Volume 6 Number 6


Honavar PU

Hygiene is the key to a healthy life. It is reflected in one’s lifestyle and is certainly linked to a person’s health and quality of life. The month of May has seen two important days related to hygiene. In the first week, 5th May was observed as ‘World Hygiene Day’ and the last week saw 28th May as ‘World Menstrual Hygiene Day’. These days help create mass awareness regarding issues related to general and menstrual hygiene respectively. Certainly, the importance of these days cannot be less emphasized as these contribute significantly in educating and training individuals with an aim of achieving good health standards. Obstetrics and gynecology is widely a surgical branch. Complications arising out of surgical procedures are often encountered inspite of possible precautions and adherence to surgical ethics and protocols. Hemorrhage, injury to surrounding viscus and their sequelae, need for blood and blood products are some of them. Surgical site infection or sepsis is a known ghastly complication. Postoperative infective spectrum can range from skin and subcutaneous infection to bacteremia or fulminant sepsis leading to multi organ failure and even death. It is a complication that can have a catastrophic event yet, is completely preventable or effects can be minimized if protocols of surgical asepsis are followed. Surgery has seen evolution in many aspects, right from surgical techniques, suturing methods, evolution of anesthesia to asepsis and disinfection. Asepsis has evolved from operating with bare or ungloved hands to washing with simple soap water solutions from wide mouthed basins and eventually to use of antiseptics for pre procedural scrubbing and automated sensor operated taps. Use of protective wear like gowns, footwear, caps and masks, sterilization of  instruments and disinfection of operating surfaces have proved their role in asepsis. It was Joseph Lister, ‘The Father of Modern Surgery‘ who promoted the idea of sterile surgery by introducing phenols to sterilize instruments and clean wounds. He noted that sepsis is caused not only due to contamination from the environment or patient but also from the health care individuals coming in contact with the patients that caused contamination of the wounds, catheters and surfaces. Hence, the emphasis is on hand hygiene. World Health Organization (WHO) has widely advocated hand hygiene and asepsis. Their module promotes the five moments of hand hygiene that are; before touching a patient, before clean or aseptic procedures, after body fluid exposure, after touching a patient and after touching patient surroundings. It has been observed that religious incorporation of these moments of hand hygiene in health care setup has reduced contaminations, infections and septic foci by huge numbers. Hence, it is widely promoted. Menstrual hygiene is another important aspect that needs open discussion.  Menstruation is a monthly reality yet linked with orthodox practices and seen as a taboo in many countries and traditions. This leads to many women and girls to miss work or days of school. It needs serious destigmatization. Easy accessibility of products and medical assistance, right information to youngsters and target population, provision of adequate and safe sanitation helps create equity and opportunity, which can lead to empowerment by eradication of a long standing discrimination. Many schools have incorporated menstrual hygiene tutorials contributing to the movement of women empowerment. Mass awareness through skits, demonstrations especially on ‘World Menstrual Hygiene Day’ definitely leaves an impact and feeling of acceptance and motivation. Thus, simple measures like hand hygiene or gestures of acceptance and practice of menstrual hygiene is important at individual as well as communal levels to avoid the burden of morbidity or mortality eventually to provide the best possible quality of life to health seekers.

Postpartum Acute Labial Edema

Author Information

Kulkarni A*, Parulekar SV**
(* First Year Resident ** Professor and Head, Obstetrics and Gynaecology, Seth G S Medical College and K E M Hospital, Mumbai, India.)


Labial edema is not only a cause of severe discomfort to a woman, but also a cause for concern because it can be due to a number of serious conditions. When it occurs related to a pregnancy, it is usually in the antenatal period. There are very few cases of postpartum labial edema in literature. We present a curious case of a 19-year-old primipara who developed acute labial edema in the immediate postpartum period.


Edema is found in 8-10% gravidas. But it is found in the lower limbs, hands and face. Isolated edema of the vulva is uncommon. The vulva includes structures that are visible externally from the symphysis pubis to perineum, viz. the mons pubis, clitoris, labia majora and minora, hymen, vestibule, vestibular glands and paraurethral glands. Vulvar edema can be due to a number of conditions like infection, lymphatic obstruction, preeclampsia, diabetes mellitus, hypoproteinemia, anemia and tocolytic therapy.[1-4] It is important to determine the cause of labial edema, so that appropriate treatment can be given.

Case Report

A 19-year-old primigravida presented to the obstetric emergency room in labor at term. She was our registered patient and had been attending the antenatal clinic as per schedule. Her antenatal period had been uneventful. She had taken all medications and vaccines as prescribed. Her vital parameters were in normal limits. Her general and systemic examination revealed no abnormality. The uterus was full term size. There was a single fetus in vertex presentation, with normal heart rate. Local examination of the vulva and speculum examination of the vagina revealed no abnormality. Her hemogram, plasma sugar levels, renal, liver and thyroid function tests, and serological tests for syphilis, HIV, hepatitis B and C were normal. Her medical and surgical history was not contributory. She progressed in labor spontaneously and delivered uneventfully vaginally a female child weighing 2.4 kg. A left mediolateral episiotomy was taken under local anesthesia for assisting childbirth. It was sutured in layers under all aseptic precautions with polyglactin No. 0. Her fourth stage of labor was normal and the episiotomy was healthy. She was transferred to the postnatal ward.
The patient complained of some pain at the episiotomy site 6 hours after delivery. She was afebrile and her pulse rate, respiratory rate and blood pressure were in normal limits. On local inspection there was an edematous swelling of both labia minora, more on the left side. It was not tender and its temperature was not raised. There was no erythema or pus locally. No vesicles or ulcers were seen. No lymphadenopathy was present. Per vaginal examination showed no evidence of infection and no other abnormality. The episiotomy was healthy. Her hemogram, random plasma sugar, liver and renal function tests were repeated and the results were normal.

She was given oral amoxicillin plus clavulanate, warm sitz baths and magnesium sulfate dressing twice a day. The edema subsided over the next 7 days. No other active management was done since the edema was subsiding.  She no longer complained of pain. On day 7 the edema had completely resolved. The episiotomy healed well. She was reassured, explained about perineal hygiene, advised local application of antibiotic ointment and was discharged. At the follow-up examination after 15 days, no abnormality was found on her general and systemic examination as well local examination of the genital tract.

Figure 1. Edema of labia minora.


There is loose connective tissue in the labia minora, in which edema fluid can collect. That explains involvement of labia minora more than other vulvar structures in development of edema. However labial edema does not develop as often as can be expected. When a preeclamptic woman or a nonpregnant woman with a systemic disease presents with generalized edema, the labia minora are not involved as a rule. Acute appearance of labial edema in pregnancy can be seen in severe preeclampsia with renal failure.[5-7] Our patient was normotensive during antenatal period, labor and puerperium. This it was not due o preeclampsia. Edematous and dry vagina and edematous vulva can be found in prolonged labor with obstruction. Our patient had normal progress of labor and timely delivery.

When edema develops in response to inflammation, it is at the site of inflammation. There are local signs of inflammation, like erythema, warmth and tenderness. These features were absent in our case. There was no lymphatic obstruction, because no other vulvar structure was involved and the edema resolved after 7 days, which would not occur with lymphatic obstruction. She had no systemic disease like renal failure, anemia or hypoproteinemia.  A local allergic reaction was a possibility, such as use of povidone-iodine scrub and solution for skin preparation, lignocaine for local anesthesia and polylactin for suturing the episiotomy. It could not have been povidone iodine, as no other adjacent skin covered area was involved. It was found in the right labium minus too, the side opposite to that of the episiotomy. Furthermore the local anesthetic had not been given into the labia and polyglactin suture did not pass through the labia too. These facts combined with an absence of erythema or vesicles ruled out allergic dermatitis.

The only etiological possibility in this case was local abrasion/contusion of the delicate labia minora and compression of their lymphatics by the fetal head during childbirth. Resultant tissue swelling would have blocked the lymphatics temporarily and caused edema of the labia minora. It would have probably resolved with conservative local treatment alone, in the form of warm sitz baths and magnesium sulfate compresses. We administered antibiotic as an additional safety measure and also for preventing infection of the episiotomy.

Labial edema is generally not treated by surgical decompression, though there are some reports of the same.[8,9] The edema in our case was not severe enough to warrant such a treatment, and it resolved successfully with conservative treatment. We have presented this case only to make clinicians aware that acute labial swelling can occur postpartum without any obvious cause and it resolves well.


We thank Dr Sarika Solanke for taking clinical photograph.

