Volume 2 Issue 6, June 2015

Chauhan AR

Valvi D, Parulekar SV.


The word rape, “the ravishing or violation of a woman” derives from the Latin raptus meaning “seizure of property”. Rape, along with abduction, forced prostitution, dowry death, torture, exposure to pornography, sexual harassment, molestation and trafficking, comes under the umbrella term “crimes against women”. The WHO defines sexual violence as “any sexual act, attempt to obtain a sexual act, unwanted sexual advances and acts to traffic, or otherwise directed against a person’s sexuality, using coercion, threats of harm or physical force, by any person regardless of relationship to the victim in any setting, including but not limited to home and work”. The term sexual assault is often used synonymously with rape.
Following a steady increase in both the incidence and reporting of rape, and catapulted into the public domain by the Nirbhaya case of December 2012 where a student was raped and left to die in the national capital, various new legislations and amendments to existing laws have been made. This article looks at role of the doctors in examination of cases of sexual assault, the Criminal Law (Amendment) Act, 2013 and the POCSO Act (Protection of Children from Sexual Offenses Act 2012).

The National Crime Records Bureau (NCRB) data show that a staggering 3,09,546 crimes against women were reported in 2013, an increase of more than 26% over the 2012 figures of 2,44,270. Of these, there were 33,707 reported cases of rape in 2013 compared to 24,923 cases in 2012 (increase of 35.2%). There is also a steady rise in sexual crimes against children. Many believe that these official figures are just the tip of the iceberg; missing incidents greatly outnumber reported ones, and the rate of under-reporting varies sharply by region. Dismally, only one in five perpetrators is convicted.

Victim or survivor?

The term “victim” literally means a person who suffers from a destructive or injurious action; using this word for women who have been subjected to a non- consensual sexual act (assault, rape or sexual violence), is considered disempowering and demeaning. Judgmental attitudes of police and health care providers assume that these persons are so victimized that they do not have agency hence are unable to comprehend their situation and make independent decisions. 
Replacing this terminology with “survivor” gives power back to the woman and recognizes that despite her being humiliated and traumatized, she has autonomy and is capable of making decisions.
Health consequences of sexual assault include unwanted pregnancy, sexually transmitted infections, and psychological trauma akin to posttraumatic stress disorder. The examination of such cases should form a part of compulsory training of all postgraduates. CEHAT (Centre for Enquiry into Health and Allied Themes) has developed a Sexual Assault Forensic and Medical Evidence (SAFE) Kit which ensures uniformity in examination, collection of evidence and reporting. A standard examination begins with consent for medicolegal examination and collection of forensic evidence. The health care provider is duty bound to inform the police but the survivor has the right to refuse police investigation (which should be documented); this should in no way interfere with the treatment. Recording a complete description of the incident, eliciting contraceptive history, listing the available evidence, documenting findings, collecting relevant swabs and other samples, documenting and treating injuries, testing for and treating infections, providing emergency contraception, support and referral, are the duty of the examining doctor. The doctor should be unbiased and sensitive to subjects with special needs, for example, marginalized groups like transgender, sex workers, persons with disability or those from minority religions and castes. Above all, he should collect good quality evidence and give a medical opinion (based on clinical findings), rather than a legal opinion on whether rape took place or not. Digital vaginal examination using two fingers, and comments on presence or absence of hymen and laxity of the vagina, should be avoided; terms like “habituation to sexual intercourse” should not be used as prior sexual experience has no bearing to the present case.

