GOITRE

HU Naaya
Professor of Surgery/Consultant Surgeon
University of Maiduguri/University of Maiduguri Teaching Hospital
 PRE-TEST
Probably the most reliable current laboratory test in suspected

hyperthyroidism is:

a) Serum T3 concentration

b) T3 resin uptake

c) Serum T4

d) Serum free thyroxine.

e) Free T4 index
 PRE-TEST

The most sensitive test of hypothyroidism is:

a) Free T4 index

b) Serum thyroid stimulating hormone.

c) Test of hypothalamic-pituitary axis

d) Protein bound iodine

e) Serum T3 concentration
 PRE-TEST
In thyroid scan:

a) If radioactive technetium is used, the scan is done at 30 minutes

b) If radioactive iodine is used the scan is done at 12 h

c) A cold (non-functioning) nodule may be an adenoma, a cyst or a

malignant tumour.

d) A nodule with most of the isotope concentrated in it is toxic or

autonomous

e) A nodular goiter has the isotope concentrated in the nodules

 INTRODUCTION

• Diseases of the thyroid gland invariably leads to enlargement of the

gland.

• The term GOITER is applied to any enlargement of the thyroid gland

regardless of the cause.

 INTRODUCTION
• The normal thyroid gland is impalpable. The term goitre (from the
Latin guttur = the throat) is used to describe generalised enlargement
of the thyroid gland.

• A discrete swelling (nodule) in one lobe with no palpable abnormality

elsewhere is termed an isolated (or solitary) swelling.

• Discrete swellings with evidence of abnormality elsewhere in the

gland are termed dominant nodule.
 ANATOMY
 Blood supply:

• Superior and inferior thyroid arteries.

• Superior, middle and inferior thyroid

veins.

 Lymphatic drainage:

• Upper & lower deep cervical lymph

node

• Pretracheal and paratracheal

• lymph node

 Nerve supply:
• Middle cervical ganglion

• Superior and inferior cervical ganglia

 HISTOLOGY
 2 types of cells :
• follicular & parafollicular.
 The follicular cells secrete T3 &
T4.
 T3 & T4 binds with glycoproteins
to form the thyroglobulin
(colloid).
 Most of the thyroid follicles are
full of stored Thyroglobulin
(colloid).
 Parafollicular cells/clear (C) cells
are found among the follicular
cells.
 They pale staining cells with a
granular cytoplasm.
 Unlike follicular cells, they are
not exposed to the follicular
lumen.
 They secrete Calcitonin which
help
• regulating blood calcium levels.
 HISTOLOGY

PARAFOLLICULAR CELLS

FOLLICULAR CELLS

HIGH POWER X45

HISTOLOGY
PHYSIOLOGY
 PHYSIOLOGY
• SECRETION OF THYROID HORMONES
• THYROXINE – 93%
• TRIIODOTHYRONINE – 7%

• FUNCTIONAL ANATOMY OF THYROID

• EACH FOLLICLE CONSISTS WHICH IS COMPOSED OF THYROGLOBULIN
• THE THYROGLOBULIN IS SECRETED INTO THE
• FOLLICLE BY THE CUBOIDAL EPITHELIAL CELLS
• THE BLOOD SUPPLY IS FIVE TIMES THE WEIGHT OF GLAND EACH MINUTE.

• SECRETION OF PARAFOLLICULAR CELLS

• Parafollicular cells (C CELL) SECRETE CALCITONIN
 FUNCTIONS OF THYROID HORMONES
•Regulation of basal metabolic rate
•Required for normal psychosomatic growth
• Has chronotropic & ionotropic effect on the heart
• Increases the sensitivity of receptors to catecholamines
& also increases the number of receptors
•Required for normal respiratory drive
•Required for normal haematopoiesis
• Thyroxine has opposite effect of insulin
•Increases the bone turnover
 PHYSIOLOGIC EFFECTS OF CALCITONIN

