This document discusses hyperthyroidism and its treatment. It defines hyperthyroidism as increased secretion of thyroid hormones due to various stimuli. It then describes the clinical types of hyperthyroidism including diffuse toxic goitre (Graves' disease), toxic nodular goitre, and toxic nodule. The document outlines the symptoms, diagnosis, and principles of treatment for hyperthyroidism including anti-thyroid drugs, radioactive iodine therapy, and surgery. Treatment options depend on factors like the type and severity of hyperthyroidism, patient age and preferences.

1. HYPERTHYROIDISM
DR.R.DURAI MS
ASSISTANT PROFESSOR
DEPARTMENT OF GENERAL SURGERY
MGMCRI

2. DEFENITION
 What is hyperthyroidism?
 Increased secretion of Thyroid hormones due to various
stimuli.
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 What is thyrotoxicosis??
 Symptoms and signs produced by Increased secretion of
Thyroid hormones due to various stimuli.
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3. TODAY’S MENU
 Clinical types
 Symptomatology
 Diagnosis of thyrotoxicosis
 Principles of treatment of thyrotoxicosis
 Choice of therapy
 Hyperthyroidism due to other causes
 Surgery for thyrotoxicosis
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4. CLINICAL TYPES

5. CLINICAL TYPES
 Diffuse toxic goitre (Graves’ disease);
 Toxic nodular goitre;
 Toxic nodule;
 Hyperthyroidism due to rarer causes.
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6. GUESS?
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ROBERT JAMES GRAVES
(1796-1853)
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7. DIFFUSE TOXIC GOITRE
(GRAVE’S DISEASE)
 Graves’ disease, a diffuse vascular goitre
 Younger women
 Eye signs
 Primary Thyrotoxicosis
 Family H/o Autoimmune Endocrine diseases
 Whole gland – Hypertrophy & Hyperplasia –
abnormal thyroid stimulating antibodies (TSH-
Rab) binding to TSH receptor
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8. TOXIC NODULAR GOITRE
 Plummer’s Disease
 Long duration
 Middle-aged or Elderly
 Infrequently is associated with eye
signs.
 Secondary thyrotoxicosis.
 Nodules inactive
 Inter-nodular thyroid tissue
overactive
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9. TOXIC NODULE(ADENOMA)
 Solitary overactive nodule
 Autonomous
 TSH secretion is suppressed
by the high level of
circulating thyroid
hormones
 Surrounding normal thyroid
tissue suppressed and
inactive.
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10. HISTOLOGY
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11. GRAVE’S HISTOLOGY
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12. SYMPTOMATOLOGY

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14. SYMPTOMATOLOGY
 Loss of weight despite a good
appetite
 Heat intolerance
 Palpitations.
 Tachycardia
 Hot, moist palms
 Exophthalmos
 Eyelid lag/retraction
 Agitation
 Thyroid goitre and bruit.
 Tiredness
 Emotional lability
 Weight loss
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15. PRIMARY VS SECONDARY
 Symptom 1st Goitre next
 Diffuse and vascular
 Large or small
 Firm or soft
 Thrill and a bruit
 Abrupt onset
 Frequent Remissions &
exacerbations
 More severe
 No Cardiac manifestations
 All eye signs
 Goitre 1st symptoms next
 Nodular
 Insidious
 Less severe
 Cardiac manifestations more
 Only Lid lag & Lid spasm
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16. CARDIAC RYTHM
 Fast heart rate during sleep
 Cardiac arrhythmias
 Stages Of Development Of Thyrotoxic Arrhythmias:
1. multiple extrasystoles
2. paroxysmal atrial tachycardia
3. paroxysmal atrial fibrillation
4. persistent atrial fibrillation, not responsive to digoxin.
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17. MYOPATHY
 Weakness of the proximal limb muscles
 Thyrotoxic myopathy
 Recovery proceeds as hyperthyroidism is controlled.
