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Ectopic Pregnancy Presenting as True Gestational Epilepsy

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SHYAMAL G, VIJAYALAKSHMI    10 November 2018

ABSTRACT

Ectopic pregnancy refers to implantation of fertilized egg in a location outside of uterine cavity including fallopian tube, cervix, ovary, cornual region of uterus and abdominal cavity. It is a life-threatening condition. Though it is familiar to physicians when it presents with abdominal pain, amenorrhea, vaginal bleeding, but when it gets ruptured patients present with weakness, dizziness, near syncope and low blood pressure. Ectopic pregnancy, presenting as multiple episodes of seizures, is difficult to distinguish from other causes of seizures. Here we describe a previously normal 24-year-old female, with no previous history of seizures, who presented with 8 weeks of amenorrhea and sudden onset of seizures (true gestational epilepsy).

Keywords

Ectopic pregnancy, seizures, true gestational epilepsy

Ectopic pregnancy refers to implantation of blastocyst anywhere else other than endometrial lining of uterus in the uterine cavity. It almost occurs 2 in every 100 pregnancies and over 95% involve oviduct. This is life- and fertility-threatening for further pregnancy. The rate of ectopic pregnancy was increased to 4-fold since 1970. The incidence of ectopic pregnancy for nonwhite is 1.5 times compared to whites. Although ectopic pregnancy is familiar to most of physicians, ectopic pregnancy presenting with atypical symptoms like new-onset seizures is very difficult to distinguish from other causes of seizures such as cerebral venous thrombosis, cerebrovascular accident, eclampsia, electrolyte disorders, neurocysticercosis, autoimmune encephalitis, anxiety, stress, hyperventilation, other structural disorders due to similar presentations. Here we describe a 24-year-old female with 2 months of amenorrhea who presented to emergency in altered sensorium after 7 episodes of generalized tonic-clonic seizures (GTCS) for which she was referred from a peripheral center.

CASE REPORT

A 24-year-old female presented to emergency department with altered sensorium following 7 episodes of GTCS. She had history of 2 months of amenorrhea and was a primi who was not aware of her pregnancy. On examination, her pulse rate was 95/minand blood pressure was 110/80 mmHg. Patient was pale and tachypneic. Patient was conscious and in post-ictal confusion with no other focal neurological deficits. Systemic examination was otherwise normal.Laboratory work-up revealed: Hemoglobin - 4.5 g/dL, leukocyte count - 8,900/mm3, platelet count - 1.2 lakh/µL. Blood urea levels of 48 mg/dL and creatinine level of 1.2 mg/dL. Sodium, potassium, chloride, calcium levels were 138 mEq/L, 3.3 mEq/L, 108 mEq/L, 4.0 mEq/dL, respectively; urine albumin was negative. Vanillylmandelic acid (VMA) levels were normal. Chest X-ray and CT brain with contrast were normal. Ultrasound abdomen showed an ill-defined hypoechoic lesion in pelvic region possibly due to ruptured ectopic pregnancy, 350 cc of volume collection. A diagnosis of ectopic pregnancy was made and patient was taken for emergency laparotomy. Laparotomy revealed clots and hemoperitoneum. Ampullary end of the left fallopian tube was found ruptured (Fig. 1 a and b). The clots, measuring about 550 g, were removed and around 1,000 mL of peritoneal fluid was drained. Hemostasis was achieved and tubes were transfixed and ligated. She was resuscitated with blood. Antiepileptic, injection phenytoin 100 mg t.i.d., was administered for 8 days. Antibiotic coverage was given and further course in hospital was uneventful. On further follow-up, she was seizure-free for a period lasting more than 6 months.