• Bone: Calcitonin suppresses resorption of bone by inhibiting the

activity of osteoclasts, a cell type that "digests" bone matrix, releasing
calcium and phosphorus into blood.
• Kidney: Calcium and phosphorus are prevented from being lost in
urine by reabsorption in the kidney tubules.
• Calcitonin inhibits tubular reabsorption of these two ions, leading to
increased rates of their loss in urine.
 Causes of thyroid disease

inflammatory toxic autoimmune simple neoplastic

Acute Physiological
Primary Hashimoto Benign
Subacute Colloidal
secondary Reidel thyroiditis malignant
chronic nodular
 CLASSIFICATION OF GOITRES
• Simple (Non-toxic) goitre (Endemic/sporadic)
• Diffuse colloid (or hyperplastic) goitre
• Nodular goitre
• Toxic goitre
• Diffuse toxic goitre (Grave’s disease)
• Toxic nodular goitre
• Toxic nodule
• Rarely toxic malignant tumour
• Neoplastic goitre
• Benign
• Malignant
 CLASSIFICATION OF GOITRES
• Inflammatory
• Autoimmune thyroiditis (Hashimoto’s disease)
• Acute suppurative thyroiditis
• Subacute thyroiditis
• Riedel’s thyroiditis
• Specific infective thyroiditis (e.g., tuberculosis)
 causes
• Iodine deficiency

• Dyshormonogenesis

• Goitrogens

• Neoplasia

• Inflammations
DIFFUSE GOITRE
 SOLTARY THYROID NODULE
•
MULTINODULAR GOITRE
 MULTINODULAR GOITRE
Multinodular goitre
 GRAVE’S DISEASE
• Grave’s
 PATHOPHYSIOLOGY

• Chronic absence of T4/T3 causes elevated level of TSH, which then

leads to diffuse homogenous hypertrophy and hyperplasia of
follicular cells and colloid (secretory follicles) in efforts to produces
more thyroid hormones.

• This is usually a reversible change.

• The enlarged thyroid hyper involuted with colloid is called colloid

goiter.
 PATHOPHYSIOLOGY
• Differential response to TSH leads to formation of nodules within the
gland.

• Several nodules may coalesce and lead to formation of multinodular

goitre.

• The nodules may undergo secondary changes; central necrosis, cystic

degeneration, haemorrhage, calcification and malignant changes
(3%).
 CLINICAL FEATURES
• Gradual onset of painless anterior neck swelling, usually long
standing in endemically iodine deficient areas.
• Recent onset of pain or increase in size may indicate secondary
changes.
• The enlarged gland may also affect neighbouring structures and lead
to wide range of symptoms and signs.
• Obstruction of airways, Oesophageal obstruction
• Laryngeal nerve compression
• Neck veins obstruction
 CLINICAL FEATURES

• Superior vena cava syndrome (Pemberton’s sign).

• Local compression causing dysphagia, dyspnea, stridor, plethora, or

hoarseness

• Pain due to haemorrhage, inflammation, necrosis, or malignant

transformation

• Signs and symptoms of hyperthyroidism or hypothyroidism

• Thyroid cancer with or without metastases

 INVESTIGATIONS OF GOITRES

• Thyroid function test

• thyroxine (T4),

• tri iodothyronine (T3),

• thyroid stimulating hormones (TSH)

• thyrotropin releasing hormone (TRH).

• This helps to know if the thyroid gland is normally, hyper or hypo

functioning.
 INVESTIGATIONS

• Thyroid scan with radioactive iodine (I123 or I131)

• In this investigation a traceable radioactive Iodine or Technetium is injected into the blood
stream, the thyroid gland concentrates radioactive iodine.

• The concentrated radioactive iodine can be detected by gamma camera.

• I123 has a shorter half life as compared to I131 and therefore preferred because it has less
exposure of the patient to radiation.

• Thyroid scan may show hot nodules (which takes more radioactive iodine than the rest of
gland) in secondary hyperthyroidism, however most simple goiters have normal uptake or
Cold nodules (which does not take radioactive iodine).

• Cold nodules are likely to be malignant.

INVESTIGATIONS
 INVESTIGATIONS

• Antithyroid receptors antibodies

• This type of investigation is done in patients suspected to have

stimulatory auto antibodies as is the case in Grave’s disease (primary
hyperthyroidism).
 INVESTIGATIONS

• Radiological investigations

• Normal AP and lateral chest X-

rays may demonstrate

retrosternal extension of the

goiter (retrosternal shadow)

 INVESTIGATIONS
• USG NECK
• Thyroid is homogeneous & slightly hyperechoic.
 INVESTIGATIONS
• The normal thyroid gland is 2 cm or less in both the transverse dimension and
depth, and is 4.5–5.5 cm in length& 0.5 mm isthmus.
 INVESTIGATIONS
• A diffusely enlarged thyroid gland with an isthmus width of 1.5 cm.
 INVESTIGATIONS
• Fine needle aspiration cytology
• To rule out malignancy of thyroid.
• Benign,
• Malignant,
• Suspicious malignant,
• Inconclusive or inadequate aspirate.