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18. EYE SIGNS
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19. Specific to Graves Disease
 1. Diffuse painless and firm enlargement of thyroid gland
 2. Ophthalmopathy – Eye manifestations – 50% of cases
 Classification of Eye Changes in Graves' Disease
 0) No signs or symptoms.
 1) Only signs, no symptoms. (Signs limited to
upper lid retraction, stare, lid lag.)
 2) Soft tissue involvement (symptoms and signs).
 3) Proptosis (measured with Hertel exophthalmometer)
 4) Extraocular muscle involvement.
 5) Corneal involvement.
 6 Sight loss (optic nerve involvement).
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20. Eye Signs in Toxic Goitre
In early stages, may be unilateral but later may
become bilateral.
 Order of appearance of signs
 Stellwag's sign : Absence of normal
blinking—so staring look.
 Von Graefe`s sign : Upper eye lid lags behind
the eye ball as the patient is asked to look
downwards.
 Dalrymphe's sign : Upper sclera is visible due
to retraction of upper eye lid.
 Joffroy's sign : Absence wrinkling in the
forehead on looking upwards with the face
inclined downwards.
 Moebius sign : Inability or failure to
converge the eye balls
 Gifford's sign: Difficulty in eversion of the
upper lid.
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21. Specific to Graves Disease……..
 3. Thyroid dermopathy
 consists of thickening of the skin,
particularly over the lower tibia, due to
accumulation of glycosaminoglycans
 (pre tibial myxedema)
 Is usually bilateral
 4. Thyroid Acropachy
 Thyroid acropachy is clubbing of fingers and
toes in primary thyrotoxicosis.
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22. DIAGNOSIS

23. DIAGNOSIS
 Examinations, symptoms
 Thyroid blood tests
 Thyroid function tests TSH , T4,T3
 Thyrroid antibodies TSI, ANTI TPO, ANTI Tg
 Other — nonspecific laboratory findings.
 low serum total, LDL, and (HDL) cholesterol concentrations
 normochromic, normocytic anemia
 Serum alkaline phosphatase
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24.  Thyroid imaging
 Radionuclide imaging
 Size, shape & function of gland assessed
 Increased uptake=“hot", less risk of
malignancy,<5%
 Decreased uptake=“cold" higher risk of
malignancy,15-20%
 Ultrasound
 CT/ MRI good for assessment of retrosternal
extension.
 pathology
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DIAGNOSIS
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25. Algorithm for Hyperthyroidism
Measure TSH and FT4
 TSH,  FT4
Measure FT3
Primary (T4)
Thyrotoxicosis
High
Pituitary Adenoma FNAC, N
Scan
Normal
 TSH, FT4 N  TSH,  FT4 N TSH, FT4 N
T3 Toxicosis
Sub-clinical Hyperthyroidism
Features of Grave’s
Yes
Rx.
Grave’s
No
Single Adenoma,
MNG
Low RAIU RAIU
Sub Acute Thyroiditis, I2, ↑ Thyroxine
F/u in 6-12 wks
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26. PRINCIPLES
OF
TREATMENT

27. MANAGEMENT
Approaches
• Anti thyroid
drugs,beta blockers
• Radioactive Iodine
I131
• Surgery
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28. Choice Of Therapy
• Type of thyrotoxicosis
• Age of the patient
• Co existing medical illness
• Severity of thyrotoxicosis
• Goitre size
• Presence of ophtalmopathy
• Patient preference
Factors
influencing
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29. ANTITHYROID DRUGS
 Indications for antithyroid drugs:
 Patients with high likelihood of remission
 the elderly or others with comorbidities increasing
surgical risk or with limited life expectancy
 Toxicity in pregnant women
 moderate to severe active Graves’ ophthalmopathy
(GO)
 Before surgery, to make the patient euthyroid
 Soon after starting radioactive I131therapy for 6 to 12
weeks
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30. How long to give ATD ?
 improved symptoms in 2 weeks and euthyroid in about 6 weeks
 Check TSH and FT4 every 4 to 6 weeks
 In Graves, remission after 12-18 months
 Monitor every 3 months for the 1st year, and then annually after ATD
 40% recurrence in 1 yr.
