3. Introduction
•Thyrotoxicosis:- clinical state that results from inappropriately high
thyroid hormone action in tissues generally due to inappropriately
high tissue thyroid hormone levels
•Hyperthyroidism:- a form of thyrotoxicosis due to inappropriately
high synthesis and secretion of thyroid hormone(s) by the thyroid
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4. Introduction Cont.
•Thyrotoxicosis can occur
• Thyroid is inappropriately stimulated by trophic factors;
• Activation of thyroid hormone synthesis and secretion leading to
autonomous release of excess thyroid hormone;
• Thyroid stores of preformed hormone are passively released in
excessive amounts owing to autoimmune, infectious, chemical or
mechanical insult;
• Exposure to extra-thyroidal sources of thyroid hormone
• Endogenous (struma ovarii, metastatic differentiated thyroid cancer) or
• Exogenous (factitious thyrotoxicosis).
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5. Introduction Cont.
•Depending on the biochemical severity of the hyperthyroidism
• Overt or Subclinical
•Overt hyperthyroidism:- subnormal serum TSH with elevated serum
levels of T3 and/or free T4 estimates.
•Subclinical hyperthyroidism:- low or undetectable serum TSH with values
within the normal reference range for both T3 and free T4 estimates.
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6. Epidemiology
•All over the world prevalence 1-2%
•US:- app 1.2% (0.5% overt and 0.7% subclinical)
• Common causes include
• Graves’ disease : 60% to 80%
• Toxic multinodular goiter and
• Toxic adenoma
•Ethiopia
• A prospective study of 110 Ethiopians with thyrotoxicosis in TASH
• 48.2% Graves’ hyperthyroidism
• 33.7% TMNG
• 12.7% TA
•More in females and affects 4-5% Female of population
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7. Causes of Thyrotoxicosis
•Graves’ Disease:- autoimmune disorder in which thyrotropin receptor
antibodies (TRAbs) stimulate the TSH receptor, increasing thyroid
hormone production.
• Strong familial predisposition
• Female preponderance (5:1)
• Peak incidence between the ages of 40 and 60 years
• Remission without treatment up to 30% of patients
• Orbitopathy: 50% of patients
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8. Causes of Thyrotoxicosis Cont.
•Toxic MNG:-
• Occur in older individuals
• Often have a prior history of a nontoxic multinodular goiter
• The natural history includes growth of established nodules, new nodule
formation and development of autonomy over time.
•Toxic Adenoma:- autonomous hormone production can be caused
by somatic activating mutations of genes regulating thyroid hormone
synthesis.
• Occurs in younger patients
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9. Causes of Thyrotoxicosis Cont.
•Painless and subacute thyroiditis:- inflammation of thyroid tissue
with release of preformed hormone into the circulation.
•Painless thyroiditis is the etiology of hyperthyroidism in about 10% of
patients
• Postpartum period (postpartum thyroiditis)
• Lithium or cytokine therapy
• 5–10% of amiodarone-treated patients
•Subacute thyroiditis:- caused by viral infection and is characterized
by fever and thyroid pain
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14. Evaluation of Thyrotoxic Patients Cont.
•Determination of Etiology
• Clinical presentation and initial biochemical evaluation
• Diagnosis of GD
• Symmetrically enlarged thyroid, recent onset of orbitopathy and moderate to
severe hyperthyroidism
• Measurement of TRAb
• Determination of RAIU
• Measurement of thyroidal blood flow on ultrasonography
• A 123I or 99mTc pertechnetate scan should be obtained when the clinical
presentation suggests a TA or TMNG
15. Evaluation of Thyrotoxic Patients Cont.
•RAIU and thyroid scan:- distinguishes causes of thyrotoxicosis having
elevated or normal uptake over the thyroid gland from those with
near-absent uptake
• GD:- Elevated diffuse uptake
• TA:- Focal uptake in the adenoma with suppressed uptake in the surrounding
and contralateral thyroid tissue
• TMNG:- multiple areas of focal increased and suppressed uptake
•Ultrasonography with color flow Doppler can distinguish thyroid
hyperactivity from destructive thyroiditis
• Useful when RAI is contraindicated such as during pregnancy or breastfeeding.