The Criminal Law (Amendment) Act 2013

Some important highlights of this act are:
·        Various sections of the Indian Penal Code, the Code of Criminal Procedure, the Indian Evidence Act and the Protection of Children from Sexual Offences Act have been amended, incorporating suggestions of the Justice JS Verma Committee, formed after the Nirbhaya gang-rape in December 2012
·        Sections 326A and B of Indian Penal Code (IPC) detail about acid attacks and punishment
·        Sections 354A, B, C and D have been rewritten respectively, to include sexual harassment, assault or force to disrobe a woman, voyeurism and stalking, and their punishments
·        Section 375 has expanded the definition of rape to include all forms of sexual violence, penetrative or non- penetrative. Penetrative may be peno –vaginal (including labial), oral or anal, including use of fingers, objects or weapons, and non-penetrative includes sexual touching of genital, anal or oral areas by penis, finger, mouth or other objects
·        With an aim of providing a strong deterrent against rape, section 376 details the punishments for sexual assault. An offender can be sentenced to rigorous imprisonment for a term which shall not be less than 7 years.
o       Section 376A give punishment of up to 20 years to life in case of death of the victim or vegetative state
o       Section 376B give punishments to a husband who rapes his wife while they are separated (2  to 7 years imprisonment)
o       Section 376C outlines punishments for persons in authority like police officers or public servants who commit sexual crimes (5 – 10 years imprisonment and a fine)
o       Section 376D outlines punishments for perpetrators of gang rape, which is 20 years to life
o       Repeat offenders may be given life imprisonment or handed the death sentence (section 376E)
·        The act recognizes the right to treatment for all survivors by public and private health care facilities; failure to administer treatment is now an offence under the law
·        No reference should be made to past sexual practices of the survivor
·        The age for consensual sex is 18 years as fixed by the law
·        Criticisms of this act have come from many human rights groups and are:
o       Marital rape and men as victims of rape has not been addressed
o       Reduction in age of consent to 16 so as to protect couples having consensual sex
o       Amending the Armed Forces Act so that armed forces personnel accused of sexual crimes can be prosecuted without sanction

POCSO Act (Protection of Children from Sexual Offenses Act 2012)

Along with an increase in the number of rape cases, sexual crimes against children less than 18 years has also been on the rise. Prior to this act, children who were victims of sexual abuse had no legal mechanism in place, especially for crimes like harassment, stalking, trafficking and child pornography.
At the centre of the act is the physical, emotional and social health and well being of the child; reporting of sexual offenses is mandatory and non- reporting is punishable. Similar to the Criminal Law (Amendment) Act, punishments for sexual offenses range from few years to life imprisonment, and a fine, with aggravated sexual assault being described in cases of abuse of a mentally ill child or abuse by persons in positions of authority or trust (parents, teachers, doctors, wardens).
Unique features of the POCSO Act are that it places the responsibility of safety and security of the child on the police, who coordinate activities between hospital, shelter home, Child Welfare Committee (CWC) and judiciary. The medical examination is conducted in privacy, in a sensitive manner without causing undue distress to the child. Special courts are appointed to conduct the trial, and the child need not appear in court but may record his or her statement with the help of a parent, teacher or special educator. The special court also fixes an amount which is given as compensation to the child. The POCSO Act is a landmark legislation that protects children from sexual crimes.

Placenta Increta Masquerading as Uterine Artery Pseudoaneurysm

Author Information

Valvi D*, Parulekar SV **
(*Assistant Professor, ** Professor and Head of Department, Department of Obstetrics and Gynecology, Seth G. S. Medical college and KEM hospital, Mumbai, India)


Adherent placenta is a not uncommon condition at term in modern times, owing to a high incidence of cesarean section. It is much less commonly seen early in pregnancy. We report a case of placenta increta, which was diagnosed six months after a first trimester termination of pregnancy. The patient presented with symptoms suggestive of a pseudoaneurysm of a uterine artery. Investigations supported that diagnosis. However the presence of a mass and her reluctance to undergo uterine artery embolization led to performance of an abdominal hysterectomy. Pathological examination of the uterus revealed the diagnosis of a placenta increta in the upper cervical region.