 MNG and Toxic Adenoma will not get cured by ATD.
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31. Adjuvants
 Beta blockers
 Inhibit adrenergic effects
 Indications
 Prompt control of symptoms;
 treatment of choice for thyroiditis;
 first-line therapy before surgery, radioactive iodine, and
antithyroid drugs;
 Contraindications
 Use with caution in older patients and in patients with pre-
existing heart disease, chronic obstructive pulmonary disease,
or asthma
 Propranolol is the most commonly prescribed medication in
doses of about 20 to 40 mg four times daily
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32.  Iodides
 Block the conversion of T4to T3 and inhibit hormone release
 Indications
 preoperatively when other medications are ineffective or
contraindicated;
 to reduce gland vascularity before surgery for Graves’ disease
 during pregnancy when antithyroid drugs are not tolerated;
 Complications
 Paradoxical increases in hormone release with prolonged use;
 common side effects of sialadenitis, conjunctivitis, or acneform rash;
Adjuvants
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33. RADIOIODINE THERAPY
 Radioactive iodine
 Concentrates in the thyroid gland and destroys thyroid
tissue
 High cure rates with single-dose treatment (80 percent);
 treatment of choice for
 Graves’ disease
 Multi nodular goitre, toxic nodules in patients older
than 40 years, and
 In recurrent thyrotoxicosis
 It is effective, safe, and does not require hospitalization.
 Given orally as a single dose in a capsule or liquid form.
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34. RADIOIODINE THERAPY………
 Drawbacks
 Delayed control of symptoms;
 post treatment hypothyroidism
 contraindicated - pregnant or breastfeeding;
 transient neck soreness, flushing, and decreased taste;
radiation thyroiditis in 1 percent of patients;
 may exacerbate Graves’ ophthalmopathy;
 may require pre treatment with antithyroid drugs in
older or cardiac patients
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35. Surgical Treatment
 Surgical treatment is reserved
 patient preference
 Pregnant women who can’t tolerate ATD
 child or adolescent intolerant of ATDs
 large goiter, with or without compressive
symptoms
 severe Graves’ ophthalmopathy
 the presence of suspicious nodules
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36. SURGICAL………..
 GRAVES DISEASE
 Near-total or total thyroidectomy is the procedure of
choice
 TMNG
 Near- total or total thyroidectomy should be performed
 TOXIC ADENOMA
 an ipsilateral thyroid lobectomy, or
 isthmusectomy
 In patients with coexisting eye disease,
 total thyroidectomy
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37. Other causes of Hyperthyroidism
 Thyrotoxicosis factitia
 Jod–Basedow thyrotoxicosis
 Subacute/acute forms of autoimmune thyroiditis or of de
Quervain’s thyroiditis
 Secondary carcinoma
 Neonatal thyrotoxicosis
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38. SURGERICAL
PROCEDURE

39. Preoperative Preparation
 Standard preparation
 make the patient euthyroid/ near euthyroid using antythyroid drugs
 Alternative method
 rapid control of thyroid status can be achieved with a combination of
thionamides, SSKI, dexamethasone (1 to 2 mg twice daily), and beta
blockers
 very rapid control=> operation within a week
 Lugol’s iodide solution or saturated potassium iodide( three
drops twice daily) for 7 to 10 days
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40. SURGICAL TECHNIQUE
 Extent of thyroidectomy
 controversial, and determined by the desired outcome
 Risk of recurrence Vs hypothyroid, and surgeons experience
 Total or near thyroidectomy
 for patients with coexistent thyroid cancer, sever ophthalmopathy, life
treating reactions to antythyroid drugs
 Subtotal thyroidectomy is recommended for the rest
 bilateral subtotal thyroidectomy in which 1–2 grams of thyroid tissue is
left on both sides.