  1. Owa OO, Aderoba AA, Akintan AL. Spontaneous massive vulva swelling in pregnancy: a case report. Tropical Journal of Obstetrics and Gynaecology 2015;32:157–160.
  2. Brittain C, Carlson JW, Gehlbach DL, Robertson AW. A case report of massive vulvar edema during tocolysis for preterm labor. Am J Obstet Gynecol 1991;165:420–422.
  3. Trice L, Bennert H, Stubblefield PG. Massive vulvar edema complicating tocolysis in a patient with twins. A case report. J Reprod Med 1996;41:121–124.
  4. Mizock G, Siegel I. Acute edema of the vulva in pregnancy. Am J American Journal of Obstet Gynecol 1963;86:483-484.
  5. Gerdhzhikov B, Kozovski G. Massive vulvar edema in severe preeclampsia. Akush Ginecol. 2005;44:44.
  6. Daponte A, Skentou H, Dimopoulos KD, Kallitsaris A, Messinis IE. Massive vulvar edema in a patient with preeclampsia. J Reprod Med. 2007;52:1067–1069.
  7. Moulin B, Hertig A, Rondeau E. Kidney and preeclampsia. Ann Fr Anesth Reamin. 2010;29:83–90.
  8. Bracero LA, Didomenico A. Massive vulvar edema complicating preeclampsia: a management dilemma. J Perinatol 1991;11:122–125.
  9. Deren O, Bildirici I, Al A. Massive vulvar edema complicating a diabetic pregnancy. European Journal of Obstetrics Gynecology and Reproductive Biology 2000;93:209–211.

Kulkarni A, Parulekar SV. Postpartum Acute Labial Edema. JPGO 2019. Vol 6 No. 6. Available from: https://www.jpgo.org/2019/06/postpartum-acute-labial-edema.html

Recurrent Ipsilateral Live Ectopic Pregnancy After Ipsilateral Partial Salpingectomy

Author Information

Solanke SS*, Parulekar SV**.
(* Second Year Resident, ** Professor and Head, Department of Obstetrics and Gynecology, Seth G S Medical College & K E M Hospital, Mumbai, India.)


A patient with a history of 6 weeks, 1 day of amenorrhea, with a history of right partial salphingectomy for tubal ectopic gestation 5 months ago presented with another right tubal ectopic pregnancy. The epidemiology, etiology and management of ipsilateral ectopic pregnancies is discussed.


Ectopic pregnancy is 1-2% of all pregnancies.[1] The commonest site of implantation of an ectopic pregnancy, primary as well as recurrent, is the fallopian tube.[2] There is 11-15% chance of recurrent ectopic pregnancy.[2] We present the a case describing a recurrent ectopic pregnancy with a cardiac activity after ipsilateral salpingectomy that led to tubal rupture.

Case Report

A 26-years-old woman, underwent exploratory laparotomy with right partial salpingectomy for ruptured right tubal ectopic pregnancy. She returned to our hospital 5 months later as gravida 3, previous one ectopic pregnancy and one spontaneous abortion with 6 weeks and 1 day of amenorrhea. She had lower abdominal pain for 2 days. She had done her own pregnancy test at home, which was positive. Her general condition was fair. Her vital parameters were in normal limits. General and systemic examination revealed no abnormality. Abdominal examination showed a 5 cm long midline vertical infraumbilical scar. Bimanual pelvic examination showed a normal sized uterus and mild tenderness in the right vaginal fornix. Transvaginal ultrasonography revealed no intrauterine gestational sac but a right adnexal mass containing gestational sac of diameter 10.1 mm and fetus of crown-rump length of 3.3 mm. Fetal cardiac activity was present. Her serum beta-hCG  level was 13240 mIU/ml. A diagnosis of right tubal ectopic pregnancy was made. Her investigations for fitness for anesthesia showed normal results. A diagnostic laparoscopy was performed, which showed an ectopic pregnancy in the medial remnant of the right fallopian tube. Omental adhesions were seen to the lateral part of the pelvic peritoneum. Mild hemoperitoneum was seen, which was suggestive of recent rupture of ectopic pregnancy. An exploratory laparotomy was done and excision of right fallopian tubal stump attached to the uterus along with ectopic gestational sac was done. The lateral part of the tube was absent. Modified Coffey’s stitch was taken to cover right cornual stump. The patient's postoperative recovery was uneventful. The histopathology report showed chorionic villi, confirming the diagnosis of an ectopic pregnancy.

Figure 1. Ectopic pregnancy (arrows) in the right tubal medial stump (FT). The right ovary (O) and uterus (U) are also seen.


The occurrence of a tubal pregnancy in the remnant of a fallopian tube after ipsilateral salpingectomy for an ectopic pregnancy is very rare, there being only sixteen cases in the literature.[3] This is the seventeenth such case in the world literature. The residual stump of the fallopian tube left attached to the uterus after partial salpingectomy is likely to be small, usually the isthmic portion of the tube. Maternal mortality is much higher with isthmic ectopic pregnancy than with ectopic pregnancy in the other parts of the fallopian tube.[4] In the case presented, the ectopic pregnancy was indeed in the isthmic part of the fallopian tube.

When a tubal ectopic pregnancy is managed by removing the affected segment of the fallopian tube (partial salpingectomy), the medial and lateral segments left behind remain separate in most of the cases. However, a pregnancy may still occur through that fallopian tube, due to recanalization or tuboperitoneal fistula formation (of the medial segment).[5] If the opening in the recanalization or fistula is too small to permit the passage of a fertilized ovum, it gets arrested lateral to that opening and a tubal pregnancy results. Another explanation is transmigration of the fertilized ovum from the other side.[6] Occurrence of an ectopic pregnancy after surgical removal of a tubal ectopic pregnancy in the past is more common on the contralateral side.[7,8]

Our patient was found to have undergone a partial salpingectomy, and had an isthmic stump.  There was no lateral part of the tube. This ruled out a tubo-tubal recanalization as a cause of the ectopic pregnancy. The ectopic was just lateral to the lateral end of the medial segment, suggesting that the cause was tuboperitoneal fistula formation. This risk would have been avoided by covering the cut and ligated ends of the fallopian tube with peritoneum after partial salpingectomy in the past. A modified Coffey’s stitch would have avoided it too.

We recommend partial salpingectomy for the management of a tubal ectopic pregnancy, keeping the cut ends separate, followed by modified Coffey’s stitch or peritonization of the cut and ligated ends of the fallopian tube. This preserves the potential for a future tubotubal anastomosis should the need arise due to loss of the other fallopian tube and the patient desires a pregnancy. Assisted reproduction would be a better option than a tubal reconstructive surgery, but the cost prevents a lot of poor patients from opting for that form of treatment. Adequate peritonization prevents occurrence of an ectopic pregnancy on that side.


We thank Dr Durga Valvi for taking operative photograph.

  1. Farquhar C.M. Ectopic pregnancy. Lancet. 2005;366(August 13–19(9485)):583–591.
  2. Bouyer J., Coste J., Fernandez H., Pouly J.L., Job-Spira N. Sites of ectopic pregnancy: a 10-year population-based study of 1800 cases. Hum. Reprod. 2002;17:3224–3230.
  3. Abraham C, Seethappan V. Spontaneous live recurrent ectopic pregnancy after ipsilateral partial salpingectomy leading to tubal rupture. Int J Surg Case Rep. 2014;7C:75–78. doi:10.1016/j.ijscr.2014.12.028
  4. Lau S., Tulandi T. Conservative medical and surgical management of interstitial ectopic pregnancy. Fertil. Steril. 1999;72(2):207–215.
  5. Kaplanoğlu M, Kaplanoğlu D, Yüce T, Kiran H. Ruptured ipsilateral ectopic pregnancies: a rare emergency case series. Clin Exp Obstet Gynecol. 2015;42(1):67-8.
  6. Ross JA, Davison AZ, Sana Y, Appiah A, Johns J, Lee CT. Ovum transmigration after salpingectomy for ectopic pregnancy. Hum Reprod. 2013 Apr;28(4):937-41.
  7. Liang C, Li X, Zhao B, Du Y, Xu S. Ruptured ipsilateral ectopic pregnancies: a rare emergency case series. J Obstet Gynaecol Res. 2014 Mar;40(3):849-52.
  8. Longoria TC, Stephenson ML, Speir VJ. Live unilateral twin ectopic pregnancy in a fallopian tube remnant after previous ipsilateral salpingectomy. J Clin Ultrasound. 2014 Mar-Apr;42(3):169-71.

Kulkarni A, Parulekar SV. Recurrent Ipsilateral Live Ectopic Pregnancy After Ipsilateral Partial Salpingectomy. JPGO 2019. Vol 6 No. 6. Available from: https://www.jpgo.org/2019/06/recurrent-ipsilateral-live-ectopic.html

Ovarian Mass Or Uterine Mass – A Diagnostic Quandary

Author Information
Jain P*, Shah R**, Mali K**, Warke HS***.
(* Junior Resident, ** Assistant Professor, *** Associate Professor, Department of Obstetrics and Gynecology, Seth G S Medical College and K E M Hospital, Mumbai, India.)
Ovarian fibroma is a rare and benign tumor of the ovary. Most commonly it is found in women during the perimenopausal or postmenopausal age group. It has a variable presentation and is generally asymptomatic. Although the tumor is benign, it closely resembles malignant tumors. We describe here a case of a 55year old woman with a pelvic mass diagnosed preoperatively on Magnetic Resonance Imaging (MRI) to be a large pedunculated uterine fibroid. She underwent total abdominal hysterectomy with bilateral salpingoopherectomy as the frozen section was suggestive of an ovarian fibroma. This case reveals the diagnostic dilemma in cases with pelvic mass.