• If follicular pattern is seen, lobectomy is done to exclude follicular

carcinoma, because the can only be differentiated by demonstrating
capsular invasion.
 TREATMENT AND PREVENTION OF SIMPLE GOITRE

• Dietary

• Iodine supplementation in iodine deficient areas, food iodine

fortification is one of the best preventive measures of goitre.

• Medical

• Thyroxin supplementation

• In patients with diffuse hyperplastic goitre for several months (0.1 to

0.2mg per day).
 SURGERY INDICATIONS
• In patients with obstructive symptoms,

• When malignancy is suspected clinically or after FNAC,

• Hyper functioning nodules

• For cosmetic reasons

 HYPOTHYROIDSM

• Hypothyroidism is a condition characterized by abnormally low

thyroid hormone production.

• Because thyroid hormone affects growth, development, and many

cellular processes, inadequate thyroid hormone has widespread
consequences for the body.
 AETIOLOGY

• Medications and food (GOITROGENS)

• Pituitary or hypothalamic disease

• Severe iodine deficiency

• Thyroid destruction (from radioactive iodine or surgery)

• Hashimoto's thyroiditis

• Lymphocytic thyroiditis (which may occur after hyperthyroidism)

 GOITROGENS

DRUGS FOOD

• Anti-thyroid • Soybeans
• Cough medicines • Millet
• Sulfonamides • Cassava
• Lithium • Cabbage
• Phenylbutazone • Excess iodine or lithium
• PAS ingestion, which decrease
• iodine release of thyroid hormone
• Oral hypoglycemic agents
 HASHIMOTO'S THYROIDITIS

• In this condition, the thyroid gland is usually enlarged (goiter) and

has a decreased ability to make thyroid hormones.

• Hashimoto's is an autoimmune disease in which the body's immune

system inappropriately attacks the thyroid tissue.

• Hashimoto's is 5 to 10 times more common in women than in men

 HASHIMOTO’S THYROIDITIS

• Increased antibodies to the enzyme, thyroid peroxidase (anti-TPO

antibodies).

• Patient with Hashimoto's thyroiditis has one or more other

autoimmune diseases such as diabetes or pernicious anemia

• Hashimoto's can be identified by detecting anti-TPO antibodies in the

blood
 THYROID DESTRUCTION SECONDARY TO RADIOACTIVE
IODINE OR SURGERY

• The likelihood of this depends on a number of factors including the dose

of iodine given, along with the size and the activity of the thyroid gland.

• If there is no significant activity of the thyroid gland six months after the
radioactive iodine treatment, it is usually assumed that the thyroid will
no longer function adequately. The result is hypothyroidism.

• Similarly, removal of the thyroid gland during surgery will be followed by

hypothyroidism.
 PITUITARY OR HYPOTHALAMIC DISEASE

• If for some reason the pituitary gland or the hypothalamus are unable to
signal the thyroid and instruct it to produce thyroid hormones, a decreased
level of circulating T4 and T3 may result, even if the thyroid gland itself is
normal.

• If this defect is caused by pituitary disease, the condition is called "secondary

hypothyroidism."

• If the defect is due to hypothalamic disease, it is called "tertiary

hypothyroidism."
 PITUITARY INJURY

• A pituitary injury may result after brain surgery or if there has been a
decrease of blood supply to the area. In these cases of pituitary injury,
the TSH that is produced by the pituitary gland is deficient and blood
levels of TSH are low.
• Hypothyroidism results because the thyroid gland is no longer stimulated
by the pituitary TSH. This form of hypothyroidism can, therefore, be
distinguished from hypothyroidism that is caused by thyroid gland
disease, in which the TSH level becomes elevated as the pituitary gland
attempts to encourage thyroid hormone production by stimulating the
thyroid gland with more TSH.
 SEVERE IODINE DEFICIENCY:

• In areas of the world where there is an iodine deficiency in the diet,

severe hypothyroidism can be seen in 5% to 15% of the population.
 SYMPTOMS OF HYPOTHYROIDISM
• The symptoms of hypothyroidism are often subtle. They are not
specific (which means they can mimic the symptoms of many other
conditions) and are often attributed to aging.

