PRESENTER : DR.

MWANGA

SURGICAL ANATOMY
Thyroid gland = shield like
site lower part of the anterior and lateral
sides of the neck.
Gland contains right and left lobe joined by
Isthmus.
Vertebral level C5,6,7,T1.
Each lobe extends from middle of thyroid
cartilage to the 4th or 5th tracheal ring.
Isthmus2nd and 3rd tracheal ring.

Contd
Dimensions lobe -5cms x 2.5cm x2.5cm.
Isthmus 1.5cm x1.5cms.
Weight 20 to 25 grams in adults.
Functional unit is lobule.
Each lobule is supplied by an arteriole.
2 capsules True capsule.
False capsule.

Normal anatomy of the recurrent laryngeal nerve. Note that on the right
side the recurrent laryngeal nerve hooks around behind the subclavian
artery, while on the left side this nerve passes around behind the aortic
arch before ascending in the neck.
B) When there is a vascular anomaly of the right subclavian artery, the r
ecurrent laryngeal nerve no longer "recurs" around this artery but
proceeds from the vagus nerve in a more transverse direction to the
larynx. In such a situation, the nerve is much more likely to be damaged
during operation unless care is taken to visualize its course in the neck.
(From Skandalakis et al,:4 w ith permission.)

BLOOD SUPPLY
1. Superior thyroid artery first anterior branch of
the external carotid artery.its in close relation
with external laryngeal nerve. It divides in to
anterior and posterior branches. Supplies
upper 1/3rd of lobe and upper of isthamus.
2. Inferior thyroid artery branch of thyrocervical
trunck.its terminal part is in close relation with
recurrent laryngeal nerve.supplies lower 2/3rd
of lobe and lower of isthamus.

Venous drainage
Superior thyroid vein drains in to internal
jugular vein or common facial vein.
Middle thyroid vein into internal jugular
vein .
Inferior thyroid vein Lt brachiocephalic
vein.
Thyroid vein of kocher in to internal
jugular vein.

Lymphatic drainage
Upper deep cervical lymph nodes .
Lower deep cervical lymph nodes.
NERVE SUPPLY:
mainly by middle cervical ganglion and
partly from superior and inferior cervical
ganglia.

PHYSIOLOGY

The hormones T3 and T4 are bound to

thyroglobulin within the colloid.
Synthesis within thyroglobulin complex is
controlled by several enzymes in
different steps1. Trapping
2.oxidation
3.coupling
4.Release

THYROID HORMONES
Iodine & tyrosine form both T3 & T4
under TSH stimulation. However, 10%
of T4 production is autonomous and is
present in patients with central
hypothyroidism.
When released into circulation T4
binds to:
Globulin TBG
75%
Prealbumin TBPA
20%

THYROID HORMONES (2)

Less than 1% of T4 & T3 is free in
plasma.
T4 is deiodinated in the tissues to
either T3 (active) or reverse T3
(inactive).
At birth T4 level approximates
maternal level but increases rapidly
during the first week of life.
High TSH in the first 5 days of life can
give false positive neonatal screening

THYROID HORMONES IN SERUM

NAME

SYMBOL

NORMAL RANGE

Total serum
thyroxine

T4

55 150 nmol/I

Total tri
iodothyronine
Free thyroxine

T3

1.2 3.1 nmol/I

t4

8 26 pmol/I

Free triiodothyronine

t3

3 9 pmol/I

THYRIOD FUNCTION TEST

1.
2.
3.
4.
5.
6.
7.
8.

serum T3, T4.

Serum TSH
Serum creatinine
Serum cholesterol
Serum calcitonin
Thyroid autoantibody levels.
Thyroid scintigraphy .
TRH

INVIVO TESTS
1. Radio iodine active uptake test.
2. Thyroid scan.

Thyroid disorders.
1.
2.
3.
4.
5.

Hypothyroidism
Goitres
Hyperthyroidism
Neoplasams of the thyroid .
Thyroiditis .

HYPOTHYROIDISM
ETIOLOGY AND CLASSIFICATION
1. Failure of thyroid development
a. complete- sporadic cretinism.
b.Partial
2.Endemic cretinism
3.Iatrogenic a. After thyroidectomy
b.after radio iodine therapy
c.After pituitary ablation
d.Drug induced eg PAS, Iodide

Contd
4 .Auto immune thyroiditis
a.Non- goitrous[ primary
myxedema ]
b. Goitrous [Hashimoto goitre]
5. Dyshormonogenesis
6.Goitrogens
7.Vascular damage to anterior pituitary.

