HYPERTHYROIDISM

Increased serum levels of thyroid hormones,

Surgical correction is frequently appropriate

HYPERTHYROIDISM
Common causes:
- diffuse toxic goitre (Graves’s disease),
- toxic multinodular goitre (Plummer’s disease),
- toxic solitary nodule,
- exogenous thyroid hormone excess,
- thyroiditis
HYPERTHYROIDISM
Rare causes:

- metastatic thyroid carcinoma,

- pituitary tumour secreting TSH
GRAVES’S DISEASE
The most common cause of hyperthyroidism
It is an immunological disorders
Thyroid stimulating antibodies (Ig G type) bind to the
TSH receptor of the thyroid cells- excess of the
thyroid hormones
The thyroid gland hypertrophies
Diffuse enlargement
GRAVES’ DISEASE
Clinical Diagnosis

Symptoms and signs of thyrotoxicosis result from

excess thyroid hormones:
Cardio vascular
Neurological
Metabolic
Exophtalmos
Diffuse enlargement of the thyroid
GRAVES’ DISEASE
Ophthalmopathy- two major components:
-Non-infiltrating ophthalmopathy
-sympathetic activity - upper lid retraction,
- a stare,
- infrequent blinking
-Infiltrating ophthalmopathy- edema of the orbital contents,
lids, periorbital tissue, cellular infiltration within the orbit
Surgical specimen
Recurrent Grave’s disease after subtotal
thyroidectomy, nodule at the piramidal lobe
 Right thyroid nodules after subtotal
thyroidectomy
Nodules with cystic degeneration after
subtotal thyroidectomy
Left upper nodule with cystic degeneration
GRAVES’ DISEASE
INVESTIGATIONS
Laryngoscopy- mobility of vocal cords
CXR, ECG
Measurement of free T3, T4, TSH
Isotope scanning not essential but necessary in the
assessment of toxic solitary and multinodular goitre-
the site of nodular overactivity
Radioactive iodine uptake- increased uptake in the
thyroid gland
GRAVES’ DISEASE
TREATMENT

To restore the euthyroid state:

Antithyroid drugs+ beta-blockers
Radioactive iodine- distroys overactive tissue
Surgery- bilateral subtotal/total thyroidectomy
Grave’s disease
Multiple nodules and hypervascularity
Grave’s disease
Pressure symptoms
TOXIC MULTINODULAR GOITRE
TREATMENT

ATD- waste of time

Radioactive iodine- not indicated
Surgery- total thyroidectomy appropriate
TOXIC SOLITARY NODULE
TREATMENT

This condition is caused by a single autonomous

thyroid nodule

Best option- Surgery- unilateral thyroid lobectomy

Thyroid scintigram
Autonomous adenoma in the
right lobe of the struma.
The test substance
accumulates almost
exclusively in the range of
the autonomous adenoma.
The other areas of the struma
show a considerable reduced
accumulation of activity.

Toxic compressive goiter
Toxic nodular goiter
Thyroid USS:
 LTL-vol. 86,98 ml., RTL- vol. 5,54 ml.
TSH=0,1 mcg/ml (0,4-7)
CT- expansive solid nodule LTL
ENT exam.- laryngoscopy- left recurent nerve palsy
AP- nodular goiter with cystic degeneration and areas
of hyperfunction
HYPERTHYROIDY
PREOPERATIVE PREPARATION

Surgery must be done in the euthyroid state

 ATD for a period then discontinue
Betablockers to control cardiac symptoms
Lugol’s solution,10 days, will diminish the peroperative
hemorrhagic risk
POSTOPERATIVE COMPLICATIONS
1. Postoperative bleeding
2. Postoperative thyrotoxic crisis
3.Postoperative voice changes
4. Hypoparathyroidism
5. Hypothyroidism
POSTOPERATIVE BLEEDING
Postoperative bleeding
there is always a risk of postop.bleeding,
it is rare but sometimes dramatic
The bleeding may occur in one of two sites,
- deep to the myofascial layer in relation to thyroid
vessels-evacuation must be done quickly
- deep to the skin flaps, from veins
Compressive hematoma- respiratory
embarrasment- evacuation is mandatory
POSTOPERATIVE
THYROTOXIC CRISIS