• Patients with mild hypothyroidism may have no signs or symptoms.

• The symptoms generally become more obvious as the condition

worsens and the majority of these complaints are related to a
metabolic slowing of the body.
 COMMON SYMPTOMS

• Fatigue • Dry skin

• Depression • Muscle cramps

• Modest weight gain • Increased cholesterol levels

• Cold intolerance • Decreased

• Excessive sleepiness concentration

• Dry, coarse hair • Vague aches and pains

• Constipation • Swelling of the legs

 COMMON SYMPTOMS

• As the disease becomes more severe, there may be puffiness around

the eyes, a slowing of the heart rate, a drop in body temperature,
and heart failure.

• In its most profound form, severe hypothyroidism may lead to a life-

threatening coma (myxoedema coma).

• In a severely hypothyroid individual, a myxoedema coma tends to be

triggered by severe illness, surgery, stress, or traumatic injury.
HYPOTHYROIDISM
 DIAGNOSIS OF HYPOTHYROIDISM

• A diagnosis of hypothyroidism can be suspected in patients with

fatigue, cold intolerance, constipation, and dry, flaky skin.

• A blood test is needed to confirm the diagnosis.

• When hypothyroidism is present, the blood levels of thyroid

hormones can be measured directly and are usually decreased.

• However, in early hypothyroidism, the level of thyroid hormones (T3

and T4) may be normal.
 DIAGNOSIS OF HYPOTHYROIDISM

• Thyroid stimulating hormone (TSH) assays are the most sensitive screening
tool for primary hypothyroidism.
• The generally accepted reference range for normal serum TSH is 0.40 – 4.2
mlU/L.
• If the levels are above the reference range then the next step is to
measure free Thyroxine (T4).
• Patients with primary hypothyroidism usually have elevated TSH levels and
decreased free hormone levels.
• In patients with hypothalamic or pituitary dysfunction, TSH levels do not
increase in appropriate relation to the low free T4 levels
 TREATMENT OF HYPOTHYROIDISM

• Treatment of hypothyroidism requires life-long levothyroxine (T4) therapy.

• This is a more stable form of thyroid hormone andrequires once a day

dosing, whereas T3 is much shorter-acting and needs to be taken multiple
times a day.

• Synthetic T4 is readily and steadily converted to T3 naturally in the

bloodstream,

• 100 to 150 micrograms per day

 CRETINISM
• Hypothyroidism developing in infancy/early childhood

• Severe mental retardation occurs in iodine deficient areas of world

(i.e., Himalayas, inland China, Africa)

• May also be sporadic, owing to enzyme deficiencies of thyroid

hormone synthesis
 CRETINISM
• Clinical features:
• Impaired skeletal development
• Impaired CNS development
• Inadequate maternal thyroid hormone prior to foetal thyroid gland
formation
• SEVERE mental retardation
• Normal brain development if maternal thyroid deficiency occurs after
foetal thyroid gland development
CRETINISM
 TOXIC GOITRE, THYROTOXICOSIS OR
HYPERTHYROIDISM
• Hyperthyroidism is a condition in which an overactive thyroid gland is
producing an excessive amount of thyroid hormones that circulate in the
blood.

• Thyrotoxicosis is a toxic condition that is caused by an excess of thyroid

hormones from any cause.

• Thyrotoxicosis can be caused by an excessive intake of thyroid hormone or

by overproduction of thyroid hormones by the thyroid gland.

• Hyperthyroidism can be primary or secondary depending on the aetiology.

 CAUSES OF HYPERTHYROIDISM
• Graves' Disease

• Functioning adenoma ("hot nodule") and toxic multinodular goiter

(TMNG)

• Excessive intake of thyroid hormones

• Abnormal secretion of TSH

• Thyroiditis (inflammation of the thyroid gland)

• Excessive iodine intake

 PRIMARY HYPERTHYROIDISM GRAVE’S DISEASE

• Graves’s disease is an autoimmune disease of the thyroid gland, in which

there is a circulating autoantibody which resembles TSH.

• The autoantibody binds to and stimulates g-protein coupled thyrotropin

receptors on thyroid gland leading to thyroid hormone release and
hyperplasia.

