Pandey N*, Jamdade K**,
(* Second Year Resident, ** Assistant Professor *** Professor. Department of Obstetrics and Gynecology,
Seth G. S. Medical College & K.E.M.
Hospital, .) Mumbai, India
Thyroid storm is a known complication in a case of complete vesicular mole, although an uncommon one. This emergency situation can prove hazardous if proper and immediate corrective measures are not taken. Anesthesia and surgical procedures are known to precipitate a thyroid storm in a patient with clinical hyperthyroidism. In our present case, a patient of complete vesicular mole went into a thyroid storm without any obvious precipitating factors. Even though corrective measures were taken on a war footing, the patient developed dilated cardiomyopathy with congestive heart failure secondary to the brief episode. Patient eventually developed torrential bleeding for which emergency suction and evacuation was performed after which the patient stabilized. This case highlights the importance of being prepared for this complication in a case of complete vesicular mole even when obvious clinical features of thyrotoxicosis are absent.
Cases of hyperthyroidism in a patient of complete vesicular mole are mentioned in literature but thyroid storm is a rare complication.[2,3] Patients whose clinical course has been unsupervised can land up with this complication when precipitating factors are present such as infection, anesthesia or a surgical intervention performed on them without proper prophylactic treatment.
A 32 year old Gravida 4, Para3, Live 3, with 14 weeks’ gestation was referred to our tertiary care center with vaginal bleeding in a diagnosed case of vesicular mole. The patient had been bleeding on and off for 25 days, due to which she had received 5 units of blood over two days at a private center. The patient gave history of passing grape like mass on the day of referral. Other medical, surgical and past obstetric history was non-significant.
On examination, the patient’s general condition was fair. She had tachycardia with a pulse of 110/min and BP was 160/80 mm Hg. She was pale. Her respiratory and cardiac examination findings were within normal limits. On abdominal examination the uterus was 20 weeks in size, firm and relaxed. Per speculum examination showed bleeding through os. On vaginal examination the os was closed and fornices were free.
On investigations Hb was 10.9gm/dl, platelet count was 0.16 million/mm3 and total WBC count was 5,500/mm3. Her serum β-HCG level was 4.5 million mIU/ml. Thyroid function tests were sent. Ultrasonography (USG) of the pelvis was suggestive of a complete vesicular mole. Chest radiograph was within normal limits. Her liver, renal function tests and coagulation profile were within normal limits.
She was scheduled to undergo suction and evacuation in view of persistent vaginal bleeding. When the patient was connected to the cardiac monitors prior to administration of any medications, T wave inversion was noted in V3 and V4 chest leads. Serum electrolytes were sent and were normal. All of a sudden patient developed severe tachycardia with a pulse of 156 beats per min and a blood pressure of 170/110 mm of Hg. On auscultation of the chest, crepitations in all lung fields were heard. A clinical suspicion of a thyroid storm was made and the thyroid function test reports were requested urgently from the routine laboratory. Serum TSH levels were not detectable, T3 was 346 ng/dl and T4 was 27 mcg/dl. The diagnosis of thyroid storm was confirmed and an urgent cardiac and endocrine opinion was taken. She was administered a loading dose of 80 mg of neomercazole, 20 mg of propranolol and 300 mg of parenteral hydrocortisone. 2D Echo was done which showed an ejection fraction of 20%, left ventricular dysfunction and dilated cardiomyopathy. The patient developed torrential vaginal bleeding during her 2D Echo and was immediately shifted for emergency suction and evacuation after obtaining high risk consent (Grade IV anesthesia risk). Suction and evacuation was done under controlled general anesthesia. Estimated Blood loss was 1.2 L. Two units of blood were transfused. She was put on Continuous Positive Airway Pressure (CPAP) and shifted to ICCU for subsequent monitoring. She was managed with frusemide and spironolactone, ramipril 2.5mg OD, carvedilol 3.15mg BD, propanolol 10mg TDS and neomercazole 10mg TDS. The patient’s condition stabilized twenty four hours post procedure. Thyroid function tests were repeated daily. Free T3 levels fell from 4.04 nmol/L post procedure to 2.86 nmol/L one week after the procedure. Free T4 levels fell from 2.03 mcg/dl post procedure to 1.45 mcg/dl one week after procedure. Serum β-HCG levels fell from 0.616 million mIU/ml 48 hours post procedure to 0.141 million mIU/ml one week after the procedure. The patient was discharged and advised to follow-up regularly with the endocrinologist and gynecologist and to obtain serial β-HCG levels.
Complete vesicular moles leads to hyperthyroidism due to β -HCG component that stimulates the thyroid gland, although clinical hyperthyroidism occurs in only 7% of the cases.[1-5] Thyroid storm is an even rarer albeit serious complication of this condition. Anesthesia and surgical interventions are known to precipitate thyroid storm. In the present case, the patient went into a spontaneous thyroid storm without any obvious precipitating factor, probably due to very high β-HCG levels of 4.5 million mIU/ml. Cardiac failure developed secondary to dilated cardiomyopathy precipitated by the tachycardia. Once the molar tissue is evacuated, hyperthyroidism also settles secondary to the fall in β-HCG levels over a few weeks.[4,5]
We can conclude that every case of complete vesicular mole should be worked up for thyroid function tests and prophylactic measures should be taken against development of thyroid storm before any sort of surgical intervention is done on the patient.
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3. Klisiewicz AM, Teckie G, Raal FJ. Gestational trophoblastic neoplasia and disorders of thyroid function. JEMDSA. July 2008, Vol 13(2): 72-74.
4. Padmanabhan LD, Mhaskar R, Mhaskar A, Vallikad E. Trophoblastic Hyperthyroidism. JAPI. October 2003, Vol 51: 1011-1012.
5. Higgins HP, Hershman JM, Kenimer JG, Patillo RA, et al. The thyrotoxicosis of hydatidiform mole. Ann Intern Med. 1975 Sep;83(3):307-11.