CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 5, September/October 2022 AFRICA 279 Case report 2 A 60-year-old female patient was admitted to the intensive care unit due to sudden convulsions accompanied by unconsciousness during an out-patient visit. The patient had had a normal fullterm vaginal delivery with significant postpartum haemorrhage 35 years earlier. She had been diagnosed with Sheehan’s syndrome and had been taking thyroid hormones and hydrocortisone, but had discontinued hormone replacement therapy in the previous 15 days. There was no history of sudden cardiac death or cardiovascular disease in the patient’s family. At admission, the ECG monitoring showed TdP and ventricular fibrillation. By administering 300 J of asynchronous electrical cardioversion, she was successfully converted to sinus rhythm. After cardioversion, the patient’s heart rate was 66 beats per minute and her blood pressure was 113/70 mmHg. Laboratory examination revealed abnormalities, including a decreased serum potassium level of 2.6 mmol/l, serum sodium level of 135 mmol/l, ACTH level of less than 1 pg/ml and elevated urinary free cortisol level of more than 3 240 µg/24 hours. The TSH level was 0.515 mIU/l, FT3 was 2.77 pmol/l, FT4 was 5.8 pmol/l, T3 was 1.35 nmol/l and T4 was 54.7 nmol/l, which suggested secondary thyroid dysfunction. Myocardial biomarkers, blood glucose, pituitary prolactin, GH, LH and FSH levels were in the normal range. A baseline ECG showed a prolonged corrected QT (QTc) interval of 692 ms with T-wave inversion in leads I, avL and V2–V6 (Fig. 4A). Due to recurrent episodes of polymorphic ventricular tachycardia, a temporary pacemaker was placed for ventricular overdrive pacing (Fig. 4B). Transthoracic echocardiography revealed preserved systolic function with a 56% EF and regional ventricular wall motion abnormality. Cerebral computed tomography (CT) showed empty sella (Fig. 5), confirming the diagnosis of Sheehan’s syndrome. Ventricular fibrillation and Sheehan’s syndrome were diagnosed according to the patient’s medical history and symptoms, experimental evidence, ECG findings and the entire disease course. After giving intravenous potassium, the patient’s potassium level improved to 4.1 mmol/l. Meanwhile, she was treated with intravenous esmolol for anti-arrhythmia. For hypopituitarism, intravenous steroids (hydrocortisone 100 mg tid and gradually reducing the amount) and thyroid hormone (levothyroxine 50 ug qd) were administered. With the normalisation of the QT interval on ECG (Fig. 4C), no additional ventricular tachycardia was observed and the temporary pacemaker was removed. The patient suffered severe brain damage and did not recover consciousness. She was discharged from our hospital after one month and given steroids (prednisone 5 mg bid) and thyroxine replacement therapy continually. Fig. 3. Brain MRI with longitudinal relaxation time (T1) weighted saggital position showed empty sella (red arrow). Fig. 4. ECG examination of case 2. A. Baseline ECG revealed a prolonged QTc interval of 692 ms with T-wave inversion in leads I, avL and V2–V6. B. The ECG after temporary pacemaker implantation indicated a ventricular pacing rate of 100 beats per minute. C. The ECG before discharge demonstrated a normal QTc interval of 422 ms. A B C
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