• These antibodies include

• Thyroid stimulating immunoglobulin (TSI antibodies),

• Thyroid peroxidase antibodies (TPO), and

• TSH receptor antibodies

 PRIMARY HYPERTHYROIDISM GRAVE’S DISEASE

• Graves' disease is hereditary and is up to five times more common

among women than men

• Female: male ratio is 9:1

• Grave’s disease tends to affect young than older women

• It causes about two third of all cases of hyperthyroidism

• These antibodies also react with retrobulbar auto antigens to cause

periorbital oedema and protrusion of eye ball (exophthalmos).
 THE TRIGGERS FOR GRAVE'S DISEASE INCLUDE:

• Stress,

• Smoking,

• Radiation to the neck,

• Medications,

• Infectious organisms such as viruses.

 SECONDARY HYPERTHYROIDISM

• In patients with secondary hyperthyroidism, there is a pre existing

thyroid pathology for example goitre or inflammatory condition

which leads to excess production of thyroid hormones or there is an

extra thyroid source of hormone production.

• Secondary hyperthyroidism has high predilection to involve

cardiovascular system
 MULTINODULAR GOITER

• In this form of secondary hyperthyroidism, there is hypersecreting

toxic nodule in the background of multinodular goitre (Plummer’s
disease);

• This tends to occur in iodine deficient areas (endemic goitres).

 TOXIC ADENOMA

• This form of secondary hyperthyroidism is characterized by presence

of benign glandular nodule in the thyroid gland, usually follicular

which secrets excess hormones.

 ECTOPIC THYROID HORMONE
• In this form of secondary hyperthyroidism, there is a hormone
producing tumor elsewhere in the body.

• For example metastatic follicular thyroid carcinoma, choriocarcinoma

which produces β-hCG whose alpha chain resembles TSH and thyroid
tissue containing teratoma.

• The excess thyroid hormones lead to clinical features typical of

hyperthyroidism.
 EXOGENOUS CAUSES

• In this form, excess hormone has been introduced into the body.

• An example is what is called thyrotoxicosis factitious which is due to

excess intake of thyroxine hormone and Jod-Basedow which is
caused by excessive intake of iodine in endemic goitre.
 TSH PRODUCING PITUITARY ADENOMA

• This is another cause of excess thyroid hormone production; an adenoma

in the pituitary gland (which normally controls the thyroid gland)
produces TSH which in turn leads to excess T4 and T3.
 OTHER CAUSES

• Post viral thyroiditis with transient self limiting thyrotoxicosis

(Subacute de Quervain’ thyroiditis); this form of hyperthyroidism is
usually painful and may be associated with other systemic symptoms.

• Radiation induced thyroiditis with release of preformed thyroid

hormones is commonly seen in patients undergoing neck radiation
 THYROIDITIS

• Inflammation of the thyroid gland may occur after a viral illness (Subacute
thyroiditis).

• This condition is associated with a fever and a sore throat that is often painful
on swallowing.

• The thyroid gland is also tender to touch.

• There may be generalized neck aches and pains.

• Inflammation of the gland with an accumulation of white blood cells known as

lymphocytes (lymphocytic thyroiditis) may also occur.
 CLINICAL FEATURES OF HYPERTHYROIDISM

• Central nervous system

• Central nervous system features are very common in patients with

primary thyrotoxicosis.

• Tremors which can be observed on the tongue and fingers,

• Nervousness,

• Emotional liability (patients become irritated easily), they may also

be lethargic or agitated and usually they have warm and moist hands.
 INCREASED METABOLIC RATE

• Weight loss,

• Heat intolerance,

• Excessive sweating, and

• Tiredness cause by muscle weakness as a result of proteolysis.

 CARDIOVASCULAR

• Very common in patients with secondary hyperthyroidism.

• They include:
• Awareness of heart beats (palpitation) due to tonic and chronic effect of
excess thyroid hormones,
• Irregular heartbeats (arrhythmia),

• Sleeping tachycardia,

• High output heart failure and

• Thyroid bruit due to excess blood flow to the gland.

GASTRO INTESTINAL TRACT (GIT);

• Loss of body weight despite having good or increased appetite, and

Increase bowel motions (diarrhoea).

 GENITAL URINARY TRACT (GUT)

• Irregular menstruation,

• Amenorrhea,

• Loss of libido and

• Erectile dysfunctions
 OPHTHALMOLOGICAL FEATURES

• Eye symptoms as is the case for central nervous system are common in
Grave’s disease.