A morbidly adherent placenta develops secondary to uterine scarring from past surgery like cesarean section and other uterine surgeries. A placenta previa is associated with placenta accreta in 3%, 11%, 40%, 61%, and 67% cases with prior 1, 2, 3, 4, and 5 or more cesarean sections respectively.[1] Risk of placenta accreta is 1–5% in placenta previa without previous uterine surgery. Other risk factors include advanced maternal age, multiparity, previous myomectomy, Asherman syndrome, submucous leiomyomas, endometrial thermal ablation, and uterine artery embolization.[2,3,4] It is not commonly reported after a first or second trimester pregnancy termination. When it does, the modern imaging techniques like ultrasonography (USG) and magnetic resonance imaging (MRI) help make a diagnosis quite accurately.[5,6,7] A pseudoaneurysm of a uterine artery results from trauma leading to extraluminal collection of blood with turbulent flow communicating with the lumen of the uterine vessel.[8] It causes recurrent vagina hemorrhage. A painful hematoma forms if it is surrounded by myometrium. The 3 layers of arterial wall are absent and surrounding tissues comprise the wall. We present an unusual case in which the vaginal bleeding was like that from a pseudoaneurysm, but there was a palpable mass measuring about 3 cm in diameter in the lateral part of the cervix. USG and contrast enhance CT supported this diagnosis. After hysterectomy, it turned out to be placenta increta.

Case Report

A 31 years old female presented with bleeding per vaginam for one and half month with soakage of 6 to 7 pads per day and passage of clots. There was a history of termination of 3 months' pregnancy 53 days back by suction and evacuation. Her obstetric history was para1, live 1, spontaneous abortion1, and MTP 1. On examination her general condition was fair, mild pallor was present, pulse and Blood pressure were normal. Abdomen was soft and nontender, pfannensteil scar was present. On per speculum examination, fresh as well as altered coloured bleeding seen. On per vaginal examination, uterus was 8 weeks size, soft, approximately 3×3cm nontender nodule felt in the right fornix.
All routine blood investigations were within normal limits. Serum beta HCG level was less than 50 mIU/ml. Ultrasongraphy and MRI reports were suggestive of placenta increta with no obvious parametrial involvement but CT angiography showed right uterine artery pseudoaneurysm in the distal portion with surrounding hematoma. The patient was counseled about the two treatment options - uterine artery embolization (UAE) and hysterectomy. In view of possibility of the lesion being placenta increta despite a CT angiography report being to the contrary, the inability of the UAE to remove the mass present and her inability to afford UAE, she opted for hysterectomy.

An exploratory laparotomy was performed. Intraoperative finding were uterus enlarged to 6-8 weeks' size, ballooned out area at the junction of isthmus and cervix, and normal adnexae. A total hysterectomy was performed. Specimen was cut opened showed 5×4cm adherent mass at the junction of isthmus and cervix. Postoperative recovery was uneventful. Histopathology report showed placenta increta.

Figure 1. MRI showing the lesion in right part of the supravaginal cervix (arrows).

Figure 2. CT angiography showing the pseudoaneurysm (arrow).

Figure 3. Hysterectomy specimen cut open, showing placenta increta (arrow).

Figure 4. Dilated aneurysmal blood vessels under serosa of the right aspect of the supravaginal cervix (arrows).


A morbidly adherent placenta develops secondary to uterine scarring from past surgery like cesarean section and other uterine conditions like previous myomectomy, Asherman syndrome, submucous leiomyomas, endometrial thermal ablation, and uterine artery embolization. Usually the diagnosis is made when the patient delivers vaginally or by cesarean section, and the placenta is retained. If an attempt is made to remove it, it may lead to partial separation and severe hemorrhage. With high degree of suspicion in cases with risk factors, antenatal diagnosis is now sought with the help of USG and MRI. It is unusual for the condition to be missed after delivery or abortion. The patient in the case reported presented 53 days after a first trimester pregnancy termination. She had normal menses in between. Her USG and MRI showed uterine artery pseudoaneurysm and formation of a blood clot in the cervix. However the mass felt firm rather than soft on bimanual pelvic examination, and did not fit the diagnosis. An embolization would not have rid the patient of that mass. After counseling the patient opted to undergo a hysterectomy. Gross and microscopic examination confirmed the diagnosis of placenta increta, which had been missed at the time of the pregnancy termination. The reason the imaging tests suggested the diagnosis of a pseudoaneurysm was evident on gross inspection of the specimen (figure 3), which showed localized large dilatation vessels just under the uterine serosa, on the outer aspect of the posterior intracervical mass. A rupture of the vessel would have resulted in massive intraperitoneal hemorrhage. Attempt at surgical removal of the mass by curettage would have proved equally catastrophic.