16. Evaluation of Thyrotoxic Patients Cont.
•Ratio of total T3 to total T4:-
• >20 in GD and toxic nodular goiter
• <20 in painless or postpartum thyroiditis
•Thyroglobulin:- distinguishes factitious ingestion of thyroid hormone from
other causes of thyrotoxicosis
• Released in subacute, painless and palpation thyroiditis
• Suppressed in exogenous thyroid hormone administration.
•Measurement of fecal T4:- alternative to TG measurement in the
presence of antithyroglobulin antibodies
17. 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 Hyper
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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18. Management
•Symptomatic management
• Beta-adrenergic blockade
• All patients with symptomatic thyrotoxicosis
• Thyrotoxic patients with resting heart rates in excess of 90 bpm or coexistent
cardiovascular disease
• Decrease in heart rate, systolic blood pressure, muscle weakness and tremor
• Improves the degree of irritability, emotional lability and exercise intolerance
• CI: bronchospastic asthma
• Calcium channel blockers are alternative
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20. Overt Hyperthyroidism Management in GD
•Modalities
• 131I therapy,
• Antithyroid medication
• Thyroidectomy
•The long-term quality of life following treatment for GD was found
to be the same in patients randomly allocated to one of the three
treatment options.
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21. 131I Therapy
•Factor favoring 131I therapy
• Females planning a pregnancy in the future( >6months)
• Comorbidities increasing surgical risk
• Previously operated or externally irradiated necks
• Lack of access to a high-volume thyroid surgeon
• Contraindications to ATD use
• Patients with periodic thyrotoxic hypokalemic paralysis, right heart
failure pulmonary hypertension, or congestive heart failure
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22. 131I Therapy Cont.
•Contraindications for 131I therapy:
• Pregnancy and lactation
• Coexisting thyroid cancer or suspicion of thyroid cancer
• Individuals unable to comply with radiation safety guidelines and
• Females planning a pregnancy within 4–6 months.
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23. 131I Therapy Cont.
•Preparation:
• Beta-adrenergic blockade
• Patients at increased risk for complications due to worsening of hyperthyroidism
• Elderly patients and patients with comorbidities
• Pretreatment with methimazole
• Patients at increased risk for complications due to worsening of hyperthyroidism
• Extremely symptomatic or
• Free T4 estimates 2–3 times the upper limit of normal
• Elderly and those with substantial comorbidity
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24. 131I Therapy Cont.
• MMI/Carbimazole
• Discontinue 3–5 days before the administration
• Restarted 3–7 days later
• Tapered over 4–6 weeks as thyroid function normalizes.
• Medical therapy of any comorbid conditions should be optimized prior
to administering radioactive iodine.
•Administration:- Sufficient radiation should be administered in a
single dose (typically 10–15 mCi) to render the patient with GD
hypothyroid.
•Complication:- Thyroid storm, worsening of hyperthyroidism,
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25. 131I Therapy Cont.
•Follow-up after 131I therapy
• First 1–2 months should include an assessment of free T4 and total T3
• If the patient remains thyrotoxic, biochemical monitoring should be
continued at 4–6 week intervals.
• When hyperthyroidism persists after 6 months, or if there is minimal
response 3 months after therapy, retreatment with 131I is suggested.
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26. Anti-Thyroid Drugs
•Factor that favors ATDs:
• High likelihood of remission (females with mild disease, small goiters, and
negative or low-titer TRAb);
• Elderly or others with comorbidities increasing surgical risk or with limited
life expectancy;
• Individuals who are unable to follow radiation safety regulations;
• Previously operated or irradiated necks;
• Lack of access to a high-volume thyroid surgeon
• Patients with moderate to severe active GO
• Need more rapid biochemical disease control
•CI: Previous known major adverse reactions to ATDs.
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27. Anti-Thyroid Drugs Cont.
•Do not cure Graves’ hyperthyroidism rather render the patient euthyroid
•Initiation
• Methimazole/Carbimazole should be used in virtually every patient who
chooses ATD therapy
• Exception:- PTU
• During the first trimester of pregnancy,
• In the treatment of thyroid storm, and
• In patients with minor reactions to methimazole who refuse RAI therapy or surgery.