• Eye protrusion or exophthalmos can be true when it is caused by

retrobulbar cellular infiltration and mucopolysaccharide depositions or
false exophthalmos when it is caused by elevation of superior eye lid
due to hyper activity of levator pulpebral superioris muscle or Muller
muscle.

• The later is caused by increased sympathetic tone.

 TRUE EXOPHTHALMOS :

• Protrusion of the eyeballs.

• It is an autoimmune disease =>

Infiltration of retro bulbar tissue

with inflammatory cells &
accumulation of fluids and
mucopolysaccharides.
 EYE SIGNS
1. Stellwag's sign :
• Staring look with infrequent blinking.

2. Dalrymple's sign :
•Rim of sclera is seen between
cornea and the upper lid.

3. Von graef's sign :

• Lagging of the upper eye lid

4. Joffroy's sign :
•Loss of forehead corrugation when looking up

5. Moebius' sign :
• Lack of convergence (due to ocular myopathy )
 EYE SIGNS

• Exophthalmos can lead to

• Exposure conjunctivitis,

• Keratitis (corneal ulceration) and

• Perforation.

• Ophthalmoplegia or eye paralysis can be caused by cellular infiltration.

• Ophthalmoplegia can be bilateral or unilateral and can be associated

with diplopia (double vision).
 GRAVE’S OPTHALMOPATHY

• Class 0 — No symptoms or signs

• Class I — Only signs, no symptoms

• (e.g., lid retraction, stare, lid lag)

• Class II — Soft tissue involvement

• Class III — Proptosis

• Class IV — Extraocular muscle involvement

• Class V — Corneal involvement

• Class VI — Sight loss (optic nerve involvement)

 CONTRAST BETWEEN PRIMARY AND SECONDARY
HYPERTHYROIDISM
Clinical features Primary Secondary
Hyperthyroidism (Grave’s) Hyperthyroidism (Plumer)

Age Young age Elderly

Onset Abrupt Gradual
Course Remissions & Steady course
exacerbations

Nervous symptoms +++ +

Metabolic manifestations +++ +

Eye signs +++ FALSE

CV manifestations + +++
Thyroid gland Diffuse Nodular
 THYROID STORM (THYROTOXIC CRISIS)
• A rare presentation of thyrotoxicosis, there is extreme signs of
thyrotoxicosis associated with severe metabolic disturbances.
• It occurs in patient with hyperthyroidism who has not been well
prepared (hyperthyroidism is not controlled) before surgery.
• It may also occur in patients with major stress eg major trauma and
infection.
• Clinical features includes;
• hyper-thermia,
• tachycardia,
• irritability,
• profuse sweating and
• diarrhoea.
 TREATMENT OF THYROTOXICOSIS

• Medical treatment

• Symptomatic treatment

• Antithyroid treatment

• Surgical treatment
 MEDICAL TREATMENT

• Medications which either target the thyroid hormones or symptoms.

• Indications include;

• primary thyrotoxicosis in small gland,

• primary thyrotoxicosis in young age,

• pre-operative preparation,

• post-operative recurrence and

• patient’s refusal of surgery.

 SYMPTOMATIC TREATMENT

• This targets central nervous system and cardiovascular symptoms.

• Beta adrenergic blockers are the mainstay of symptomatic therapy

for thyrotoxicosis.

• Propranolol in range of 40mg twice or thrice a day has been used

with greatest success due to additional benefit of inhibition of
peripheral conversion of T4 to T3
 SYMPTOMATIC TREATMENT
• Fevers are treated with cooling measures and antipyretics.

• Intravenous glucocorticoids are indicated if adrenal insufficiency is

suspected.

• Aggressive hydration of up to 3 – 5 L/d of crystalloid compensates for

potentially profound GI and insensible losses.

