Volume 3 Issue 9, September 2016

Chauhan AR

Pregnancy Following Ileal Augmentation Cystoplasty
Agrawal N, Pai K, Parulekar SV.

Implantation Of Silastic Band On Ovary
Valvi D, Parulekar SV.

An  External Os Stitch As Emergency Cerclage:  A Last Ditch Effort
Sonawane PK, Nanavati AM.

Combined Oral Contraceptive Induced Pancreatitis In A Case Of Polycystic Ovarian Syndrome
Agarwal N, Daigavane M, Samant PY.

Primary Anterior Vaginal Wall Leiomyoma
Lahade V, Shah NH, Khadkikar R.

Intracranial Bleed In Pregnancy
Satia MN, More V, Madhavi J.

Ruptured Ectopic Pregnancy In Communicating Rudimentary Horn Of Unicornuate Uterus
Shende D, Amin K, Chauhan AR.

Cesarean Scar Ectopic: Genesis Of Morbidly Adherent Placenta
Pardeshi SH, Thosar MA, Gupta AS.

Uterine Artery Embolization In The Management Of Retained Products Of Conception
Saxena N, Deshmukh P, Chauhan AR.


Chauhan AR

Neurological problems in pregnancy though rare, are associated with significant maternal morbidity and mortality, especially cases of stroke and epilepsy. In developed countries, they contribute to approximately 20 % of maternal deaths. Neurological conditions may pre-exist, occur for the first time in pregnancy or may be exacerbated by pregnancy. Neurological manifestations are seen in eclampsia, amniotic fluid embolism and acute fatty liver which are unique to pregnancy, while infective conditions like hepatitis E and falciparum malaria may have increased severity of neurological symptoms in pregnancy. Patients with pre-existing conditions like chronic hypertension or intracranial lesions may deteriorate in pregnancy or puerperium.
The obstetrician is most familiar with eclampsia and its management. Neurological manifestations include cerebral edema, subarachnoid hemorrhage, microinfarctions, hypertensive encephalopathy and changes in the visual cortex. Cerebral imaging, either computerized tomography (CT) scan or magnetic resonance imaging (MRI) reveal cerebral edema or PRES, i.e. posterior reversible (leuko-) encephalopathy syndrome, characterized by bilateral symmetrical cerebral edema of the white matter usually in the parieto - occipital area. Cerebral imaging should be reserved for those cases of eclampsia where the presentation is atypical, prior to 20 weeks of gestation or > 48 hours postpartum, and patients with focal deficits or prolonged coma.
Apart from pregnancy - specific causes, etiology of altered mental state and coma in pregnancy include vascular causes such as infarction, intracerebral bleed, cerebral venous sinus thrombosis and hypertensive encephalopathy, infections like meningitis and cerebral malaria, tumors like meningiomas, tuberculomas and pituitary tumors, metabolic conditions like hypoglycemia, hyponatremia and hepatic encephalopathy, and drugs and toxins.
Neurological conditions in women of child bearing age are numerous but usually categorized in four broad unrelated groups: epilepsy, stroke, multiple sclerosis and headache/ migraine, which are described briefly below.
Epilepsy is the most common; approximately 7 % of epileptic patients conceive, and 0.5 % of all pregnancies are complicated by epilepsy. Even well controlled cases may have at least one convulsion in pregnancy; in a third of cases, there is a worsening of seizure control. This is attributable to a variety of causes, mainly poor control peri- conceptionally, change of medication, non- compliance due to fear of teratogenicity, physiological changes of pregnancy, stress and sleep deprivation. Pregnant women should ideally be managed on only one anti- epileptic drug in the least dose in pregnancy. Solitary convulsion may not cause problems to mother and fetus but status epilepticus or convulsions during labor are associated with high maternal and perinatal mortality. Incidence of congenital malformations is reported to be 4 - 6 %; phenobarbital is probably the least teratogenic anti- epileptic.
Stroke, an acute neurological impairment that may be either ischemic or hemorrhagic, is a rare but serious complication of pregnancy, with a 4 - 5 times increased incidence as compared to non pregnant women. Hypercoagulable state of pregnancy and venous stasis are important physiological risk factors, along with uncontrolled systolic hypertension and eclampsia. Co - morbidities like obesity, diabetes, renal and heart disease and vasculopathies increase the incidence of vascular events. Sudden onset weakness of face or limbs, confusion, difficulty in speech, vision or walking, loss of balance or severe headache may indicate infarction or hemorrhage and warrant neuroimaging to confirm the diagnosis. Stroke should be treated aggressively and fibrinolytic treatment with tissue plasminogen activator should be instituted, ideally within 1 - 3 hours of presentation.
Multiple sclerosis (MS) is a progressive demyelinating disease of the central nervous system characterized by neuro-inflammation and neuro- degeneration; incidence is 3.6 per 100,000 and is more common in Western countries. The disease is usually diagnosed in the 20s and 30s, and has a long course (onset to death is about 38 years). Hence most women will become pregnant prior to worsening of their symptoms. These patients are usually on disease modifying drugs like interferons and synthetic polypeptides like glatiramer acetate, which ideally should be stopped pre- conceptionally. Additionally they may be on  antidepressants and antimuscarinics which also require close monitoring. Though pregnancy may have a favorable effect on MS in first and second trimesters, spasticity and relapse may occur postpartum. Treatments with corticosteroids and intravenous immunoglobulins have been tried.
Neuroimaging in the form of CT scan and MRI form the mainstay in diagnosis. Most practitioners and patients are reluctant to perform these tests in pregnancy, but the risk of fetal exposure with CT scan is < 0.0005 rad; this can be further minimized with abdominal shield. In suspected cases of intracerebral hemorrhage, the benefits far outweigh the risks and timely treatment can be instituted after imaging. In most cases, MRI or MR venogram is preferred as it offers better resolution, however it is time consuming and cumbersome to perform, especially in latter stages of  pregnancy. Women have difficulty remaining supine for any length of time due to aortocaval compression, and experience claustrophobia. Other interventional radiological procedures like digital subtraction angiography (DSA) may be advised to visualize cerebral or spinal vessels in suspected aneurysms or arteriovenous malformations; clinicians should weigh the benefits of complete diagnosis against the potential risk of radiation to the fetus.
Previous issues of the journal have carried reports on some of these conditions in pregnancy, like myasthenia gravis, pituitary macroadenoma and acoustic schwannoma. This issue carries an interesting case of stroke in the third trimester which we hope will be of use to the reader.

Pregnancy Following Ileal Augmentation Cystoplasty

Author Information

Agrawal N*, Pai K**, Parulekar SV***.
(Third Year Resident, ** Assistant Professor, *** Professor and Head, Department of Obstetrics and Gynecology, Seth G S Medical College & KEM Hospital, Mumbai, India.)


Paraganglioma of the urinary bladder is found not commonly during pregnancy. Its management often involves excision of the urinary bladder, which may require an augmentation cystoplasty at a later date. Management of pregnancies after an augmentation cystoplasty can be quite challenging. We present such a case managed successfully.


Though pregnancies following urological procedures have increased significantly, little information is available regarding pregnancy outcome in women who have undergone augmentation cystoplasty.[1] We report a case of previous Lower Segment Caesarean section (LSCS) with augmentation cystoplasty done after paraganglioma excision which had resulted in Vesicoaginal Fistula (VVF).VVF was then corrected at a later date by Martius flap after which the symptoms  had subsided but not completely resolved .Our patient underwent emergency LSCS for previous LSCS with previous VVF repair surgery at term. The obstetrician should work along with urologists in management of such cases.

Case Report

A 27 year old , Gravida 3 Para2 Living 1 IUFD1 with 38 weeks’ gestation was admitted for safe confinement. She was a known case of paraganglioma excision with partial cystectomy with augmentation cystoplasty followed by VVF repair. She was diagnosed with bladder paraganglioma 2 years ago when she was pregnant with her second child. Ultrasonography (USG)  and  magnetic resonance imaging (MRI) of the abdomen and pelvis had revealed a 6.5 x 5.5 cm mass in inferior wall of bladder, a 10.8 x 5.6 cm hematoma within the bladder with intrauterine gestation of 12 weeks. Partial cystectomy with paraganglioma exicion was done at 3rd month of gestation after transurethral biposy of tumor showed a paraganglioma of the bladder. She made an uneventful recovery thereafter though she continued to dribble some urine all the time. She underwent LSCS at 38 weeks for breech presentation, delivering a 2.8 kg baby.  Patient had continuous dribbling of urine, 6 months after the LSCS, due to small capacity of bladder for which she underwent augmentation cystoplasty using ileal segment. Her symptoms had not relieved  and perspeculum examination showed leakage of urine along left anterolateral wall of the vagina about 4 cm from introitus suggestive of a vesocovaginal fistula (VVF).VVF repair with Martius flap interposition was done by vaginal approach. One month following VVF repair, she conceived and she was advised medical termination of pregnancy(MTP) in view of  recent major VVF repair, possibility of injury to augmented bowel, intestinal obstruction during delivery, and recurrence of VVF after delivery. She deferred her decision for some time after which she was beyond the legal limit for termination and she continued her pregnancy. She followed up regularly in the antenatal and urology clinics. Her renal function tests (RFT), urine routine microscopy and culture sensitivity were regularly monitored. Her plasma free normetanephrine level was also normal. She was  admitted for safe confinement at term. Her RFT, urine routine microscopy and urine culture sensitivity were within normal limits. She  underwent emergency LSCS in view of previous LSCS with previous VVF repair surgery. Urologist were informed and kept standby. A liberal infraumblical vertical incision was given. Intraoperatively uterovesical fold was seen densely adherent to the lower uterine segment.A segment of ileal loop was seen near the lower segment of uterus. A transverse incision was taken 3 cm above the uterovesical fold without dissecting adherent uterovesical fold and disturbing augmentation cystoplasty and its blood supply. Exteriorizing the uterus revealed a bicornuate uterus with rudimentary left horn. LSCS was uneventful and she delivered female child of 2.4 kg. Postoperative course of the patient was uneventful and on discharge she was advised to follow up in postnatal and urology clinics.