The possibility of morbid placental adhesion must be kept in mind when a patient presents with abnormal uterine bleeding after a pregnancy and imaging techniques do not show retained products of conception. If there is a mass arising from the lower part of the uterus or upper part of the cervix, one should consider it to be a morbidly adherent placenta, even in presence of an angiography showing a pseudoaneurysm.

  1. Silver RM, Landon MB, Rouse DJ, Leveno KJ, Spong CY, Thom EA, et al. Maternal morbidity associated with multiple repeat cesarean deliveries. National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network. Obstet Gynecol 2006;107:1226–32.
  2. Al-Serehi A, Mhoyan A, Brown M, Benirschke K, Hull A, Pretorius DH. Placenta accreta: an association with fibroids and Asherman syndrome. J Ultrasound Med 2008;27:1623–8.
  3. Hamar BD, Wolff EF, Kodaman PH, Marcovici I. Premature rupture of membranes, placenta increta, and hysterectomy in a pregnancy following endometrial ablation. J Perinatol 2006;26:135–7.
  4. Pron G, Mocarski E, Bennett J, Vilos G, Common A, Vanderburgh L. Pregnancy after uterine artery embolization for leiomyomata: the Ontario multicenter trial. Ontario UFE Collaborative Group. Obstet Gynecol 2005;105:67–76.11).
  5. Comstock CH. Antenatal diagnosis of placenta accreta: a review. Ultrasound Obstet Gynecol 2005;26:89–96.
  6. Warshak CR, Eskander R, Hull AD, Scioscia AL, Mattrey RF, Benirschke K, et al. Accuracy of ultrasonography and magnetic resonance imaging in the diagnosis of placenta accreta. Obstet Gynecol 2006;108:573–81
  7. Palacios Jaraquemada JM, Bruno CH. Magnetic resonance imaging in 300 cases of placenta accreta: surgical correlation of new findings. Acta Obstet Gynecol Scand 2005;84:716–24.
  8. Cooper B., Hocking-Brown M., Sorosky J, Hansen W. Pseudoaneurysm of the Uterine Artery Requiring Bilateral Uterine Artery Embolization. Journal of Perinatology (2004) 24, 560–562.

Valvi D, Parulekar SV. Placenta Increta Masqurading as Uterine Artery Pseudoaneurysm
JPGO 2014 Volume 2 Number 6 Available from: http://www.jpgo.org/2015/06/placenta-increta-masquerading-as.html

Congenital Chloride Diarrhoea

Author Information

Vora P*, Jassawalla MJ**, Bhalerao S***, Nadkarni T****
(* Third Year Resident, ** Head of Department, *** Honorary, **** Associate Professor,
Department of Obstetrics and Gynaecology, Nowrosjee Wadia Maternity Hospital, Parel, Mumbai, India)


A case of congenital chloride diarrhea in a patient with recurrent polyhydramnios was suspected antenatally, confirmed postnatally and managed successfully.


Congenital chloride diarrhea is a rare autosomal recessive disorder caused by abnormality in the active transport of chloride from the distal ileum and colon. It is characterized by hypokalemia, hypochloremia, hyponatremia, metabolic alkalosis and dehydration in the newborn.