• Charcoal hemoperfusion has been shown to be effective in treatment

of iatrogenic or intentional ingestion of excessive doses of
levothyroxine
 ANTITHYROID TREATMENT

• These drugs either blocks iodine binding to tyrosine and decrease

antibody titres (Carbimazole) or block iodine binding and prevent

conversion of T4 to T3 (propylthiouracil).
 ANTITHYROID DRUGS

• Inhibitors of hormone synthesis

• [Link] (PTU)

• [Link] (Tapazole)

• Blockade of hormone release

• Lopanoic acid

• Saturated solution of potassium iodide

• Lugol's solution
 PROPYLTHIOURACIL (PTU)

• The drug of choice

• Recommended as DOC for women who are pregnant or
breastfeeding.
• Dosage:
• HYPERTHYROIDSM:
• 300 – 450 mg/day 8 hrly (3 divided doses) initially (may require up to
600 – 900 mg/day)
• Maintenance: 100 – 150 mg/day (3 divided doses) 8hrly
 PROPYLTHIOURACIL (PTU)
• THYROTOXIC CRISES:
• Initial 200 – 300 mg PO q4 – 6hr initially on day 1 (may require 800 –
1200mg/day),
• Then reduce gradually
• Some practitioners propose an initial dose of 600 – 1000mg with gradual
dose reduction after initial response.
• Maintenance: 100 – 150mg/day PO divided q8 – 12hr
• GRAVES DISEASE:
• 50 – 150mg PO initially
• Maintenance: 50mg PO q8 – 12hr for up to 12 – 18 months, then taper and
discontinue if TSH is normal
 SURGICAL TREATMENT

• All patients must be euthyroid before embarking in surgery, ECG,

CXR, and Echocardiogram must be done to rule out arrhythmia and
heart failure.

• Thoracic inlet X-ray in huge goitres to rule tracheal deviation and

compression as discussed above.

• Lugol’s iodine reduces risk of haemorrhage.

 INDICATIONS FOR SURGICAL INTERVENTION

• Graves disease in young,

• Large gland or in patients with exophthalmos,

• Multi-nodular or solitary nodule,

• Unresponsive, poor compliance to medical treatment and when

there is contraindication to drug e.g. Hypersensitivity.

 TYPES OF SURGERY

• Subtotal thyroidectomy; leaves about 8-10 gram of thyroid tissue,

either 4-5gram on each side or 8-10 gram on one side.
• Near total thyroidectomy removes nearly all thyroid tissue leaving
only about 4gm thyroid tissue;
• Lobectomy removes the entire lobe one side with isthmectomy e.g.
in solitary toxic nodule;
• Total thyroidectomy; remove of the whole of the thyroid gland
 COMPLICATION OF THYROID SURGERY
• Haemorrhage
• Primary is a type of bleeding which occur during surgery due to
arterial or venous cut,
• Reactionary bleeding occurs when a patient’s blood pressure comes
to normal after waning of hypotensive aesthetic drugs or due to pain
and
• Secondary bleeding which occurs 7 days to 2 weeks after surgery,
usually due to infection of wound.
 RESPIRATORY OBSTRUCTION

• Apart from hematoma formation, the following can also cause airway
obstruction post thyroidectomy period;

• Traumatic laryngeal oedema,

• Bilateral recurrent laryngeal nerve injury leading to vocal cords paralysis,

especially in patients with huge thyroid complicated by difficult surgery,

• Tracheomalacia occurs in patients with huge goitres or those with

retrosternal extension.
 RECURRENT LARYNGEAL NERVE INJURY

• Recurrent laryngeal nerve injury can be

• unilateral leading to hoarseness of voice & dyspnoea on exertion,

• bilateral incomplete in which the patient can present with stridor

(due to irritation of adductor fibres)

• bilateral complete with voice loss (aphonia).

• Airway obstruction
 SUPERIOR LARYNGEAL NERVE DAMAGE

• Superior laryngeal nerve injury may also occur in difficult surgery,

• loss of function of this nerve leads to loss of high pitched voice

(cricopharyngius paralysis).
 HYPOTHYROIDISM

• Thyroid insufficiency

• Thyroid insufficiency following thyroidectomy may occur 2 to 5 years

later, it may occurs as high as 20 to 45% in patients who have

undergone total thyroidectomy

 HYPOPARATHYROIDISM
• Parathyroid insufficiency
• Hypoparathyroidism occurs when both parathyroid glands are
accidentally traumatized, devascularized or damaged.
• If seen after removal, the glands must be reimplanted on deltoid
muscles or sternocleidomastoid muscles.
• The incidence of hypoparathyroidism occurs in less than 0.5% of
all patients underwent thyroidectomy.
• Parathyroid hormone is responsible for calcium homeostasis
(increases GIT calcium reabsorption, resorbs bone, reduces renal
calcium excretion and enhances phosphorus renal excretion). In
absence causes hypocalcaemia.
 KELOID SCAR AND HYPERTROPHIC SCARS

• Keloid and hypertrophic scars are late complication of thyroidectomy,

occurring several years after surgery.