DISCUSSION

Ectopic pregnancy, the implantation of a fertilized ovum outside the uterine cavity, has been increasing in numbers and now accounts for 2% of all pregnancies in the United States.1 Worldwide, ectopic pregnancy remains the leading cause of maternal death in the first trimester.2 Ectopic pregnancy continues to be an important contributor to maternal mortality, morbidity and early fetal wastage in the first trimester of pregnancy.3The incidence is higher in women between 35 and 44 years of age and it is counted as 27 per 1,000 reported pregnancies.4Distribution of cases in percentage according to predisposing factors are pelvic inflammatory disease (47.5%), infertility treatment (22.5%), previous ectopic pregnancy (25%), tubal surgery (10%), lower-segment cesarean section (12.5%) and intrauterine contraceptive device (IUCD) insertion (12.5%).5 No single clinical feature accurately indicates ectopic pregnancy. Less than half of women with ectopic pregnancy exhibit the classic triad of a history of amenorrhea, abdominal pain and irregular vaginal bleeding. And, unfortunately, these features are seen commonly in patients with both viable (50%) and nonviable (25%) intrauterine pregnancies, as well as in threatened abortion, cervical irritation, infection and trauma.6Abdominal pain and vaginal bleeding are highly sensitive for ectopic pregnancy, but are not specific for the disorder. Pain located in the hypogastrium or iliac fossa may be mild-to-severe. Vaginal bleeding, present in 50-80% of patients with ectopic pregnancy, can be mistaken for a normal menstrual period. Pregnancy-associated symptoms of nausea and vomiting, breast tenderness and fatigue may be present. Lower abdominal and adnexal tenderness can be elicited in most women with ectopic pregnancy. Cervical motion tenderness, peritoneal signs and adnexal masses are most specific for ectopic pregnancy, but are not sensitive. An adnexal mass is palpable in less than 10% of cases; when it is detected, one-third of patients will have a contralateral ectopic pregnancy on ultrasonography. Symptoms of hemodynamic compromise (orthostasis, hypotension, shock) are becoming uncommon with earlier diagnosis of ectopic pregnancy, facilitated by improved detection methods.6The above-mentioned clinical features make the diagnosis of ectopic pregnancy easy, but when it presents with none of above-mentioned symptoms it, like our case, makes the diagnosis difficult. True gestational epilepsy is one of cause for seizures in pregnancy. An ectopic pregnancy can present as true gestational epilepsy like in our case. It is well-known fact that estrogens activate seizure foci and lower seizure threshold and progesterones dampen the seizure foci.7 Differential diagnosis of convulsion diagnosed for the first time during pregnancy include: eclampsia, thrombotic thrombocytopenic purpura,8 pheochromocytoma, neurofibromatosis, oxytocin infusion, water intoxication, cerebral vein thrombosis, neurocysticercosis,9 autoimmune encephalitis and anti-NMDA (N-methyl-D-aspartate) receptor encephalitis during pregnancy.10 Other metabolic and structural causes of seizures were ruled out from relevant investigations.During pregnancy, seizures presenting first time is called true gestational epilepsy.10 In our case, she did not have any past history of epilepsy and all above-mentioned and possible structural and metabolic causes were ruled out. In our patient, after removal of ectopic products of conception, there were no further episodes of seizures and at follow-up till now about 6 months, no further complications occurred. So, the convulsions could be attributed to ectopic pregnancy, which is very unusual.CONCLUSIONThere are many causes of seizures in pregnancy. Ectopic pregnancy, autoimmune encephalitis and neurocysticercosis have to be considered as some of the important differential diagnosis after ruling out common causes of seizures in pregnancy mentioned above. Early recognition of the disease and prompt treatment of the condition will be a lifesaving and fertility preserving measure.

REFERENCES

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  7. Gerard N Bamboo, Thomas P Duffy. Medical Complications During Pregnancy. 5th Edition, 411.
  8. Kafali H, Harma M, Harma M. Pseudoeclampsia: convulsion diagnosed for the first time during pregnancy; eclampsia versus epileptic or psychogenic seizures. Artemis. 2004;5(1):70-2.
  9. Suarez VR, Iannucci TA. Neurocysticercosis in pregnancy: a case initially diagnosed as eclampsia. Obstet Gynecol. 1999;93(5 Pt 2):816-8.
  10. Dalmau J, Gleichman AJ, Hughes EG, Rossi JE, Peng X, Lai M, et al. Anti-NMDA-receptor encephalitis: case series and analysis of the effects of antibodies. Lancet Neurol. 2008;7(12):1091-8.

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