CRETINISM

MYXOEDEMA
A very advanced form of adult hypothyroidism.
CLINICAL FEATURES
SYMPTOMS 1.Tiredness
2.mental lethargy
3.cold intolerence
4.increase in weight
5.constipation
6. menstrual disturbances

Contd

1.
2.
3.
4.
5.
6.
7.
8.
9.

Signs:
Carpal tunnel syndrome
Slow pulse rate
Dry skin
Dry hair
Cold extremeties
Periorbital puffiness
Hoarse voice
Slow movements
Sluggish ankle jerk

Cont.

1.
2.
3.

Investigations:
Serum T4 levels below 55 nmol/l
Free T4 8 pmol/l
Radioiodine studies shows reduced
thyroid uptake and increased renal
excretion- less than 12% at 24 hours is
diagnostic
4. ECG T wave flattened or inverted
5. TSH raised

Treatment:
L-thyroxine is curative
A dose of 0.15 -0.2 mg/day
In elderly patients with Myocardial
insufficiency the initial dose should be as
low as 0.05 mg per day.
If rapid or short lived response is essential,
then triiodothyronine is used

GOITRE
ENLARGED THYROID GLAND
Classifications of goitre
1. SIMPLE GOITRE (EUTHYROID)
Diffuse hyperplastic goitre
Nodular goitre
Colloid goitre
Iron deficiency goitre
Multinodular goitre

Cont.
2. TOXIC GOITRE
Diffuse toxic goitre (Graves disease)
Toxic nodular goitre
Toxic nodule
Secondary thyrotoxicosis in MNG
3. NEOPLASTIC GOITRE (BENIGN &
MALIGNANT)

CLASSIFICATION OF THYROID NEOPLASM

BENIGN

FOLLICULAR ADENOMA

NEOPLASMS
MALIGNANT

METASTATIC
(BLOOD BORNE)
SECONDARY
LOCAL INFILTRATION
PRIMARY

CARCINOMA

DIFFERRENTIATED

PAPILLARY

MALIGNANT LYMPHOMA

UNDIFFERENTIATED
(ANAPLASTIC)

FOLLICULAR

MEDULLARY CA

4. INFLAMMATORY GOITRE
Autoimmune
Chronic lymphocytic thyroiditis
Hashimotos disease

Granulomatous
De- Quervains thyroiditis
Fibrosing
Riedels thyroiditis

Infective
Acute
Chronic

Others
Amyloid

SIMPLE GOITRE
-Due to hyper stimulation of thyroid gland by anterior
pitutary

1.

Aeitiology
Iodine deficiency
-daily iodine requirement is 100-125 mcg
-low iodine areas
-goitrogenic area
-failure of intestinal absorption
2. Defects in synthesis of thyroid hormone
-enzyme deficiency within thyroid gland
-goitrogens:- vegetables of brassica family e.g.
cabbage, kale, rap

STAGES IN GOITRE FORMATION

1.

2.

3.
4.
5.

Due to fluctuating TSH level a mixed pattern develops

(active and inactive lobules)
Active lobules become more vascular and hyperplastic
until haemorrhage occurs causing central necrosis and
leaving only a surrounding ring of active follicles
Necrotic lobules coalesce to form nodules.
Persistent TSH stimulation causes diffuse hyperplasia
and it is reversible if TSH stimulation ceases
Continual repetition of this process results in nodular
goitre

Apart from TSH Growth stimulating immunoglobulin is also

responsible for this process

COLLOID GOITRE-SMOOTH SURFACE AND ROUND BORDERS

DIFFUSE HYPERPLASTIC GOITRE

Children are affected in endemic areas
Sporadic cases in puberty where
metabolic demands are high
Stress and pregnancy
If TSH stimulation ceases the goitre may regress

TREATMENT
L-thyroxine is given in maximum doses
0.2mg/day for several months and then
very slowly tail off to 0.1mg/day which
should be continued for many years
Surgery indicated for cosmetic reasons,
pressure symptoms and no response for
medical treatment
Prevention fortified salt

