Children's goiter

Definition

 * enlargement of the thyroid gland above the norm for the given age (in an ultrasound examination, the thyroid volume is greater than 2 standard deviations).

By function

 * eufunctional goiter,
 * hypofunctional goiter,
 * bradycardia, weight gain, growth retardation, failure to thrive, dry skin and hair, facial flushing, eyelid swelling, drowsiness, fatigue, inefficiency, constipation, pseudopubertas praecox.
 * hyperfunctional goitre,
 * tachycardia, weight loss, failure to thrive, warm, sweaty skin, heat intolerance, exophthalmos, diarrhea.

By character

 * 1) diffuse goiter:
 * 2) *lack of iodineu ("iodopenic goiter" - does not occur in the Czech Republic)
 * 3) *congenital disorder of hormone synthesis (dyshormonogenesis)
 * 4) *autoimmune inflammation (Hashimoto's lymphocytic thyroiditis, Graves-Based thyroiditis)
 * 5) multinodular goiter:
 * 6) * sometimes occurs in AI inflammations of the SŽ
 * 7) localized node:
 * 8) *thyroid carcinoma (most commonly differentiated papillary or medullary C-cell carcinoma - familial).
 * 9) *solitary nodule in 3/4 benign - cystic mass

Diffuse parenchymatous goiter

 * right hyperplasia of the thyroid gland caused by chronic hyperstimulation, especially in chronic iodine deficiency (intake < 40 μg/day) and in morbus Basedow.

Goiter neonatorum

 * etiology : insufficient intake of iodine during pregnancy; transplacental transfer of strimogenic substances (PAS, resorcinol); treatment of pregnant thyrostatics; transmission of TRAK antibodies in a mother with Basedow's disease;
 * intrauterine lack of thyroid hormones → increased secretion of TSH → goiter;
 * visible enlargement of the thyroid gland → stridor, difficulty breathing.

Juvenile euthyroid goiter

 * iodine deficiency or familial iodine utilization disorder;
 * development of goiter during puberty, more often in girls;
 * eufunctional goiter, homogeneously enlarged → necrosis, cysts, nodules;
 * thyroid hormones at the lower limit of normal, TSH normal, normal TRH test, thyroid antibodies negative;
 * optimization of iodine supply (200 μg/day) if the goiter is refractory to iodine – suppression of TSH with thyroxine.

Congenital hypothyroidism

 * most common congenital endocrine disease (prevalence 1:4000);
 * thyroid hormones play a key role in brain development, especially up to 8 months of age (a little less then up to 3 years of age);
 * without replacement treatment, irreversible brain damage occurs – at the time of clinical diagnosis, the brain is already irreversibly damaged;
 * since 1985, nationwide newborn screening has been introduced - determination of the TSH level;
 * etiopathogenesis: dysgenesis of the thyroid gland (agenesis, aplasia, hypoplasia, hemithyroid, cystic malformation, ectopia) or dyshormonogenesis (disorder of any level of synthesis or secretion of hormones), or rare isolated congenital central hypothyroidism (congenital TSH defect - cannot be detected by newborn screening);
 * clinical picture without treatment: protracted neonatal icterus, failure to thrive, delayed growth rate and bone maturation – late closure of fontanels, delayed eruption of milk dentition, macroglossia, muscle hypotonia, omphalocele, constipation, hoarse cry;
 * neonatal goiter or normal-sized thyroid gland;
 * laboratory findings: ↑TSH, ↓fT4; (for the central form ↓TSH and fT4);
 * therapy : lifelong L-thyroxine replacement therapy (started as soon as possible).

