Vnitr Lek 1994, 40(1):40-43

[Thyrotoxic crisis].

J Hrnciar: Interná klinika nemocnice F. D. Roosevelta, Banská Bystrica.

A thyrotoxic Crisis is an acute or subacute metabolic explosion caused by uncontrolled release of tyronines from the thyroid gland (more frequently a diffuse thyroid gland) following its injury: strumectomy, administration of a therapeutic dose of I131, inflammations, or excessive stimulation (massive release of TSIg by stress lympholysis, low iodine doses). Concurrently a massive conversion of T4 to T3 in tissues must occur which is enhanced by discontinuation of beta-blockers, thyrostatics, synthetic glucocorticoids and administration of drugs replacing T4 from the bond to plasma carries (salicylates, sodantone, furosemide, barbiturates etc.) during stress. The trigger mechanism of the crisis is any severe stress (surgery, accidents, infection, childbirth) and the administration of iodine preparations. Their effect depends, however, on the dose, period of administration and the functional and morphological state of the thyroid gland. Small doses of iodine administered for a short period stimulate hormonogenesis, large doses (more than 10 mg/day), on the other hand, block the iodine pump, T4 and T3 secretion by the thyroid gland and conversion of T4 to T3 in tissues. In therapy specific procedures are involved: I. Block of T4, T3 synthesis and secretion a) ipodate, ioipanoic acid, Lugol's solution i.v. b) propycil, methimasol c) in iodine-basedowized goitres perchlorate and lithium II. Block of T4 to T3 conversion (iodine preparations, incl. amiodarone, beta-blockers, propycil, dexamethasone). III. Reduction of hypermetabolism (beta-blockers, Ca inhibitors) IV. Reduction of free T4 and T3 in blood stream (by plasmapheresis, haemoperfusion, haemodialysis) V. General provisions in intensive therapy (control of hyperpyrexia, dehydration, hypoxia, supraventricular arrhythmia and circulatory decompensation).