Case Report

A 26 year old, gravida 5, para 4, living 2, intrauterine fetal death 1, neonatal death 1, second degree consanguineous marriage, was referred with an ultrasound (USG) findings of polyhydramnios with dilated fetal bowel loops at 33 weeks of gestation in preterm labor. Her first pregnancy was an intrauterine fetal demise at 7 months of gestation with history of polyhydramnios. Her second pregnancy also had history of polyhydramnios with neonatal death at 2 months. Her third and fourth pregnancies had been uneventful normal deliveries with both fetuses alive and well. Her antenatal investigations including plasma sugar levels were within normal limits. She had received steroid therapy to cause fetal lung maturation. USG suggested fetus with cephalic presentation with a composite gestational age of 33 weeks, an estimated weight of 2.1 kg with amniotic fluid index of 28 cm and dilated bowel loops with peristalsis without fetal ascites, intraperitoneal calcifications and fetal structural anomalies. Due to cord presentation with fetal distress the woman was taken up for lower segment cesarean section. She delivered a female child of 2.18 kg with an APGAR at 1 & 5 minutes of 7/10 & 8/10 respectively. After birth neonate had a distended abdomen with visible peristalsis and watery diarrhoea (figure 1) and was immediately transferred to the neonatal intensive care unit. Hemogram was normal. Stool chloride level was increased (90 mmol/l) [normal range 6-17 mmol/l]. Polyuria and diarrhoea persisted and an USG of the abdomen on day 2 of life revealed dilated bowel loops with normal peristalsis. Serum electrolytes revealed hyponatremia, hypocalcemia, hypokalemia, and hypochloremia. Twenty four hour urinary levels of sodium, potassium, calcium and creatinine were corresponding to the serum levels. Serum renin levels were markedly increased (> 500 IU/ml). Hence a diagnosis of congenital chloride diarrhoea was established. The neonate gradually started accepting feeds well and electrolyte imbalance was corrected with 3% NaCl, calcium gluconate and KCl respectively along with maintenance fluids and broad spectrum antibiotics for 21 days. The neonate was discharged on day 26 of life.

Figure1. Distended abdomen of the neonate at birth


Congenital chloride diarrhea was first described in 1945 and is also known as Darrow Gamble disease.[1] Around 250 cases have been reported so far, mainly in Saudi Arabia, Finland and Poland. Congenital chloride diarrhea is a rare autosomal recessive disorder affecting both the sexes caused by mutation in the solute carrier family 26 member 3 genes mapped to chromosome 7. The pathogenic feature is defect in the chloride/bicarbonate channels affecting the distal ileum and colon resulting in fecal chloride loss and osmotic diarrhea which if untreated leads to dehydration and death.[2] Sodium and potassium in stool is not abnormally high but profuse diarrhea leads to absolute loss manifesting as hyponatremia and hypokalemia. Excessive loss of H+ through the kidneys leads to alkalosis. Hyperaldosteronism occurs as a compensatory mechanism to conserve sodium. ‘Urine like diarrhea’ leads to polyhydramnios which in turn causes preterm delivery.[3] Antenatal ultrasound features include dilated bowel loops with polyhydramnios without fetal ascites, intraperitoneal calcifications and fetal structural anomalies. Hence a differential diagnosis of jejunal and ileal obstruction (increased peristalsis), meconium peritonitis (ascites and intraperitoneal calcification) and cystic fibrosis (hyperechoic bowel loops) can be ruled out on USG.[4,6] Amniocentesis may show increased levels of alpha fetoprotein, bilirubin and chloride in the amniotic fluid but these are not diagnostic.[1,5] Most children become toilet trained at a normal age, social adjustment is not impaired and they can live a perfectly normal life.[7] The long term prognosis is generally favorable but complications like renal disease, inflammatory bowel disease, hyperuricemia, inguinal hernias, spermatoceles and male subfertility are possible.[2,8] Hence we conclude that careful evaluation of the differential diagnosis on ultrasound can help point towards such life threatening rare neonatal disorders. Uncommon causes of recurrent pregnancy losses can also be elucidated by offering the parents genetic analysis.

