Child goiter

Definition

 * an enlargement of thyroid gland above the norm for the age (during the ultrasound examination volume of thyroid gland 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 leakage, eyelid swelling, somnolence, fatigue, inefficiency, constipation , premature puberty
 * hyperfunctional goiter ,
 * tachycardia, weight loss, failure to thrive, warm, sweaty skin, heat intolerance, exophthalmos, diarrhea

If hyperthyroidism is suspected, the patient must be sent to hospital - there is a risk of heart failure.

By character

 * 1) diffuse goiter:
 * 2) *lack of iodine (does not occur in the Czech Republic)
 * 3) *congenital hormone synthesis disorder (dyshormonogenesis)
 * 4) *autoimmune inflammation ( Hashimoto's lymphocytic thyroiditis, Graves-Based thyroiditis)
 * 5) multinodular goiter:
 * 6) *sometimes associated with autoimmune inflammation of thyroid gland
 * 7) localized node:
 * 8) *thyroid carcinoma (most often differentiated papillary carcinoma or medullary C-cell carcinoma - familial occurrence)
 * 9) *3 / 4 of the solitary nodules are benign - cystic lesion

Diffuse parenchymal goiter

 * real thyroid hyperplasia caused by chronic hyperstimulation, especially in chronic iodine deficiency (intake <40 μg / day) and in Basedow's disease.

Struma neonatorum

 * etiology : insufficient iodine intake during pregnancy;transplacental transmission of strumigenic substances (PAS, resorcinol); treating the pregnant patient by thyrostatics; transmission of TRAK antibodies from a mother with Basedow's disease;
 * intrauterine thyroid hormone deficiency → increased TSH secretion → goiter;
 * visible enlargement of the thyroid gland → stridor, breathing difficulties.

Juvenile euthyroid goiter

 * iodine deficiency or familial disorder of iodine usage
 * development of goiter in puberty, more often in girls;
 * eufunctional goiter, homogeneously enlarged → necrosis, cysts, nodules;
 * lower amount of thyroid hormones, TSH normal, normal TRH test, thyroid antibodies negative;
 * optimization of iodine intake (200 μg / day), if the goiter is refractory - suppression of TSH by thyroxine is indicated.

Congenital hypothyroidism

 * the most common congenital endocrine disease (prevalence 1: 4000);
 * thyroid hormones play a key role in brain development, especially by 8 months of age (slightly less so by 3 years of age);
 * without substitution treatment, irreversible brain damage occurs - at the clinical diagnosis, the brain is already irreversibly damaged;
 * nationwide neonatal screening has been introduced since 1985- determination of TSH level
 * etiopathogenesis: thyroid gland dysgenesis (agenesis, aplasia, hypoplasia, hemithyroiditis, cystic malformation, ectopy) or dyshormonogenesis (disorder of any stage of hormone synthesis or secretion) or rare isolated congenital central hypothyroidism (congenital TSH defect - cannot be detected by neonatal screening);
 * clinical picture without treatment: prolonged neonatal jaundice, failure to thrive, delayed growth rate and bone maturation - late closure of the fontanel, delayed eruption of the lactic dentition, macroglossia, muscle hypotension, omphalocele, constipation, hoarse screaming;
 * neonatal goiter or thyroid gland of normal size;
 * laboratory findings: ↑ TSH, ↓ fT 4 ; (the central form- ↓ TSH and fT 4 );
 * therapy : lifelong L-thyroxine replacement therapy (started as soon as possible).

Autoimmune thyroid gland disease

 * the most common acquired thyroid disease in children and adolescents; more often in girls;
 * Mostly lymphocytic (Hashimoto's) thyreoiditis;
 * often associated with other autoimmune diseases (type 1 diabetes mellitus, celiac disease) and chromosomal aberrations (Down syndrome, Turner syndrome);
 * soft diffuse goiter, USG: diffusely 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: the first is the stage of euthyroidism, then the stage of permanent hypothyroidism; there may also be transient hyperthyroidism ("hashitoxicosis");
 * without treatment : growth retardation, dyslipidemia, obesity, impaired school achievement, anemia, dry and rough skin, premature pseudopuberty or delayed puberty, myxedema, constipation, bradycardia;
 * laboratory findings : ↑ TSH, ↓ fT 4;
 * therapy : lifelong L-thyroxine replacement therapy.

Neonatal hyperthyroidism (thyrotoxicosis)

 * a rare disorder that can be life-threatening for newborns;
 * transplacental transmission of maternal antibodies against the TSH receptor in Graves-Basedow-type maternal thyrotoxicosis;
 * clinical picture : hyperthyroidism since the fetal period - IUGR, tachycardia, accelerated bone maturation, goiter, exophthalmos, risk of metabolic breakdown and heart failure;
 * laboratory finding : ↑ fT 4 ;
 * therapy : antithyroid therapy until maternal antibodies disappear, ie in a descending dose for 2-3 months. [3]

Graves-Basedow thyrotoxicosis

 * the most common cause of hyperthyroidism in children; especially in adolescent girls;
 * etiopathogenesis : anti-TSH receptor autoantibodies (TRAb, rTSH-ab) that have a thyroid stimulating effect;
 * clinical picture : hyperkinetic circulation with tachycardia and systolic hypertension with increased pressure amplitude, weight loss, impaired school achievement, irritability, nervousness, gentle hand tremor, diarrhea, sweating, in 60% orbitopathy with exophthalmos- caused by proliferation of retrobulbar connective tissue by autoimmune stimulation;
 * in 75% goiter - strongly perfused, warm, tactile swirl;
 * laboratory findings : ↓ TSH, ↑ fT 4 ;
 * therapy : thyrostatics (methimazole, carbimazole, propithiouracyl), if there are repeated relapses recurrent total thyroidectomy and lifelong L-thyroxine replacement therapy is indicated.

Iodopenic goiter

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

Clinical examination

 * palpation of the thyroid gland (between the jugular socket and the beginning of the trachea)
 * WHO criteria:
 * GRADE 0: the thyroid gland is not palpable
 * GRADE 1: The thyroid gland is palpable but not visible in the normal position of the neck
 * GRADE 2: the thyroid gland is palpable and visible at 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) - increased anti-TPO ​​indicate autoimmune thyroiditis
 * anti-hTG (human thyroglobulin)
 * TRAK / TRAb (TSH receptor stimulating antibodies) - Graves-Basedow disease

Ultrasound examination of tyroid gland

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

FNAC under ultrasound control

 * thin needle aspiration biopsy for subsequent cytological examination

Differential diagnosis of goiter in children

 * medial and lateral cervical cysts ,
 * lymphangioma,
 * hemangioma,
 * thyroiditis,
 * thyroid adenoma,
 * thyroid cancer.

Therapy

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

Complication

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

Related articles in czech

 * Onemocnění štítné žlázy: Hypotyreóza • Hypertyreóza
 * Vyšetření u chorob štítné žlázy • Vyšetření funkce štítné žlázy
 * Symptomatické duševní poruchy při endokrinopatiích