Evaluation and management of

multi-nodular goiter
By: Ahmad Heikal
Student no.: 211511142

Abstract
Nodular goiters are encountered commonly in clinical practice by primary care
physicians, endocrinologists, surgeons, and otolaryngologists. Epidemiologic data
suggest that in the United States, the incidence of such goiters is approximately 0.1% to
1.5% per year, translating into 250,000 new nodules annually. Nodular goiters are more
common in women than in men, with advancing age, and after exposure to external
irradiation. These goiters may be asymptomatic, with normal TSH levels (nontoxic), or
may be associated with systemic thyrotoxic symptoms (toxic MNG or Plummer's
disease). Diagnostic evaluation of patients with nodular goiters consists of clinical
evaluation, biochemical testing, FNA, and imaging studies. The serum TSH level is a
sensitive and reliable index of thyroid function. FNA results are pivotal to assess cancer
risk in patient management for prominent palpable and suspicious nodules. Chest
radiography, high-resolution ultrasonography, and computed tomography help to
delineate the size and extent of a goiter in evaluating compression symptoms.
Indications for treatment in patients with MNG include hyperthyroidism, local
compression symptoms attributed to the goiter, cosmesis, and concern about malignancy
based on FNA results. The use of levothyroxine suppression therapy to effectively
decrease and control MNG size is controversial. Thyroid hormone should not be used,
however, in patients with suppressed serum TSH levels, to avoid the development of
toxic symptoms. Management of toxic MNG by surgery is well established. Radioiodine
is also effective therapy for many of these patients. When treatment is necessary for
nontoxic MNG, surgical excision is preferred. Our recommendations are as follows. For
patients who have small, nontoxic multinodular goiters that are clinically asymptomatic,
who are biochemically euthyroid according to serum TSH levels, and who have
prominent palpable or suspicious nodules benign by FNA, yearly evaluation with serum
TSH determinations and thyroid palpation is sufficient. Patients with modest but stable
MNG size and normal serum TSH levels may also be managed by yearly clinical
observation. In this second group, levothyroxine suppression therapy is often
unsuccessful and has the potential for untoward effects from exogenous
hyperthyroidism. For large nontoxic multinodular goiters with local compression
symptoms, the preferred treatment is surgery. In patients with toxic MNG, treatment
with either surgery or radioiodine is recommended, although patients with large goiters
and large, autonomously functioning nodules become euthyroid more quickly following
surgery.

Introduction
Goiter means enlargement of the thyroid gland and is a general term that conveys the
information that the volume of the thyroid gland is larger than normal. The presence of
goiter can be determined by inspection, palpation, or by an imaging study.
Normal thyroid gland measures 4 to 4.8 cm in sagittal, 1 to 1.8 cm in transverse, and 0.8
to 1.6 cm in anteroposterior dimensions. This corresponds to a volume of 7 to 10 mL on
ultrasonography calculations and 10-20 grams in weight. Thyroid size increases with age
and body size. It is larger in males as opposed to females. The size decreases with higher
iodine intake.
The thyroid gland can enlarge due to a variety of physiological or pathological stimuli.
Goiter during adolescence and pregnancy are two causes of a physiological goiter.
Goiter can be associated with euthyroidism, hypothyroidism, or hyperthyroidism. It can
be diffuse, nodular, or multi nodular. The thyroid gland usually grows anteriorly in the
neck, because the enlarging thyroid is not constrained by the weak anterior cervical
muscles, subcutaneous tissue, or the skin. The term goiter is usually used to denote
cervical goiter. If the thyroid gland enlarges inferiority and passes through the thoracic
inlet, then it is called a substernal or retrosternal goiter.

What is a simple goiter?

A simple goiter is an enlargement of the thyroid gland, with a lack of thyroid
malfunction or thyroid cancer being apparent. Most goiters are non-cancerous and
goiters are not tumors. The thyroid gland islocated at the front of the neck where the
collarbones meet. It is an important gland in the endocrine system, as it makes the
hormones which control many processes in our bodies.
How is a simple goiter caused?
Goiters are most commonly caused by iodine deficiency. Iodine is paramount in
producing hormones through the thyroid. Thus if there is not enough iodine in the body,
the thyroid increases in size as it tries to get more iodine. A goiter can also be caused by
an infection, a reaction to the immune system attacking the thyroid, smoking, and certain
foods and medications. Goiters are more common in those who have a family history of
them, people aged over 40, and women.

What are the symptoms of a simple goiter?

The main symptom of a goiter is an enlarged thyroid gland, which may range in size,
from looking like a small spot or nodule to a large lump. In very rare cases a goiter can
put pressure on the trachea (windpipe) and esophagus, which can cause breathing
problems, a cough, and problems swallowing.

How can goiters be prevented?

Goiters cannot often be prevented, but as they are sometimes connected to lack of
iodine, it is important to make sure you get enough in your diet. A lot of the salt we
consume is iodides, which means iodine is added to it. However, it is important to
regulate the amount of salt consumed. Other ways of getting enough iodine include
eating seaweed or seafood, such as shellfish. Too much iodine can also cause a goiter to
form, so be mindful of how much you consume.