  1. Kim SH, Kim SH. Congenital chloride diarrhoea: Antenatal ultrasound findings in siblings. J Ultrasound Med 2001;20:1133-1136.
  2. Höglund P. SLC26A3 and congenital chloride diarrhoea. Novartis Found Symp. 2006;273:74-86; discussion 86-90, 261-4.
  3. Parikh B, Khubchandani RP, Amdekar YK, Ugra D, Patel A, Nardekar J. Congenital chloride diarrhoea. Indian J Paediatrics 1993;30:811-813.
  4. Elrefae F, Elhassanein AF. Congenital chloride diarrhoea: A review of 12 arabian children. Dove press journal 2013;6:71-75.
  5. Lee DH, Park YK. Antenatal diagnosis of congenital chloride diarrhoea. J Obstet Gynaecol Res. 2012;38(6):957-61
  6. Boopathy Vijayaraghavan S, Lalitha R, Jaleel Ahamed A. Antenatal diagnosis of congenital chloride diarrhoea. Ind J Med Ultrasound 1998;3 & 4:17-18
  7. Holmberg C. Congenital chloride diarrhoea. Clinics in Gastroenterology 1986;15(3):583-602.
  8. Gürakan F, Baysoy G, Wedenoja S, Uslu N, Ozen H, Ozaltin F, et al. Three cases of a rare disease, congenital chloride diarrhoea, summons up the variation in the clinical course and significance of early diagnosis and adequate treatment in the prevention of intellectual disability. Turk J Pediatr 2011;53(2):194–8.

Vora P, Jassawalla MJ, Bhalerao S, Nadkarni T.Congenital Chloride Diarrhoea. JPGO Volume 2 No. 6. Available from: http://www.jpgo.org/2015/06/congenital-chloride-diarrhoea.html

Spontaneous Resolution Of Meconium Peritonitis

Author Information

Jain P*, Tiwari N**, Goel A***, Chauhan AR****.
(* First Year Resident, **Assistant Professor, *** Second Year resident **** Additional Professor. Department of Obstetrics and Gynecology, Seth G S Medical College and KEM Hospital, Mumbai, India.)


Meconium peritonitis is a nonbacterial, chemical inflammation of the peritoneum caused by escape of meconium into the peritoneal cavity, either in fetal life, at the time of delivery, or very shortly after delivery. This escape of meconium is due to a breach somewhere in the intestine and may be associated with bowel obstruction due to imperforate lumen, congenital bands, or other anomalies. We report a case of antenatally diagnosed meconium peritonitis without obstruction, with no definite etiology found, which resolved spontaneously; the neonate remained asymptomatic in the postnatal period.


Meconium peritonitis, a noninfectious chemical peritonitis due to perforation of small intestine and leakage of meconium into the fetal peritoneal cavity,[1,2] is seen in about 1 in 35,000 live births in the USA.[3] Its prevalence in the Indian scenario is unknown. Earlier such cases were incidentally diagnosed during X- ray pelvimetry for suspected fetal macrosomia and congenital malformations.
Meconium peritonitis may occur without any underlying cause, or the cause may be innocuous and intervention may not be required. The common bowel disorders leading to meconium peritonitis in utero are those resulting in bowel perforation due to obstruction and ischemia such as small bowel atresia, congenital bands, volvulus and meconium ileus, of which intestinal atresia appears to be the most common cause.[4] Cystic fibrosis may be a possible etiological factor in 7.7 – 40 % of cases. Therefore parents should be counseled regarding this possibility and ideally such newborns must be screened.[5]