Figure 1. Ileal loop near the lower uterine segment.

Figure 2. LSCS scar in a bicornuate uterus with left rudimentary horn.


VVF is still one of the common uro-gynecological problems in developing countries. Though obstetric causes commonly result in VVF in developing countries, our case was following an elective urological procedure of partial cystectomy for excision of a paraganglioma of the urinary bladder. Pregnant women with VVF or history of VVF repair should be managed in a tertiary center where facilities of LSCS, senior consultants and urologists are available. All patients with history of VVF repair should be posted for elective LSCS or an emergency LSCS, in case patient is in labor. There are very few case reports of pregnancy following abdominal cystoplasty procedure.[2,3] There are some anatomical changes occurring after bladder augmentation. Ileo-cystoplasty involves fixing it cranially by the mesentery, laterally by ureter, and caudally by the trigone and urethra.[1] When the uterus enlarges, mesentery shifts to one side reaching the anterior abdominal wall. There is possibility of damage to augmentation or its blood supply in a cesarean section. Previous pelvic surgery may also lead to dense adhesions. For these reasons, some authors recommend the upper-segment cesarean section rather than the LSCS in such cases.[4] A urologist should be kept standby before the LSCS is started as they are well versed with an augmented bladder. In the case presented, as no dense adhesions were found near the lower uterine segment after taking a liberal midline infraumbilical vertical incision, a decision to go ahead with a LSCS was taken. The bladder dissection away from the lower uterine segment which is a standard step in a routine LSCS can be avoided if possible as it may disrupt the repair already done. As the ileum is mobilized for maintaining the vascularity, risk of bowel injury during LSCS should be kept in mind. The cesarean section should be performed by senior consultants not only to prevent such injuries but also to detect them in case inadvertent injury occurs. Proper antenatal care should be given to all women who have undergone augmentation cystoplasty. Early registration, identification of high risk factors like urinary tract infection(UTI) and its aggressive management, and monitoring of renal function, diagnosing hydronephrosis on USG is important in optimum management of these patients.[5]


The goal of management of patients with augmentation cystoplasty is safe delivery resulting in a healthy baby, while preserving of urinary tract integrity and renal function. The problems frequently encountered in these patients are urinary infections, hydronephrosis, or deterioration in renal function. The obstetrician and the urologist should work in unison in managing the problems of such women, preferably in a tertiary center.

  1. Hautmann RE, Volkmer BG. Pregnanacy and urinary diversion. Urol Clin N Am.2007;34(1):71–88. 
  2. Quenneville V, Beurton D, Thomas L, Fontaine E. Pregnancy and vaginal delivery after augmentation cystoplasty. BJU Int. 2003;91(9):893–4.
  3. Shaikh A, Ahsan S, Zaidi Z. Pregnancy after augmentation cystoplasty. J Pak Med Assoc. 2006;56(10):465–7. 
  4. Greenwell TJ, Venn SN, Creighton S, Leaver RB, Woodhouse CR. Pregnancy after lower urinary tract reconstruction for congenital abnormalities. BJU Int. 2003;92(7):773–7.
  5. Deepa Kapoor, Saurabh Sudhir Chipde, Shalini Agrawal, Surabhi Chipde, and Rakesh KapoorDelivery after augmentation cystoplasty: Implications and precautions J Nat Sci Biol Med 2014 Jan;5(1):206-209.

Agrawal N, Pai K, Parulekar SV. Pregnancy Following Ileal Augmentation Cystoplasty. JPGO 2016. Volume 3 No. 9. Available from: http://www.jpgo.org/2016/09/pregnancy-following-ileal-augmentation.html

Implantation Of Silastic Band On Ovary

Author Information

Valvi D*, Parulekar SV**.
(* Assistant (Professor, ** Professor and Head, Department of Obstetrics and Gynecology, Seth GS Medical College & KEM Hospital, Mumbai, India.)


Silastic band or falope ring application is the most popular technique of laparoscopic tubal ligation in India. Once mastered, the technique is straightforward to use. However the learning curve is quite steep, and there can be a number of errors in the learning phase. Losing silastic bands in the peritoneal cavity is one such error. We present a case in which such a lost silastic band got implanted on an ovary secondarily. This is the first case of this type in the world literature.


Falope rings are made of a combination of silicone and rubber which allows specific elasticity with a solution of 5% barium sulphate.  Barium sulphate allows identification of ring on radiologic imaging.[1] These rings has high degree of elasticity and 97 to 100% memory.  These are biocompatible and bio durable. They do not cause foreign body reaction or infection. As the falope ring contracts due to its elasticity, it constricts the base of the loop and blocks the fallopian tube. Deprived of its blood supply, the constricted loop is resorbed. With use of falope ring risk of complication and the subsequent pregnancies are lowest and benefit is greatest.  Full visualization of fallopian tubes and proper instrumentation eliminate the risk of misapplication of rings to the ligaments or bowel.

Case Report

A 48years old woman Para 1 living 1 abortion1 presented with abnormal uterine bleeding which was found to be due to uterine leimyomas enlarging the uterus to 18 weeks’ size. She had undergone laparoscopic tubal ligation 15 years back. Records and details of tubal ligation were not available. An abdominal hysterectomy was performed on her after ultrasonography for confirmation of the diagnosis and investigations for fitness for anesthesia. During hysterectomy it was found that one falope ring was adherent to the left ovary (figures 1 and 2). Tubal ligation sites were normal and falope rings were seen at the tubal ligation site, one on each fallopian tube. There were no falope rings lying free in the peritoneal cavity.

Figure 1. Falope ring adherent to the surface of the left ovary.

Figure 2. Falope ring adherent to the surface of the left ovary, another view.


Laparoscopic female sterilization with falope rings is a minor procedure. However it is not simple and the learning curve is quite steep. The operator must be skilled and well acquainted with the instruments and every part of the procedure of laparoscopic sterilization using falope rings. Complication like misapplication of ring to uteroovarian or round ligament, or mesosalpinx can occur, leading to failure of the sterilization procedure and a pregnancy. If it is applied to the bowel, there is risk of perforative peritonitis. Nonapplication of rings is seen when the operating surgeon is inexperienced or during learning period. Loss of rings in the peritoneal cavity can also occur during procedure.[2] Severe inflammatory reaction and peritonitis are noted following falope ring tubal ligation reported in the review of literature.[3] Postoperative salphingitis causing detachment of falope ring also reported in review of literature.[4] In our case a falope ring was adherent to the left ovary. It could not have been primarily applied to the ovary, because the firm and smooth tissue of the ovary cannot be drawn into the falope ring applicator by the prongs of the applicator. Any such effort would result in the prongs cutting through the ovary during application of ring. Falope rings are inert, biocompatible and bio durable and do not cause foreign body reaction. Hence they do not get adherent to any structure in the body.  Adherence of the falope ring to the ovary may be explained by positioning of a free lying intraperitoneal ring over the stigma of an ovarian follicle after ovulation, and its entanglement in subsequent healing process. Another explanation is that pelvic inflammation and subsequent fibrosis could have trapped a free lying intraperitoneal ring over the surface of the ovary. In our case there was no evidence of past pelvic infection and fibrosis. So the former explanation seems to be the most likely cause of the falope ring getting adherent to the ovary.
Though free lying falope rings are not reported to cause any complications, they indicate lack of expertise in performing the procedure, and that in the evnt of failure of sterilization, may contribute to evidence of negligence. Our case report helps to draw attention to occurrence of loss of falope rings in the peritoneal cavity and its implications.

  1. Laparoscopic sterilization: prevention of failure; Schmidt, E, Diedrich, J. Glob libr women's med 2014; DOI 10.3843/GLOWM.10402\
  2. Phipps JH, Drife JO. Postoperative salphingitis causing detachment of a falope ring; Journal of Obstetrics and Gynecology 1988:l8(4),367.
  3. Aubert JM, Garcia A. Improving falope-ring application in laparoscopy training. J  Reprod Med 1987 May: 32(5):340-2.
  4. Severe pelvic inflammatory disease and peritonitis following falope ring tubal ligation; LoBue C., J Reprod Med1981;26(11):581-4.