Serious complication-where there has not been

adequate preop.preparation
It occurs within the first 24 hours of thyroidectomy
Symptoms: confusion, hyperactive, fever, profuse
sweating, rapid PR.
Treatment: beta-blockers, iv steroids, iodine
POSTOPERATIVE VOICE CHANGES
Rare due to any damage to recurrent laryngeal nerves- this
occurs in less than 1%
Probably minor changes in the muscles around the cricoid
and thyroid cartilages are the most important, inevitable
with the mobilization of the gland
Trauma to external laryngeal nerve- cricothyroid muscle-
voice change- difficulty in achieving vocal cord tension
Trauma t the internal laryngeal nerve can occur where
there is difficulty in mobilizing the superior pole
POSTOPERATIVE
HYPOPARATHYROIDISM
Hypocalcemia- usually a consequance of a metabolic
changes- re-entry of calcium into bone demineralized
by hyperthyroidism (“hungry bones”)
Parathyroids are small and are not always easy to
identify
The incidence of hypoparathroidism after surgery
shoud be less than 1%
Hipoparathyroidism and hypocalcemia
Transient or definitive- 1%-15%
Manipulation of the PT glands- neck dissection
Single vs. 3 glands preserved for normal PT fct.
Non-capsular dissection technique- risk of injury
Incidental removal with thyroid gland
PT- reimplant into the SCM muscle
Identification of PT- avoid injury risk
Hypoparathyroidism
THYROID CANCER
Tumors of thyroid follicular epithelium
Papillary carcinoma
Follicular carcinoma
Anaplastic carcinoma
Tumors of parafollicular cells
Medullary carcinoma
Tumors of lymphoid cells
Lymphoma
PAPILLARY CARCINOMA
The commonest thyroid tumor
Previous neck irradiation-risk factor-thy.ca.
Hard whitish nodule
Lymphatic spread
Three types based on tu. size and extent:
Minimal lesion<1cm
Intrathyroid lesion>1cm.within the thyroid
Extrathyroid lesion-locally advanced
FOLLICULAR CARCINOMA
Encapsulated, solitary nodule
Usually firm, but soft when intratumor hg.
Spread via the boodstream
Two main types after histopathology:
Minimally invasive-slight capsular or vascular invasion
Frankly invasive-venous extension into thyroid and
jugular veins
The TNM stages of thyroid cancer

 “TNM” stands for Tumour, Node, Metastasis.

 T1 - the tumour is entirely inside the thyroid and is less than 2cm
across in any direction
 T2 - The tumour is entirely inside the thyroid and is more than 2cm
but no more than 4cm across in any direction
 T3 - The tumour is entirely inside the thyroid and is more than 4cm
across in any direction
 T4a - The cancer has grown outside the thyroid gland into the
surrounding tissue.
 T4b - The cancer has grown outside the thyroid gland into the area
surrounding the bones of the spine, or one of the main blood vessels
nearby.
TNM staging
 N0- no lymph nodes contain cancer cells
 N1a - there are lymph nodes containing cancer cells on one side of the
neck only (on the same side as the cancer)
 N1b - there are lymph nodes containing cancer cells anywhere else
(usually the other side of the neck or in the chest)

 M0- no distant MTS

 M1 - present distant MTS
TNM staging
Differentiated thyroid cancer: papillary and
folicular thyroid cancer
Under 45years of age:
Stage 1 - cancer is only inside the thyroid, or the
thyroid and the lymph glands

Stage 2 - cancer has spread presenting metastases

TNM staging for differentiated thyroid
cancer, over 45 years of age

Stage 1 - cancer is only inside the thyroid and is less

than 2cm across
Stage 2 - cancer is any size, but is only inside the
thyroid
Stage 3 - cancer has grown beyond the thyroid
capsule, or there are cancer cells in the lymph nodes
Stage 4 - cancer has spread to other parts of the body,
such as lungs or bones
TREATMENT OF DIFFERENTIATED THYROID
CANCER

Thyroidectomy is the treatment of choice

Objectives- to eradicate primary tumor
- to reduce the incidence of recurrence
Papillary cancer-multifocality-total thyroidectomy is
the best option plus clearance of cervical lymph nodes
Follicular cancer- if minimal-lobectomy
- If invasive-total thyroidectomy
POSTOPERATIVE TREATMENT
Thyroxine after total thyroidectomy
Thyroglobuline measurement-sensitive indicator of
residual or recurrent differentiated thyroid cancer
after total thyroidectomy
Radioactive iodine is a useful means of detecting
metastatic disease after total thyroidectomy
ANAPLASTIC CARCINOMA
Highly aggressive tumor, affects the elderly
Rapidly infiltrates local structures
Metastases via bloodstream, lymphatics
Long history of goitre that suddenly starts to grow
rapidly
Voice change, dysphagia, dyspnea
Resection is rarely possible
Survival within six months
Staging for anaplastic thyroid cancer
There is no number staging system for
anaplastic thyroid cancer.
This is because there is a high risk of the cancer
spreading.
If the cancer is only in the neck - complete removal
If the patient is fit enough - surgery or radiotherapy
MEDULLARY CARCINOMA
Incidence-8% of thyroid malignancies
Solid non-follicular carcinoma
Arises from the parafollicular cells, C-cells which
secretes calcitonin- hypocalcemia
In the upper 2/3rds, multicentric, bilateral
Spreads by lymphatics to regional nodes
Spreads via bloodstream to liver, lungs, bones
MEDULLARY CARCINOMA
This tumor produces calcitonin- tu.marker
CEA- another tu.marker
This tu. can secrete a range of hormones and
peptides: prostaglandins, 5-hydroxitryptamine,
ACTH.
Diagnosis- FNAC, serum calcitonin
Association with pheochromocytoma- urinary VAM
and metanephrines
MEDULLARY CARCINOMA
TREATMENT
Total thyroidectomy is the best option
Central and paratracheal lymph nodes clearance,
Carotid sheath nodes removed, if involved with tu.-
modified radical neck dissection, preserving IJV, SCM,
spinal accessory nerve.
Bilateral lymph nodes clearance is advised
Medullary thyroid cancer