Ovarian fibroma is a tumor of stromal cell origin. It accounts for around 4% of all ovarian tumors and usually occurs in perimenopausal and postmenopausal women. These tumors are usually unilateral, solid, hard and have a bosselated external surface. It may be associated with ascites and right sided hydrothorax known as Meig’s syndrome. However, due to variation in presentation, differences in shape and size of the tumor, it is often misdiagnosed as a uterine myoma.[1-3] In cases where tumor size is large and associated with ascites or hydrothorax and elevated CA-125 levels, it is misdiagnosed as a malignancy.[4]

Case Report
A 55 year old nulligravida, married for 35 years presented with complaints of pain in abdomen and distension since 4 years. Pain was dull aching, generalized and intermittent in nature. Patient was menopausal since 10 years. On examination, her general condition was fair, she was afebrile, pulse was 84 per minute and blood pressure was 120/80 mm of Hg. Abdominal examination revealed a palpable mass of around 26 weeks size which was hard in consistency, had irregular surface and was mobile. On speculum examination, cervix and vagina was healthy with minimal white discharge. Bimanual examination revealed a 26 weeks hard ballotable mass arising from the pelvis with irregular surface was felt. Chest radiograph showed minimal infiltrates in the basal portions of the lung and increased bronchovascular markings raising a possibility of tuberculosis causing elevated CA-125 levels. On pelvic ultrasound (USG), uterus was normal in shape and size. A vascularised solid looking mass occupying whole of the pelvis and extending upto the supraumblical region was seen. Differential diagnosis of an ovarian mass or a pedunculated fibroid along with moderate ascites was given. MRI pelvis suggested a large pedunculated uterine fibroid with moderate ascites.[Fig.1] Tumor markers revealed raised CA 125 (208.8 U/ml) and LDH (378 U/L). Pap smear was inflammatory. USG guided ascitic fluid tapping was done, which showed predominantly lymphocytes and no evidence of malignant cells. Ascitic fluid protein was 5.15, ADA levels of ascitic fluid were in the normal range. Hence the possibility of abdominal tuberculosis was ruled out. Consent for total abdominal hysterectomy SOS bilateral salpingo oopherectomy was taken. Exploratory laparotomy revealed a large solid multilobulated mass of 15x20 cm arising from right ovary occupying the entire peritoneal cavity which had undergone torsion.[Fig.2] The mass was separate from the fallopian tube. Uterus was less than normal size. Around l.5 liters of ascitic fluid was drained. Frozen section of the ovarian mass was sent and frozen section revealed spindle cell tumor of the ovary. No evidence of malignancy was seen. Total abdominal hysterectomy with bilateral salpingoophorectomy was done. Contralateral ovary and fallopian tube was normal. Postoperatively the patient had an uneventful course. The histopathology report confirmed the findings of ovarian fibroma.
Fig.1 . MRI pelvis showing a large uterine fibroid.
Fig.2 . Large solid multilobulated ovarian mass.
Ovarian fibromas are tumors which are of stromal cell origin. They are composed of spindle cells, oval or round cells that are capable of producing collagen.[5] Fibromas are mostly solid, spherical, lobulated encapsulated grey white masses which are covered by ovarian serosa.[6] Fibromas occur at all ages, but mostly present during perimenopausal and postmenopausal age group. Very rarely they may also present with peritoneal implants without any atypical feature in the primary tumor.[7] Removal of these tumors by surgical intervention is recommended because of the probability of malignancy.[8] The surgical approach can be done either by open or via laparoscopic method, but surgeons are generally reluctant to use laparoscopic approach as the benign nature of the disease cannot be definitely diagnosed preoperatively and it might be difficult to resect the tumor safely with preservation of ovarian function. CA-125 has been used as a tumor marker for the diagnosis of ovarian carcinoma to distinguish it from benign lesions. But unfortunately, it has not proved to be a reliable predictor to distinguish between them[4]. In this case, there was a strong suspicion of large uterine fibroid, the only test that created the diagnostic quandary was the raised CA 125 levels which suggested that the mass could be large ovarian mass with or without malignant lesions, leiomyosarcoma and even the possibility of abdominal Koch’s could not be completely ruled out. Therefore, surgery was planned with the possibility of malignant lesion and decision of frozen section to be sent intraoperatively was taken. Intraoperatively, a large ovarian mass of around 15x18 cm was seen along with torsion which was sent for frozen section, which revealed spindle cell tumor of ovary i.e fibroma and patient uneventfully underwent total abdominal hysterectomy with bilateral salpingoopherectomy. The histopathology report also turned out to be fibroma. The choice of treatment would have been the same for a young patient, but consent would have been changed to exploratory laparotomy with myomectomy SOS right salpingoopherectomy. This case emphasizes the importance of variable presentation of the tumor and also highlights the non specificity of CA -125 as a poor marker of ovarian malignancy. Hence, the role of histopathological examination should not be underestimated even in very obvious cases. MRI is used as a diagnostic tool in diagnosis of ovarian tumors. But it also shows variable appearances. On MRI T2 images ovarian fibromas can have 3 patterns of appearance. They can be seen as homogenous hypointense masses, heterogenous masses with isointense and few patchy hyperintense areas or heterogenous masses with predominantly hyperintense and few isointense parts. On T1 weighted images, mostly they present as homogenous masses with cystic degeneration. After contrast, they may show homogenous mild enhancement in all phases. At times the diagnosis of the pelvic masses remains a dilemma. The role of radiological modalities in diagnosing such tumors has to be correlated with other diagnostic modalities and clinical findings to reach an appropriate diagnosis and the final diagnosis is obtained on histopathology.

  1. Li X, Zhang W, Zhu G, Sun C, Liu Q, Shen Y. Imaging features and pathologic characteristics of ovarian thecoma. J Comput Assist Tomogr. 2012 Jan-Feb;36(1):46–53.
  2. Zhang Z, Wu Y, Gao J. CT diagnosis in the thecoma-fibroma group of the ovarian stromal tumors. Cell Biochem Biophys. 2015 Mar;71(2):937–43.
  3. Zhang H, Zhang GF, Wang TP, Zhang H. Value of 3.0T diffusion-weighted imaging in discriminating thecoma and fibrothecoma from other adnexal solid masses. J Ovarian Res. 2013;6(1):58.
  4. Paladini D, Testa A, Van Holsbeke C, Mancari R, Timmerman D, Valentin L. Imaging in gynecological disease (5): clinical and ultrasound characteristics in fibroma and fibrothecoma of the ovary. Ultrasound Obstet Gynecol. 2009 Aug;34(2):188–95.
  5. Tavassoli FA, Mooney E, Gersell DJ, McCluuggage WG, Konishi I, Fuji S, et al. Sex-cord stromal Tumors. In: World Health Organisation Classification of Tumors. Pathology and Genetics of Tumors of the Breast and Female Genital Organs. Lyon, France: IARC Press; 2003. p. 149-51.
  6. Crum CP. The Female Genital Tract. In: Kumar V, Abbas AK, Fausto N, editors. Robbins and Cotran Pathologic basis of disease. 7 thed. Philadelphia: WB Saunders Company; 2004. p. 1059-117.
  7. Young RH, Scully RE. Sex Cord-Stromal, Steroid Cell and other ovarian tumors with Endocrine, Paraendocrine and Paraneoplastic manifestation. In: Kurman RJ, editors. Blausteins Pathology of the Female Genital Tract. 5 th ed. India: Springer Private Limited; 2004. p. 923-5.
  8. Leung SW, Yuen PM. Ovarian fibroma: A review on the clinical characteristics, diagnostic difficulties and management option in 23 cases. Gynecol Obstet Invest 2006; 62:1-6.
Jain P, Shah R, Mali K, Warke HS. Ovarian Mass Or Uterine Mass – A Diagnostic Quandary. JPGO 2019. Vol. 6 No.6. Available from: https://www.jpgo.org/2019/06/ovarian-mass-or-uterine-mass-diagnostic.html

Syringomyelia In Pregnancy

Author Information

Kumari H*,  Pardeshi S**,  Gupta AS***.
(* Junior resident, ** Assistant Professor, *** Professor, Department of Obstetrics & Gynecology, Seth G S Medical College and K E M Hospital, Parel, Mumbai, India).


Syringomyelia is a rare neurological condition in which there is cyst formation within the spinal cord. If the cyst expands it compresses the nerve tissue and patient becomes symptomatic with features like progressive pain, stiffness and weakness, loss of temperature sensation, etc. Causes of Syringomyelia include trauma, meningitis, hemorrhage, tumor, and arachnoiditis. Syringomyelia is also found associated with Arnold Chiari type 1 malformation. Treatment of syringomyelia depends on cause. 


