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Surgery thyroid

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Surgery thyroid

  1. 1. THYROID GLAND
  2. 2. Topics discussed: • Anatomy & Physiology • Congenital Anomalies • Examination of Thyroid • Goiter • Hyperthyroidism & Thyrotoxicosis • Hypothyroidism • Thyroiditis • Neoplasm • Thyroidectomy
  3. 3. 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
  4. 4. DEVELOPMENT • 1st endocrine gland to develop in body. • Mainly develops from thyroglossal duct.
  5. 5. 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
  6. 6. Capsules of Thyroid
  7. 7. 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.
  8. 8. Arterial Supply Of Thyroid
  9. 9. Venous drainage of Thyroid KOCHER’S VEIN:-Present between inferior & middle thyroid vein. Very rare.
  10. 10. Nerves IN RELATION TO THYROID
  11. 11. Riddle’s Triangle
  12. 12. Lymphatic drainage 1.Level III & IV nodes 2.Level VI nodes 3.Level VII nodes
  13. 13. Histology
  14. 14. Physiology
  15. 15. Feed back mechanism
  16. 16. 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
  17. 17. 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
  18. 18. CONGENITAL ANOMALIES OF THYROID
  19. 19.  Ectopic thyroid  Lingual thyroid  Thyroglossal cyst  Thyroglossal fistula  Lateral aberrant thyroid  Agenesis  Dyshormonogenesis Types of congenital anomalies of THYROID
  20. 20. 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.
  21. 21. 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.
  22. 22. ECTOPIC THYROID
  23. 23. 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.
  24. 24. 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]
  25. 25. position of lingual thyroid
  26. 26. Thyroid swelling of lingual thyroid may cause’s- 1. DYSPHAGIA 2. PAIN 3. SPEECH IMPAIRMENT 4. RESPIRATORY OBSTRUCTION 5. HAEMORRHAGE
  27. 27. DIFFERENTIAL DIAGNOSIS FOR LINGUAL THYROID • Carcinoma of posterior third of tongue • Angiofibroma • Sarcoma • Hypertrophid lingual tonsil
  28. 28. 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.
  29. 29. TREATMENT 1. L-THYROXINE is given daily orally. 2. Require surgical excision. 3. Radio isotope therapy for ablation
  30. 30. 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.
  31. 31. 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
  32. 32. THYROGLOSSAL CYST
  33. 33. 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
  34. 34. 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
  35. 35. 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
  36. 36. 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.
  37. 37. THYROGLOSSAL FISTULA
  38. 38. •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.
  39. 39. 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
  40. 40. 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
  41. 41. 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
  42. 42. 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.
  43. 43. THYROGLOSSAL FISTULA
  44. 44. •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.
  45. 45. INVESTIGATION • RADIOISOTOPE STUDY • FISTULOGRAM TREATMENT • SISTRUNK OPERATION
  46. 46. 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.
  47. 47. LATERAL ABERRANT THYROID
  48. 48. 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.
  49. 49. 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.
  50. 50. DYSHORMONOGENESIS
  51. 51. 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.
  52. 52. INVESTIGATION • CT-SCAN OF TEMPORAL BONE- shows “abnormal bony labyrinth” This condition shows “THYROID PEROXIDASE DEFICIENCY”.
  53. 53. CLINICAL EXAMINATION OF THYROID SWELLING
  54. 54. GOITRE • Swelling of neck resulting from thyroid enlargement is GOITRE. • It can be euthyroid, hyperthyroid, or hypothyroid.
  55. 55. CAUSES • More common in women than men • Physiological • Iodine deficiency • Autoimmune thyroid conditions
  56. 56. • Radiotherapy • Radioactivity • Unusual dietary habits • Drugs
  57. 57. 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
  58. 58. 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.