 Hartley Dunhill procedure
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41. TYPES OF
THYROIDECTOMY
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42. Features
Control of toxicity
Return to euthyroid
state
Recurrence
Thyroid failure
Hypoparathyroidism
Followup
Total Thyroidectomy
Immediate
Immediate
None
100%
5%
Minimal
Subtotal
thyroidectomy
Immediate
Variable
5%
25%
1%
lifelong
Surgical options
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43. Postoperative management
 Following surgery, thyroid hormone replacement should be
started
 TSH should be measured every 1–2 months until stable, and
then annually
 RAIT should be used for retreatment of persistent or
recurrent hyperthyroidism following inadequate surgery
 Following thyroidectomy, serum calcium hormone levels be
measured, and oral calcium supplementation be
administered based on these results
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44. NOVEL MINIMALLY INVASIVE
THERAPIES
 Percutaneous Ethanol Injection (PEI) for Nodules
 Injections of ethanol can be administered directly to toxic thyroid
nodules, cysts and large nontoxic thyroid nodules
 Ultrasound-Guided Laser Thermal Ablation (LTA) for
Nodules
 Percutaneous laser thermal ablation is used to reduce both
hyperfunctioning and compressive nodule
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45. Treatments Under Investigation
 Arterial Embolization
 Indicated in patients with severe hyperthyroidism who cannot tolerate or
who prefer not to use conventional treatment methods
 The Novel Molecule
 a small-molecule antagonist that directly inhibits or prevents TSI antibodies from
activating the TSH receptor.
 The small-molecule antagonist has not yet been studied in clinical trials
 Therapeutic Peptides
 antagonistic peptides that interfere with the action of TSH receptor antibodies as
well as peptides that bind to TSH receptor antibodies, preventing them from
reacting with the TSH receptor
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46. CHOICE OF THERAPY

47. Choice of therapy
Diffuse toxic goitre
 over 45 years, radioiodine.
 under 45 years,
 surgery for the large goitre and
 anti-thyroid drugs or radioiodine
for the small goitre
 Toxic nodular goitre
 Surgery
 Toxic nodule
 Surgery or radioiodine(>45)
 Recurrent thyrotoxicosis after surgery
 radioiodine is the treatment of choice,
but anti-thyroid drugs may be used in
young women intending to havechildren.
Further surgery has little place.
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48. COMPLICTIONS OF
THYROID SURGERY

49. IMMEDIATE COMPLICATIONS
 HEMORRHAGE
 INFECTION
 RECURRENT LARYNGEAL NERVE PALSY
 THYROID CRISES OR STORM
 RESPIRATORY OBSTRUCTION
 PARATHYROID INSUFFICIENCY OR TETANY
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50. LATE COMPLICATIONS
 THYROID INSUFFIENCY
 RECURRENT THROTOXICOSIS
 PROGRESSIVE EXOPHTHALMOS
 HYPERTROPHIC SCAR OR KELOID.
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51. HEMORRHAGE
 Incidence – 0.3-1%
 Two types -
 Deep to deep fascia
 Subcutaneous
 May be primary or reactionary
 A deep bleeding produces tension hematoma. Usually due to slipping of
the ligature of the superior thyroid artery, though it can also be from a
thyroid remnant or a thyroid vein. This compresses on the airway &
potentially life threatening unlike the subcutaneous bleeding.
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52. HEMORRHAGE
 GOOD INTRAOPERATIVE HEMOSTASIS
 Don’t traumatize the thyroid
 Avoid too much neck dressings
 Suction drain ??
 Do not waste time on imaging
 A tension hematoma requires opening of the
wound, evacuation of hematoma & ligature of the
bleeding vessels
 A subcutaneous hematoma can be aspirated.
