[Dr.Vad]

Уважаемая Галина Афанасьевна!

Согласен, что поражение именно голосовой связки при тиреотоксикозе - крайне редкое заболевание, вот что удалось разыскать:

Retrospective review of cases with concurrent diagnosis of vocal cord paralysis and benign thyroid disease. Eight cases found, all with documented vocal cord paralysis, by laryngoscopy. Two patients were thyrotoxic: one had Graves' disease and the other had subacute thyroiditis.
Из Collazo-Clavell ML, Gharib H, Maragos NE. Relationship between vocal cord paralysis and benign thyroid disease. Head Neck. 1995 Jan-Feb;17(1):24-30

Все же, кажется, что родственники могли и сагравировать увиденное, гораздо важнее на мой взгляд, все же наличие клиники пипокалиемии, которая может быть потенциально фатальной, но и не всегда просто ее купировать.
Приведу фрагменты описания еще одного случая thyrotoxic periodic paralysis:

A 22-year-old Hispanic man was carried into the Emergency Department (ED) by family members with a chief complaint of paralysis beginning the night before. The patient awoke at 2:00 a.m. unable to walk without assistance due to lower extremity weakness. By morning his condition had deteriorated to paralysis of all four extremities. The patient had a history of binge drinking 2 days before presentation, followed by a 2-day history of diarrhea. The patient was not taking any medications. There was no family history of neuromuscular or endocrine disease.

On arrival the patient was awake and alert with a generalized flaccid paralysis. The patient was tachycardic to 127 beats/min, with a blood pressure of 126/56 mm Hg. The temperature was 37.6°C (99.6°F) and respiratory rate was 22 breaths/min. Examination of the head and neck did not reveal evidence of thyromegaly. Eye examination showed slight proptosis with midrange, reactive pupils. Cardiac examination showed tachycardia with good peripheral perfusion. The lungs were clear bilaterally and the abdominal examination was unremarkable. Motor examination was significant for flaccid paralysis of the lower extremities above the toes and of the upper extremities above the wrists. The patient's grip strength remained 5/5 bilaterally. Cranial nerves were intact as was sensation to light touch and pin prick. Deep tendon reflexes were diminished without clonus.

During the initial electrocardiogram (EKG), done within 5 min of arrival, the patient went into stable ventricular tachycardia closely followed by unstable ventricular tachycardia and, later, asystole. Advanced Cardiac Life Support protocols were initiated. Cardiopulmonary resuscitation was performed, the patient was intubated and defibrillated. The patient received a round of lidocaine, and was started on an amiodarone drip as well as intravenous KCl (40 mEq over the first 1/2 hour), the latter on the basis of a bedside stat-electrolyte potassium of 1.5 mmoles/L. After resuscitation the patient's rhythm returned to sinus tachycardia at 118 beats/min.

Initial laboratory investigation (drawn during the initial resuscitation) revealed a potassium level of 1.3 mmol/L, a sodium of 142 mmol/L, chloride 107 mmol/L, bicarbonate 18 mmol/L, glucose 174 mg/dL, blood urea nitrogen 16 mg/dL, creatinine 0.6 mg/dL, and calcium 9.0 mg/dL.

Despite intravenous potassium replacement the patient's potassium level continued to drop. Two hours after presentation, and despite another 40 mEq of intravenous replacement, the patient's potassium had fallen to 1.1 mmol/L. He was then given another 40 mEq of potassium intravenously, and 2 h later the patient remained profoundly hypokalemic with a potassium level of 1.5 mmol/L. He then received 20 mEq of potassium via a nasogastric tube for a total of 140 mEq in the first 3 h.

Over his ED course the patient became febrile, tachycardic at 179 beats/min, and agitated despite significant sedation. Further questioning of the patient's family members revealed a history of a "problem with his thyroid." The patient had been hospitalized 3 years prior and took medication for only 4 to 5 months after discharge. Given the additional medical history and a clinical picture consistent with thyrotoxicosis, the patient was given two 1-mg doses of intravenous propranolol. Less than an hour after the two doses of propranolol, the patient's heart rate had come down to 119 beats/min, and the potassium had increased to 4.6 mmol/L.

The patient was transferred to the Intensive Care Unit in critical condition where the potassium continued to climb to a peak of 7.5 mmol/L. Thyroid function tests returned and showed hyperthyroidism with undetectable levels of thyroid stimulating hormone (reference range 0.35–5.50 IU/mL), T4 was 23.5 g/dL (reference range 4.5–10.9 g/dL), T3 was 6.5 ng/mL (reference range 0.6–1.8 ng/mL). He was extubated the following day, and discharged in stable condition 3 days later.