• Baseline CBC and a liver profile including bilirubin and transaminases
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28. Anti-Thyroid Drugs Cont.
•Methimazole
• Longer duration of action, allowing for once daily dosing, more rapid efficacy,
and lower incidence of side effects
◦ 5–10 mg if free T4 is 1–1.5 times
10–20 mg for free T4 1.5–2 times
30–40 mg for free T4 2–3 times
the upper limit of normal
•PTU
• Shorter duration of action, two or three times daily dosing and higher
incidence of side effects
•Adverse effects of ATDs
• Divided as minor and major
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29. Anti-Thyroid Drugs Cont.
•Major adverse effects
• Agranulocytosis
• More common in PTU
• Hepatotoxicity
• 2.7% of patients taking PTU and 0.4% of patients taking MMI
• MMI- cholestatic
• PTU- hepatocellular
• Vasculitis
• Antineutrophil cytoplasmic antibody (pANCA)-positive small vessel vasculitis as well
as drug-induced lupus
• More common in PTU
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30. Anti-Thyroid Drugs Cont.
•Monitoring
• Assessment of serum free T4 and total T3
• Serum TSH not a good parameter for monitoring therapy in the early
course.
• Once the patient is euthyroid, the dose of MMI can usually be decreased
by 30%–50%
• A differential WBC count should be obtained during febrile illness and at
the onset of pharyngitis
• Liver function and hepatocellular integrity should be assessed in patients
who experience pruritic rash, jaundice, light-colored stool or dark urine,
joint pain, abdominal pain or bloating, anorexia, nausea, or fatigue.
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31. Anti-Thyroid Drugs Cont.
•Duration
• The medication should be continued for approximately 12–18 months,
• Discontinuation is considered if the TSH and TRAb levels are normal
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32. Surgery
•Indications:
• Symptomatic compression or large goiters (≥80 g);
• Relatively low uptake of radioactive iodine;
• Thyroid malignancy is documented or suspected
• Large thyroid nodules greater than 4 cm or nonfunctioning or hypofunctioning
• Coexisting hyperparathyroidism requiring surgery;
• Females planning a pregnancy in <4–6 months
• Patients with moderate to severe active GO.
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33. Surgery Cont.
•Contraindications:
• Substantial comorbidity such as cardiopulmonary disease, end-stage
cancer, or other debilitating disorders.
• Pregnancy is a relative contraindication
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34. Surgery Cont.
•Preparation:
• Pt should be rendered euthyroid with ATDs with or without β-adrenergic
blockade
• Potassium iodide should be given in the immediate preoperative period
• Decreases thyroid blood flow, vascularity, and intraoperative blood loss
• Potassium iodide can be given as 5–7 drops Lugol’s solution (8 mg iodide/drop) or
1–2 drops SSKI (50 mg iodide/drop) three times daily mixed in water or juice for 10
days before surgery.
• Supplementing oral calcium, vitamin D or both preoperatively may
reduce the risk of postoperative hypocalcemia due to parathyroid injury
or increased bone turnover
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35. Surgery Cont.
•Procedure of choice
• Near-total or total thyroidectomy
• High cure rate
• Total thyroidectomy has a nearly 0% risk of recurrence
• Subtotal thyroidectomy may have an 8% chance of persistence or recurrence of
hyperthyroidism at 5 years
• Most common complications
• Hypocalcemia (transient or permanent),
• Recurrent or superior laryngeal nerve injury (temporary or permanent),
• Postoperative bleeding
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36. Surgery Cont.
•Postoperative care
• Serum calcium or intact parathyroid hormone levels be measured, and
that oral calcium and calcitriol supplementation be administered based
on these results.
• Antithyroid drugs should be stopped at the time of thyroidectomy and
beta-adrenergic blockers should be weaned following surgery
• L-thyroxine should be started at a daily dose appropriate for the
patient’s weight (1.6 µg/kg), and serum TSH measured 6–8 weeks
postoperatively.
• Once stable and normal, TSH should be measured annually or more
frequently if clinically indicated.