• The two can be differentiated because the former forms mass which
crosses an incision line and the later does usually cross the incision
line.
 MANAGEMENT OF SOME IMPORTANT POST OPERATIVE
COMPLICATIONS

• Hematoma and bleeding

• This is one of the most common complications in thyroid surgery.

When suspected, reopen the wound immediately and ligate any
bleeding vessel (wound exploration and bleeder ligation).

• Such treatment should start at bed side if bleeding is severe or when

hematoma is obstructive.

• Give IV fluids using large bore canula and transfuse if necessary.

 MANAGEMENT OF SOME IMPORTANT POST OPERATIVE
COMPLICATIONS

• Respiratory obstruction and recurrent laryngeal nerve damage

• Intubate the patient immediately if obstruction is severe, or

• perform cricothyroidotomy if intubation is not convenient.

• Ventilate or give high flow oxygen 8 L/second and make sure an

intravenous line is established with crystalloids.

 HYPOPARATHYROIDISM

• Symptoms and signs of hypocalcaemia include circumoral

paraesthesias, mental status changes, tetany, carpopedal spasm,

laryngospasm, seizures, QT prolongation on ECG, and cardiac arrest.

• In such condition, a patient is given IV 10mls of 10% Calcium

Gluconate over 10 minutes, or calcium carbonate 2.5g to 5g orally.

 THYROID STORM

• Supportive measures which includes IV fluids ice packs and

antipyretics, oxygen mask 8litres per second, and sedatives.

• Specific treatment include giving propranolol 1mg IV as drip repeated

if needed, oral Carbimazole or propylthiouracil and Digoxin if heart
failure is diagnosed.
 RETROSTERNAL GOITRE
• RG
 WHAT IS RETROSTERNAL GOITRE
• RG
• A goitre with a portion of its mass
located in the mediastinum
 PRIMARY RETROSTERNAL GOITRE

• Primary intra-thoracic goitres arise from aberrant thyroid tissue

which is ectopically located in the mediastinum, receive their blood
supply from mediastinal vessels and are not connected to the cervical
thyroid. They are rare, representing less than 1% of all RGs
 SECONDARY RETROSTERNAL GOITRE
• Secondary RGs develop from the thyroid located in its normal cervical site.

• Downward migration of the thyroid into the mediastinum is facilitated by:

• negative intra-thoracic pressure,

• gravity,

• traction forces during swallowing and

• the presence of anatomical barriers preventing the enlargement in other directions

(thyroid cartilage, vertebral bodies, strap muscles, especially in patients with a short,
large neck).
 SECONDARY RETROSTERNAL GOITRE

• These secondary RGs are, characteristically, in continuity with the

cervical portion of the gland and receive their blood supply,
depending on cervical vessels, almost always through branches of the
inferior thyroid artery.
 TYPES

• Plunging goitre : rise with deglutition and then descent again through
the thoracic inlet

• Mediastinal goitre : lie wholly in the chest but are connected with the
thyroid and supplied by thyroid vessels through narrow band

• Intrathoracic goitre : lie wholly in the chest but completely separated

from the gland supplied by mediastinal vessels
 SYMPTOMS

• May remain symptomless for years

• Dyspnoea due to displacing and compressing on the trachea

• The Dyspnoea aggravated by any posture that reduces the thoracic

inlet as lying down or flexion the neck

• The patient prefer to spend the night in a chair

• Some time they miss diagnosed as asthmatic

• Sometimes there is dysphagia

 SIGNS
• Retrosternal goitre • Retrosternal goire
 SIGNS
• Percussion of the sternum may reveal retrosternal dullness
 INVESTIGATIONS

• X-ray
 INVESTIGATIONS

• X-ray
 INVESTIGATIONS

CT SCAN
 INVESTIGATIONS

• Tc99m SCAN
 TREATMENT
• Thyroidectomy is the only line of treatment

• Mostly via cervical approach , rarely a median sternotomy is required

• Devascularization is done via the neck from which the retrosternal

portion derived its blood supply

• Special care should be exerted to avoid injury of the recurrent

laryngeal nerves during the delivery of retrosternal goter
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