Valvi D, Parulekar SV. Implantation Of Silastic Band On Ovary. JPGO 2016. Volume 3 No. 9. Available from: http://www.jpgo.org/2016/09/implantation-of-silastic-band-on-ovary.html

An External Os Stitch As Emergency Cerclage: A Last Ditch Effort

Author Information

Sonawane PK*, Nanavati AM**.
(* Associate Professor, ** Registrar, Department of Obstetrics and Gynecology, K. J. Somaiya Hospital And Research Centre, Mumbai, India)


A 28 year old G2P1L1 with previous lower segment cesarean section (LSCS) done in view of breech presentation came at 26 weeks of gestation with 4-5 cm dilated fully effaced cervix with membranes bulging out of external os. Emergency cerclage was performed. With good postoperative care the pregnancy reached till term after which a healthy child was delivered by LSCS, thus justifying that rescue cerclage can be attempted as a last ditch effort.


Rescue cerclage is a cerclage performed emergently after the cervix is found to be dilated, effaced, or both, in the absence of labor pains prior to 28 weeks of gestation.[1] Usually a cerclage is performed in the following two situations: history indicated cerclage  done at 12 -14 weeks gestation for those with a high risk for preterm birth and midtrimester miscarriage, or an ultrasound indicated cerclage done when a transvaginal USG suggests cervical length less than 25 mm.

Case Report

Our patient was a 28 year old G2P1L1 with previous LSCS done in view of breech presentation. She presented at 26 weeks of gestation with a feeling of heaviness in lower abdomen and something giving way through vagina. She had no complaints of pain in abdomen, leaking or bleeding PV. There was no history of abnormal vaginal discharge or fever. She had undergone a hysteroscopic resection for  uterine polyp one year prior to this pregnancy. On abdominal examination, uterus was corresponding in size, fetal heart sounds were present and there was no uterine activity. On per vaginal examination, cervix was found to be fully effaced, 4-5 cm dilated with membranes bulging out of the external os. On per speculum examination the findings were confirmed.

Figure 1. Membranes bulging out of cervix.

After ruling out fetal anomalies on ultrasonography, the patient and relatives were counseled thoroughly. Decision for rescue cerclage was taken. Preoperative tocolytic was given and steep head low given under general anesthesia. Membranes were pushed back with sponge dipped in liquid paraffin with the help of a sponge holder. Purse string suture was taken with No. 1-0 monofilament nylon over external os, with the knot tied at 12 o'clock position.

Figure 2. Purse string suture at external os.

The patient was advised complete bed rest, perioperative tocolytics, antibiotics and vaginal progesterone tablets. A laxative  was prescribed to prevent unnecessary straining during passage of stools. After hospitalization for 2 weeks, she was discharged at 28 weeks on  request. She followed up regularly during the rest of her antenatal period which was uneventful. At 38 weeks an elective LSCS was performed in view of previous LSCS, and a 2.5 kg healthy female child was born. Knot was cut just before the cesarean section.


The decision of performing a rescue cerclage depends mainly on correct case selection, however one must remember the following factors contraindicate the procedure: active preterm labor, evidence of chorioamnionitis, rupture of membranes, evidence of fetal defects, fetal death and continuing vaginal bleeding.[2] The two known procedures for rescue cerclage are Espinosa Flores and Wurm procedures. Espinosa Flores procedure involves displacing the herniated membranes inside the uterus with a Foley catheter, and after grasping the anterior and posterior aspect of the cervix with ring forceps, a mersilene tape or polypropylene suture is inserted from anterior to posterior direction at 9 o'clock position of cervix and the other end of the tape is taken out through a bite from posterior to anterior direction at 3 o'clock position; the knot is tied anteriorly. In the Wurm procedure two “U” stitches of polypropylene sutures are taken, one vertically (from 12 to 6 o'clock and back to 12 o'clock) and the other horizontally (from 3 to 9 o'clock and back to 3 o'clock) through the cervix.[3] 
Reposition of the membranes during the procedure is an extremely important step in a cerclage procedure. This is sometimes made easier by tilting the operating table in a head down position and filling the bladder with 600 ml of saline, but this procedure carries the cervix further cephalad making the procedure difficult to perform. Some advocate using a No. 18 Foley catheter and inflating the balloon to 30 ml, where the balloon is used to push the membranes inside the cavity and then the balloon is deflated gradually as the cervical suture is being placed. Reposition can also be achieved by giving steep head low to the patient and using a gauze dipped in lignocaine jelly or liquid paraffin to avoid frictional injury to membranes while the sutures are placed over the cervix.[1] 
Perioperative tocolysis and antibiotic coverage have been advocated to improve the outcome. While there are not many randomized controlled trials (RCT) regarding the choice and dosage of antibiotics and tocolytics to be used, a few uncontrolled retrospective studies do support the use of both perioperatively.[4,5] Sometimes the complications during a rescue cerclage are difficult to separate from the risks that are inherent to the underlying condition; risk of premature rupture of membranes with or without preterm delivery, neonatal morbidity and mortality are some of the common risks associated with rescue cerclage.[2] 
There are not many studies done with regards to the effectiveness of rescue cerclage, however the few studies available do suggest rescue cerclage to be a better option than expectant management by bed rest for patients with dilated cervix and bulging membranes. Daskalakis et al. evaluated the efficacy of emergency cerclage in cases with dilated cervix and protruding membranes and found that the mean prolongation of pregnancy (8.8 weeks) and the mean birth weight (2101 g) after cerclage placement was significantly higher from those of the bed rest group (3.1 weeks and 739 g, respectively).[6] Only a third of the patients  undergoing cerclage had preterm delivery before 32 weeks of gestation, while 94% of the patients belonging to the bed rest group delivered prematurely before 32 weeks. One RCT evaluating  rescue cerclage and bed rest against bed rest alone included 23 women who were confirmed to have cervical dilatation and bulging membranes on per speculum examination at a mean gestation of 22-23 weeks. Eight of 13 women in the cerclage group required emergency suture removal for maternal or fetal  indications prior to 36 weeks of gestation. Women in the cerclage group could prolong the pregnancy by  4 weeks more than those in the bed rest group (mean interval between randomization and delivery 54 days versus 20 days), there were significantly less number of preterm deliveries before 34 weeks of gestation (53%  in cerclage group as against all the patients in the bed rest group who delivered before 34 weeks). There was an improvement in neonatal survival (56% in cerclage group as compared to only 28% in the bed rest group) and a significant reduction in  neonatal morbidity.[7]   


There have been conflicting opinions regarding performing a rescue cerclage for prolongation of pregnancy and more RCTs and case studies are required to support the decision to perform a rescue cerclage, however with proper case selection, absence of obvious signs of infection and uterine activity and with sound technical expertise one can attempt a rescue cerclage as a last ditch effort in advanced cases.

  1. Mahmud G, Tasnim N, Abbas S. Rescue cerclage: A Ray of hope in advanced cervical incompetence. JSOGP. 2011; 1(1): 24-32.
  2. Royal College of Obstetrician and Gynaecologists. Cervical Cerclage: Green-top Guideline No. 60. 2011.
  3. Arias F. Cervical insufficiency. In: Daftary SN, Bhide AG. Practical Guide to High-Risk Pregnancy and Delivery. Noida, UP, India: Elsevier; 2008; 262-274.
  4. Abo-Yaqoub S, Mohammed AB, Saleh H. The effect of second trimester emergency cervical cerclage on perinatal outcome. J Matern Fetal Neonatal Med. 2012; 25(9): 1746 -9.
  5. Fuchs F, Senat MV, Fernandez H, Gervaise A, Frydman R, Bouyer J. Predictive score for early preterm birth in decisions about emergency cervical cerclage in singleton pregnancies. Acta Obstet Gynecol Scand. 2012; 91(6): 744-9. 
  6. Daskalakis G, Papantoniou N, Mesoqitis S, Antsaklis A. Management of cervical insufficiency and bulging fetal membranes. Obstet Gynecol. 2006; 107(2pt1): 221-6.
  7. Althuisius SM, Dekker GA, Hummel P, van Geijn HP. Cervical incompetence prevention randomized cerclage trial: emergency cerclage with bed rest versus bed rest alone. Am J Obstet Gynecol 2003; 189(4): 907-10.

Sonawane PK, Nanavati AM. An  External Os Stitch As Emergency Cerclage:  A Last Ditch Effort. JPGO 2016. Volume 3 No. 9. Available from: http://www.jpgo.org/2016/09/an-external-os-stitch-as-emergency.html

Combined Oral Contraceptive Induced Pancreatitis In A Case Of Polycystic Ovarian Syndrome

Author Information

Agarwal N*, Daigavane M**, Samant PY***
(* Third Year Resident, ** Assistant Professor, ***Additional  Professor, Department of Obstetrics and Gynecology, Seth G.S. Medical College and K.E.M. Hospital, Mumbai, India.)


Drug induced pancreatitis is a rare entity whose incidence is subject to physicians reporting cases after exclusion of other causes. The incidence has risen over years as new drugs continue to be invented. We report a case of acute pancreatitis induced by drospirenone containing oral contraceptive pill that recurred after self-readministration, thus confirming the etiology. Patient recovered well after supportive medical therapy.


Oral contraceptive (OC) pills have been implicated as causing acute pancreatitis (AP). Mortality in acute pancreatitis is 2.1–7.8 %.[1] In our case the patient had an attack of pancreatitis due to OCs and pancreatitis recurred on resumption of the drug. The patient was taking OCs for polycystic ovarian disease.