Syringomyelia prevalence is about 8.4 cases per 1 lakh population. It is more common in males after 40 years. In pregnancy with syringomyelia, the main challenge is labor analgesia, anesthesia for cesarean section and immobility of the patient. Here we present a case of syringomyelia who had previous two LSCS and partial motor deficit of lower limbs.

Case Report

A forty year old female, in her sixth pregnancy with two living issues, one intrauterine fetal death and two MTP’s was admitted for elective lower segment cesarean section in view of previous two lower segment cesarean sections. She was admitted at 38.3 weeks of gestation.
She was a known case of syringomyelia (post traumatic) with lumbar disc prolapse and hyperthyroidism. She had a fall in 2005, which resulted in a fracture of D12 vertebra and she was advised bed rest. However her symptoms did not get relieved and hence MRI was done which was suggestive of disc prolapse at the level of L4-L5. She underwent a laminectomy for the same. In 2008, she had a fall again with right intertrochanteric fracture of femur for which she underwent ORIF (open reduction and internal fixation). Subsequently she developed weakness in the lower limbs and a repeat MRI was performed which showed a syrinx from D2-3 to D9. She was advised physiotherapy and vocational therapy.
During the same time frame, she was also diagnosed with hyperthyroidism having toxic and visual symptoms and anterior neck swelling. She was started on tablet carbimazole 60 mg. During pregnancy dose was tapered to 10 mg with which she had a normal thyroid profile.
She was admitted for elective lower segment cesarean section. Orthopedic and endocrine opinion was taken. Neurologist was consulted and she had bilateral upper limb power of 5/5, right lower limb power was 3/5, and left lower limb power was also 3/5. Fitness for general anesthesia was given and avoidance of spinal anesthesia was advised as syringomyelia had involved lumbar region. She underwent elective lower segment cesarean section under general anesthesia. She tolerated the procedure well. She delivered a male baby with an Apgar score of 9/10. She was discharged on D5 of post surgery. Her subsequent recovery was unremarkable.    


Syringomyelia is a rare, slowly progressive neurological condition where there is a syrinx within the spinal cord. The safest mode of delivery and anesthetic management in patients with syringomyelia is still controversial. There are concerns regarding worsening of syrinx in vaginal delivery but there is no evidence to prove the same.[1] In a case study done by Ghaly, there was difficulty in intubating the patient for general anesthesia prior to cesarean section as syringomyelia had involved the cervical cord, which was not the case with our patient.[2]
In a case report by Margarido, the patient who had post traumatic syringomyelia was given epidural anesthesia instead of general anesthesia and her outcome was good.[3]                                     
In a case report by Acosta Diez the patient who only had low sensory perception had an instrumental vaginal delivery and even though she had received epidural analgesia she did not show any worsening of neurological symptoms whereas in our case as patient was for elective lower segment cesarean section labor analgesia was not indicated.[4]
In a case report by Park and Jason D patient had associated Arnold Chiari malformation with syringomyelia and she had worsening of neurological symptoms in labor. She underwent cesarean section with epidural anesthesia and postpartum there was no worsening of neurological symptoms. In contrast our patient who had post traumatic syringomyelia with no associated malformation general anesthesia was given as her syrinx was involving the lumbar area. In another case report by Jason D patient had associated Arnold Chiari malformation and patient underwent operative vaginal delivery with epidural anesthesia.[5]
Hasaballa, reported a patient of syringomyelia with paresthesia’s and weakness who was managed conservatively, her neurological symptoms regressed and she conceived and delivered uneventfully vaginally thereafter.[6]
By and large syringomyelia doesn’t start de novo and is usually secondary to traumatic insult or infection. The route of delivery is decided considering the degree of motor deficit in the lower limbs. As such pregnancy does not alter the course of syringomyelia. There is much concern regarding route of anesthesia as spinal anesthesia is best avoided in order to prevent further trauma to the spinal cord which may alter the course of the disease. It is universally accepted that epidural anesthesia or general anesthesia is best suited for these patients as can be seen in above mentioned case reports. Epidural analgesia can be safely used in most of the patients with syringomyelia for labor analgesia.[7,8,9]  

  1. Garvey GP, Wasade VS, Murphy KE, Balki M. Anesthetic and Obstetric Management of Syringomyelia During Labor and Delivery. A Case Series and Systematic Review.  Anesthesia & Analgesia. 2017;125(3):913-924.
  2. Ghaly RF, Candido KD, Sauer R, Knezevic NN. Anesthetic management during Cesarean section in a woman with residual Arnold-Chiari malformation Type I, cervical kyphosis, and syringomyelia. Surgical Neurology International. 2012;3:26.
  3. Margarido C, Mikhael R, Salman A, Balki M. Epidural anesthesia for cesarean delivery in a patient with posttraumatic cervical syringomyelia. Canadian Journal of Anesthesia.  2011; 58(8):764–768.
  4. Diez J A; Santos CP. Syringomyelia and pregnancy: A case report and review. Journal of Maternal-Fetal and Neonatal Medicine.2010;23(S1):219.
  5. Parker JD, Broberg JC, Napolitano PG. Maternal Arnold-Chiari Type I malformation and syringomyelia: A labor management dilemma. American Journal of Perinatology. 2002;19(8):445-450.
  6. Hassaballa MM, Vaughan H, Akhtar S, Tahir A. O303 management of syringomyelia in pregnancy - a case presentation. International Journal of Gynecology & Obstetrics. 2012;119(53):S367-S367.
  7. Margarido C, Mikhael R, Salman A, Balki M. Epidural anesthesia for Cesarean delivery in a patient with post-traumatic cervical syringomyelia. Can J Anaesth. 2011;58(8):764-8.
  8. López R, Nazar C, Sandoval P, Guerrero I, Mellado P, Lacassie HJ. [Neuraxial analgesia during labor in a patient with Arnold-Chiari type I malformation and syringomyelia]. Rev Esp Anestesiol Reanim. 2007;54(5):317–21.
  9. Roelofse JA, Shipton EA, Nell AC. Anaesthesia for caesarean section in a patient with syringomyelia. A case report. S Afr Med J. 1984;65(18):736–7.

Kumari H,  Pardeshi S,  Gupta AS.  Syringomyelia In Pregnancy. JPGO 2019. Vol 6 No. 6. Available from: https://www.jpgo.org/2019/06/syringomyelia-in-pregnancy.html

Maternal Near Miss: Uterine Perforation Or Cesarean Scar Pregnancy?

Author Information

Madge H*, Shah R **, Mali K**.
(* Senior Resident, ** Assistant Professor. Department of Obstetrics and Gynecology, Seth GS Medical College and KEM Hospital)


Maternal near miss in first trimester is usually due to obstetric hemorrhage resulting from pregnancy loss, uterine perforation or ruptured ectopic pregnancy. Cesarean scar pregnancy (CSP) is an unusual and rare form of ectopic pregnancy with complications relating to both; prior uterine scar and obstetric hemorrhage.


Development of gestational sac in a cesarean scar is on the rise due to the increase in the number of cesarean sections. It is seen in 0.15 % of women with prior cesarean section and 1 in 1800 to 1 in 2500 pregnancies overall.[1,2] Around 6.1 % of ectopic pregnancies are CSP’s.[3] Though rare, awareness of the diagnostic and treatment modalities is vital as it poses high risk for uterine rupture and uncontrollable hemorrhage. We present a case of maternal near miss occurring due to perforation of a prior scarred uterus during MTP which lead to precipitous deterioration of her condition due to likely failure to suspect a CSP in its early stages.

Case Report

A 38 year old female gravida 4, parity 3, living 1, intra uterine fetal death 2, with previous 2 LSCS was brought to our casualty by a local gynecologist and her relatives in view of intractable bleeding following medical termination of pregnancy. The accompanying doctor gave history that she presented with sonography suggestive of a gestational sac of 5 weeks in the lower uterine segment, cervical length of 3.49 cm and cardiac activity not appreciated due to early pregnancy.  However, as the sac was in the lower segment, a diagnosis of missed abortion was made and she was prescribed MTP pills. However, she had excessive vaginal bleeding for which 2 units packed red blood cells and 2 units fresh frozen plasma were transfused and an emergency check curettage was done at the private clinic. As bleeding was still not controlled an intra vaginal pack was kept and antifibrinolytics were started. On soakage of pack with blood, she was further transfused 5 units of packed red blood cells and 6 units of fresh frozen plasma and was referred to our tertiary center for further management.
On admission, she was in a state of shock, not maintaining her vital parameters. She was immediately started on inotropic drugs. Her vital parameters were revived to pulse 60/ min. and BP 100/70 mm Hg and respiratory rate to 24/ min. Abdomen was guarded. Per vaginal examination revealed uterus of 10-12 weeks in size with clots in situ and 3 blood soaked intravaginal packs were removed. Her hemoglobin (Hb) was 6.7 gm/dL, Total leucocyte count (TLC) was 20,000/ cubic mm and platelet count was 77,000/ cubic mm. A presumptive diagnosis of DIC with septic abortion was made. She was started on parenteral meropenem, piperacillin-tazobactam, metronidazole and vancomycin.
However on imaging, sonography revealed raised vascularity of the myometrium and an organized hematoma in the lower uterine segment. CT scan suggested significant findings, all in the lower uterine segment; 184 cc of collection, tortuous prominent vessels in the anterior wall and severely thinned out walls with 4-5 mm foci suspicious of a uterine rent. The diagnosis was revised to uterine perforation with DIC and she was taken up for an exploratory laparotomy.
Figure 1. CT scan showing (arrow) collection in the lower uterine segment

Intra-operatively lower uterine segment was found to be bluish and discolored with ongoing bleeding and severely thinned out anterior wall; only serosa remained. An obstetric hysterectomy was performed in view of irreparably damaged uterus. Three units packed red blood cells and 4 units fresh frozen plasma were transfused intra-operatively. She recovered gradually under observation in ICU and was discharged on post-operative day 14 in a stable condition.