Autoimmune thyroid disease

 * the most common acquired thyropathy in children and adolescents; more often in girls;
 * mostly lymphocytic (Hashimoto's) thyroiditis';
 * often associated with other autoimmune diseases (diabetes mellirus type 1, celiac disease) and with chromosomal aberrations (Down's syndrome, Turner's syndrome);
 * soft diffuse goiter; USG: diffuse inhomogeneous texture (“pepper and salt”); histology: lymphocytic infiltration of the gland;
 * etiopathogenesis : autoantibodies against thyroid peroxidase (anti-TPO) and against human thyroglobulin (anti-hTG);
 * clinical picture : first phase of euthyroidism, then phase of permanent hypothyroidism; there may also be transient hyperthyroidism ("hashitoxicosis");
 * without treatment : growth retardation, dyslipidemia, obesity, impaired school performance, anemia, dry and rough skin, premature pseudopuberty or delayed puberty, myxedema, constipation, bradycardia;
 * laboratory findings : ↑TSH, ↓fT4;
 * therapy : lifelong L-thyroxine replacement therapy.

Neonatal hyperthyroidism (thyrotoxicosis)

 * a rare disorder that can endanger the life of a newborn;
 * etiopathogenesis : transplacental transfer of maternal antibodies against the TSH receptor in maternal thyrotoxicosis of the Graves-Basedow type;
 * clinical picture : hyperthyroidism from the fetal period – IUGR, tachycardia, acceleration of bone maturation, goiter, exophthalmos, risk of metabolic disruption and heart failure;
 * laboratory finding : ↑fT4;
 * therapy : antithyroid treatment until the maternal antibodies disappear, i.e. in a decreasing dose for 2-3 months.

Graves-Basedow thyrotoxicosis

 * most common cause of hyperthyroidism in children; especially in adolescent girls;
 * etiopathogenesis : autoantibodies against the TSH receptor (TRAb, rTSH-ab), which have a stimulating effect on the thyroid gland;
 * clinical picture : hyperkinetic circulation with tachycardia and systolic hypertension with increased pressure amplitude, weight loss, impaired school performance, irritability, nervousness, mild hand tremors, diarrhea, sweating, in 60% orbitopathy with exophthalmos - occurs by the proliferation of retrobulbar connective tissue due to autoimmune stimulation;
 * in 75% goiter – heavily perfused, warm, palpable vortex;
 * laboratory findings : ↓TSH, ↑fT4;
 * therapy : thyrostatics (methimazole, carbimazole, propithiouracil), in case of repeated relapses total thyroidectomy and lifelong replacement therapy with L-thyroxine.

Iodopenic goiter

 * our natural diet is low in iodine → iodization of table salt since the 1950s;
 * iodine deficiency → reduced production of thyroid hormones → ↑TSH → iodopenic goiter;
 * endemic cretinism - eradicated.

Clinical examination

 * palpation examination of the LV (between the jugular fossa and the beginning of the trachea)
 * WHO criteria :
 * GRADE 0: the thyroid gland is not palpable or palpable
 * GRADE 1: thyroid gland is palpable but not visible in normal neck position
 * GRADE 2: thyroid gland is palpable and visible in normal head position

Laboratory examination

 * TSH
 * immeasurably low – hyperthyroidism
 * slightly elevated – subclinical hypothyroidism
 * significant increase (tens of mIU/l) – hypothyroidism,
 * fT4
 * significantly increased – hyperthyroidism
 * significantly reduced – hypothyroidism
 * antibodies
 * anti-TPO (thyroid peroxidase) – elevated values indicate autoimmune thyroiditis
 * anti-hTG (human thyroglobulin)
 * TRAK/TRAb (TSH receptor stimulating antibodies) – Graves-Basedow disease

Ultrasound examination of the spine

 * we evaluate the size, echotexture of the gland and look for focal changes.

FNAC under USG control

 * fine needle aspiration biopsy for subsequent cytological examination

Differential diagnosis of goiter in children

 * medial and lateral neck cysts,
 * lymphangioma,
 * hemangioma,
 * thyroiditis,
 * thyroid adenoma,
 * thyroid carcinoma.

Therapy

 * prevention of endemic goiter: fortification of salt with iodine
 * iodine substitution
 * at volume +80ml: surgical thyroidectomy or radioablation

Complications

 * risk of oppression of surrounding structures : dyspnoea, dysphagia, superior vena cava syndrome

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