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53. INFECTION
 Cellulitis – erythema, warmth & tenderness
around the wound
 Abscess – superficial / deep
 Deep abscess associated with fever,
leucocytosis, tachycardia
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54. INFECTION
 Pus for Gram’s stain & culture
 CT for deep neck abscess
 Can be prevented by proper hemostasis at the time
of surgery & using suction drain.
 Per-operative antibiotics not recommended.
 Once established
 Antibiotics
 Drainage of abscess.
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55. RECURRENT LARYNGEAL
NERVE PARALYSIS
 Temporary paralysis is due to pressure of hematoma on
the nerve. Recovers in 3 weeks to 3 month.
 Permanent paralysis is rare (<2%) and is due to undue
stretching or its inclusion in a ligature.
 Unilateral –
 1/3 rd are asymptomatic
 Change in voice
 Improves due to compensation by the healthy cord.
 Bilateral- dyspnea & biphasic stridor
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56. RECURRENT LARYNGEAL
NERVE PARALYSIS
 Prevent injury to the nerve by
 Identify
 ITA ligated far from lobe
 Posterior layer of pretracheal fascia kept intact.
 Laryngoscopy, laryngeal EMG
 For unilateral paralysis no treatment is required.
 For bilateral paralysis
 Tracheostomy (with speaking valve.
 Lateralization of cord
 Arytenoidectomy
 Through endoscope
 Thyroplasty type 2
 Cordectomy
 Nerve muscle implant
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58. COMBINED PARALYSIS
 Unilateral
 Vocal cord lies in cadaveric position
 Hoarseness of voice & aspiration of liquids.
 Ineffective cough
 Bilateral
 Aphonia
 Aspiration
 Ineffective cough
 Bronchopneumonia
 ONLY superior laryngeal nerve palsy also occurs rarely & presents with
hoarseness & loss of voice stamina.
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59. COMBINED PARALYSIS
 Unilateral
 Speech therapy
 Medialise of cord
 Teflon paste injection
 Thyroplasty type 1
 Muscle or cartilage implant
 Arthrodesis of arytenoid joint
 Bilateral
 Tracheostomy
 Epiglottopexy
 Vocal cord plication
 Total laryngectomy
 SLN: speech therapy
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60. THYROID CRISIS / STORM
 Acute exacerbation of hyperthyroidism as the patient has
not been brought to the euthyroid state before
operation.
 Tachycardia, fever(>1050C) , restlessness, delirium
 Mortality is 10%
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61. THYROID CRISIS / STORM
 Ensure euthyroid state before
operation
 Sedation – morphine / pethidine
 Hyperpyrexia – ice bags. Tepid
sponging, hypothermic blanket,
rectal ice irrigation
 Oxygen administration
 IV glucose-saline for dehydration
 Potassium for tachycardia
 Cortisone – 100mg IV
 Carbimazole – 10- 20 mg 6th hourly
 Lugol’s iodine 10 drops 8th hourly by
mouth or potassium iodide 1g IV
 Propranolol – 20-40mg 6th hourly
 Digoxin for atrial fibrillation
 Diuretics for cardiac failure
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62. RESPIRATORY
OBSTRUCTION
 Laryngeal edema due to
 Tension hematoma
 Endotracheal intubation & surgical handling
 More chance in vascular goiters.
 Collapse / kinking of the trachea
 Bilateral recurrent nerve paralysis can aggravate
obstruction if edema is present.
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63. RESPIRATORY
OBSTRUCTION
 Open the wound & release the tension hematoma
 Endotracheal tube if no improvement. INTUBATION TO
BE DONE BY AN EXPERIENCED ANESTHETIST as repeated
attempts cause more edema leading to cerebral anoxia.
 The tube is left in place for several days & steroids given
to reduce the edema.
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64. PARATHYROID
INSUFFICIENCY
 Due to removal of parathyroids or the parathyroid end artery.