Figure 2. Intra-operative image of uterus. Artery forceps points towards the underlying hematoma in the lower uterine segment just beneath the remaining uterine serosa.
Figure 3. Rent in lower uterine segment at the site of previous scar

Histopathology report of the uterus revealed endometrium in proliferative phase except for the lower uterine segment which showed decidual changes with trophoblastic tissue. Myometrium showed thick walled vessels. The combined findings of histopathology, sonography and CT pointed towards a likely diagnosis of cesarean scar pregnancy. Evidence of pregnancy in the lower uterine segment with empty uterus and empty cervical canal, thinned out anterior wall of lower uterine segment with presence of trophoblastic tissue exclusively at the site of lower uterine segment suggested a scar pregnancy as our final diagnosis.[3,4] The final diagnosis was detailed as a case of maternal near miss with inadvertent uterine perforation in a case of missed cesarean scar pregnancy.


Cesarean scar pregnancies can present at any time from implantation to term but have been reported to present more commonly in the first trimester. It can sometimes be difficult to distinguish it from a failed pregnancy or miscarriage.[5] CSP often presents with vaginal bleeding, abdominal pain or may have no symptoms.[1] Similar symptoms are also seen in failed pregnancy. Sonographically, both may show gestational sac in the lower uterine segment thus adding to the confusion. However, an empty uterus, thinned anterior wall and raised peritrophoblastic flow in lower uterine segment on USG and bulging of the gestational sac through the myometrium on MRI indicate CSP, while positive “sliding sign”, lack of color flow on doppler and failure to grow on ultrasound (USG) confirm failed pregnancy.[3,5] In our case myometrial vascularity was also raised on USG. However as the gestational sac was already evacuated before she presented at our hospital, findings such as raised peritrophoblastic flow in lower uterine myometrial area on doppler and histopathological evidence of gestational sac invading the scar could not be verified for confirmation.[3,4]
Our patient was managed on the lines of an early failed pregnancy while the intractable bleeding that followed suggested CSP.  She had also presented with a scan of only 5 weeks pregnancy while the mean gestational age for diagnosis of CSP is 46 days (>6 weeks).[6] With the added USG findings of adequate cervical length and empty uterus it may have been worthwhile in this patient to follow up with β HCG, cardiac activity and rule out invasion of myometrium by gestational sac to confirm the diagnosis of pregnancy failure before prescribing MTP pills. The additional intervention of curettage after suspected pill failure also adds to the likelihood of scar dehiscence and rupture. The culmination of risks involved in the case ultimately resulted in a maternal near miss. Inadvertent use of MTP pills followed by curettage in a likely case of CSP may have lead to both the catastrophic consequences of rupture and life-threatening hemorrhage.
Manoharan et al reported an increased risk of uterine rupture of 5.6 % with the use of misoprostol in a previously scarred uterus.[7] Cesarean scar pregnancies can also lead to rupture uterus as well as morbidly adherent placenta, severe hemorrhage and preterm labor.[8] Various researchers suggest that CSP can be managed conservatively by systemic or local methotrexate, local injection of embryocides, uterine artery embolization; or surgically by dilatation and curettage, laparoscopic/ hysteroscopic removal, open hysterotomy or hysterectomy but highest number of complications are seen with systemic methotrexate, dilatation and curettage and uterine artery embolization.[1] It goes on to prove the caution one needs to take when prescribing MTP pills in the first trimester to a woman with previous cesarean section as the complications can be multiple and even catastrophic.


In prior cesarean section, CSP should be ruled out if gestational sac is implanted in the lower uterine segment. Prescribing MTP pills to such patients can be catastrophic and life-threatening. Simple investigation like USG can diagnose the condition and is the imaging modality of choice, MRI is an adjunct.[1] Treatment needs to be tailored depending on the patient’s hemodynamic status and need for fertility preservation. Finally, all patients should be managed in tertiary care setup with availability of emergency services and blood products.

  1. Seah SC, Laili SAL, Hairiah A, Ab Rahim AG. Catching an ectopic caesarean scar pregnancy – Radiological perspective. Med J Malaysia. 2018;73(1):51-53.
  2. Tang JAWK, Wong EMF, Shu W. Caesarean scar ectopic pregnancy: Imaging findings of this rare but potentially life-threatening condition. Hong Kong Med J. 2018;24:636.e1-2.
  3. Gozdemir E, Simavli S. Cesarean Scar Pregnancy: Diagnosis and Treatment. J Nurs Care. 2014;3:182.
  4. 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;21(3):220-227.
  5. Osborn DA, Williams TR, Craig BM. Cesarean scar pregnancy: Sonographic and magnetic resonance imaging findings, complications, and treatment. J Ultrasound Med. 2012;31(9):1449-56.
  6. Grechukhina O, Deshmukh U, Fan L, Kohari K, Abdel-Razeq S, Bahtiyar MO, et al.Cesarean Scar Pregnancy, Incidence, and Recurrence: Five-Year Experience at a Single Tertiary Care Referral Center. Obstet Gynecol. 2018 Nov;132(5):1285-1295.
  7. Manoharan M, Wuntakal R, Erskine K. Uterine rupture: a revisit. The Obstetrician & Gynaecologist. 2010;12:223-230.
  8. Kaelin AA, Cali G, Monteagudo A, Oviedo J, Ramos J, Timor-Tritsch I. The clinical outcome of cesarean scar pregnancies implanted "on the scar" versus "in the niche". Am J Obstet Gynecol. 2017;216(5):510.e1-510.e6.

Madge H, Shah R, Mali K. Maternal Near Miss: Uterine Perforation Or Cesarean Scar Pregnancy? JPGO 2019. Vol 6 No. 6. Available from: https://www.jpgo.org/2019/06/maternal-near-miss-uterine-perforation.html

Atypical Presentation Of Chronic Ectopic Pregnancy

Author Information

Shinde S*, Madge H*, Mali K**.
(* Senior Resident, ** Assistant Professor, Department of Obstetrics and Gynecology, Seth G S Medical College and K E M Hospital, Mumbai, India.)


Ectopic pregnancy is a leading cause of maternal morbidity and mortality in early pregnancy. The clinical features of chronic ectopic pregnancy are variable. We present a case of chronic ectopic pregnancy mimicking pyosalpinx which is a diagnostic dilemma.


An ectopic pregnancy is one in which the fertilized ovum gets implanted in a site other than the normal uterine cavity. The incidence of ectopic pregnancy has increased over the last 20 years. It is around 8.1 for 1000 deliveries.[1] It turns chronic with the formation of a pelvic hematocele due to multiple minute hemorrhages into the peritoneal cavity. Amenorrhea, vaginal bleeding and abdominal pain are the classic features of chronic ectopic pregnancy which are seen in at least 50% of the cases.[2] Diagnosis depends mainly on history-taking, clinical physical examination, laboratory investigations (urine pregnancy test, serum beta hCG) and radiological investigations.[3] Although ultrasonography (USG) has high sensitivity, large adnexal mass can be a challenge in arriving at a correct diagnosis. It can be reported falsely as a large hematosalpinx [4] or abdominopelvic lump mimicking an ovarian tumor.[5] In this case, patient presented with pain in abdomen, spotting per vaginum, negative urine pregnancy test and radiological findings suggestive of a pyosalpinx.