Case Report

A 20-year-old woman was admitted in surgery department with diagnosis of acute pancreatitis treated in a private clinic, who presented with recurrence. She was referred to us for complaint of irregular heavy vaginal bleeding off and on since menarche. For regularization of menses, she had been prescribed numerous 3 month regimes with various combined oral contraceptive (OC) pills containing ethinyl estradiol 0.05 mg + levonorgestrel 0.25 mg, ethinyl estradiol 0.03 mg + drospirenone 3 mg, ethinyl estradiol 0.02 mg + desogestrel 150 mcg, in last 10 years. Two years ago, she had been diagnosed with polycystic ovarian disease. At presentation to our hospital, the patient was on drospirenone containing pills for 3 months, last pill taken prior to the first episode and between two episodes of pancreatitis at interval of 43 days.
The patient had an episode of acute abdominal pain and was admitted in a private hospital. In view of raised ascitic fluid amylase and lipase, she was diagnosed as acute pancreatitis. She had no history of hyperlipidemia, food intolerance, smoking or drinking alcohol, gall stone disease, infection or abdominal trauma. There was no family history of coronary heart disease and hypertension.
Her investigations during the first attack showed hemoglobin: 9.2g/dl, white blood cell count: 8800 cmm, platelets: 4.0 lakhs. Thyroid function tests, liver enzymes, renal functions, lipid profile were normal, alkaline phosphatase: 273 U/L, ascitic fluid amylase: 462 U/L (range 25-125 IU/L), ascitic fluid lipase:1230 U/L (range 40- 290 U/L). Ascitic fluid cytology revealed lymphocytic rich effusion negative for malignancy, ascitic fluid bile salts and bile pigment were absent. Ascitic fluid polymerase chain reaction for tuberculosis was negative. Chest X-ray showed bilateral costophrenic angle haziness, with mild pleural effusion. Ultrasound showed polycystic ovaries and ascites. Abdominal computerized tomography (CT) scan showed bilateral basal pleural effusion with basal atelectasis, moderate ascites, and suspicious disruption of pancreas with pancreatitis.
She was treated with antibiotics and intravenous fluids. She recovered and was discharged after 10 days. The patient restarted OC pills on her own and after 13 days, developed similar acute abdominal pain and distension. She was brought to our hospital for the same. There was no vomiting or fever. She was pale, afebrile, and normotensive with mild tachycardia. She was tachypneic, air entry was decreased bilaterally. Severe tenderness was present in umbilical region.  She was admitted in surgery ward. CT scan confirmed pseudo cyst in lesser sac and pancreatitis with ascites. Her serum amylase was 39 U/L, serum lipase was 129 U/L. Gynecological reference was taken. In absence of other contributory factors, OC pills were considered as etiological factor for AP. She was advised to discontinue them. She was put on nasojejunal feed and supportive treatment. She was discharged after 10 days on full nasojejunal feed. She was advised medroxyprogesterone 10 mg /day from 16th to 25th day of menstrual cycle and follow up.
At follow up after 1 and 3 months, patient was asymptomatic. Nasojejunal tube was removed after 2 months. Patient took medroxyprogesterone for 1 cycle and had moderate withdrawal bleeding. From the next cycle she did not take progesterone. Her cycles were normal. She was put on tablet pancrelipase, which contains enzymes lipase, protease and amylase. At 3 months, her serum amylase was 43.7 U/L and lipase was 169 U/Lit.  Her only complaint was severe hair loss.


Pancreatitis may be caused due to alcohol abuse, gallstones, endoscopic retrograde cholangiopancreatography, trauma, hyperlipidemia, HIV infection, chronic hypercalcemia and certain medications.[2] A national survey in Japan in 1999 reported that 1.2 % of all cases of AP were drug induced.[1] Grendell cited studies from Czech republic and France that reported drugs to be the most likely cause in 5.3 % and 6.5 % cases respectively. Drugs may be the etiological factor in a patient with idiopathic acute pancreatitis.[3] Diagnosis of drug-induced acute pancreatitis is made after exclusion of other causes. Medications causing pancreatitis have been broadly classified into five categories: Ia, Ib, II, III, and IV, by Badlov and colleagues according to number of published case reports, evidence like positive rechallange test, exclusion of other causes of pancreatitis and latency period.[4] OC pills are classified in group Ib and ІI. There are two mechanisms by which hormonal pills lead to acute pancreatitis. First is hypertriglyceridemia, either an exacerbation due to drugs or it may occur de novo. Another mechanism is pill induced hypercoagulable state, leading to pancreatic necrosis. Other mechanisms include accumulation of metabolic toxins and hypersensitivity reaction.[5] Blake and Pitcher reported a case with normal lipids, who developed acute recurrent pancreatitis after being on conjugated estrogen (class Ia) for menopause.[6] In 2011, FDA approved fourth generation OC pill containing ethinyl estradiol and drospirenone. Drospirenone pill users have 6 times higher risk of thromboembolism compared to women who do not use OCs. The risk is twice that in women who take pills containing levonorgestrel.[7] Both ingredients estrogen and drospirenone have tendency for thrombosis. They may increase triglycerides, they also have mild diuretic property; both these properties may increase the risk of pancreatitis.[8] Pancreatitis leads to malabsorption syndrome and fatty acid deficiency which leads to hair loss as was seen in our patient on follow up.  Most women on OCs are young and healthy, and pancreatitis is otherwise unlikely in them. Hence drug-induced acute pancreatitis is diagnosed with history of drug use and possibly re-challenge.


In a young, healthy woman taking oral contraceptives and presenting with acute severe abdominal pain, the possibility of acute pancreatitis should be considered. Many cases are underreported or not published so the incidence of OC pills causing pancreatitis is unknown at present. Diligent history taking and exclusion of other causes clinches the diagnosis and helps prevent future administration of the drug.

  1. Sekimoto M, Takada T, Kawarada Y, Hirata K, Mayumi T, Yoshida M, Hirota M, Kimura Y, Takeda K, Isaji S, Koizumi M, Otsuki M, Matsuno S,  JPN guidelines for the management of acute pancreatitis: epidemiology, etiology, natural history, and outcome predictors in acute pancreatitis. J Hepatobiliary Pancreat Surg. 2006;13(1):10–24.
  2. Kaurich T. Drug-induced acute pancreatitis.  Proc (Bayl Univ Med Cent). 2008; 21(1):77–81
  3. Grendell JH. Editorial: Drug-induced acute pancreatitis: uncommon or commonplace? Am J Gastroenterol. 2011; 106(12): 2189–2191
  4. Badalov N, Baradarian R, Iswara K, Li J, Steinberg W, Tenner S. Drug-induced acute pancreatitis: an evidence-based review. Clin Gastroenterol Hepatol. 2007; 5(6): 648–61.
  5. Jones MR, Hall OM, Kaye AM, Kaye AD. Drug-induced acute pancreatitis: a review. Ochsner J. 2015;15(1):45–51. 
  6. Blake WE, Pitcher ME. Estrogen-related pancreatitis in the setting of normal plasma lipids: case report. Menopause. 2003; 10(1): 99-101.
  7. Wu CQ, Grandi SM, Filion KB, Abenhaim HA, Joseph L, Eisenberg MJ. Drospirenone-containing oral contraceptive pills and the risk of venous and arterial thrombosis: a systematic review. BJOG. 2013;120(7): 801-10. 
  8. Yasmin pancreatitis Lawsuit. https:// www.schmidtlaw.com/yasmin-pancreatitis-lawsuit.

Agarwal N, Daigavane M, Samant PY. Combined Oral Contraceptive Induced Pancreatitis In A Case Of Polycystic Ovarian Syndrome. JPGO 2016. Volume 3 No. 9. Available from: http://www.jpgo.org/2016/09/combined-oral-contraceptive-induced.html

Primary Anterior Vaginal Wall Leiomyoma

Author Information

Lahade V*, Shah NH**, Khadkikar R***.
(* Consulting Obstetrician and Gynecologist, ** Director, *** Consulting Obstetrician and Gynecologist, Vardann Multispeciality Hospital, Mumbai, India.)


Vaginal leiomyoma is an extremely rare benign smooth muscle tumor in the vagina. The etiology is unknown. It arises most commonly in smooth muscle layer of midline anterior vaginal wall. Patients are asymptomatic initially. Symptoms start with the growth of the leiomyoma due to compression when it grows larger in size. Most vaginal leiomyomas are not diagnosed clinically but only on histopathology. Sometimes they can be associated with leiomyomas at other locations in the body. The imaging findings are that of a well-defined enhancing soft tissue mass arising from the vagina. They may be confused with other vaginal tumors and even urethrocoele. A preoperative diagnosis is essential to decide the surgical plane and surgical route. We report a case of primary leiomyoma of the vagina arising from its anterior wall and presenting with complaints of lower abdominal pain and something coming out per vaginum.


