Goiter

GOITER
DR SYED UBAID
Associate professor of surgery

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.

GOITER
 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.

Causes of thyroid disease
inflammatory
Acute
Subacute
chronic
toxic
Primary
secondary
autoimmune
Hashimoto
Reidel thyroiditis
simple
Physiological
Colloidal
nodular
neoplastic
Benign
malignant

Classification of thyroid swellings
 Simple goitre (euthyroid)
 Toxic goiter
 Neoplastic
 Inflammatory
 Other (Amyloid)

 Simple goitre (euthyroid)
1.Physiological
Pubertal ,Pregnancy
2.Diffuse hyperplastic
Multinodular goitre
 Toxic goiter
1.Diffuse (Graves’ disease)
2.Multinodular
3.Toxic adenoma
 Neoplastic
1.Benign 2.Malignant

Inflammatory
1. Autoimmune
Chronic lymphocytic thyroiditis Hashimoto’s
disease
2.Granulomatous
(De Quervain’s thyroiditis)
3. Fibrosing (Riedel’s thyroiditis)
4. Infective
Acute (bacterial thyroiditis,viral thyroiditis, ‘subacute
thyroiditis’)
Chronic (tuberculous, syphilitic)

Simple goiter
Aetiology
Simple goitre may develop as a result of stimulation of the
thyroid gland by TSH,
 Inappropriate secretion from the anterior pituitary a
microadenoma
 In response to a chronically low level of circulating thyroid
hormones.
1. The most important factor in endemic goitre is dietary
deficiency of iodine, Goitrogens in food.
2. Defective hormone synthesis
(Dyshormonogenesis) probably accounts for many
sporadic goitres.

Simple goiter
 There is chronic deficiency of Thyroxine (T4) and or
triiodotrynine (T3) in the body which in turn causes
compensatory elevation of TSH because of the lack
of necessary negative feedback.
 Prolonged stimulation of TSH in attempt to bring
normal thyroid hormones level leads to simple
goiter.
 Such phenomenon may occur in the following
settings;
physiological e.g. puberty, pregnancy, lactation
Iodine deficiency
Enzymatic deficiency for example in Pendred’s
syndrome which is caused by peroxidase deficiency,

Classification of simple goiter
simple diffuse goiter
simple colloid goiter
simple nodular goiter

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 goiter.
The nodules may undergo secondary changes;
central necrosis, cystic degeneration,
hemorrhage, calcification and malignant
changes (3%).

Clinical presentation
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
neighboring structures and lead to wide
range of symptoms and signs.

Clinical presentation
• Obstruction of airways
• Laryngeal nerve compression
• Esophageal obstruction
• Neck veins obstruction
• Superior vena cava syndrome
(Pemberton’s sign).

Investigation in simple goiter
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.

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.

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).

Radiological investigations
Normal AP and lateral
chest X-rays may
demonstrate
retrosternal extension
of the goiter
(retrosternal shadow)

Thoracic inlet X-rays
may demonstrate
compression or
deviation of the
trachea, this
important to
anesthetist if surgery
is contemplated
(difficult intubation).

USG NECK
Thyroid is homogeneous & slightly hyperechoic.

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 ithmus.

A diffusely enlarged thyroid gland with an isthmus width
of 1.5 cm.

Computed tomography
may be indicated if
more details are
needed before surgery
or there is suspicion of
malignancy
transformation.

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
goiter
Dietary
• Iodine supplementation in iodine deficient
areas, food iodine fortification is one of the
best preventive measures of goiters.
Medical
Thyroxin supplementation
• In patients with diffuse hyperplastic goiter 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

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.
HYPOTHYROIDSM

 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)
Aetiology

DRUGS
Anti-thyroid
Cough medicines
Sulfonamides
Lithium
Phenylbutazone
PAS
iodine
Oral hypoglycemic agents
GOITROGENS

FOOD
Soybeans
Millet
Cassava
Cabbage
Excess iodine or lithium ingestion, which
decrease release of thyroid hormone
GOITROGENS

Goitrogens(cassava, lima beans, maize, bamboo
shoots, and sweet potatoes)

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
Hashimoto's thyroiditis

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.
Thyroid destruction secondary to
radioactive iodine or surgery

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 or Hypothalamic disease

 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.
Pituitary injury

• 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.
Severe iodine deficiency:

 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.
Symptoms of hypothyroidsm

 Fatigue
 Depression
 Modest weight gain
 Cold intolerance
 Excessive sleepiness
 Dry, coarse hair
 Constipation
 Dry skin
 Muscle cramps
 Increased cholesterol
levels
 Decreased
concentration
 Vague aches and pains
 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 (myxedema coma).
• In a severely hypothyroid individual, a
myxedema coma tends to be triggered by
severe illness, surgery, stress, or traumatic
injury.

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 requires life-long
levothyroxine (T4) therapy.
This is a more stable form of thyroid hormone
and requires 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
Treatment of hypothyroidism

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   thyroid hormone synthesis

Cretinism
Clinical features:
 Impaired skeletal development
 Impaired CNS development
 Inadequate maternal thyroid hormone prior to
fetal thyroid gland formation
 SEVERE mental retardation
 Normal brain development if maternal thyroid
deficiency occurs after fetal thyroid gland
development

Toxic goiter, 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 etiology.