Case Report

34 year lady P2L2 referred from a private practitioner with symptoms of abdominal pain and spotting per vaginum since 2 months and USG suggestive of left adnexal space occupying lesion of 6.8x4.3 cm. Her menstrual cycles were regular and she gave no history of amenorrhea. There was no history of vaginal discharge, tuberculosis or use of contraceptives. On examination, her pulse was 90/min and blood pressure was 110/60 mm of Hg. She had no pallor. Abdomen was soft with no guarding, tenderness or rigidity. On speculum examination, cervix and vagina looked healthy. On bimanual examination, uterus was of 6wks size, anteverted, deviated to the right and a 3x4 cm cystic mass was felt in the left fornix. The mass was mobile and left forniceal tenderness was present. There was no cervical motion tenderness. The urinary pregnancy test was negative and beta hCG value was low (3.58 mIU/ml). USG was repeated which showed a thick walled convoluted cystic tubular structure with dense echoes within forming a mass of 6.6x5x4 cm in the left adnexa suggestive of left sided pyosalpinx. Endometrial thickness was 9 mm. In view of pyosalpinx, investigations to rule out tuberculous focus (chest x-ray, Mantoux test, sputum AFB) were done and found to be negative. Computed tomography (CT) of the pelvis showed dilated tubular structures with multiple hypodensities with a maximum diameter of 3.1 cm in left adnexa likely to be left sided pyosalpinx [figure 1]. Minimal free fluid was also noted in the pelvis. She was started on oral cefixime, doxycycline and metronidazole followed by intravenous ceftriaxone and metronidazole for 5 days. Despite antibiotics, her symptoms persisted. Hence, consent for exploratory laparotomy with left salpingectomy SOS left salpingo oophorectomy was taken. Intraoperatively, left fallopian tube showed 3x6cm organized congested mass with blood clots and left ovary was normal. Right fallopian tube and ovary were normal [fig.2]. Thus left sided salpingectomy was done. Histopathology of the specimen showed a fallopian tube wall with dense chronic inflammation and focally multinucleated giant cells. One of the sections showed occasional necrotic villi in the lumen amidst hemorrhage. Final diagnosis of chronic ectopic pregnancy with chronic salpingitis was made. Postoperative period was uneventful. Her symptoms were relieved and she was discharged after 7 days.

Figure 1. CT scan pelvis suggesting pyosalpinx.

Figure 2. Left chronic ectopic pregnancy with normal right fallopian tube and ovary.


Chronic ectopic pregnancy is when implantation occurs outside the endometrial cavity, there are multiple recurrent minute hemorrhages into the peritoneal cavity. At times bleeding can be confined to the fallopian tube resulting in hematosalpinx. In other cases, it can also lead to adhesion formation with adjacent structures presenting clinically as an abdominal or pelvic lump. Thus, clinical acumen, laboratory investigations and imaging all can be misleading and the diagnosis can be confused with hematosalpinx, pyosalpinx, ovarian tumor or abdomino pelvic lump. In this case, there was an inability to diagnose an ectopic pregnancy pre operatively as she gave no history of amenorrhea, urine pregnancy test was negative similar to 17.65% of cases of ectopic pregnancies studied by Swami et al,[6] serum beta hCG was normal similar to study conducted by Surampudi and Gundabattula.[7] USG and CT pelvis reported pyosalphinx. Screen for tuberculosis in the view of pyosalphinx was negative. As laparotomy was done for refractory symptoms, the final diagnosis was made aided with histopathology.


The preoperative diagnosis of chronic ectopic pregnancy is often difficult. Laboratory and imaging can be misleading in diagnosing chronic ectopic pregnancy. Laparoscopy or laparotomy followed by histopathology can help in confirming a chronic ectopic pregnancy.

  1. Sudha VS, Delphine RT. A retrospective study on ectopic pregnancy: a two year study. Int J Reprod Contracept Obstet Gynecol. 2016 Dec;5(12):4365-68.
  2. Asuri SS, Kalpana P. A clinical study of ectopic pregnancy. Int J Reprod Contracept obstet Gynecol. 2016 Nov;5(11):3750-53.
  3. Mehta A, Jamal S, Goel N, Ahuja M. A retrospective study of ectopic pregnancy at a tertiary care centre. Int J Reprod Contractor Obstet Gynecol. 2017 DeC;6(12):5241-46.
  4. Nacharaju M, Vellanki VS, Gillellamudi SB,Kotha VK,Alluri A. A Rare Case of Chronic Ectopic Pregnancy Presenting as Large Hematosalpinx. Clin Med Insights Reprod Health 2014;8:1-4.
  5. Tigga MP, Chakraborty SB, Ray J, Debbarma S, Debbarma A. A rare case of chronic ectopic pregnancy mimicking ovarian tumor: a diagnostic dilemma. Int J Reprod Contracept obstet Gynecol. 2015 Jun;4(3):918-20.
  6. Swami MB, Sharma P, Tyagi M, Kuswaha R, Harit J. Clinical Study of Ectopic Pregnancy. Journal of Evolution of Medical and Dental Sciences 2015 Oct;4(86):15057-62.
  7. Surampudi K, Gundabattula SR. The Role of Serum Beta Hcg in Early Diagnosis and Management Strategy of Ectopic Pregnancy. J Clin Diag Res. 2016 Jul;10(7):QC08-QC10.

Shinde S, Madge H, Mali K. Atypical Presentation Of Chronic Ectopic Pregnancy. JPGO 2019. Vol. 6. No. 6. Available from: https://www.jpgo.org/2019/06/atypical-presentation-of-chronic.html

Florid Genital Warts In Pregnancy

Author Information

Mahanti S*, Chaudhari HK **.
(* Senior Resident, ** Associate Professor, Department of Obstetrics and Gynecology, Seth G S Medical College and K E M Hospital, Mumbai, India.)


Genital warts are commonly acquired viral genital mucosal lesions. These lesions generally get aggravated during pregnancy due to the increased mucosal vascularity and the apparent suppressed cell-mediated immunity. Here we present a case of a young primigravida at 18 weeks of gestation who presented with complaints of swelling in the genital region on routine antenatal examination which was diagnosed as genital warts or condyloma acuminata. The maternal and perinatal outcome of the same has been elaborated here.


Warts are cauliflower like growths that affect mucosal surfaces including the oral cavity, larynx, anal canal, vaginal canal, cervix and uncommonly the nasal cavity. Warts are caused by Human Papilloma Virus (HPV) and are a part of the spectrum that range from benign papilloma to precancerous lesions of the cervix including low and high grade squamous intraepithelial lesion to obvious malignant lesions of the cervix and vagina.[1] Here we have described a case of florid genital warts in second trimester pregnancy and its management.

Case Report

A 24 year old primigravida at 18 weeks of gestation presented to the antenatal out-patient department (OPD) with complaints of leukorrhea. She had registered at 10 weeks of gestation, but had no gross perineal lesions or complaints. General, cardiovascular and respiratory system examination was within normal limits. On abdominal examination, uterus was 16 weeks size corresponding to the period of gestation. On local perineal examination, two papillomatous whorled growths of around 4 cm largest dimension consistent with genital warts were seen in the posterior commissural area extending up to the anal margin. In view of her complaints of leukorrhea, a speculum examination was done which revealed florid papillomatous growth involving the cervix and vagina.[Fig. 1,2] The growths were coated with a layer of white discharge which was non-foul smelling. She was admitted for the management of florid genital warts. The diagnosis was established on visual examination alone. Dermatology opinion was taken and they confirmed the diagnosis and she was advised to follow up for local cryotherapy with liquid nitrogen of the larger lesions and local application of tri-chloroacetic acid on the smaller lesions. She underwent six sessions of local cryotherapy at weekly intervals each lasting around 15-20 minutes as provided by the dermatologists. She also followed up in antenatal OPD for the entire duration of pregnancy. At around 32 weeks, after completion of all the sessions of cryotherapy and treatment from dermatological point of view, patient was re-examined. On local examination, the two large whorled warts of 4cm largest dimension involving the posterior commissure had resolved completely.[Fig.3]On speculum examination, there were no growths in the vagina or at the cervical os.[Fig.4] However, vaginal pessaries of clotrimazole were advised for vaginal candidiasis and metronidazole tablets for 7 days for bacterial vaginosis. Fetal growth was corresponding to the period of gestation and she appreciated good fetal movements. At 37 completed weeks, dermatology reference was taken. In view of complete resolution of genital and perianal lesions, they opined that she could be given trial of normal labor. She went into spontaneous labor at 40 weeks. However, emergency lower segment cesarean section was done in view of thick meconium stained amniotic fluid with fetal distress in first stage of labor. Patient and the neonate had an uneventful postnatal course. The neonate did not have any lesions on gross physical examination and was advised to follow up in OPD after 6 months or earlier if symptoms such as hoarse cry or respiratory difficulty or the presence of fleshy growths on nasal and oral mucosa was noted. Patient was discharged on the fifth postoperative day with advice to follow up in OPD for Pap smear and HPV DNA testing after 6 weeks. Pap smear was inflammatory and HPV DNA was negative for the high-risk types.

Fig. 1. Pre-treatment exophytic lesions in cervix and vagina obliterating vaginal canal.

Fig. 2. Pre-treatment lesions at the cervix and vagina and a large exophytic lesion at the introitus posteriorly.

Fig. 3. Post treatment image of vulva showing no lesions.

Fig. 4. Post treatment resolution of cervical and vaginal warts with candidiasis is seen.


