Very rare in children. 

Causes include :

-        the most common: Graves-Basedow disease, which is autoimmune in nature. Anti-TSH and anti-TSH receptor antibodies develop, causing hypersecretion of TSH and considerable hyperstimulation of the thyroid gland, which becomes enlarged (goiter); exophthalmos can also occur, which can compromise visual function. 

-         toxic adenoma (Plummer's), rare in children;

-         acute infectious thyroiditis, bacterial in nature; 

-         Hashimoto's thyroiditis (chronic lymphocytic thyroiditis) of autoimmune origin, causing progressive lymphocytic infiltration of the gland, leading initially to hyperthyroidism but eventually to destruction of thyroid cells and hypothyroidism;

-         subacute thyroiditis (De Quervain's), a thyroid inflammation probably viral in origin;

-         familial non-immune hyperthyroidism [MIM 609 152](see this term): autosomal dominant familial hyperthyroidism syndrome caused by mutation of the TSH receptor gene, leading to its constitutional activation and expressed in early childhood;

-         iodine overload (particularly long-term amiodarone therapy);

-         excessive ingestion of thyroid hormones (e.g. anti-obesity diets) ;

-         lithium overload.

Hyperthyroidism causes increased metabolism, with accelerated heart rate, weight loss, hyperactivity and even agitation, heat intolerance, tremors and loss of sleep. At the onset of symptoms, children are often considered hyperactive with attention deficit. In Graves' disease, inflammation of the connective tissue and extraocular muscles leads to exophthalmos, in addition to the diffuse, homogeneous enlargement of the thyroid gland (goiter).

The diagnosis is based on biology: increased serum thyroid hormone levels with a drop in TSH, except in the case of Graves' disease, where there is TSH hypersecretion.

The first line of treatment is based on synthetic anti-thyroid drugs such as methimazole (0.4 mg/kg/d in 3 doses) or propyl-thio-uracyl (5 to 10 mg/kg/d in 3 doses, but little used due to its hepatotoxicity). This treatment is usually combined with a β-blocker (propranolol 2 mg/kg/d in 2 doses in infants; 10 mg/kg/d in 3 doses in older children). In the event of intolerance, failure or recurrence of hyperthyroidism, radioactive iodine treatment or surgical removal may be proposed, with the effect of rendering the child hypothyroid.

Thyrotoxic crisis or thyroid storm : brisk increased secretion of thyroid hormons following an infection, surgical stress or interruption of the medical treatment. It can lead to cardiovascular complications (tachycardia and hypertension, atrial fibrillation, cardiac decompensation, myocardial ischemia) and neurological complications (convulsions), with a risk of mortality.

Anesthetic implications: 

Children must be made euthyroid before surgery. Since anti-thyroid drugs take 6 to 8 weeks to effectively block thyroxine synthesis, in an emergency, iodine treatment with high oral doses of lugol (4 to 8 drops every 8 h) or potassium iodide (3 to 5 drops every 6 h) can rapidly reduce thyroid hormone synthesis by inhibiting thyroperoxidase. Children on β-blockers: increased risk of bradycardia and hypoglycemia. The hypermetabolic state increases the volume of distribution, clearance and metabolism of many anesthetic agents.

In case of thyrotoxic crisis: IV esmolol, MgSO4, hydrocortisone, sometimes dantrolene.

Post-operative: risk of hypocalcemia and hypothyroidism.

References : 

-        Knighton JD, Crosse MM.
Anaesthetic management of childhood thyrotoxicosis and the use of esmolol.
Anaesthesia 1997; 52:67-70.

-        Bonannoa J, Grannell T, Maves G, Tobias JD.
Perioperative care of a child with hyperthyroidism. 
J Med Cases 2024;15:49-54.

Updated: December 2024