Other causes of goiter include:

The body's immune system attacking the thyroid gland (autoimmune problem)
Certain medicines (lithium, amelioration) Infections (rare) Cigarette smoking
Eating very large amounts of certain foods (soy, peanuts, or vegetables in the broccoli
and cabbage family)
Toxic nodular goiter, an enlarged thyroid gland that has a small growth or many growths
called nodules, which produce too much thyroid hormone
Simple goiters are more common in:
People over age 40
People with a family history of goiter
People who are born and raised in areas with iodine deficiency
Etiology

Several pathogenic mechanisms can cause goiter. It can be caused by iodine deficiency,
which is often seen in countries that do not have a public health intervention to prevent
iodine deficiency. In this instance, the terminology is an endemic goiter. Inflammatory
disorders of the thyroid gland such as autoimmune thyroiditis, postpartum thyroiditis,
silent thyroiditis, radiation thyroiditis, subacute thyroiditis, and suppurative thyroiditis
can cause thyroid enlargement, hence goiter.
As the enlargement of the thyroid is the consequence of the inflammatory process and
abates after the inflammation resolves, the term "goiter" is not used to describe the
disorder. Goiter is among the symptoms and signs of inflammatory thyroid disorder.
Thyroid diseases that cause hyperthyroidism, such as Grave disease, toxic nodular
goiter, and toxic multinodular goiter can cause goiter. Goiter can include one or more
nodules and is termed as nodular goiter or nontoxic multinodular goiter; in these entities,
the enlarged thyroid is associated with euthyroidism. Other causes can be thyroid cancer
and granulomatous and infiltrative diseases of the thyroid.

Epidemiology

The most common cause of goiters worldwide is iodine deficiency that affects an
estimated 2.2 billion people. The prevalence and incidence of goiter are based on the
degree of iodine deficiency. With mild iodine deficiency, the incidence of goiter is 5% to
20%. With a moderate deficiency, the prevalence increases to 20% to 30%, and with
severe iodine deficiency, the incidence increases to greater than 30%. Even with the use
of iodine, there has been an increase in the incidence of thyroid nodules. It is not clear
the increase in prevalence represents a true increase or an increased detection. One of
the causes of this could be the increased utilization of radiological imaging and more
frequent screening with ultrasound.
At this time, ultrasonography can detect even the smallest of nodules, causing the
incidence of nodules to be 60% to 70% in adults. However, imaging and screening are
not the sole causes of the increase in incidence. It has been thought that obesity, insulin
resistance, and metabolic syndrome may be factors that have caused an increased
incidence of goiter. Females are approximately four times more likely to develop goiter
as compared to males. There is no racial difference in goiter prevalence.

Pathophysiology
Enlargement of thyroid, i.e. goiter is an adaptive reaction of thyroid follicular cells to
any process that blocks thyroid hormone production. The most common cause of goiter
is iodine deficiency. In countries that use iodized salt and in others where iodine
deficiency is not a problem, Hashimoto thyroiditis is an important cause of goiter.
However, iodine deficiency still remains the most common cause worldwide. Goiters
have various morphological, hormonal, and clinical presentations and not all causes of
goiter can be attributed to iodine deficiency. Genetic, demographic, and environmental
factors are also responsible for the development of goiter. Other causes include Graves
disease, inborn errors of thyroid hormone synthesis, congenital hypothyroidism,
inflammatory thyroid diseases like postpartum thyroiditis, infiltrative diseases of thyroid
like sarcoidosis, and amyloidosis, TSH secreting pituitary adenomas, and others.

Conclusion
Nontoxic and toxic multi nodular goiter are the main etiologies of goiter in patients aged
55 years and older. Thyroid size is the main factor influencing the appearance of signs
and symptoms, although age and sex are related with the presence of retrosternal goiter
and tracheal deviation. Iodine deficiency is not the etiological factor behind the large
volume of multi nodular goiter cases admitted in government medical college
Trivandrum, Kerala, India as only 2% of cases evaluated showed iodine deficiency. The
limitations of the study included the fact the study period is limited to one year only and
that this being tertiary care center based study, may not exactly represent the actual
situation in the community. Also, the difficulty in quantifying goitrogens intake and
inability to estimate water and soil iodine levels from the community could be other
confounding factors. While the concept of iodine deficiency still dominates most
discussions about the parthenogenesis of multi nodular goiter, we think it is time to
dwell on the fundamental process of goitrogenesis, which operates through mechanisms
innate to the hereditary and acquired heterogeneity among the thyrocytes themselves. In
this view, goiter nodules and nodular goiters are true benign neoplasms arising by
mechanisms common to all benign endocrine and non-endocrine neoplasms. May be,
superimposed iodine shortage does enhance the incidence of goiters. However, we do
reiterate that continued supplementation of edible salt fortified with iodine should be
monitored carefully, and supplementation programs should be tailored to the particular
region. Funding: No funding sources Conflict of interest: None declared Ethical
approval: The study was approved by the institutional ethics committee.