Genital warts are benign lesions most often caused by HPV types 6 or 11, which are categorized as the ‘low risk’ type of Human Papilloma Viruses; implying low risk of progression to frank malignancy. Detection of high risk type of HPV from these lesions, i.e. type 16, 18, 31, 33, or 35 are usually associated with type 6 or 11 coinfection.[2] The diagnosis of genital warts is however made on visual inspection only and serological testing or HPV DNA testing is usually not recommended since they are expensive tests and do not alter the clinical course or management of the patient. Biopsy is not recommended for the diagnosis alone and only indicated in the atypical appearances of warts, excessive friability with bleeding on touch, non-responsive to usual line of management or worsening despite therapy.[3] Biopsy performed in such cases comes with the significant risk of bleeding from these lesions however, becomes necessary in order to rule out occult malignancy. Exophytic cervical warts may undergo biopsy to rule out malignancy before empiric treatment is initiated and specially in cases where there is no response to empirical management.[3] This patient had multiple florid condylomata acuminata which subsided on empirical management alone and hence biopsy was not performed. Cesarean delivery does not lower the risk of neonatal or juvenile laryngeal papillomatosis.[4,5] Cesarean section may be indicated in cases where there is obstruction of the vaginal outlet with warts or the presence of gross cervical and vaginal warts, but such cases are very rare. Congenital HPV infection from vertical transmission apart from temporary skin colonization is quite unheard of. Conjunctival, perianal or oropharyngeal warts in the first three years of life is most often due to perinatal vertical transmission of maternal HPV serotypes. Juvenile-onset recurrent respiratory papillomatosis (JoRRP) is a benign neoplasm of the larynx that causes hoarseness and respiratory distress in children and is caused by HPV 6 or 11. Risks for infection are maternal genital HPV infection and prolonged labor.[6] The rate of vertical transmission of HPV to the neonate from mothers with subclinical infection with HPV can be 1-18%. However, elective cesarean section in these cases does not reduce the risk of infection. There is a role of serial follow up of neonates born to mothers with genital HPV infection but they rarely demonstrate persistent HPV DNA positivity. HPV vaccination may ultimately decrease rates of JoRRP in the future. Symptomatic management of the genital warts is necessary for the amelioration of symptoms such as leukorrhea or pruritis. This does not eradicate the infectivity of HPV associated with these lesions and the patients should be explained about the need for regular screening procedures such as Pap smear and liquid based cytology with HPV DNA testing. Management of the genital warts is categorized to patient and provider applied treatments. This patient was managed with provider based applications of cryotherapy with a cryoprobe and trichloroacetic acid 80 to 90 percent solution, and it resulted in complete resolution of the lesions. Alternative methods of treatment in pregnancy include laser ablation and surgical excision of the lesion. Podophyllin, podophyllotoxin and sinecatechins are not recommended for treatment of anogenital warts during pregnancy.[3] The eradication of the genital warts in pregnancy is not essential unless it is symptomatic and therapy is aimed at managing the symptomatic warts with minimal maternal and fetal toxicity. Even if the management is suboptimal and lesions do not subside completely during pregnancy, the lesions most often regress rapidly in the postpartum period possibly due to recovery of cell mediated immunity.


Condylomata acuminata are benign lesions of the lower genital tract that are seen in the reproductive age group and is the benign manifestation of Human Papilloma Virus infection. Pregnant women with genital warts may vertically transmit it to the neonate but the chances of such transmission are very less. Adequate treatment of the lesions is required to ameliorate symptoms of the mother. There is a need for educating all women of the reproductive age group of the clinical spectrum of HPV infections ranging from subclinical infection to carcinoma cervix and emphasize on the role of effective screening procedures available. 

  1. Hamouda T, Freij MA, Saleh M . Management of genital warts in pregnancy. Clin Exp Obstet Gynecol. 2012;39(2):242-4.
  2. Beutner KR, Reitano MV, Richwald GA, Wiley DJ. External genital warts: report of the American Medical Association Consensus Conference. AMA Expert Panel on External Genital Warts. Clin Infect Dis. 1998 Oct;27(4):796–806.
  3. Workowski KA, Bolan GA. Sexually transmitted diseases treatment guidelines, 2015. MMWR Recomm Rep. 2015 Jun 5;64(RR-03):1-137.
  4. British Association for Sexual Health and HIV guideline on the Management of Anogenital Warts, 2015.
  5. The Society of Obstetricians and Gynecologists of Canada. Canadian Consensus Guidelines on Human Papillomavirus. J Obstet Gynaecol Can. 2007 Aug;29(8):S24.
  6. Niyibizi J, Rodier C, Wassef M, Trottier H. Risk factors for the development and severity of juvenile-onset recurrent respiratory papillomatosis: a systematic review. Int J Pediatr Otorhinolaryngol. 2014 Feb;78(2):186-97.

Mahanti S, Chaudhari HK. Florid Genital Warts In Pregnancy. JPGO 2019. Vol. 6 No. 6. Available from:  https://www.jpgo.org/2019/06/florid-genital-warts-in-pregnancy.html

Chronic Placental Abruption And Its Consequences

Author Information

Khare A*, Samant PY**,Mane A ***
(* Junior resident, **Associate Professor, Department of Obstetrics & Gynecology, ***Assistant Professor, Department of Pathology, Seth G S Medical College and K E M Hospital, Parel, Mumbai, India).


Placental abruption is often multifactorial. Associated perinatal outcomes are intrauterine growth restriction, preterm birth, chronic fetal asphyxia and even intrauterine fetal death. In chronic abruption, since the presentation is less dramatic, it is tempting to buy time so that the neonatal outcome is better; but acute abruption frequently occurs in these cases and may jeopardize life. At the same time, neonatal consequences of the long term seepage of blood from subchorionic and retroplacental hematoma into the amniotic fluid are grave. We report a case of multigravida with chronic abruption and subchorionic hematoma from early second trimester; who presented with chronic thrombocytopenia and preeclampsia.


Chronic abruption and subchorionic hemorrhage usually start in the first trimester at a slow rate and continue into the later trimesters. Underlying medical conditions such as hypertension, gestational diabetes mellitus, hyperhomocysteinemia, hyperlipidemia, thrombophilias either genetic or acquired, cocaine abuse or chronic smoking, certain placental developmental pathologies, placentomegaly and placental circulatory disturbances can cause placental hematomas.[1]
Elliott et al defined chronic abruption as delay of at least 7 days after initial hemorrhage before delivery and described a syndrome of chronic abruption oligohydramnios sequence (CAOS). CAOS is when abruption occurs more than 7 days before delivery, there is a documentation of normal amniotic fluid index (AFI) 5-25, and eventual oligohydramnios (AFI < 5) without evidence of spontaneous rupture of membranes is detected.[2] Most frequent condition associated with abruption whether acute or chronic is some form of hypertension in pregnancy. Subchorionic hematoma in first trimester increases risk of abortions, chronic and acute placental abruption, preterm births and even intrauterine fetal deaths. Also fetal lung injury occurs, because of chorioamnionic hemosiderosis due to leak of blood in the amniotic cavity.

Case Report

A 26 year old 4th gravida with previous 3 full term normal deliveries was referred from a peripheral hospital in view of gestational thrombocytopenia to our institute for antenatal registration at 32 weeks of gestation. She had vaginal bleeding at 14 weeks gestation for which she consulted a private practitioner and was treated conservatively. Her sonography (USG) was suggestive of a large retroplacental hematoma of 45x30 mm and also a subchorionic hematoma of 45x40x17 mm. A week later, she had fever which was diagnosed as Dengue and she was treated for the same at a peripheral hospital. Her hemoglobin at that time was 7.8 gm%, platelet count was 58,000/ cmm and total count was 5,800/ cmm. USG at 18 weeks was suggestive of retroplacental hematoma of 80x24 mm. Liquor was adequate. There was growth lag of 1 week. In her subsequent USG scans the hematoma gradually increased in size to 139x130x91 mm. The cord was seen eccentrically inserted at the lower pole of the placenta.

Figure 1. Fetal surface of the placenta with thrombosed blood vessels and marginal cord insertion.

The placental edge was 9 cm away from the internal os. There was also intrauterine fetal growth lag of 1 week. On presentation to our outpatient department, the woman had high blood pressure for the first time; 150/90 mm Hg, with proteinuria and normal deep tendon reflexes. She did not have any premonitory symptoms. Her fundal height corresponded to 28 weeks of gestation. The lie was unstable. Her complete blood count was suggestive of anemia and thrombocytopenia. Hemoglobin was 9.5 gm% and platelet count was 87,000/ cmm. Serum glutamic oxaloacetic transaminase was 89 u/l and glutamic pyruvic transaminase was 22 u/l. INR was 0.9.  Her plasma fibrinogen was 296 mg% and renal function tests were normal. She was diagnosed to have iron deficiency anemia and pseudothrombocytopenia by the hematologist. She was started on tablet labetalol 200 mg twice a day. On day 2 of admission, after steroid coverage; and after confirming availability of adequate blood and blood products, lower segment cesarean section was done for intrauterine growth restriction (IUGR) with transverse lie with pregnancy induced hypertension and chronic abruption in early labor. On the operation table, she had spontaneous rupture of membranes with passage of blood stained liquor and passage of clots per vaginum. Intraoperatively dark red to brown colored liquor was noted after amniotomy, indicative of acute placental abruption superimposed on chronic abruption. She was transfused 2 units of packed red blood cell’s intraoperatively. Intraoperative blood loss was 1000 ml. Prophylactic per rectal misoprostol 800 micrograms was administered. She delivered a preterm female child of 1296 gms. The child had Apgar score of 9/10 at 1 minute but was shifted to neonatal intensive care unit for prematurity and later developed respiratory distress and complications of hypoxia.
After delivery, the placental examination revealed a ‘crater’ which was occupied by a chronic blood clot. The placenta was sent for histopathological examination.