There are 4 number stages for medullary thyroid cancer

. These are:
Stage 1 - cancer is less than 2cm across
Stage 2 - cancer is between 2cm and 4cm across
Stage 3 - There is spread to cervical lymph nodes
Stage 4 - The cancer cells have spread to another part
of the body
 
MEDULLARY CARCINOMA
FOLLOW-UP

Follow-up: calcitonin, CEA

If raised- persistent or recurrent disease
Ultrasonography, CT, MRI,scintigraphy
External irradiation- last chance
Chemotherapy is disapointing
Present lymph nodes metastases-survival rate is 45%
at 10 years
THYROIDITIS

Subacute thyroiditis
Autoimmune thyroiditis
Riedel’s thyroiditis
Acute suppurative thyroiditis
SUBACUTE THYROIDITIS
Granulomatous or de Quervain’s thyroiditis
Probably viral origin
Painful swelling of one or both thyroid lobes,
malaise, fever
Preceding history of sore throat or viral infection
a week or two before the onset of thyroid
symptoms
Symptoms and signs of hyperthyroidism
Thyroid hormone levels raised but low uptake of
radioactive iodine, ESR is raised
SUBACUTE THYROIDITIS
The disease process is self-limiting with resolution of
local sy. and thy. dysfunction
Few pts. pass through a mild hypothyroid phase
Local sy.-aspirin, steroids
Transient hyperthyroidism does not require
antithyroid drugs
AUTOIMMUNE THYROIDITIS
Diffuse process throughout the thyroid gland-
Hashimoto’s disease
Infiltration of thyroid by lymphocytes and plasma
cells
Immunological disorder- serum thyroid ab.
Hypothyroidism- thyroxine, steroids
Nodule present- FNAC to rule out lymphoma
RIEDEL’S THYROIDITIS

Invasive fibrous thyroiditis- dense fibrous

inflammatory infiltrate throughout the thyroid
extended extracapsular
Rare condition, can mimic malignancy
Tamoxifen, or surgery for pressure sy.
 ACUTE SUPPURATIVE THYROIDITIS

The thyroid can be infected by bacterial or fungal agents

Acute painfully inflammed gland
Needle aspiration- dg. & bacteriology
Appropriate antibiotics
PRIMARY HYPERPARATHYROIDISM
Symptoms: renal lithiasis, osteitis fibrosa cystica,
peptic ulcer, cholelithiasis, weakness, constipation
Lab. tests: elevated serum calcium, serum PH
high, decreased serum phosphorus,
hyperphosphaturia
Radiology: skull XR- ground-glass appearance
Localization: USS, CT, MRI
Surgery- removal of adenoma
DISORDERS OF THE PARATHYROID GLAND
PTH- regulator of calcium metabolism
Acts in conjunction with calcitonin
Serum Ca falls- PTH increases
Serum Ca rises- PTH decreases
Increased PTH secretion:
Hypercalcemia
Hypocalciuria
Hypophosphatemia
hyperphosphaturia
PRIMARY HYPERPARATHYROIDISM
May occur as:
- part of a multiple endocrine adenomatosis syndrome,
- familial hyperparathyroidism,
- ectopic tumor
90% due to a solitary adenoma
10% due to four-gland hyperplasia
1%- due to parathyroid carcinoma
Osteita fibrosa cystica- parathyroid
adenoma
Left parathyroid adenoma
Left parathyroid adenoma
Right parathyroid adenoma
Right parathyroid adenoma
Parathyroid adenoma
Surgical specimen
What is abnormal at this face??
Myasthenia gravis
Motor end-plate in MG
Which organ is involved in the patholopgy
of MG??
Where the thymus is located??
Pneumomediastinography
A.Gh. 65 years old, 3 w. of severe myasthenia, Oss.III
CT-calcified thymoma adherent to the left mediastinal pleura, op.
2003, histology- type A, medullary thymoma without capsular
invasion, chemotherapy CP+PDN, obvious improvement
CT, 60 years old, thymoma+MG, Oss.IV, op. 2002,
Lymphocitic thymoma (type I malignant thymoma)-Masaoka II ( well
encapsulated but microscopic capsular invasion), adhesions to left M.
pleura which was resected
Radiotherapy 44 Gy, chemotherapy, 1 year CP+PDN
Pericarditis and mixedema at 1 year postRxT
Remission of MG for 5 years, 2008- AChE
Different approaches to the
thymus
Position of the patient for thymectomy
Sterile field
Median complete sternotomy
Dissection
Intradermic suture
OP.IAN.2009
Longitudinal incision
Sternotomy
Sternal retracter
Dissection
Dissection
Dissection
Dissection
Dissection
Dissection
Left innominate vein
Mediastinal aspect after tumor resection+pleurectomy
Sternoraphy- 3 metalic wires
Specimen
CT-2009
Presternal fascial closure
Skin sutured
Right eye ptosis