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37. Hyperthyroidism Management in TMNG or TA
•Two effective and relatively safe treatment options are 131I therapy
and thyroidectomy
•On occasion, long-term, low-dose treatment with methimazole may
be appropriate.
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38. 131I Therapy
•Indication:
• Advanced patient age,
• Significant comorbidity,
• Prior surgery or scarring in the anterior neck,
• Small goiter size,
• RAIU sufficient to allow therapy, and
• Lack of access to a high-volume thyroid surgeon
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39. 131I Therapy Cont.
•Contraindications:
• Pregnancy or lactation
• Coexisting thyroid cancer
• Individuals unable to comply with radiation safety guidelines, and
• Females planning a pregnancy within 4–6 months.
•Preparation
• Beta-blockade and Pretreatment with Methimazole
• Pts older than 60 years of age and those with cardiovascular disease or severe
hyperthyroidism
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40. 131I Therapy Cont.
•Administration
• Sufficient radiation should be administered in a single dose to
alleviate hyperthyroidism
•Follow-up
• Assessment of free T4, total T3 and TSH within the first 1–2 months
• Repeated at 1–2 month intervals until stable results are obtained, then
at least annually
• Retreatment with radioactive iodine is suggested if hyperthyroidism
persists beyond 6 months
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41. Surgery
•Indications:
• Presence of symptoms or signs of compression within the neck,
• Concern for coexisting thyroid cancer,
• Coexisting hyperparathyroidism requiring surgery,
• Large goiter size (>80 g), substernal or retrosternal extension,
• RAIU insufficient for therapy
• Need for rapid correction of the thyrotoxic state
•Contraindications:
• Significant comorbidity such as cardiopulmonary disease, end-stage cancer,
or other debilitating disorders.
• Pregnancy is a relative contraindication
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42. Surgery Cont.
•Preparation:
• Risks of surgery are increased in the presence of thyrotoxicosis.
• Thyrotoxic crisis during or after the operation can result in extreme
hypermetabolism, hyperthermia, tachycardia, hypertension, coma, or death.
• Pt should be rendered euthyroid prior to the procedure with methimazole
pretreatment with or without beta-adrenergic blockade.
•Procedure of choice
• Near-total or total thyroidectomy should be performed for TMNG
• Recurrence can be avoided in TMNG if a near-total or total thyroidectomy is
performed initially.
• Reoperation for recurrent or persistent goiter results in a 3- to 10-fold
increase in risk for permanent vocal cord paralysis or hypoparathyroidism
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43. Surgery Cont.
•An ipsilateral thyroid lobectomy, or isthmusectomy if the adenoma is
in the thyroid isthmus, should be performed for TA.
• A preoperative thyroid ultrasound is useful
• Detects the presence of contralateral nodularity
• Total thyroidectomy may be more appropriate in the presence of
contralateral nodularity
• Lobectomy has low complication rates and higher risk of postoperative
hypothyroidism occurs in pts with positive antithyroid antibodies
preoperatively
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44. Surgery Cont.
•Postoperative care
• Following thyroidectomy for TMNG
• Serum calcium or intact PTH levels should be measured, and oral calcium and
calcitriol supplementation should be administered based on these results.
• Severe or prolonged preoperative hyperthyroidism and larger size and greater
vascularity of the goiter increases the risks of postoperative hypocalcemia.
• Thyroid hormone replacement should be started at a dose appropriate for the
patient’s weight (1.7 mcg/kg) and age
• Methimazole should be stopped at the time of surgery for TMNG or TA.
• Beta-adrenergic blockade should be slowly discontinued following
surgery.
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45. Surgery Cont.
•Persistent or recurrent hyperthyroidism following surgery is
indicative of inadequate surgery.
•Remedial thyroid surgery has significantly increased risk of
hypoparathyroidism and RLN injury and should be avoided
•Radioactive iodine therapy is option of treatment.
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46. Role of ATD Therapy in Pts with TMNG or TA
•ATDs do not induce remission in pts with nodular thyroid disease
and discontinuation results in relapse
•Long-term methimazole treatment of TMNG or TA should be
avoided, except in some elderly or otherwise ill patients with limited
longevity who are able to be monitored regularly, and in patients
who prefer this option.