 Incidence – 1-3%
 Occurs 2 – 5% after operation. Can be delayed for 2-3 weeks or hypocalcemia may be
asymptomatic.
 Classic triad –
 Carpopedal spasm
 Stridor
 Convulsions
 Latent tetany
 Trousseau’s sign
 Chvostek’s sign
 Persistant – grand mal epilepsy, cataracts, psychosis, calcification of basal ganglia,
papilledema.
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65. PARATHYROID
INSUFFICIENCY
 Correct identification of the gland
 Ligate vessels distal to the parathyroids.
 Recognition of the parathyroid glands, which appear in a variety of shapes
and have a caramel-like color, is critical. When they lose their blood supply,
they turn black. The devascularized gland should be removed, cut into 1 to
2mm pieces, and reimplanted in the sternomastoid muscle or the forearm.
 Monitor serum Ca for 72 hrs post-operatively.
 20 ml 10% solution of calcium gluconate IV
 10 ml injected IM
 2.5-5 G calcium carbonate / day
 PTH is unsatisfactory.
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66. THYROID INSUFFICIENCY
 INCIDENCE :20-25% of patients subjected to subtotal thyroidectomy for diffuse
toxic goiter & toxic nodular goiters with internodular hyperplasia
 Time: <2 yrs. May be delayed >5yrs.
 Transient hypothyroidism may occur within 6 months which is asymptomatic.
 Due to change in nature of autoimmune response.
 More chance if less residual thyroid tissue
 Cold intolerance, fatigue constipation, weight gain, myxedema.
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67. THYROID INSUFFICIENCY
 Thyroxine – start with 50 mcg/d, 100mcg/d after 3 weeks,
and 150 mcg/d thereafter. Taken as a single daily dose.
 Monitoring –
 TSH in the lower end of reference range (0.15-3.5 mU / l)
 T 4 normal or slightly raised. (10 – 27 pmol / l)
 Manage ischemic heart disease with beta blockers &
vasodilators
 Increase thyroxine during pregnancy. (50 mcg)
 Myxedema coma: IV thyroxine 20mcg 8th hourly
followed by oral.
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68. RECURRENT
THYROTOXICOSIS
 Incidence 5 – 10%
 Due to inadequate removal or hyperplasia of
remaining thyroid tissue.
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69. RECURRENT
THYROTOXICOSIS
 Less than 40 yrs – carbimazole
 0-3wks 40-60mg/d
 4-8wks 20-40mg/d
 18-24 months 5-20mg/d
 More than 40 yrs – radioiodine
 5-10mCi oral; 75% respond in 4-12 weeks
 Repeated after 12-24 weeks if no improvement.
 Beta blocker / carbimazole cover during lag period.
 Long term follow-up for hypothyroidism.
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70. PROGRESSIVE / MALIGNANT
EXOPHTHALMOS
 Occurs even when thyrotoxic features are regressing.
 Steroids & radiotherapy.
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71. HYPERTROPHIC SCAR /
KELOID
 Platysma to be divided at a higher level
 Occurs if scar overlies the sternum
 Some persons are more susceptible.
 May follow wound infection.
 Intradermal steroids, repeated monthly.
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72. References
 HYPERTHYROIDISM AND OTHER CAUSES OF THYROTOXICOSIS: MANAGEMENT
GUIDELINES OF THE ATA AND AACE Baskin HJ, Cobin RH, Duick DS, et al
(American Association of Clinical Endocrinologists) 2011
 Klein I, Becker D, Levey GS.Treatment of hyperthyroid disease. Ann Int
Med.1994;121:281-288.
 Schwartz’s Principles of Surgery, 9th ed.
 William’s Text Book Of Endocrinology, 11th ed.
 Bailey & Loves’ Short Practice of Surgery, 25th ed.
 Greenspan’s Basic & Clinical Endocrinology, 8th ed.
 Uptodate
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73. Thank u !!!