT 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.

DYSHORMONOGENESIS

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• MULTINO

DULAR• NODULE• RECURRE

NT

NON TOXIC

• DIFFUSE• MULTINODUL

AR• NODULE• RECURRENT

NEOPLASM

• PAPILLARY

• MEDULLARY

• FOLLICULAR

• ANAPLASTIC

INFLAMMATORY

• REIDEL’S• HASHIM

OTO• 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.

PRESENTING COMPLAINTS

• Swelling :Long standing swelling: benign conditionShort duration with rapid growth:

malignant conditionSudden increase in size with pain:

hemorrhage

• Rate of growth:Slow growingRapid growing

• Dyspnoea: Anaplastic caRetrosternal goiterLong standing MNGSecondary thyrotoxicosis

• Hoarseness of voice:Malignancy

• Toxic features: of hyperthyroidismCNS symptoms:- tremors

sweatingintolerance to heatpreference to coldexcitabilityirritability

CVS symptoms:- palpitations precordial chest paindyspnoea on exertion

HISTORY TAKING

• Swelling : onsetdurationrate of growthpain

• Local effects: dyspnoeadysphagiahoarseness of voicepain

• Toxicity: CNSCVSGITMenstrual

• Hypothyroidism:LethargyDeposition of fatDeep, husky voiceIntolerance to cold

ON EXAMINATION

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 thyroidNodular: MNG

• Borders: usually round.

• With deglutition:Swelling which move-A. thyroid swellingB. subhyoid bursitisC. pretracheal and prelaryngeal LNsD. thyroglossal cystE. Laryngocoele

Restricted in-A. Malignancy B. Retrosternal goiterC. Large goiter

• Protrusion of tongue: thyroglossal cyst

PALPATION• Local temperature• Size, shape, surface, border

• Consistency:1. Soft: grave’s ds. ,colloid goitre2. Firm: adenoma, MNG3. 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

Lahey’s method

Pizillo’s method

Kocher’s test

pemberton’s sign

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 FASCIA3. 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 nodule4. 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

Grave’s Disease

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.

PATHOGENESIS :

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 state2. Iodine excess3. Lithium therapy4. Infection- bacterial and viral5. 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) diarrhea2. 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 reflex4. 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.

von Graefe’s sign

(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

CLINICAL FEATURES OF THYROTOXICOSIS

2.Cardiac ManifestationTachycardia is commonPulsus paradoxousWide pulse pressureMultiple extrasystolesParoxysmal atrial tachycardiaParoxysmal atrial fibrillationPersistent atrial fibrillation

3.Myopathy

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.

4.Pretibial MyxoedemaUsually 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

5.Thyroid Acropachy

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

6.other

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

Investigation for Thyrotoxicosis

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.

TREATMENT• Thyrotoxicosis may be treated by THE

FOLLOWING treatment modalities —

1. Antithyroid drugs2. 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 Thyrotoxicosis2. Autonomous toxic nodule3. 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.

THYROIDITIS

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 T4NO 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 +ve TPO -ve

OTHERSHASHIMOTO

T4 REPLACEMENT ANNUAL FU

THYROID NEOPLASMS

CLASSIFICATION BENIGN

Follicular adenoma

MALIGNANT PRIMARY

Follicular epithelium-Differentiated Follicular Epi.Undifferentiated

Para follicular cells

Lymphoid cells

Follicular papillary

Anoplastic

Medullary

Lymphoma

SECONDARYMetastatic Local infiltration

INCIDENCE AND SPREADAnnual incidence of thyroid cancers is 3.7 per

100000 populationSex 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. Intrathyroidaliii. 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 FEATURESo It can be soft, firm, hard, cystico Can be solitary or multinodularo 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

TNM STAGINGTUMOURTX Primary cannot be assessedT0 No evidence of primaryT1 Tumour <2 cm T1a <1 cm T1b >1 cm- <2 cm T2 Limited to thyroid, >2 cm but < 4cmT3 Limited to thyroid, >4 cm or any tumour with

minimal extra thyroid extensionT4 Any size with extensive extra thyroidal extension T4a moderately advanced T4b very advanced

NODESNX Cannot be assessedN0 No regional node metastasisN1 Regional node metastasis N1a level VI N1b any/all other levels

METASTASISMX Cannot be assessedM0 No metastasisM1 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

TREATMENTIt can be discussed under three headings –Treatment of the primary, treatment of the secondries in

the lymph nodes & suppression of lymph nodesI. 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 THYROIDIt is 10-15% of casesCommon in females TYPES: a)Non invasive- blood spread not common b)Invasive- blood spread commonTypical 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.

TREATMENTI .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)

TREATMENTSurgery 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

THYROIDECTOMY

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

THYROIDECTOMY

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

HEMI THYROIDECTOMY

• 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

SUBTOTAL THYROIDECTOMY

• 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

NEAR TOTAL THYROIDECTOMY

• 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.

PARTIAL THYROIDECTOMY

• Here, entire gland is removed.

• Indications- 1)Follicular Carcinoma 2)Medullary Carcinoma

TOTAL THYROIDECTOMY

• 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)

HARTLEY-DUNHILL OPERATION

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.

complications1) 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-eclampsiaFeatures: • 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 500mgPropanolol 80mg orally.Propylthiouracil 200mg or Methimazole 20mg followed

by Lugols iodine or KI after 1 hour.Cholestyramine 4gm Digitoxin along with cardiac monitoringOther 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

Total thyroidectomy for multinodular goitre (1).mp4

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

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