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47. Alternative Techniques of Management of TMNG or TA
•US guided percutaneous ethanol injection (PEI)
• Effective and safe
• Demonstrated an overall cure rate (absent uptake in the nodule) of
93%, and a major complication rate of 3%
• Average reduction in the volume of nodules was 66%
• Complications: transient laryngeal nerve damage, abscess and
hematoma
•Radiofrequency ablation and laser therapy
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48. Subclinical Hyperthyroidism
•Prevalence and Causes
• U.S.:- 0.7% had suppressed TSH levels (<0.1 mU/L), and 1.8% had low
TSH levels (<0.4 mU/L)
• DDx :- exogenous thyroid hormone use, nonthyroidal illness, drug effects
and pituitary/hypothalamic disease
• Natural history is variable
• 0.5%–7% progress to overt hyperthyroidism annaully
• 5%–12% reversion to normal TSH levels
• TMNG, GD, solitary autonomously functioning nodules and various forms
of thyroiditis
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49. Subclinical Hyperthyroidism Cont.
•When to treat SH?
• Treatment of SH is controversial
• When TSH is persistently <0.1 mU/L treatment is recommended
• In all individuals > 65 years of age
• In patients with cardiac risk factors, heart disease or osteoporosis;
• In postmenopausal women who are not on estrogens
• In individuals with hyperthyroid symptoms.
• There are insufficient data for or against treatment of SH in younger
persons or premenopausal women with SH and serum TSH <0.1 mU/L
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50. Thyroid Storm
•Precipitated by abrupt cessation of antithyroid medications,
infection, thyroid or nonthyroid surgery, and trauma in patients with
untreated thyrotoxicosis.
•Diagnosis is made clinically
• Severely thyrotoxic patient with evidence of systemic decompensation
•Sensitive diagnostic system can be considered
• Burch–Wartofsky Point Scale
• Japanese Thyroid Association (JTA) categories of thyroid storm
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52. Thyroid Storm Cont.
•Treatment strategy for thyroid storm
• Therapy directed against thyroid hormone secretion and synthesis
• Measures directed against the peripheral action of thyroid hormone at
the tissue level
• Reversal of systemic decompensation
• Treatment of the precipitating event or intercurrent illness; and
• Definitive therapy
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53. Thyroid Storm Cont.
Decrease De Novo Synthesis and Release
• Propylthiouracil
• 500–1000mg load, then 250mg
every 4 hours
• Blocks new hormone synthesis
• Blocks T4-to-T3 conversion
• Methimazole
• 60–80 mg/d
• Blocks new hormone synthesis
•Inorganic iodine (SSKI/Lugol’s
solution)
• 5 drops (0.25mL or 250 mg) orally
every 6 hours
• Blocks new hormone synthesis
• Blocks thyroid hormone release
•Oral cholecystographic agents:
ipodate and iopanoic acid
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54. Thyroid Storm Cont.
•Prevent peripheral effects:
• Propranolol
• 60–80 mg every 4 hours
• Consider invasive monitoring in
congestive heart failure patients
• Blocks T4-to-T3 conversion in high doses
• Esmolol infusion
• Alternative drug
•Other consideration
• Hydrocortisone
• 300mg IV load, then 100 mg TID
• May block T4-to-T3 conversion
• Prophylaxis against relative adrenal
insufficiency
• Dexamethasone
• Cooling with acetaminophen and
cooling blankets
• Volume resuscitation and nutritional
support
• Respiratory care and monitoring in ICU
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56. Positioning and preparation
• Positioning and skin preparation
• sandbag b/n scapula
• Eyes protected
• ETT is strapped firmly in position
• Gentle traction of the arms
• alongside the body
• Placing in 20° reverse
• Trendlenburg position
• Surgeon stands on the opposite
• side to the lobe to be removed
• Skin prepped and draped
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57. Incision and mobilization of skin layers
•A Kocher transverse incision, 2 to 3cm above the sternal notch,
through the platysma.