The vaginal mucosa is a nonkeratinized, stratified squamous epithelium. Vaginal submucosa is composed of connective tissue with elastic fibers, lymphatics and venous plexus. The submucosa is surrounded by muscularis having a circular layer of muscle overlaid by a longitudinal layer. A layer consisting of loose connective tissue covers the muscularis. Tumors arising from the vaginal tissue include papilloma, haemangioma, polyp and rarely leiomyoma.
Leiomyomas are the most frequent gynaecological tumors that are seen in about 20-40% of women after 35 years of age. Commonly leiomyomas arise from uterus, however they may arise from extrauterine sites including cervix, vagina, round ligament, ovary, fallopian tubes, and uterosacral ligament. A firm single, globular or polypoidal mass appearing in the vagina is usually a leiomyomatous polyp arising from the cervix or from within the uterine cavity. Other conditions mimicking a vaginal leiomyoma include urethral diverticulum, cystocele, Skene duct abscess or vaginal malignancy. Vaginal leiomyomas are benign, solitary, smooth muscle masses, and when they enlarge in size, symptoms may include vaginal discharge, intermenstrual bleeding, dyspareunia, something coming out of vagina and urinary retention.[1] Diagnosis is usually difficult preoperatively but can be confirmed with the help of better imaging techniques such as magnetic resonance imaging (MRI). Diagnosis also can be confirmed either by frozen section or postoperative histopathology.

Case Report

A 40 year old female reported to our OPD for something coming out of vagina since six months. She had previous three full term vaginal deliveries and last delivery was 10 years back. She gave history of something coming out of vagina since six months, dyspareunia, white watery discharge since 6 months.  On examination, a mass of 8 x 8 cm was felt from the vagina anteriorly extending from urethral meatus to external os of cervix. It was single, non tender, firm to hard in consistency with a decubitus ulcer on it. The uterus could be felt separate from the mass and cervix could be visualized separately. Diagnosis of vaginal wall cyst or anterior vaginal wall leiomyoma was made.

Figure 1: Anterior vaginal wall leiomyoma.

Her routine biochemical and hematological investigations were within normal limits. Excision of vaginal leiomyoma under spinal anesthesia was planned. Bladder was catheterized and vaginally the extent of bladder was assessed by bladder sound. Vertical incision was made on the mass after infiltration with adrenaline and normal saline. Plane of cleavage was good with a defined capsule and the mass could be enucleated completely. The mass looked like a leiomyoma and was sent for histopathological examination.

Figure 2:  Enucleation of anterior vaginal leiomyoma.

On gross pathological examination, the mass was grayish white, 10 x 10 cm with whorled appearance. Microscopic examination showed fascicles and interlacing bundles of smooth muscle cells having elongated to oval nuclei with eosinophilic cytoplasm, the section also consisted of hypercellular areas. Intervening stroma showed inflammatory infiltrates with lymphocytes, polymorphs and few plasma cells. The diagnosis of leiomyoma was confirmed.


A leiomyoma of vagina is a rare condition. Majority of leiomyomas arise from the body of the uterus and sometimes from the cervix. Extrauterine sites include round ligament, uterosacral ligament, ovary and very rarely vagina and vulva.  Most of these cases are not diagnosed primarily as leiomyomas, and diagnosis can be established only by histopathology.
In the vagina, a leiomyoma usually presents as a single, intramural or pedunculated, solid or cystic, well-circumscribed mass arising most commonly from the midline anterior wall and less commonly from the posterior or  lateral walls  in women between 35-50 years of age. Ultrasonography usually diagnoses it to be a cervical leiomyoma. MRI shows it as a well-delineated solid lesion of low signal intensity in T1- and T2-weighted images, with homogenous contrast enhancement similar to myometrium.[2] 
These rare lesions are asymptomatic initially. Symptoms may arise due to compression from the growing tumor varying with the size and location of leiomyoma. Leiomyomas of vagina commonly are slow in growth and solitary in number. Presentation can be as urinary symptoms like increased frequency, urge and urinary retention due to pressure on the urinary bladder.[3] Other symptoms include dyspareunia and pelvic pain. Low back pain occurs due to pressure on the pelvic ligaments. If situated superiorly, they can involve the distal ureters to cause hydronephrosis, which can be assessed by intravenous urography. Large lesions may interfere with vaginal delivery. Though the lesion is usually benign, sarcomatous changes have been reported. There are case reports of leiomyosarcoma in the posterior wall of vagina.[4] Histopathology is the gold standard of diagnosis to rule out malignant change. 
On gross examination, it is firm, well circumscribed homogenous mass resembling its uterine counterpart. On cut section it is white to tan with a whorled pattern like any other leiomyoma. On microscopy, it consists of fascicles of uniform smooth muscle cells having a typical spindle shape with less prominent cell borders and pale eosinophilic cytoplasm. Cystic degeneration visualized as watery collection in the interstitium is seen in larger tumors.
Surgical management is always indicated, the only problem being the most effective approach. Excision and enucleation is the treatment of choice. Surgical removal of the tumor through vaginal route, preferably with urethral catheterization, is usually preferred as there is availability of good surgical plane. Sometimes vaginal approach may cause severe hemorrhage if the whole leiomyoma  is not approachable. It is advisable to choose abdominal route for such cases. For huge tumors, an abdominoperineal approach is needed to perform complete excision. Preoperative embolization may be helpful in reducing vascularity of such tumors before excision as these tumors at times present with life-threatening hemorrhage due to hypervascular nature.
Recurrences have been reported. Patients need to be followed up after surgery for chance of recurrence. The tumor is hormone-dependent and usually regresses after menopause. Though location of a leiomyoma in the vagina is rare, it should be considered in the differential diagnosis of a vaginal swelling.

  1. Chakrabarti I, De A, Pati S. J Midlife Health. 2011; 2(1): 42–43.
  2. Shimada K, Ohashi I, Shibuya H, Tanabe F, Akashi T. MR imaging of an atypical vaginal leiomyoma. AJR Am J Roentgenol. 2002;178(3): 752–4. 
  3. Leron E, Stanton SL. Vaginal leiomyoma- an imitator of prolapse. Int Urogynecol J Pelvic Floor Dysfunct. 2000; 11(3):196-8. 
  4. Sim CH, Lee JH, Kwak JS, Song SH. Necrotising ruptured vaginal leiomyoma mimicking a malignant neoplasm. Obstet Gynecol  Sci. 2014; 57: 560-563.

Lahade V, Shah NH, Khadkikar R. Primary Anterior Vaginal Wall Leiomyoma. JPGO 2016. Volume 3 No. 9. Available from: http://www.jpgo.org/2016/09/primary-anterior-vaginal-wall-leiomyoma.html

Intracranial Bleed In Pregnancy

Author Information

Satia MN*, More V**, Madhavi J***.
(* Professor, ** Assistant Professor, *** Third Year Resident, Department of Obstetrics and Gynecology, Seth G. S. Medical College and K.E.M. Hospital, Mumbai, India)


Acute neurological diseases complicating pregnancy are rare, yet they lead to devastating complications if not treated in time. Intracranial hemorrhage (ICH) leading to stroke is a life -threatening complication which is even more devastating when it occurs in a young patient of childbearing age. We report a case of a young woman who presented in third trimester with severe headache, acute confusional state and right -sided hemiparesis and was diagnosed as a case of intracerebral bleed on MRI brain. She required an emergency LSCS in maternal interest as the chances of the intracranial bleed increasing in size or the chances that an aneurysm if present, would rupture, were higher if she were allowed to progress spontaneously into normal labor. Patient was discharged with no neurological deficit.


Stroke, the sudden onset of brain dysfunction from a cause involving blood vessels is one of the most common causes of long-term disability.[1] It is defined as acute onset of focal neurological dysfunction without any other etiology. Diseases of the cerebral blood vessels are the most common causes of death in the developed world after cardiac diseases and cancer.  Differential diagnosis in a patient with acute focal stroke is primary /secondary cerebral tumors, subdural hematoma, cerebral abscess, Todd’s paresis, demyelination, hypoglycemia, encephalitis and hysterical conversion especially in patients who are likely to become pregnant.[2] In pregnancy, stroke is commonly seen in the late third trimester and immediate postpartum period. Intracranial hemorrhage leading to stroke is a life threatening complication carrying a 35 – 83 % maternal mortality risk.[3] The incidence of ischemic and hemorrhagic stroke is similar, being 3.5 - 5 per 1,00,000 pregnancies in developed countries.[4] Various causes of stroke described in literature include those that occur in young non-pregnant patients, and those that are seen only due to pregnancy. Diagnosis that are specific to pregnancy are pregnancy induced hypertension, amniotic fluid embolism and postpartum vasculopathy[5,6] and those not specific to pregnancy include venous sinus thrombosis, embolism due to cardiac or CNS causes or SLE  and rupture of an arteriovenous malformation or a cerebral aneurysm rupture; the last two causes being most common.[7,8]