Multinodular goitre
Is the end stage result of diffuse
hyperplastic goitre
Aetiopathogenesis
-Puberty goitre
-Pregnancy goitre
-Iodine deficiency goitre
All these 3 types of goitres if left untreatred
will change into multinodular goitre

PUBERTY

GENETIC FACTORS

GOITROGENS

IODINE DEFICIENCY

LOW LEVELS OF T3 AND

T4

Feed back mechanism

TSH STIMULATION

DIFFUSED HYPERPLASIA

MIXED PATTERN

NECROSED FOLLICLES

MULTINODULAR GOITRE
After a few years
MALIGNANCY

TOXIC MULTINODULAR GOITRE

Clinical features and diagnosis

Common in females
Female : male ratio is 10:1
Age group is 20-40
Long duration of swelling in front of the neck
Dyspnoea, dysphagia
Gland is nodular, firm
Hard areas- calcification; soft areas- necrosis
Sudden increase in size with pain-haemorrhage
The most common site of a nodule is at the junction of
isthmus with one lobe

Investigations

Thyroid profile
X-ray of the neck
-

AP and lateral view

Calcifications
Deviation of trachea
To rule out retrosternal extension-soft tissue

Isotope scan
- can demonstrate 3 patterns:
a) Hot nodule- glands no uptake, nodule takes
b) Warm nodule- entire gland takes up isotope e.g typical of
Graves disease
c) Cold nodule-nodules doesnt take up isotope

Only 10% of the cold nodules are malignant

Ultrasound scan
FNAC

PEMBERTONS SIGN

TOXIC GOITRE
(thyrotoxicosis)
DEFINITION:
Its a complex disorders which occurs due
to increased levels of thyroid hormones
and manifests clinically with various signs
and symptoms involving many body
systems.

CLINICAL TYPES
Diffuse toxic goitre - Graves diseaseprimary thyrotoxicosis
Toxic nodular goitre- secondary
thyrotoxicosis
Toxic nodule
others

GRAVES DISEASE

1.

2.
3.
4.
5.

The exact aetiopathogenesis is not known but

some positive aetiological factors
Autoimmune disorder-abnormal thyroid
stimulating antibodies
Familial
Thyroid stimulating immuoglobulins and long
acting thyroid stimulators
Exopthalmos- opthalmopathy
Female, emotions, stress, young age

PATHOLOGY
As a result of continous stimulation acinar
hypertrophy and hyperplasia takes place.
Acinar cells which are usually flat
becomes tall columnar. The normal colloid
disappears and the cells are empty
however, rich vascularity is seen.
Thus, small follicles with hyperplastic columnar
epithelium is characteristic.

CLINICAL FEATURES
Primary thyrotoxicosis is more common in
females than males
Age: 15- 25 yrs
Loss of weight inspite of good apetite
Diarrhoea occurs due to smooth muscle
activity of small intestine
Intolerance to heat
Preference to cold

Cont.

Fine tremors
Excitability
Excessive sweating
Oligomenorrhoea free steroid hormones
level decrease in graves disease, this
results in decreased effective estrogen at
the cellular level which in turn causes
oligomenorrhoea

GRAVES DISEASE

SIGNS

Uniformly enlarged thyroid gland

Smooth surface, no nodules
Gland is soft or firm in consistency
It is warm- highly vascular
Auscultation a bruit is usually heard

Cont.
CNS signs
tremors of the tongue and the tongue is
within the oral cavity
- tremors of the outstretched hand
- extensors are weak compared to flexors
- always a moist warm hand (shake hand
and see)

CVS signs:
Pulse rate is always raised and rapid
indicating tachycardia
Depending upon the pulse rate
thyrotoxicosis is classified as follows:
Mild- 90 100/ min
Moderate 100 110/min
Severe - >110/min
Palpitations and extra systoles
Fibrillations and cardiac failure are rare

EYE SIGNS:
Prominent eyeballs-proptosis and lid retraction
result in exophthalmos
Lid spasms
Classical stare
Sclera is visible beyond limbus
Typically seen in Graves disease
Rare in secondary thyrotoxicosis
In late stages optic nerve damage and blindness
can occur