  59. 59. PRESENTING COMPLAINTS
  60. 60. • 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
  61. 61. • Dyspnoea: Anaplastic ca Retrosternal goiter Long standing MNG Secondary thyrotoxicosis • Hoarseness of voice: Malignancy
  62. 62. • 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
  63. 63. HISTORY TAKING
  64. 64. • Swelling : onset duration rate of growth pain • Local effects: dyspnoea dysphagia hoarseness of voice pain
  65. 65. • Toxicity: CNS CVS GIT Menstrual • Hypothyroidism: Lethargy Deposition of fat Deep, husky voice Intolerance to cold
  66. 66. ON EXAMINATION
  67. 67. 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
  68. 68. • Borders: usually round. • With deglutition: Swelling which move- A. thyroid swelling B. subhyoid bursitis C. pretracheal and prelaryngeal LNs D. thyroglossal cyst E. Laryngocoele
  69. 69. Restricted in- A. Malignancy B. Retrosternal goiter C. Large goiter • Protrusion of tongue: thyroglossal cyst
  70. 70. 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”
  71. 71. • SCM contraction test • Chin test (neck fixation test) • Position of trachea • Palpation of LNs • Palpation of CCA • Evidence of toxicity
  72. 72. • Special tests: 1. Crile’s method
  73. 73. Lahey’s method
  74. 74. Pizillo’s method
  75. 75. Kocher’s test
  76. 76. pemberton’s sign
  77. 77. 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.
  78. 78. Systemic examination • CNS examination • Eye examination • Examination of Skeletal system • CVS examination • Deep tendon reflexes
  79. 79. 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
  80. 80. 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
  81. 81. INVESTIGATIONS • Blood tests • X-rays • Ultrasound scan • Fine needle aspiration cytology (FNAC) • Radioactive iodine scan
  82. 82. TREATMENT This may involve one or several of the following: • surgery • radioactive iodine • antithyroid medication • levothyroxine tablets
  83. 83. GOITRE Presented By:- ANURADHA SAINI
  84. 84. Definition Any enlargement of thyroid gland irrespective of its pathology .
  85. 85. GOITRE- - Diffuse hyperplastic goitre - Multinodular goitre - Discrete thyroid nodule - Solitary nodule - Retrosternal goitre
  86. 86. DIFFUSE HYPERPLASTIC GOITRE • Persistent increase in TSH level Diffuse active lobules • In late stage • TSH stimulation decrease
  87. 87. Follicle become inactive filled with colloid colloid goitre - Reversible stage Treatment- L-thyroxine
  88. 88. • 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
  89. 89. Iodine deficiency goitre Goitrogens Dyshormogenesis Pathogenesis- Discordant growth with functionally and structurally altered thyroid follicles due to fluctuation in TSH level
  90. 90. 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
  91. 91. Nodule formation Centre of nodule inactive and only margine active formation of many nodules Multinodular goitre
  92. 92. 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
  93. 93. On examination- - asymmetrical in shape - nodular surface - soft to hard consistency - kocher’s test positive
  94. 94. Complications- 1. Secondary thyrotoxicosis 2. Follicular carcinoma of thyroid 3. haemorrhage in a nodule 4. Tracheal obstruction 5. Cosmetic problem
  95. 95. 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
  96. 96. 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
  97. 97. DISCRETE THYROID NODULE - Clearly palpable nodule - Solitary (Isolated) OR Dominant nodule - Common in females - Solid or cystic
  98. 98. 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
  99. 99. 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
  100. 100. 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
  101. 101. 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
  102. 102. 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.
  103. 103. 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
  104. 104. - 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
  105. 105. RETROSTERNAL GOITER Defined as having >50% goiter below suprasternal notch. Classification- 1. Primary - rare 2. Secondary – common
  106. 106. 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
  107. 107. - 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
  108. 108. Thyrotoxicosis/ hyperthyroidism
  109. 109. Hyperthyroidism : State of excessive production of thyroid hormone by thyroid gland. Thyrotoxicosis : State of excessive thyroid hormone in the body due to any cause.
  110. 110. 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.
  111. 111. 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
  112. 112. (c) Autoimmune/ de Quervain’s thyroiditis (d) Malignant goiter (e) Neonatal thyrotoxicosis (f) TSH secreting tumors of pituitary (g) Struma ovarii (h) Drugs- amidarone
  113. 113. Grave’s Disease
  114. 114. 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.