•Clamps applied on the dermis to facilitate dissection
•First cephalad in a subplatysmal plane to the level of `thyroid cartilage
notch
•Then caudad to `suprasternal notch
•Self retaining retractors are applied
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58. Midline dissection and mobilization of strap muscles
•Start incision at the suprasternal notch
and extend to the thyroid cartilage
•Dissect strap muscles from the thyroid
gland until middle thyroid vein(S) are
encountered
•Retract `thyroid anteriorly and medially
and the carotid sheath laterally
•Divide the middle thyroid veins
•NB: Division of the strap muscles is not
done routinely.
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59. Division of the isthmus
•During thyroid lobectomy
•The isthmus is divided b/n clamps
•The thyroid tissue that remains is oversewn
•It minimizes :
•Chance of invasion into the trachea
•Midline visible mass due to hypertrophy
•Pyramidal lobe also mobilized
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60. Mobilization of the gland and identification of
vital structures
•Dissect superiorly, laterally, and
posteriorly
•superior thyroid artery and veins
identified & ligated (transfixed) on
the capsule of the gland
•Berry’s (suspensory) ligament
•ELN
•Identification of RLN & lower PTGs
•Inf. Thyroid vessels
•Thyroid ima if present
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61. 3/18/2024 61
Management of complications
1. General complications are rare
2. Bleeding and air way obstruction
3. Recurrent laryngeal nerve injury
• Causes:-stretching, bruising, ligation, division, burn, compromised bld supply.
Consequence:- VC paresis or paralysis
Incidence:-permanent < 1% of all & 30% of injured nerves.
-transient =2-4%,for wks to mths
Risk factors:-nerve not identified, anatomic variations, recurrent dis., type of
dis.
62. Recurrent laryngeal nerve injury
• Unilateral:-
• reintubation
• temporary:-observe for 6-12 min
• if function not return in 6-12 min Teflon inj
ection
• speech therapy
• = definitive Rx not until 6 months
• -medialization and reinnervation
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63. 3/18/2024 63
Recurrent laryngeal nerve injury
•Bilateral :-
Could be temporary
reintubation, paralyzed
hydrocortisone 100mg tid
wound re-explord for reversible cause
If extubation fails after 48 hrstracheostomy
Principal goal of Surgery is to improve AW patency, cordotomy &
atytenoidectomy
64. 3/18/2024 64
Nerve injury
•External br. Of superior laryngeal nerve
-difficult to shout or sing high tones
-hoarseness, weakness, decreased range of pitch, fatigue after exessive use
-prevention=> superior thyroid vessels ligated individually on gland
65. 3/18/2024 65
Hypoparathyroidism
• After all operations Ca2+ decreases by 1mg/dl.
•Usually is transient (reportedly 2-53%)
•Cause is not clearly understood, attributable to:-
1) damage to PT gland --- < 0.5%
2) reversible ischaemia through damage to PTG
end artery---most common cause
3) Hypothermia to the glands
4) Release of endothelin 1 ( suppresses PTH)
5) ”hungry bone dis.” In preoperative hyperthyroidism.
•10% solution of calcium gluconate, containing 90 –180 mg elemental calcium in 50 mL of 5% dextrose, over
10 to 20 minutes followed by a slower infusion of calcium gluconate, 0.5 to 1.5 mg/kg/h over an 8- to 10-
hour period
66. References
1. 2016 ATA Guidelines for Diagnosis and Management of Hyperthyroidism and
Other Causes of Thyrotoxicosis,
https://www.liebertpub.com/doi/pdfplus/10.1089/thy.2016.0229
2. Schwartz’s Principles of Surgery 11 Ed
3. Sabiston Textbook of Surgery 20 Ed
4. Medical management of Thyroid disease, David S. cooper, 2nd ed
5. Atlas of Endocrine Surgical Techniques
6. Maria Luisa Brandi, John P. Bilezikian, Dolores Shoback, Roger Bouillon, Bart
L. Clarke, Rajesh V. Thakker, Aliya A. Khan, John T. Potts, Jr, Management of
Hypoparathyroidism: Summary Statement and Guidelines, The Journal of
Clinical Endocrinology & Metabolism, Volume 101, Issue 6, 1 June 2016,
Pages 2273–2283, https://doi.org/10.1210/jc.2015-3907
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