SEVERE GRAVES OPTHALMOPATHY

THYROTOXIC MYOPATHY
Mild weakness of proximal limb muscles in
common difficulty in climbing steps do
occur
Weakness of extraocular muscles results
in double vision (Diplopia)
Myopathy responds to antithyroid
treatment
Features suggestive of myasthenia gravis
and periodic paralysis can be found

SKIN CHANGES

Pretibial myxoedema- non pitting

Pruritis
Palmar erythema
Thinning of hair
Skin is dry and course
Thyroid acropachy

WAYNES CLINICAL DIAGNOSTIC INDEX

Symptom score + sign score = diagnostic
index
INDEX-UNDER 11 = non toxic
11 19 = Equivocal
> 19 is toxic

INVESTIGATIONS
Routine inv- CCP, RBG,FBG, postprandial Blood sugar, urinalysis, CXR,
neck xray, indirect laryngoscopy
Serum T3, T4 are high and TSH is low
Thyroid antibodies are elevated
Sleeping PR remains high
Thyroid scan will show warm gland

OF PRIMARY THYROTOXICOSIS
AIMS OF TREATMENT
1. To reduce the functioning thyroid mass
to a very critical level (about 6-8 gms of
thyroid tissues)
2. To minimize complications

To restore the patient to euthyroid state:

DRUGS

DOSE

PRECAUTION & SIDE

EFFECT

Carbimazole

10 mg 6 hrly
*M-10mg 2-3/day

Takes 2-3 wks for its

action

Propranolol

10-20 mg BD / TDS

CCF,Bronchial asthma

Lugols iodine

10-20 drops TDS 10

days before surgery

Bitter taste, to be used

with orange juice

Potassium
perchlorate

200 mg TDS
* M 200-400 mg OD

Propyl thiouracil 200 mg TDS

*M- maintanance

PLEASE NOTE
Iodine containing anti-arrhythmic drug
AMIODARONE may worsen
thyrotoxicosis.
Propyl thiouracil is safe in pregnancy with
Graves disease.
Role of Lugols iodine is doubtful.

TO REDUCE THE FUNCTIONING

THYROID MASS
Subtotal thyroidectomy
Radio iodine therapy

TO MINIMISE COMPLICATIONS
Good pre-op preparation

ANTITHYROID DRUGS
ADVANTAGES:
No surgery
No radio active materials
DISADVANTAGES:
Treatment is prolonged
failure rate is 50%
Some goitres become vascular and
enlarge
rarely dangerous drug reactions

SURGERY
ADVANTAGES
Goitre is removed
cure is rapid
cure rate is high with adequate surgery
DISADVANTAGES
Recurrence of thyrotoxicosis in < 5%
Post op thyroid insufficiency in 20 -45%
parathyroid insufficiency < 0.5%
nerve injury (ELN , RLN)

surgery
1.
2.
3.
4.
5.
6.

Hemi thyroidectomy
Total thyroidectomy
Near total thyroidectomy
Subtotal thyroidectomy
Lobectomy
Isthumusectomy

complications
1.
2.
3.
4.
5.
6.
7.
8.
9.

Haemorrage
Respiratory obstruction
Recurrent laryngeal nerve paralysis
Thyroid insufficiency
Parathyroid insuficiency
Throtoxic storm
Wound infection
Keloid scar
Stitch granuloma

Post op follow up
1.indirect laryngoscopy
Serum calcitonin at 6 wks
Observation every 6 months for
recurrence

RADIO IODINE
ADVANTAGE:
No surgery
no prolonged drug therapy
DISADVANTAGE:
unavailability
thyroid insufficiency-70-80% after 10yrs
an indefinite follow up is essential

CHOICE OF THERAPY
Diffused toxic goitre
over 45yrs-radioiodine
under 45 yrs surgery for large goitre
drugs for small goitre
Toxic nodular goitre surgery
Toxic nodule surgery is mainstay radioiodine
for >45yrs
Recurrent thyrotoxicosis after adequate surgery:
> 45 yrsradioiodine, <45 yrs drugs
Failure of previous Rx with antithyroid drug or
radio iodine surgery or thyroid ablation