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.

Grave’s disease
These antibodies include
– thyroid stimulating immunoglobulin (TSI
antibodies),
– thyroid peroxidase antibodies (TPO), and
– TSH receptor antibodies

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 edema 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.

In patients with secondary hyperthyroidism,
there is a pre existing thyroid pathology for
example goiter 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
Secondary hyperthyroidism

In this form of secondary hyperthyroidism,
there is hypersecreting toxic nodule in the
background of multinodular goiter (Plummer’s
disease);
This tends to occur in iodine deficient areas
(endemic goiters).
Multinodular goiter

• This form of secondary hyperthyroidism
is characterized by presence of benign
glandular nodule in the thyroid gland,
usually follicular which secrets excess
hormones.
Toxic adenoma

• 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.
Ectopic thyroid hormone

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 goiter.
Exogenous causes

• 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.
TSH producing pituitary adenoma

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
Other causes

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.
Thyroiditis

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.
Clinical features of hyperthyroidism

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 (diarrhea).

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 rid
due to hyper activity of levator pulpebral
superioris muscle or Muller muscle.
The later is caused by increased sympathetic
tone.

True exophthalmos :
actual protrusion of the eyeballs.
It is an autoimmune disease
Infiltration of retro bulbar tissue with
inflammatory cells & accumulation
of inflammatory fluids.
Probably due to cross- reaction of thyroid antigen & eye (Schwartz )
C.T showing infiltration of
Retro bulbar spaces
True exophthalmos

B. Certain 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 )

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
(eg, 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)

Clinical features Primary
Hyperthyroidism (Grave’s)
Secondary
Hyperthyroidism (Plumer)
Age Young age Elderly
Onset Abrupt Gradual
Course Remissions &
exacerbations
Steady course
Nervous
symptoms
+++ +
Metabolic
manifestations
+++ +
Eye signs +++ FALSE
CV manifestations + +++
Thyroid gland Diffuse Nodular

 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
 diarrhea.
Thyroid storm (thyrotoxic crisis)

1. Medical treatment
2. Symptomatic treatment
3. Antithyroid treatment
Treatment of thyrotoxicosis

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.
Medical 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

These drugs either blocks iodine binding to
tyrosine and decrease antibody titers
(Carbimazole) or block iodine binding and
prevent conversion of T4 to T3
(propylthiouracil).
Antithyroid treatment

Antithyroid drugs
Inhibitors of hormone synthesis
1.Propylthiouracil (PTU)
2.Methimazole (Tapazole)
Blockade of hormone release
Lopanoic acid
Saturated solution of potassium iodide
Lugol solution

• The drug of choice
• Recommended as DOC for women who are
pregnant or breastfeeding.
• Dosage:
– HYPERTHYROIDSM:
• 300 – 450 mg/day 8 hrly initially (may require up to
600 – 900 mg/day)
• Maintenance: 100 – 150 mg/day 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

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 goiters to rule
tracheal deviation and compression as
discussed above.
Lugol’s iodine reduces risk of hemorrhage.
Surgical treatment

 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.
Indications for surgical intervention

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
isthmusectomy eg in solitary toxic nodule;
Partial thyroidectomy; bilateral partial lobectomy
eg in multinodular toxic goiter involving both
lobes.
Types of surgery

Hemorrhage
• 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 anesthetic drugs or due to pain
and
• Secondary bleeding which occurs 7 days to 2
weeks after surgery, usually due to infection of
wound.
Complication of thyroid surgery

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
goiters or those with retrosternal extension.

Recurrent laryngeal nerve injury
• Recurrent laryngeal nerve injury can be
– unilateral leading to hoarseness of voice &
dyspnea on exertion,
– bilateral incomplete in which the patient can
present with stridor (due to irritation of
adductor fibers)
– bilateral complete with voice loss (aphonia).

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).

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

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 hypoparthyroidisim occurs in less
than 0.5% of all patients underwent thyroidectomy.
• Parathyroid hormone is responsible for calcium
homeostasis (increases GIT calcium reabsorbtion,
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.

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 paresthesias, 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 sedatatives.
• Specific treatment include giving
propranolol 1mg IV as drip repeated if
needed, oral Carbimazole or
propylthiouracil and Digoxin if heart failure
is diagnosed.

What is Retrosternal goiter
• a goitre with a portion of its mass located in
the mediastinum

Why
 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 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). 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 goiter : rise with deglutition and then
descent again through the thoracic inlet
• Mediastinal goiter : lie wholly in the chest but
are connected with the thyroid and supplied
by thyroid vessels through narrow band
• Intrathracic goiter : lie wholly in the chest but
completely separated from the gland supplied
by mediastinal vessels

How
• Short-necked individuals
• Usually after middle age
• Intrathracic goiter more common in men

Symptoms
• May remain symptomless for years
• Dyspnea due to displacing and compressing on
the trachea
• The Dyspnea 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
• Palpation : thyroid gland enlarged

Signs
• Percussion of the sternum may reveal
retrosternal dullness

Treatment
• Thyroidectomy is the only line of treatment
• Mostly via cervical approach , rarely a median
sternotmy 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

Goiter

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