Case Report

A 26 year old woman, second gravida with previous full term normal delivery was referred to our casualty at 36 weeks of gestation in view of acute confusional state with right sided hemiparesis. Patient was antenatally registered with a local municipal hospital with regular antenatal visits and had no significant medical or surgical illness. She had history of sudden onset of headache followed by loss of speech and inability to use right upper and lower limbs. Patient was brought to our hospital in a drowsy state, responding only to deep pain. She was immediately admitted to the medical intensive care unit. On examination her general condition was poor, she was drowsy and responding only to deep painful stimuli; vital parameters were stable, with pulse of 94/min and BP of 110/80 mm of Hg. Per abdomen examination revealed uterus corresponding to 34 weeks size with cephalic presentation, regular fetal heart rate of 140 bpm with minimal activity. Per vaginal examination findings were suggestive of early labor. Cardiovascular and respiratory system examination were within normal limits. Neurological examination was suggestive of a Glasgow Coma Scale (GCS) score of 6/15, with normal muscle power in all muscles except for right upper and lower limbs, where it was 2/5. Complete blood count showed hemoglobin of 10 gm%; platelet count was 2.5 lakh /mm3. Her INR was 1.1. Liver and renal function tests were within normal limits. Urgent MRI brain was done which was suggestive of large hemorrhage of 6.5 x 2.9 x 4.7 cm in the frontal region of the left cerebral hemisphere causing a midline shift of 6 mm to the right side. MR venogram of cerebral venous sinuses was done which was normal. Urgent neurosurgery opinion was sought and emergency LSCS was advised in maternal interest as the chances of the intracranial bleed increasing in size or the chances that an aneurysm if present would rupture were more if patient was allowed to progress spontaneously. Neurosurgical intervention was not advised. Patient was evaluated by the anesthesiology team and emergency LSCS under general anesthesia was done with very high risk consent. She delivered a male child of 2.1 kg with an Apgar score of 9/10 at one minute of life. The procedure was uneventful and she was shifted back to the medical intensive care unit for further medical management. Patient was on ventilator in the post-operative period. Medical care included intravenous antibiotics in the form of Piperacillin and Tazobactam to prevent ventilator associated pneumonia, along with fluid therapy and injection mannitol to control the intracranial tension. Supportive physiotherapy was also instituted. Patient remained in the same condition for almost seven days after which she started showing signs of improvement. Her GCS improved to 8/15. CT scan of brain on the tenth post-operative day revealed a marked decrease in the size of the hemorrhage to 4.7 x 1.3 cm. Patient was managed conservatively with no neurosurgical operative intervention as advised by neurosurgeons. Gradual weaning was done from the ventilator as there was improvement in her GCS score and she was extubated on day 22 post- LSCS. Her muscle power in the right upper and lower limbs improved to 4/5 and patient was completely conscious, oriented to time, place and person and was able to perform her daily activities. No active neurosurgical intervention was advised. She was discharged and asked to follow up with interventional radiologist after two months.

Figure 1. MRI plate on admission: Red arrow demonstrates the intracranial bleed in the left frontal area.

Figure 2. MR venogram showing all the normal cerebral venous sinuses.

Figure 3. CT scan post-delivery: A decrease in the size of the bleed as shown by the red arrow.


Various studies have found that pregnancy induced hypertension and AV malformations are the most common identifiable causes of ICH in pregnancy.[8,11] Of the 15 % of cases caused by hemorrhage, about half of them occur due to breach in the continuity of a blood vessel within the brain parenchyma, i.e. primary intracranial hemorrhage resulting in stroke, as seen in our patient. The other possible differential diagnoses in this patient could be either rupture of a small micro-aneurysm or AV malformation, but MR venogram done at the time of admission showed normal venous sinuses. Hence these diagnoses and that of any thromboembolism were ruled out. If the artery ruptures into the brain parenchyma and also into the subarachnoid space it is said to be a case of subarachnoid hemorrhage; these patients may present with acute focal stroke.[1] Hemorrhage frequently occurs into an area of brain infarct and clinical presentation of such patients is practically similar to those patients with primary intracerebral hemorrhage. 
ICH can be extradural, subdural, subarachnoid or intra-parenchymal. Intracerebral hemorrhage contributes to maternal mortality to a large extent. The risk of ICH associated with pregnancy is greatest in the postpartum period [9] and is responsible for 5–12 % of all maternal deaths.[10] Brain MRI and MR venogram are generally considered as the most important diagnostic tools in patients with ischemic stroke and cerebral venous thrombosis, respectively. The gestational age and the risk–benefit ratio should be taken into consideration before planning these tests. The risk from MRI is generally considered lower in the second trimester. A suspicion of subarachnoid hemorrhage is made in pregnancy when patients present with sudden onset headache with altered sensorium, vomiting and neurological deficit. These symptoms may be mistaken for preeclampsia, more so if they are associated with albuminuria.  To confirm the diagnosis CT scan should be done after adequate hydration and with abdominal shield to prevent fetal hazard. Severe PIH is the most common cause of PRES i.e. posterior reversible leuko encephalopathy syndrome, which is usually associated with reversible vasogenic edema, typically in the posterior portion of the brain. Most likely cause of PRES syndrome is auto- regulation abnormalities.[12] PIH also has been associated with the group of reversible cerebral vasoconstriction syndromes, where patients present with clinical symptoms like thunderclap headache which sometimes may be associated with neurologic deficits, along with reversible arterial segmental vasoconstriction.[13] These two reversible syndromes may go undiagnosed because the primary manifestation may be headache and visual scotomas, and priority in these patients is induction of labour and delivery.[14] These postpartum vasculopathies may be seen in patients totally uncomplicated and without the history of PIH. Investigations include cerebrospinal fluid analysis that is usually normal and imaging studies like angiography that may show multifocal narrowing in vasculature giving a picture similar to vasculitis. Maternal morbidity and mortality associated with postpartum angiopathy may be due to the associated infarction / hemorrhage.
The risk of rupture of small aneurysms or arteriovenous malformations during pregnancy is due to increased plasma volume, cardiac output, and changes in the vessel wall.[15]   Also other rare causes in pregnancy may be due to metastatic choriocarcinoma or substance abuse like alcohol and amphetamines,[16] postpartum cardiomyopathy that can result in embolism, or less commonly, watershed infarction from hypotension. 
Prevention of stroke during pregnancy in high-risk patients is similar to that used for thrombo-prophylaxis, with either unfractionated or LMWH in the 1st trimester, followed by warfarin, then heparin until delivery and warfarin in the postpartum period. Successful reperfusion is the treatment of choice. In the near future recombinant tissue plasminogen activator may be used to treat pregnant patients with acute stroke as interventional radiologists discover novel imaging modalities like MRI perfusion. In addition to these, direct thrombin inhibitors like dabigatran may be used in pregnancy for women who cannot be given heparin or warfarin. Dabigatran is currently US FDA category C drug and experimental research in humans will be required to find out the safety profile and the risk–benefit ratios.


Intracerebral bleed is a major cause of maternal morbidity and mortality and though the incidence of this devastating condition is variable, it presents special challenges in diagnosis and management. Research is required to formulate guidelines for prevention and treatment in pregnancy, since there is paucity of data available regarding the safety profile of common drugs, such as aspirin, aspirin/extended-release dipyridamole and clopidogrel. Multidisciplinary approach involving neurosurgeons, intensivists and obstetricians is of prime importance in the management of ischemic stroke or hemorrhage.

  1. Tate J, Bushnell C. Pregnancy and stroke risk in women. Women’s Health (London). 2011; 7(3): 363-74.
  2. Mc Allen, Leuck J. Diseases of nervous system. In: Walker B.R,  Colledge N.R, Ralston S.H, and Penman I editors.Davidson’s principles and practice of medicine.22nd edition. London: Churchill Livingstone 2014; 924-1006.
  3. Feske S. Stroke in pregnancy. Semin Neurol. 2007; 27(5): 442–452.
  4. Liu X, Wang S, Zhao Y, Teo M, Guo P, Zhang D et al. Risk of cerebral arteriovenous malformation rupture during pregnancy and puerperium. Neurology.  2014; 82: 1798-1803.
  5. Jaigobin C, Silver FL. Stroke and pregnancy. Stroke. 2000; 31: 2948–51. 
  6. Liang CC, Chang SD, Lai SL, Hsieh CC, Cheuh HY, Lee TH. Stroke complicating pregnancy and the puerperium. Eur J Neurol. 2006; 13:1256–1260.
  7. Davie CA, O’Brien P. Stroke and pregnancy. J Neurol Neurosurg Psychiatry. 2008; 79: 240–245.
  8. Tiel GA, Rinkel GJ, Van der Bom JG, Algra A, Klijn CJ. The risk of aneurysmal subarachnoid hemorrhage during pregnancy, delivery, and the puerperium in the Utrecht population: case-crossover study and standardized incidence ratio estimation. Stroke. 2009; 40: 1148–11.  
  9. Petitti D, Sidney S, Quesenberry CJ, Bernstein A. Incidence of stroke and myocardial infarction in women of reproductive age. Stroke. 1997; 28: 280–283.
  10. Dias M, Sekhar L. Intracranial hemorrhage from aneurysms and arteriovenous malformations during pregnancy and the puerperium. Neurosurgery. 1990; 27: 855–65. 
  11. Jeng JS, Tang SC, Yip PK. Stroke in women of reproductive age: comparison between stroke related and unrelated to pregnancy. J Neurol Sci. 2004; 221:25–29. 
  12. Lee V, Wijdicks E, Manno E, Rabinstein A. Clinical spectrum of reversible posterior leukoencephalopathy syndrome. Arch Neurol. 2008; 65: 205–210.
  13. Calabrese L, Dodick D, Schwedt T, Singhal A. Narrative review: reversible cerebral vasoconstriction syndromes. Ann Intern Med. 2007; 146: 34–44. 
  14. Bushnell C, Chireau MV. Preeclampsia and stroke: risks during and after pregnancy. Stroke Research and Treatment. 2011; v 2011:1-9. 
  15. Treadwell S, Thanvi B, Robinson T. Stroke in pregnancy and the puerperium. Postgrad Med J. 2008; 84: 238–245. 
  16. Wilterdink JL, Feldmann E. Intracranial hemorrhage. Adv Neurol. 2002; 90: 63–74.

