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).

Classification

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:
   • lack of iodine (does not occur in the Czech Republic)
   • congenital hormone synthesis disorder (dyshormonogenesis)
   • autoimmune inflammation ( Hashimoto's lymphocytic thyroiditis , Graves-Based thyroiditis)
2. multinodular goiter:
   • sometimes associated with autoimmune inflammation of thyroid gland
3. localized node:
   • thyroid carcinoma (most often differentiated papillary carcinoma or medullary C-cell carcinoma - familial occurrence)
   • 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.

Disease

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.

Examination

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

Links

Related articles in czech

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

References

1. LEBL, Jan and Jiří BRONSKÝ. Small differential diagnosis in pediatrics. 1st edition. Prague: Galén, 2012. pp. 110-114. ISBN 978-80-7262-939-8 .
2. MUNTAU, Ania Carolina. Pediatrics. 4th edition. Prague: Grada, 2009. pp. 78-79. ISBN 978-80-247-2525-3 .
3. LEBL, J, J JANDA and P POHUNEK, et al. Clinical pediatrics. 1st edition. Galén, 2012. 698 pp. 185-188. ISBN 978-80-7262-772-1 .
4. AL TAJI, E and O HNÍKOVÁ. Thyroidopathy in childhood and adolescence. Pediatrician. practice [online] . 2014, vol. 15, vol. 3, pp. 134-137, also available from <https://www.pediatriepropraxi.cz/pdfs/ped/2014/03/04.pdf>.
5. LEBL, Jan. Clinical pediatrics. 1st edition. Prague: Galén, c2012. ISBN 978-80-7262-772-1 .