Figure 2. Maternal surface of placenta; crater formed by chronic blood clot and disrupted cotyledons.

Figure 3. Placental villi with calcification (yellow arrow), extensive fibrin deposition (black arrow) and fresh hemorrhage (blue arrow).

Postoperatively she had persistent mild thrombocytopenia that normalized gradually over 15 days and at discharge the platelet count was 2 lacs/ cmm.. She was given intravenous vitamin B12 as per hematologist’s advice. She was discharged on oral iron and antihyperstenive therapy on day 15. During the neonatal intensive care unit stay, the child had respiratory distress and was diagnosed with hypoxic ischemic encephalopathy. The child was stabilized and discharged after 15 days.


Exact incidence of chronic abruption is not known. In a large Japanese retrospective study the incidence of chronic abruption was found to be 0.05 %.[3]
Our patient was a case of chronic concealed placental abruption apparent from early second  trimester with retroplacental as well as a subchorionic hematoma. It is seen that symptoms of subchorionic hematoma have a bimodal occurrence in the period of gestation and more than three fourths of the pregnancies end up in preterm labor.[4]
According to Norman et al in patients detected with subchorionic hematoma in second trimester, the risk of placental abruption is doubled irrespective of vaginal bleeding in early pregnancy.[5]
Immediately after that the patient was diagnosed with Dengue fever with low platelet counts at around 18 weeks , which probably further contributed to her subchorionic hematoma. Subsequently she developed mild intra uterine growth restriction and hypertension. There is a comparatively bad outcome if the volume of hematoma is more than 60 ml and mortality exponentially increases with placental involvement.[6]
The finding of dark red to brown colored amniotic fluid was due to escape of blood degradation products from the chronic retroplacental clot into the amniotic fluid. Such chronic seepage leads to diffuse chorioamnionic hemosiderosis (DCH).[7] When chronically exposed to degenerated red blood cells, fetal lungs and pulmonary vasculature get damaged leading to chronic lung disease and pulmonary hypertension.[8] Pulmonary complications noted in the baby in this case were attributable to the exposure to blood products. The acute episode of abruption worsened the neonatal outcome adding to the morbidity due to DCH.
Circumvallate placentae are known to be associated with peripheral placental hemorrhage. Though in our case insertion was marginal rather than circumvallate; it also is considered as a risk factor for IUGR, increased cesarean rate. [9]


There are studies showing achievement of latency period of more than 10 days with use of tocolytics in cases of chronic abruption without evidence of maternal coagulopathy; but acute abruption was noted in large number of these cases.[7] Thus close observation for acute abruption is required in maternal interest.

  1. Naftolin F, Khudr G, Benirschke K, Hutchinson DL. The syndrome of chronic abruptio placentae, hydrorrhea, and circumvallate placenta. Am J Obstet Gynecol 1973; 116(3):347–350.
  2. Elliott JP, Gilpin B, Strong TH Jr, Finberg HJ. Chronic abruption-oligohydramnios sequence. J Reprod Med. 1998;43(5):418-22.
  3. Aoki S, Inagaki M, Kurasawa K, Okuda M, Takahashi T, Hirahara F. Retrospective study of pregnant women placed under expectant management for persistent hemorrhage. Arch Gynecol Obstet 2014;289(2):307-11.
  4. Seki H, Kuromaki K, Takeda S, Kinoshita K. Persistent subchorionic hematoma with clinical symptoms until delivery. Int J Gynaecol Obstet. 1998;63(2):123-8.
  5. Norman SM, Odibo AO, Macones GA, Dicke JM, Crane JP, Cahill AG. Ultrasound-detected subchorionic hemorrhage and the obstetric implications. Obstet Gynecol. 2010;116(2 Pt 1):311-5.
  6. Nyberg DA, Mack LA, Benedetti TJ, Cyr DR, Schuman WP. Placental abruption and placental hemorrhage: correlation of sonographic findings with fetal outcome. Radiology. 1987;164(2):357-61.
  7. Yoshida S, Kikuchi A, Sunagawa S, Takagi K, Ogiso Y, Yoda T, et al. Pregnancy complicated by diffuse chorioamniotic hemosiderosis: obstetric features and influence on respiratory diseases of the infant. J Obstet Gynaecol Res. 2007;33(6):788-92.
  8. Ismail KI, Hannigan A, O'Donoghue K, Cotter A. Abnormal placental cord insertion and adverse pregnancy outcomes: a systematic review and meta-analysis. Syst Rev. 2017;6(1):242.

Khare A, Samant PY, Mane A. Chronic placental abruption and its consequences. JPGO 2019. Vol 6 No. 6. Available from: https://www.jpgo.org/2019/06/chronic-placental-abruption-and-its.html

Remembering Past Greats: Gisella Perl

Author Information

Prasad M*
(*Assistant Professor, Department of Obstetrics and Gynecology, Vydehi Institute of Medical Sciences and Research Centre, Bengaluru, India.)

The history of obstetrics and gynecology is replete with instances where lives of women have been saved from the hazardous medical conditions associated with the female genital tract. There are innumerable conditions where ‘ending of the pregnancy’ results in improvement of the health of the mother. The infamous Nazi era was associated with a similar scenario, albeit differently. This was the time where Gisella Perl, the Hungarian obstetrician was a savior to the lives of hundreds of women.
Born into a Jewish family in the first decade of the 20th century, Perl was an outstanding student in the local school. She went on to join medical school, despite initial resistance from her family. She chose gynecology as a profession and married an internist Dr Krauss. By early 1940’s, she was having a good practice in Hungary.[1] It is to be noted that during her otherwise good practice, she had refrained from offering abortions due to her religious beliefs.
During the German invasion that took place she was sent to the Auschwitz concentration camp. One of her initial tasks was to motivate the inmates of the camp for blood donations. However, when the infamous Josef Mengele came to know that she was a gynecologist, she was ordered to identify every pregnant woman and send to him. Perl’s moment of reckoning came when she noticed that every pregnant woman was systematically being executed, as per the existing barbaric norm of racial selection.[2]

Though abortion was against Perl’s religion, she had no choice but identify and abort pregnant women before it came to the knowledge of Mengele. This was the only way to prevent execution of the pregnant woman. It is believed that she had performed hundreds of abortions in the Auschwitz concentration camp with no medical equipment, instruments, gloves or medications. She resorted to manual dilatation of the cervix or rupture of the membranes, with her bare hands, being the only way to save the lives of those women. It is probably the most unique of situations in the history of humankind where the death of an unborn child prevented the death of the mother, the angelic facilitator being Gisella Perl.[3]

Eventually, when the war ended, she managed to move to America and began clinical practice at the Mount Sinai Hospital, New York. It was during this time that her endurance came to the light of the world, when she authored her biography “I was a doctor in Auschwitz”.
She blended with the chores of a normal obstetrician/ gynecologist and authored many papers. The topics she worked on included vaginal infections.[4,5]  Her estranged daughter, whom she managed to hide during the war, later reunited with her, and they moved to Israel, where she passed away at the age of 81.

Gisella Perl’s life was an example of living true to the principle that any obstetrician follows “The mother is more important than the child”. Though she lived under circumstances which no modern doctor may ever face again, her courageous behavior and actions shall serve as an inspiration to all gynecologists.

  1. Gisella Perl. Available from: https://en.wikipedia.org/wiki/Gisella_Perl
  2. Peleg R. Gisella Perl: a Jewish gynecologist in Auschwitz. J Womens Health (Larchmt). 2005;14(7):588-91.
  3. Weisz GM, Kwiet K. Managing Pregnancy in Nazi Concentration Camps: The Role of Two Jewish Doctors. Rambam Maimonides Med J. 2018;9(3):e0026
  4. Perl G. Errors in the diagnosis of trichomonas vaginalis infections as observed among 1199 patients. Obstet Gynecol. 1972;39(1):7-9.
  5. Perl G. Monilial vulvovaginitis following "the Pill". Mt Sinai J Med. 1970;37(6):699-701.

Prasad M. Remembering Past Greats: Gisella Perl. JPGO 2019. Volume 6 No.6. Available from: https://www.jpgo.org/2019/06/remembering-past-greats-gisella-perl.html