Author
Information
Pandey N*, Jamdade K**, Gupta
AS
(* Second Year Resident, ** Assistant Professor *** Professor. Department
of Obstetrics and Gynecology, Seth G. S. Medical College & K.E.M.
Hospital , Mumbai , India
Abstract
Thyroid storm is a known
complication in a case of complete vesicular mole, although an uncommon one.[1]
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.[1]
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.
Introduction
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.[1]
Case
Report
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.
Discussion
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.[1]
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]
Conclusion
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.
References
1.
Berkowitz RS, Goldstein DP. Gestational
Trophoblastic Disease. In Jonathan S. Berek,
editor. Berek
and Novak’s Gynaecology. 15th ed. New
Delhi
2.
Laurent V, Besson L, Doussin JF, Rondelet B.
Hyperthyroidism induced by molar pregnancy. Ann Fr Anesth Reanim. Pubmed.1993;
12(4):424-7.
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.
Citation