摘要
Mental changes are common in patients with thyrotoxicosis. These changes are usually mild, such as insomnia, poor concentration, anxiety and emotional lability. Severe cases, such as coma, are rare and usually happen in ”thyroid storm” according to previous literature. The diagnosis of ”thyroid storm” is a clinical one, which the cardinal criteria are high fever, severe tachycardia, gastrointestinal dysfunction and central nervous system dysfunction. Besides, as a consequence of acceleration in bone resorption, hypercalcemia may occur in thyrotoxicosis. However, the patient is rarely symptomatic due to the hypercalcemia. Herein, we report a middle-aged male who visited doctor firstly due to nausea and vomiting. Later on, hypercalcemia was found. Hyperthyroidism was not diagnosed until his condition deteriorated to coma. This 33-year-old man visited some hospital firstly due to nausea and vomiting. The endoscopy disclosed peptic ulcer. His symptoms did not improve after treatment. He visited another hospital where hypercalemia (12.4 mg/dL) was found and intact parathyroid hormone level was 32 pg/mL (normal range: 10-60). Consciousness became unclear though the hypercalcemia was ameliorated by normal saline and diuretics. He was in status of coma while arriving at our hospital. Physical examination revealed severe tachycardia (140-150/min), body temperature 36.9 and visible diffuse goiter. Laboratory data revealed mild hypercalemia (10.5 mg/dl) and prerenal azotemia (BUN: 78 mg/dL, creatinine: 1.8 mg/dL). Thyroid function test revealed TSH: ＜0.03μU/mL (normal range 0.35-5.5); T3 665.12 ng/dL (80-190); and Free T4 9.8 ng/dL (0.7-1.8). We treated the thyrotoxicosis with oral propylthiouracil 200 mg Q6H, propranolol 40 then 60 mg Q6H, diluted Lugol's solution 3 c.c. TID, intravenous hydrocortisone 100 mg Q6H, and a lot of fluid. Heart rate slowed down gradually. The serum calcium level checked on the third day was normal. Lugol's solution and hydrocortisone was discontinued after 4 days of use. The dosage of other medicine was decreased gradually, too. The serum calcium level on the 7th day was normal, too. He recovered his consciousness after 7 days of coma, but was confused for another 3 days before completely clear. There was no neurological sequela while seen after discharge. By the response to treatments, we thought the manifestations and hypercalcemia were attributed to thyrotoxicosis. This is a rare case of coma resulting from severe thyrotoxicosis, which nearly reached ”thyroid storm”, that was atypical because there was no fever. So we name it ”thyrotoxic coma”.
並列摘要
Mental changes are common in patients with thyrotoxicosis. These changes are usually mild, such as insomnia, poor concentration, anxiety and emotional lability. Severe cases, such as coma, are rare and usually happen in ”thyroid storm” according to previous literature. The diagnosis of ”thyroid storm” is a clinical one, which the cardinal criteria are high fever, severe tachycardia, gastrointestinal dysfunction and central nervous system dysfunction. Besides, as a consequence of acceleration in bone resorption, hypercalcemia may occur in thyrotoxicosis. However, the patient is rarely symptomatic due to the hypercalcemia. Herein, we report a middle-aged male who visited doctor firstly due to nausea and vomiting. Later on, hypercalcemia was found. Hyperthyroidism was not diagnosed until his condition deteriorated to coma. This 33-year-old man visited some hospital firstly due to nausea and vomiting. The endoscopy disclosed peptic ulcer. His symptoms did not improve after treatment. He visited another hospital where hypercalemia (12.4 mg/dL) was found and intact parathyroid hormone level was 32 pg/mL (normal range: 10-60). Consciousness became unclear though the hypercalcemia was ameliorated by normal saline and diuretics. He was in status of coma while arriving at our hospital. Physical examination revealed severe tachycardia (140-150/min), body temperature 36.9 and visible diffuse goiter. Laboratory data revealed mild hypercalemia (10.5 mg/dl) and prerenal azotemia (BUN: 78 mg/dL, creatinine: 1.8 mg/dL). Thyroid function test revealed TSH: ＜0.03μU/mL (normal range 0.35-5.5); T3 665.12 ng/dL (80-190); and Free T4 9.8 ng/dL (0.7-1.8). We treated the thyrotoxicosis with oral propylthiouracil 200 mg Q6H, propranolol 40 then 60 mg Q6H, diluted Lugol's solution 3 c.c. TID, intravenous hydrocortisone 100 mg Q6H, and a lot of fluid. Heart rate slowed down gradually. The serum calcium level checked on the third day was normal. Lugol's solution and hydrocortisone was discontinued after 4 days of use. The dosage of other medicine was decreased gradually, too. The serum calcium level on the 7th day was normal, too. He recovered his consciousness after 7 days of coma, but was confused for another 3 days before completely clear. There was no neurological sequela while seen after discharge. By the response to treatments, we thought the manifestations and hypercalcemia were attributed to thyrotoxicosis. This is a rare case of coma resulting from severe thyrotoxicosis, which nearly reached ”thyroid storm”, that was atypical because there was no fever. So we name it ”thyrotoxic coma”.