Cases reported "Thyroid Crisis"

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1/7. Hypokalemic thyrotoxic paralysis: a rare cause of tetraparesis with acute onset in Europeans.

    We describe a 21-year-old Italian male affected by hypokalemic tetraparesis with acute onset. In the emergency ward, the patient was agitated, with tachycardia (140/min) and systolic hypertension (180/70 mm Hg). He was not able to flex the lower extremities against a light resistance and furthermore, he was hypotonic and without tendon reflexes. One hour later he developed strength deficit of the upper extremities as well. Biochemical analyses revealed severe hypopotassemia (2.1 meg/l). After administration of 140 meq potassium phosphate, the patient began to improve, and 12 h after the onset he was able to walk normally. Successive investigations documented an undiagnosed case of Graves' disease. Thyrotoxic hypokalemic paralysis has been observed almost only in Asians, however, with this case and others reported, we believe that it should be considered as a cause of muscular paralysis also in Caucasians.
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2/7. Acute quadriplegia in a 34-year-old man.

    A 34-year-old man of Native American descent had flaccid paralysis of the extremities 2 days after a camping trip. He had no respiratory difficulty, sensory deficit, or abnormal reflexes. He was subsequently found to have a serum potassium level of 1.6 mEq/L, a thyrotropin level of <0.06 microIU/L, and a free thyroxin level of 5.30 ng/dL. Thyroid uptake and scan were consistent with those of Graves' disease. Symptoms rapidly resolved with potassium chloride, propranolol, prednisone, and antithyroid therapy. No further episodes occurred.
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3/7. Thyroid storm-induced multiple organ failure relieved quickly by plasma exchange therapy.

    We report a 54-year-old female patient in whom thyroid storm was improved dramatically by plasma exchange. The patient presented with tachycardia, high fever and pulmonary congestion, in addition to left hemiparalysis and dysarthria. serum thyroid hormone concentrations were markedly increased and computed tomography showed a fresh cerebral infarct, suggesting that she had thyroid storm precipitated by cerebral infarction. As there was no remarkable improvement even after 24 h of conventional therapy, plasma exchange was carried out using fresh frozen plasma. Consequently, her critical condition improved quickly. The half-life of thyroid hormones is so long that quick improvement is not always achieved even by sufficient doses of antithyroid drugs. Thus, plasma exchange in combination with conventional therapy appears to be effective in relieving the life-threatening state in our patient with thyroid storm precipitated by acute cerebral infarction.
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4/7. Thyrotoxic periodic paralysis associated with a mutation in the sodium channel gene SCN4A.

    Thyrotoxic hypokalemic periodic paralysis (THypoKPP) is an uncommon disorder with an unknown etiology. We describe a family in which the proband presented with paralysis and thyrotoxicosis. Because of similarities between familial hypokalemic periodic paralysis (FHypoKPP) and THypoKPP, we sequenced exon 12 of the SCN4A gene, which is known to be mutated in FHypoKPP. We identified an Arg672Ser mutation in the proband and his affected father, as well as the proband's brother. As the brother has paralysis without thyrotoxicosis, our finding suggests that the genetic spectrum of FHypoKPP and THypoKPP overlap. We speculate that thyroid hormone may exert a threshold or permissive effect in hypokalemic periodic paralysis. Non-thyrotoxic family members of individuals with THypoKPP may have an unrecognized risk for paralysis.
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5/7. Thyrotoxic periodic paralysis in a Latin-American taking acetazolamide.

    A Latin-American teenager was begun on a regimen of acetazolamide for a presumptive diagnosis of familial periodic paralysis. He presented 2 weeks later with near total body paralysis and was found to have florid manifestations of Graves' disease. Although thyrotoxic periodic paralysis occurs most frequently in Oriental males, it occasionally is found in Caucasians. Unlike familial, euthyroid, and periodic paralysis, thyrotoxic periodic paralysis may be worsened by administration of acetazolamide. Physical signs and laboratory evidence of hyperthyroidism must be sought in cases of periodic paralysis to differentiate the two diseases.
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6/7. Emergency surgery complicated by thyrotoxicosis and thyrotoxic periodic paralysis.

    A general anaesthetic was administered for emergency surgery to a patient with a bleeding gastric ulcer in the presence of undiagnosed thyrotoxicosis. The case is presented to illustrate firstly how hyperthyroidism may be masked by other acute illnesses, and secondly an unusual complication of thyrotoxicosis. The anaesthetic management of thyrotoxic patients undergoing incidental emergency surgery is discussed.
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7/7. Thyrotoxic periodic paralysis, an unusual cause of hypokalemic periodic paralysis.

    Over a two-year period two patients were admitted to the hospital with episodes of paralysis and hypokalemia. In the first patient, familial hypokalemic periodic paralysis was initially suspected. Only several months later was Graves' disease diagnosed and this diagnosis linked to thyrotoxic periodic paralysis. The second patient came to notice after treatment with thyreostatic drugs was stopped prematurely and paralysis together with hypokalemia developed. Thyrotoxic periodic paralysis, being rare outside asia, closely mimics the clinical presentation of familial hypokalemic periodic paralysis. Mainly men in the third decade with a negative family history are affected. Graves' disease is the most common cause of hyperthyroidism. This disorder is not always clinically apparent since signs of hyperthyroidism may be easily missed. Therefore thyroid function tests are part of the diagnostic workup of hypokalemic periodic paralysis. Correction of thyroid function is essential to treatment. The pathophysiology is still controversial.
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