A 52-year-old woman presented to
our emergency department with a history of progressively
increasing dyspnea on exertion and palpitation for four days.
She had been otherwise well and was not taking any medication
until two months earlier before this presentation when she
started to experience restlessness, diaphoresis and heat
intolerance. One week prior to this admission, she had
intermittent fevers, diarrhea, and cough with greenish sputum.
At the emergency department, her temperature was 39°C; blood
pressure, 124/78 mmHg; pulse rate, irregular with a rate of
156 beats per minutes; and respiratory rate, 32 respirations
per minute. Physical examination revealed a tremulous, anxious
woman in severe distress. The skin was moist. Grade 3/6
systolic murmurs at the cardiac apex and bilateral basal rales
were heard. An enlarged firm thyroid was palpable. There was
no exopthalmus, eyelid lag or stare. The remainder of the
physical examination was unremarkable. The chest radiograph
showed pulmonary congestion and cardiomegaly and ECG revealed
atrial fibrillation with rapid ventricular rate. Laboratory
results are shown in Tables. After one hour at emergency
department, she was found collapsed and required endotracheal
intubation and mechanical ventilator support in the intensive
care unit. Thyroid function test revealed thyroid-stimulating
hormone (TSH), 0.022 μIU/mL (normal, 0.4- 4), free thyroxine,
3.85 ng/dl (normal, 0.58-1.64), and triiodothyronine, 19.17
pg/ml (normal 2.5-3.9).
Thyroid storm was diagnosed.
High-dose propylthiouracil, propranolol, and intravenous
hydrocortisone followed by saturated solution of potassium
iodide were administered. Empiric antibiotic therapy for
pneumonia was also given. Thyroid sonography disclosed
bilateral diffuse enlargement of thyroid glands with
heterogenous echogenicity and increased vascularity. The
presence of thyroid auto-antibody in her serum specimen
supported the diagnosis of Graves’ disease. Fever and
tachycardia subsequently resolved and endotracheal tube was
extubated later. She was discharged home on propylthiouracil
and propranolol with a scheduled follow up at our OPD.
< Laboratory data
>
1. Hemogram
WBC |
RBC |
HB |
HCT |
MCV |
MCHC |
PLT |
K/μL |
M/μL |
g/dL |
% |
fL |
g/dL |
K/μL |
15.90 |
3.9 |
12.6 |
36.4 |
88.6 |
35.8 |
168 |
2. Biochemistries and electrolytes
ALB |
TP |
T-Bil |
AST |
ALT |
ALP |
γ-GT |
Glucose |
g/dL |
g/dL |
mg/dL |
U/L |
U/L |
U/L |
U/L |
mg/dL |
3.5 |
6.2 |
0.4 |
44 |
42 |
162 |
18 |
32 |
UN |
CRE |
Na |
K |
Ca |
CRP |
mg/dL |
mg/dL |
mmol/L |
mmol/L |
mg/dL |
mg/dL |
38.9 |
1.4 |
138 |
3.8 |
8.9 |
13 |
3. The baseline endocrinologic results
hsTSH |
FT4 |
T3 |
0.4- 4 μIU/mL |
0.58-1.64 ng/dl |
2.5-3.9 pg/ml |
0.022 |
3.85 |
19.17 |
** Abbreviations: hsTSH, high-sensitivity
thyroid-stimulating hormone; FT4: free thyroxine; T3,
triiodothyronine.
<
Discussion >
甲狀腺風暴
(thyroid
storm)是甲狀腺機能亢進非常少見的併發症,通常發生在甲狀腺亢進未治療或控制不良下,合併促發的因子而造成。合併促發的因子,包括有:感染、外傷、手術、脫水、內科疾病等種種生理壓力。至於以往因甲狀腺功能亢進而進行甲狀腺切除術所發生的甲狀腺風暴則少見,因現今術前多半已將甲狀腺功能控制到穩定且短期併服碘溶液後才開刀。甲狀腺風暴的致病機轉尚未清楚,有人認為是甲狀腺功能過高從而增加腎上腺素受體的數目及敏感度而導致身體的生理變化。臨床上,病人血中的甲狀腺荷爾蒙值並沒有明顯比其他甲狀腺功能亢進病人來得更高。甲狀腺風暴通常來得突然而進展快速,患者可能有體溫上升、心搏過快、情緒激動暴躁甚至精神混亂,有的則有胃腸道的症狀,諸如:嘔吐、腹瀉、腹痛甚至肝腫大及黃疸;而皮膚摸起來溫暖而潮濕;罹患者甚至會由於心律不整,併發心衰竭休克而死亡。診斷除了依賴臨床症狀和表徵外,實驗室檢查,包括:fT4及T3上升及thyroid
stimulating
hormone(TSH)低下。及時認知及給予適切的治療才能挽救病患的生命。其治療包括:(一)、抑制甲狀腺素之分泌與合成;
(二) 、對抗已存在血循中之甲狀腺素的效應; (三)、支持性療法;
(四)、治療誘發因子。(一)、抑制甲狀腺素之分泌與合成:抗甲狀腺藥物propylthiourecil(PTU)可抑制甲狀腺素的合成並阻斷週邊甲狀腺素(T4)轉換成較活動性的三碘甲狀腺素(T3),較無法阻止甲狀腺素週邊轉換作的methimazol為佳。服用一個小時後,施予碘溶液可阻斷甲狀腺素的釋放。另同時給予腎上腺皮質素,可阻斷甲狀腺素的釋放並抑制T4的週邊轉換T3。(二)、對抗已存在血循中之甲狀腺素的效應:
β
-腎上腺素阻斷劑,如:propranolol可控制心跳過快等心律不整;如果病患有氣喘,可改用選擇性阻斷劑,如:metoprolol或鈣離子阻斷劑,如:verapamil。(三)、支持性療法:降低體溫可採用物理性的方法,如:冰袋放在腋下和鼠蹊部、酒精擦拭
(只要不要過度退燒,造成寒顫即可);
退燒避免使用水楊酸製劑,因為水楊酸可能與甲狀腺素競爭血中結合蛋白、取代其位置而使其游離出來而加重病情。由於高熱及大量出汗,患者易發生脫水,應補充液體及電解質。另外,積極處理心衰竭,密切注意呼吸速率和尿液排出量。(四)、治療誘發因子:積極治療感染或其他疾患者。只有少數情況下因傳統的治療無效才需要血漿換置術(plasmapheresis)或血液透析。
<
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>
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