ENDEMIC (IODINE-DEFICIENT) GOITER

The most common type of goiter, encountered chiefly in geographic regions where the
natural supply of iodine is deficient (eg, the Great Lakes areas of the United States), is the so-
called simple or colloid goiter. In addition to being caused by an iodine deficiency, simple
goiter may be caused by an intake of large quantities of goitrogenic substances in patients
with unusually susceptible glands. These substances include excessive amounts of iodine or
lithium, which is used in treating bipolar disorders. Simple goiter represents a compensatory
hypertrophy of the thyroid gland, caused by stimulation by the pituitary gland. The pituitary
gland produces thyrotropin or TSH, a hormone that controls the release of thyroid hormone
from the thyroid gland. Its production increases if there is subnormal thyroid activity, as
when insufficient iodine is available for production of the thyroid hormone. Such goiters
usually cause no symptoms, except for the swelling in the neck, which may result in tracheal
compression when excessive. Many goiters of this type recede after iodine imbalance is
corrected. Supplementary iodine, such as SSKI, is prescribed to suppress the pituitarys
thyroid-stimulating activity. When surgery is recommended, the risk for postoperative
complications is minimized by ensuring a preoperative euthyroid state by treatment with
antithyroid medications and iodide to reduce the size and vascularity of the goiter. Providing
children in iodine-poor regions with iodine compounds can prevent simple or endemic goiter.
If the mean iodine intake is less than 40 fg/day, the thyroid gland hypertrophies. The World
Health Organization recommends that salt be iodized to a concentration of 1 part in 100,000,
which is adequate for the prevention of endemic goiter. In the United States, salt is iodized to
1 part in 10,000. The introduction of iodized salt has been the single most effective means of
preventing goiter in at-risk populations.

Reference: Bare, S. (2004). Brunner and Suddarths Textbook of Medical Surgical Nursing.
(10
th
Edition) Philippines: Lippincott Williams & Wilkins.






Iodine Deficiency Disorder
Cretinism
Cretinism is the most extreme manifestation of IDD. Cretinism can be divided into
neurologic and myxedematous subtypes. These subtypes have considerable clinical overlap.
Both conditions can be prevented by adequate maternal and childhood iodine intake.
Neurologic cretinism is thought to be caused by severe IDD with hypothyroidism in the
mother during pregnancy and is characterized by mental retardation, abnormal gait, and deaf-
mutism, but not by goiter or hypothyroidism in the child. Myxedematous cretinism is
considered to result from iodine deficiency and hypothyroidism in the fetus during late
pregnancy or in the neonatal period, resulting in mental retardation, short stature, goiter, and
hypothyroidism.
Mental Retardation
Worldwide, iodine deficiency is the leading cause of preventable mental retardation. This
became a renewed concern as the prevalence of moderate iodine deficiency in the United
States among women of childbearing age increased from 4% in the 1970s to 15% by the
1990s. Although children of mothers from iodine-deficient regions may have normal thyroid
function test results, they are noted to have lower language and memory performance.
Reduction in IQ has been noted in affected youth from regions of severe and mild iodine
deficiency. Mental retardation as a result of iodine deficiency can be exaggerated in the
setting of concomitant deficiencies of selenium or vitamin A.
Postnatally, as infants and children are particularly sensitive to fluctuations in iodine intake,
this population is at risk for poor mental and psychomotor development (predominantly in
language and memory skills). Unlike mental retardation that occurs because of prenatal
iodine deficiency, mental retardation from continued postnatal iodine deprivation may be
reversible with thyroid hormone replacement.

Reference: http://emedicine.medscape.com/article/122714-clinical
Author: Stephanie L Lee, MD, PhD; Chief Editor: George T Griffing, MD