Satia MN, More V, Madhavi J. Intracranial Bleed In Pregnancy. JPGO 2016. Volume 3 No. 9. Available from: http://www.jpgo.org/2016/09/intracranial-bleed-in-pregnancy.html

Cesarean Scar Ectopic: Genesis Of Morbidly Adherent Placenta

Author Information
Pardeshi SH*, Thosar MA*, Gupta AS**
(* Assistant Professor, ** Professor, Department of Obstetrics and Gynecology, Seth G. S. Medical College and K.E.M. Hospital, Mumbai, India)


Cesarean scar ectopic pregnancy and morbid adherent placenta though rare in occurrence their prevalence is constantly increasing. Both these conditions present diagnostic dilemma in early pregnancy as well as have similar finding on imaging and on histopathology. We present a case of scar ectopic in previous 2 lower segment cesarean sections (LSCS) with dilemma in diagnosis and histopathological corroboration to morbid adherent placenta.


Cesarean scar pregnancy (CSP) is defined as implantation of trophoblastic villi deep in the myometrium at the site of the previous cesarean scar  during  present pregnancy  and is a rare type of ectopic pregnancy, often leading to substantial morbidity. [1 ] Cesarean section scar pregnancies are thought to occur in 1 in 1800 pregnancies. Of all the ectopic pregnancies seen in women with past cesarean section, CSP is presumed to occur in 6 % of these women. [2 ] Morbidly adherent placenta (MAP) is a condition where placenta is adhered to the myometrium most commonly at previous LSCS scar. Misdiagnosis or delayed treatment can result in uterine rupture, intractable hemorrhage, and other complications. [3 ] The trend toward an increase in the cesarean section rate has also seen an increase in the number of cesarean section scar ectopic pregnancies as well as MAP.[4,5]  Recently multiple authors have put forth a hypothesis for both these conditions to be a part of the same spectrum of pathology progression.

Case Report

A 28 year-old graida 3 para 2 woman with previous two LSCS and 12 weeks of amenorrhea was referred to our gynecology clinic with a history of attempted suction evacuation done for a missed abortion a week back in a private hospital. During the procedure there was episodic torrential bleeding which stopped spontaneously. Procedure was abandoned but she required transfusion of two units of blood and fresh frozen plasma (FFP) each. The patient was referred to our tertiary care institute for further management.
On examination her vital parameters were within normal range. Mild pallor was noted. Abdominal examination showed a Pfannenstiel scar but no tenderness, guarding, rigidity or lump. On per speculum examination there was blood stained watery discharge, cervix was short, pulled up and cervical os was closed. On per vaginal examination uterus was 12 weeks in  size, anteverted, cervix deviated to left and lower segment was ballooned up. Ultrasound (USG) done initially in private hospital suggested a missed abortion of 12 weeks, while repeat USG done in our hospital after a week of initial USG stated the presence of a 7 × 6 cm heterogeneous hypoechoic lesion in uterus with interphase between lesion and myometrium at fundus and anterior wall obscured. MRI done to delineate detailed anatomy was suggestive of hematoma with retained products of conception. It failed to identify any adherent placenta. Serum β-HCG titers were 282 mIU/ml. The patient's hemoglobin was 8.6 gm %, rest of the reports including coagulation parameters were within normal limits.
With provisional diagnosis of missed abortion, decision for check curettage was taken. Consent was also taken for hysterectomy in view of previous history of bleeding. After cervical priming with misoprostol 400µg, check curettage was attempted during which few products of conception were removed but it was associated with torrential bleeding (figure 1).
A decision to perform obstetric hysterectomy was taken on table.  On opening the  abdomen the uterus was normal in size but the cervix was ballooned up to about 10 cm in diameter, uterovesical fold of peritoneum was extending above the mass, previous LSCS scar was thinned out and had a bluish discoloration (figure 2).

The products of conception were seen adherent to the previous scar site, which were removed and hysterectomy was done. The patient needed transfusion of 4 units of whole blood and 4 FFPs. Blood loss was about 2 L. She was discharged on day 5 of surgery with uneventful postoperative course. Histopathology of specimen showed the corpus endometrium to be proliferative, myometrium to be unremarkable. Cervix had foci of hemorrhage and numerous congested blood vessels but no chorionic villi. Excised scar that was sent separately showed myometrium with chorionic villi and adherent blood clots. No decidual tissue was seen. Products of conception that were evacuated by suction showed blood clots with infarcted chorionic villi. 

Figure 1. Products of conception removed on curettage.

Figure 2A and 2B. Ballooned out scar on the lower segment. Yellow arrows demarcate the ballooned out lower segment. Bluish discoloration is marked out by blue arrows. Black arrow delineates the previous scar. C is uterine corpus.

Figure 3. Area of the isthmus after amputation of the uterine corpus. Scar Ectopic with products of conception (P) adhered to myometrium (M) and also present in uterine (U.C.). Black arrow shows the scar area (anterior lower edge of the isthmus; scar area). Blue arrow shows the posterior lower edge of the isthmus.


Many theories explain the occurrence of intramural ectopic pregnancy. Invasion of the uterine muscle by the blastocyst through tiny, microscopic breaks or paths best explains the genesis of this condition. These are probably the  result of trauma from a previous cesarean section or any other uterine surgery or even after manual removal of the placenta.[3,6] Same mechanism is also proposed for the development of MAP. 
Vial et al proposed 2 types of scar ectopic pregnancies.[7] In the first type,  implantation of the gestational sac occurs on the uterine scar. This then progresses away from the uterine serosa and can grow either toward the cervico-isthmic space or towards the uterine cavity. Such a pregnancy may proceed to term developing in MAP, but with an increased risk of life-threatening massive bleeding from the site of implantation. In the second type pregnancy implants deeply into the scar tissue and its growth then progresses towards its external or the serosal layer. This culminates in rupture and bleeding during the first trimester of pregnancy. Some authors believe that the difference between those 2 types of pregnancy is of paramount importance to delineate development to MAP vs scar ectopic.[8] Typically, the diagnosis in both conditions is made based on ultrasound evaluation of the uterus and confirmed by MRI or during surgery. Sonography combined with Doppler flow imaging has been advocated as a useful diagnostic modality, with no need for a pelvic MRI for confirmation.[4,5] 
Timor-Tritsch et al did histological correlation in total of 58 cases (37 CSP and 21 MAP).[9] Finding of various degrees of invasion by trophoblastic villi into the uterine muscle or into the previous cesarean scar tissue associated with absent or scanty intervening deciduas as consistent with the classic definition of morbidly adherent placenta was also found in cases of CSP. 
Nagi et al reported a case of viable scar ectopic diagnosed in early pregnancy. The pregnancy was allowed to progress with meticulous follow up. By end of second trimester USG features were suggestive of placenta previa with accreta. Timor-Tritsch et al in a similar study followed 10 cases of CSP diagnosed in early pregnancy.[9] All 10 patients were diagnosed before 10 weeks gestation and subsequently exhibited signs of MAP on USG. Nine of the 10 patients delivered live born neonates between 32 and 37 weeks with cesarean hysterectomy. The 10th pregnancy was similar to our case. She had excessive vaginal bleeding requiring hysterectomy, at 20 weeks. All patients had histological features suggestive of MAP similar to histological features in our case.
We also support the hypothesis of MAP and CSP having similar origin. We feel that our patient had type 1 of scar ectopic pregnancy due to which products of conception were retrieved from the cavity during suction. Presence of chorionic villi in between the myometrium with absence of decidua suggests the formation of a MAP. As the fetal demise occurred she presented for evacuation. Had fetal demise not occurred she may have presented in advanced pregnancy with morbid adhesion of placenta. If CSP can be diagnosed in the first trimester as in our case then the woman may be able to choose to continue the pregnancy (expectant management ) or opt to terminate the pregnancy. The women willing for expectant management and continuation of pregnancy should be followed up in high risk obstetric center with facilities to manage morbidly adherent placenta. This case is being presented to highlight the fact that both these conditions could be two ends of the same spectrum.