  115. 115. PATHOGENESIS :
  116. 116. 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.
  117. 117. 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.
  118. 118. Acini with flat cuboidal epithelium filled with homogenous colloid Hyperplasic empty acini lined by columnar epithelium
  119. 119. Risk Factor 1. Postpartum state 2. Iodine excess 3. Lithium therapy 4. Infection- bacterial and viral 5. Smoking 6. Stress
  120. 120. Clinical features • It is 8 times more common in females. • Occurs at any age group.
  121. 121. 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
  122. 122. 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
  123. 123. 5. Genitourinary symptom: (a) oligo- or amenorrhea (b) occasional urinary frequency 6. Integument: (a) hair loss (b) pruritis (c) palmer erythema
  124. 124. 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
  125. 125. 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.
  126. 126. von Graefe’s sign
  127. 127. (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.
  128. 128. Naffziger’s sign Jellinek’s sign Dalrymple’s sign Enroth sign
  129. 129. (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.
  130. 130. 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)
  131. 131. 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.
  132. 132. 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
  133. 133. Tachycardia is common Pulsus paradoxous Wide pulse pressure Multiple extrasystoles Paroxysmal atrial tachycardia Paroxysmal atrial fibrillation Persistent atrial fibrillation
  134. 134. 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.
  135. 135. 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
  136. 136. Thyroid acropachy is clubbing of finger and toes in primary thyrotoxicosis.Hypertropic pulmonary osteoarthropathy can develop.
  137. 137. Thrill is felt in the upper pole of the thyroid and also bruit on auscultation. Hepatoslenomegaly.
  138. 138. 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)
  139. 139. 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.
  140. 140. 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
  141. 141. 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.
  142. 142. • Thyrotoxicosis may be treated by THE FOLLOWING treatment modalities — 1. Antithyroid drugs 2. Radioiodine Therapy 131I 3. Surgery.
  143. 143. 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.
  144. 144. 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
  145. 145. • 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.
  146. 146. • 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.
  147. 147. 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.
  148. 148. • 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.
  149. 149. AUTO ANTIBODIES ARE DIRECTED AGAINST: 1.THYROGLOBULIN (60%) 2.THYROID PEROXIDASE (95%) TPO 3.TSH RECEPTOR (60%)
  150. 150. IT IS ALSO THOUGHT TO BE ASSOCIATED WITH: • Increased intake of iodine. • Drugs such as; interferon alpha, lithium ,amiodarone.
  151. 151. 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).
  152. 152. 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.
  153. 153. 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.
  154. 154. 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.
  155. 155. 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.
  156. 156. 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
  157. 157. • 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.
  158. 158. 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.
  159. 159. • Pain is often reffered to jaw or ear. • Complete resolution is the usual outcome. • Permanent hypothroidism can occur particullary with coincidental thyroid autoimmunity.
  160. 160. 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.
  161. 161. 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.
  162. 162. 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.
  163. 163. etiology • Primary autoimmune etiology Riedel’s thyroiditis is associated with: 1.Mediastinal and retroperitoneal fibrosis 2.Periorbital and retroorbital fibrosis 3.Sclerosing cholangitis
  164. 164. 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.
  165. 165. diagnosis • Diagnosis is confirmed by OPEN THYROID BIOPSY, as the firm and fibrous nature of the gland renders FNAC INADEQUATE.
  166. 166. 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.
  167. 167. 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
  168. 168. 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
  169. 169. SIGN AND SYMPTOMS: SYMPTOMS: • COLD INTOLERANCE • PREFERANCE TO HOT THINGS • MENTAL LETHARGY • DEC. APPETITE • WEIGHT GAIN • MENORRHAGIA • CONSTIPATION
  170. 170. SIGNS: • DECREASE SWEATING • DRY SKIN • BRADYCARDIA • BRADIKINESIA • DELAYED RELAXATION OF ANKLE REFLEX:MOST IMPORTANT SIGN
  171. 171. 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.