CLASSIFICATION OF THYROID NEOPLASM

BENIGN

FOLLICULAR ADENOMA

NEOPLASMS
MALIGNANT

METASTATIC
(BLOOD BORNE)
SECONDARY
LOCAL INFILTRATION
PRIMARY

CARCINOMA

DIFFERRENTIATED

PAPILLARY

MALIGNANT LYMPHOMA

UNDIFFERENTIATED
(ANAPLASTIC)

FOLLICULAR

MEDULLARY CA

SUMMARY OF MALIGNANT TUMOUR OF THYROID GLAND

PAPILLARY

FOLLICULAR

ANAPLASTIC

MEDULLARY

Etiology

Irradiation

Endemic goitre

Unknown

Sporadic or
familial

Incidence

60%

17%

13%

6%

Age

20-40

30-50

>50

Middle age

Dx

Thyroid swelling Thyroid swelling

with LN
with metastasisbone

Thyroid
swelling, local
fixity, stridor

Difficult to Dx
clinically

Microscop Orphan Annieic

eyed nuclei,
psammoma
bodies

Angioinvasion,
capsular invasion

Poorly
differentiated
cells

Amyloid
stroma-like
carcinoid

Spread

Blood

Local
infiltration

Lymphatic,
blood

Lymphatic

PAPILLARY

FOLLICULAR

ANAPLASTIC

MEDULLARY

Invx

FNAC

FROZEN
SECTION

FNAC,
BIOPSY

FNAC,
CALCITONIN

Rx of
1O

NEAR TOTAL NEAR TOTAL

ISTHMUSECT
THYROIDECT THYROIDECTO OMY,EXT. RT
OMY
MY

TOTAL
THYROIDECTO
MY

Rx of
mets

FUNCTIONAL I 131 OR EXT RT

BLOCK
DISSECTION

PALLIATIVE
EXT. RT

RADICAL
BLOCK
DISSECTION

TSH
YES
depende
nce

YES

NO

NO

Hormon VERY RARE

al prod

VERY RARE

NO

CALCITONIN,
5-HT, ACTH

Px

GOOD

WORST

BAD

EXCELLENT

FOLLICULAR NEOPLASM

PAPILLARY CA PRESENTING AS SOLITARY NODULE

PAPILLARY CARCINOMA

PAPILLARY CARCINOMA WITH HUGE LYMPH NODE SECONDARIES

ULCERATED SECONDARIES IN THE SCALP BONE FROM

FOLLICULAR CARCINOMA THYROID

SECONDARY IN THE LEFT SECOND RIB-OCCULT

FOLLICULAR CARCINOMA

SECONDARY DEPOSIT IN THE STERNUM IN A

PATIENT WHO UNDERWENT NEAR TOTAL
THYROIDECTOMY FOR FOLLICULAR CARCINOMA 5
YEARS AGO

Based on BIOLOGICAL AGGRESIVENESS, 2 RISK groups:

Low Risk:
(F) < 50, (M) < 40 years
Papillary Ca, Follicular Ca (cytologically suspicious)
Tumour < 1.5 -2 cm, confined to one lobe, no metastases
SURGERY: LOBECTOMY
? Near total THYROIDECTOMY
Prognosis: Lobectomy ? Higher recurrence
No significant advantage in survival compared to TT
High Risk:
Age: (F) > 50, (M) > 40 years
Larger, bilateral tumours or metastases
Papillary Ca (extrathyroidal)
Follicular Ca (widely invasive)
Medullary Ca
SURGERY: TOTAL THYROIDECTOMY
? Near total THYROIDECTOMY
+Lymphnode excision of central nodes
+Modified radical neck dissection

LOW RISK
1.8% Mortality Rate

Men under 41 and Women under 51

without distant metastases
All men over 41 and women over 51 with:
Intra-thyroidal papillary cancer (papillary cancer confined
present only within the thyroid gland) OR follicular
cancer tumor with minor capsular involvement
(the tumor slightly extends into the capsule which
surrounds it) AND
Primary tumor less than 5 cm in diameter AND
No distant metastases

PROGNOSIS

HIGH RISK
46% Mortality Rate

All patients with distant metastases

All men over 41 and women over 51 with:

Extra-thyroidal papillary cancer (extends beyond the
thyroid gland) OR follicular cancer tumor with
major capsular involvement (the tumor extends
significantly into the capsule which surrounds it)
AND/OR
Primary cancer is 5 cm in diameter or larger, regardless
of the extent of the disease