  1. Nagi JB, Ofili-Yebovi D, Marsh M, Jurkovic D. First-Trimester Cesarean Scar Pregnancy Evolving Into Placenta Previa/Accreta at Term. J Ultrasound Med. 2005 Nov 1;24(11):1569–73. 
  2. Seow K-M, Huang L-W, Lin Y-H, Lin MY-S, Tsai Y-L, Hwang J-L. Cesarean scar pregnancy: issues in management. Ultrasound Obstet Gynecol. 2004 Mar;23(3):247–53. 
  3. Fylstra DL. Ectopic pregnancy within a cesarean scar: a review. Obstet Gynecol Surv. 2002 Aug;57(8):537–43. 
  4. Maymon R, Halperin R, Mendlovic S, Schneider D, Herman A. Ectopic pregnancies in a Cesarean scar: review of the medical approach to an iatrogenic complication. Hum Reprod Update. 2004 Dec;10(6):515–23. 
  5. Jurkovic D, Hillaby K, Woelfer B, Lawrence A, Salim R, Elson CJ. First-trimester diagnosis and management of pregnancies implanted into the lower uterine segment Cesarean section scar. Ultrasound Obstet Gynecol. 2003 Mar;21(3):220–7. 
  6. Cheng P-J, Chueh H-Y, Soong Y-K. Sonographic diagnosis of a uterine defect in a pregnancy at 6 weeks’ gestation with a history of curettage. Ultrasound Obstet Gynecol. 2003 May;21(5):501–3. 
  7. Vial Y, Petignat P, Hohlfeld P. Pregnancy in a cesarean scar. Ultrasound Obstet Gynecol. 2000 Nov;16(6):592–3.  
  8. Ghezzi F, Laganà D, Franchi M, Fugazzola C, Bolis P. Conservative treatment by chemotherapy and uterine arteries embolization of a cesarean scar pregnancy. Eur J Obstet Gynecol Reprod Biol. 2002 Jun 10;103(1):88–91. 
  9. Timor-Tritsch IE, Monteagudo A, Cali G, Vintzileos A, Viscarello R, Al-Khan A, et al. Cesarean scar pregnancy is a precursor of morbidly adherent placenta. Ultrasound Obstet Gynecol. 2014 Sep;44(3):346–53. 
  10. Timor-Tritsch IE, Monteagudo A, Cali G, Palacios-Jaraquemada JM, Maymon R, Arslan AA, et al. Cesarean scar pregnancy and early  placenta accreta share common histology. Ultrasound Obstet Gynecol. 2014 April;43(4):383-95.

Pardeshi SH, Thosar MA, Gupta AS. Cesarean Scar Ectopic: Genesis Of Morbidly Adherent Placenta. JPGO 2016. Volume 3 No. 9. Available from: http://www.jpgo.org/2016/09/cesarean-scar-ectopic-genesis-of.html

Uterine Artery Embolization In The Management Of Retained Products Of Conception

Author Information

Saxena N*, Deshmukh P**, Chauhan AR***
(* Ex- Registrar, ** Third Year Resident, *** Professor, Department of Obstetrics and Gynecology, Seth G. S. Medical College and K.E.M. Hospital, Mumbai, India)


Amongst the various nonsurgical techniques used for the conservative management of retained products of conception, uterine artery embolization (UAE) has shown promising results. It is an effective outpatient nonsurgical radiologic treatment. We report a case of a 23 year old P2 L2 MTP1; previous 2 LSCS who underwent dilatation and curettage (D & C) twice for persistent findings of retained products of conception with continuous vaginal bleeding. Successful conservative management of the retained products was done using uterine artery embolization and serial monitoring of β hCG levels; patient subsequently recovered with negligible β hCG levels.


Uterine artery embolization (UAE) is a noninvasive radiological modality useful as an outpatient nonsurgical treatment of uterine leiomyomas.[1] This technique was first reported by  Ravina et al  in 1995 where it was used as an effective pre-hysterectomy treatment which had a significant clinical improvement and averted many hysterectomies.[2]
We observed gradual reduction in the volume of uterine contents (retained blood clots) after undergoing uterine artery embolization (UAE) eventually resulting in disappearance of the entire products and clinical improvement of the patient.

Case Report

A 23 year old woman with two previous cesarean sections and two medical terminations of pregnancy was referred to our emergency department on day 28 post curettage with ultrasound suggestive of retained products of conception. MTP pills were consumed 4 months back when she had a viable intrauterine pregnancy of 8 weeks on ultrasound. Dilatation and curettage (D & C) was done after she bled continuously for 20 days. The bleeding continued after D & C and the patient was referred to a tertiary care in view of repeat ultrasound suggestive of retained products, with possible differential diagnoses of gestational trophoblasatic disease or arterio-venous malformation. Magnetic resonance imaging (MRI) was done which confirmed the diagnosis of retained products. 
On admission, her general condition was fair, vital parameters were normal, there was no tachycardia or pallor. Abdominal examination revealed uterus just palpable. On speculum examination, the cervical os was partially open with active bleeding. Per vaginal examination revealed uterus 12-14 weeks, mobile with slight irregularity on right wall and ballooned up lower segment.
All routine blood investigations and coagulation profile were normal (hemoglobin was 9.1 g/dL, INR was 1.08), β hCG was 481 mIU/ml,  and liver and renal function tests were normal. Ultrasound of pelvis revealed a well-defined heterogenous collection of approximately 7 x 6 x 5.5 cm in lower uterine segment with multiple vascular channels suggestive of retained products of conception. MRI confirmed the findings of retained products of conception with stretched and thinned out myometrium. 
In view of two previous unsuccessful surgical attempts to evacuate her twice- scarred uterus, the patient was unwilling to undergo a third surgical procedure. As she was stable a decision to manage her conservatively was taken, and she underwent uterine artery embolization (UAE). The patient was followed up regularly with serial ultrasonography and β hCG, which fell rapidly initially and gradually disappeared to < 2 mIU/ml.


UAE is a noninvasive radiologic modality that was first reported by Ravina et al  in 1995 where it was used as an effective pre-hysterectomy treatment. This technique resulted in significant clinical improvement and averted many hysterectomies.[2] The procedure is of short duration performed usually under conscious sedation where the branches of uterine artery are occluded using a variety of embolization substances. The most common embolization substances used for the management of post partum hemorrhage or vaginal bleeding include gelfoam particles, coils or glue like n-butyl-cyanoacrylate.[3] 
The common indications for which UAE is used are the management of intramural fibroids (causing menorrhagia, pelvic pain and pressure symptoms, infertility, or as a pre-operative measure for large fibroids), dysfunction uterine bleeding and adenomyosis. Other less common indications include uterine AV malformations and pseudoaneurysms. UAE is used in obstetric cases for morbid adherent placenta and postpartum hemorrhage; its role in retained products of conception is limited and there are very few reports for this indication. 
There was a significant clinical improvement and effective control of vaginal bleeding after UAE in our case. Cravello et al report a similar case where severe hemorrhage following abortion at 12 weeks gestation was successfully managed by UAE after ruling out cervical trauma and perforation.[4] However, persistent symptoms after UAE occur in approximately 20 % of patients who may require other procedures such as repeat embolization, myomectomy or hysterectomy.[1]
The pre procedural care includes administration of IV fluids, analgesics, anti-emetics and antibiotics which should be continued post procedure as well. A few complications include angiography complications, post-embolization syndrome and uterine artery dissection or rupture. 
The important outcomes for the management of vaginal bleeding that are achieved with UAE are alleviation for the need for emergency hysterectomy, gradual resumption of menstruation, simultaneous treatment of unsuspected abnormalities and successful pregnancy outcomes post procedure.[5]
Amongst a variety of treatment options available now days for refractory cases, conservative line of management helps to preserve future fertility in younger women. Methotrexate has emerged with promising results to treat persistent retained placental tissue. It action on the dividing trophoblastic cells of the placental tissue reduces the neovascularisation; resorption of retained placental tissue occurs over course of time. Other standard treatments include internal iliac artery ligation and emergency hysterectomy. 
In conclusion, UAE has a role to play in cases of retained products where there is hemorrhage, previous surgical attempts have failed to evacuate the uterus or in patients who are medically high risk or unfit for surgery. Where facilities are available, it may be tried for newer indications like retained products of conception.

  1. Tulandi T, Salamah K. Fertility and uterine artery embolization. Obstet Gynecol. 2010;115(4):857–860.
  2. Ravina JH, Herbreteau D, Ciraru-Vigneron N, Bouret JM, Houdart E, Aymard A et al. Arterial embolisation to treat uterine myomata. Lancet. 1995; 346(8976): 671–672.
  3. Pron G, Mocarski E, Bennett J, Vilos G, Common A, Vanderburgh L et al. Pregnancy after uterine artery embolization for leiomyomata: the Ontario multicenter trial. Obstet Gynecol. 2005; 105(1): 67-76.
  4. Cravello L, Mimari R, Agostini A, Pellegrin V, Limet L, Bartoli JM. Uterine artery embolisation to treat severe hemorrhage following legal abortion. J Gynecol Obstet Biol Reprod (Paris). 2007; 36(5): 500 -2.
  5. Hehenkamp WJ, Volkers NA, Birnie E, Reekers JA, Ankum WM. Symptomatic uterine fibroids: treatment with uterine artery embolization or hysterectomy -results from the randomized clinical Embolisation versus Hysterectomy (EMMY) Trial. Radiology. 2008; 246 (3): 823-32.

Saxena N, Deshmukh P, Chauhan AR. Uterine Artery Embolization In The Management Of Retained Products Of Conception. JPGO 2016. Volume 3 No. 9. Available from: http://www.jpgo.org/2016/09/uterine-artery-embolization-in.html