  172. 172. Myxoedema: • Severe form of hypothyroidism. • Clinical feature: all sign and symptoms of hypothyroidism + supraclavicular puffiness + malar flush(redness at cheek) + yellow tinge to skin
  173. 173. Myxedema coma: • Myxedema neglecting patient go to myxedema coma. • All features of myxedema + hypothermia + mental detoriaration
  174. 174. Treatment:  I.V levothyronine 10microgram 6th hourly  I.V steroids  Antibiotic  Slow warming  Electrolyte management.
  175. 175. ALGORITHM FOR HYPOTHYROIDISM MEASURE TSH Increased TSH TSH Normal
  176. 176. TSH NORMAL MRI CONSIDER PATHOLOGY IN PITUITARY YESNO MEASURE FREE T4 NO TEST NORMALLOW NO TESTEVALUATE PITUITARY, SICK EUTHYROID, DRUGS EFFECT
  177. 177. INCREASED TSH MEASURE FREE T4 NORMAL LOW SUB-CLINICAL HYPOTHYROIDISM PRIMARY HYPOTHYROIDISM MEASURE TPO
  178. 178. TPO TPO +ve TPO -veTPO +veTPO -ve OTHERS HASHIMOTO T4 REPLACEMENT ANNUAL FU
  179. 179. THYROID NEOPLASMS
  180. 180. 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
  181. 181. 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
  182. 182. 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
  183. 183. 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
  184. 184. 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
  185. 185. 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.
  186. 186. 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
  187. 187. 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
  188. 188. 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
  189. 189. 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
  190. 190. 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
  191. 191. 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
  192. 192. 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
  193. 193. 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
  194. 194. Follicular carcinoma appear to be macroscopically encapsulated, but microscopically, there is a invasion of the capsule & of the vascular spaces in the capsular region.
  195. 195. 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.
  196. 196. 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
  197. 197. 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
  198. 198. 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.
  199. 199. 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
  200. 200. MEN TYPE I MEN TYPE II a • Pituitary Adenoma Parathyroid adenoma • Parathyroid Adenoma Pheochromocytoma • Pancreatic Adenoma Medullary carcinoma
  201. 201. 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
  202. 202. 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)
  203. 203. 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
  204. 204. 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
  205. 205. 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
  206. 206. 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
  207. 207. 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
  208. 208. THYROIDECTOMY
  209. 209. 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.
  210. 210. TYPES • Hemi Thyroidectomy • Subtotal Thyroidectomy • Partial Thyroidectomy • Near Total Thyroidectomy • Total Thyroidectomy • Hartley Dunhill operation
  211. 211. • 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
  212. 212. • 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
  213. 213. • 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
  214. 214. • 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.
  215. 215. • Here, entire gland is removed. • Indications- 1)Follicular Carcinoma 2)Medullary Carcinoma
  216. 216. • 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)
  217. 217. 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
  218. 218. PRE OPERATIVE CONSENT • Scar • Airway obstruction • Voice changes • Hypothyroidism • Hypo parathyroidism
  219. 219. 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).
  220. 220. INCISION : Horizontal crease incision is given, two finger breadth above the sternal notch, from one sternomastoid to other (KOCHER’S thyroid incision)
  221. 221. 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.
  222. 222. 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.
  223. 223. Pretracheal Fascia: • It covers the thyroid gland. • It is opened Vertically to expose the thyroid gland.
  224. 224. 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)
  225. 225. 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.
  226. 226. 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.
  227. 227. 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)
  228. 228. 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.
  229. 229. 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
  230. 230. 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.
  231. 231. 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.
  232. 232. Post-Thyroidectomy Scar Thyroidectomy scar after 6 months.
  233. 233. 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.
  234. 234. 2)RESPIRATORY OBSTRUCTION It may occur due to  Hematoma  laryngeal Edema (Commonest Cause)  Bilateral Recurrent Nerve palsy.  T/t: Evacuation of haematoma
  235. 235. 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
  236. 236. 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.
  237. 237. 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,
  238. 238. • 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.
  239. 239. 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
  240. 240. 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
  241. 241. Thank you and have a great day!

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