Case Report

A 23 year old primigravida, married for 1 year, presented to us with 5 months’ amenorrhea and vomiting. Routine antenatal investigations were normal, blood group was O positive; liver function test (SGOT and SGPT) were elevated. Ultrasonography (USG) showed a single live fetus of 23 weeks’ gestational age and an anterior placenta. There was evidence of moderate fetal ascites with septations and echogenic foci (calcifications) over intestinal loops. There were no cerebral or hepatic calcifications. A diagnosis of meconium peritonitis was made and the patient and her relatives were counseled about possible need of operative intervention in postnatal period. In light of these findings, TORCH titers were done which were negative. Pregnancy was supervised and serial USG done in the late second and third trimester showed persistence of the multiple calcified foci over the intestinal loops with ascites as seen in the first scan. Calcific densities also developed over liver and stomach. Bowel loops were not dilated. Fetal kidney, bladder and heart were normal. No obvious perforation was identified.
Labor was induced at 37 weeks’ gestation. She delivered a female child of 3 kg with normal Apgar score. The newborn was admitted in neonatal intensive care unit for observation. The baby’s abdomen was soft and she passed meconium spontaneously within a few hours of birth. She was given breastfeed, which was well tolerated. USG of the neonatal abdomen revealed a normal scan. Radiography of the abdomen confirmed intra-abdominal calcification consistent with meconium peritonitis. The baby was also evaluated for the possibility of cystic fibrosis; immunoreactive trypsinogen test was found to be negative. The mother and the baby were discharged on day 14 after delivery and the baby was asymptomatic at 6 weeks postpartum.

Figure 1: Radiograph showing calcification of meconium peritonitis.


Meconium peritonitis is a sterile chemical peritonitis in which an intense inflammation results in calcification along the surface of bowel or peritoneum. Diagnosis of meconium peritonitis is rare before 20 weeks’ because peristalsis rarely commences before this time. Prenatal sonographic diagnosis of meconium peritonitis is extremely useful in postnatal management plan. Bilateral hydroceles, swollen vulvae, fetal ascites, polyhydramnios, intra-abdominal mass, bowel dilatation, snow storm appearance, highly echogenic linear or clumped foci which represent calcification may be seen. Fetal ascites tends to be echogenic. Therefore, such USG findings should be an indication for invasive procedures for fetal blood testing and parental testing for cystic fibrosis.
Meconium peritonitis is associated with a 20-30% incidence of prematurity and a 10-20% incidence of polyhydramnios. Pregnancy should be allowed to continue till term depending upon fetal growth and progression of any associated complication. Rarely, dystocia secondary to massive ascites or abdominal distension with meconium has been reported, for which cesarean section may be required. With the advent of prenatal diagnosis the outcome for this condition has improved, with survival rates up to 90%.[6,7] Mortality is high in cases where perforation persists postnatally.
Review of the literature shows that when only calcifications are present, the outcome is favorable. Once an antenatal diagnosis of complicated meconium peritonitis is reached, the mother should be referred to a tertiary care center for delivery where close monitoring and facilities for urgent perinatal intervention are available if needed.[8,9] The pediatrician should be vigilant to look for early signs of bowel obstruction in the neonate.
One of the important factors for improving outcome in such cases is anticipatory recognition of complications. Early recognition and treatment of acid base imbalance, superimposed bacterial peritonitis, and septic shock can prevent death. The timing of delivery should therefore be discussed with pediatrician and pediatric surgeon. Surgery performed within 24 hours in newborns with bowel obstruction may also improve their outcome. However, asymptomatic infants may develop bowel obstruction secondary to adhesions later in childhood which may need an urgent surgical intervention.
In conclusion, the infant in our case was asymptomatic and had an uneventful postnatal period. Probably the site of perforation got sealed spontaneously without any sequele, indicating a self- limiting process. Such favorable outcome has been described by some authors.[10,11]

  1. Izumi Y, Sato Y, Kakui K, Tatsumi K, Fujiwara H, Konishi I. Prenatal treatment of meconium peritonitis with urinary trypsin inhibitor. Ultrasound Obstet Gynecol 2011; 37:366–368.
  2. Salvia G, Guarino A, Terrin G, et al. Neonatal onset intestinal failure: an Italian multicenter study. J Pediatr 2008; 153: 674–6.
  3. Foster MA, Nyberg D, Mahony B, et al. Meconium peritonitis: prenatal sonographic findings and their clinical significance. Radiology 1987; 165:661–665. 
  4. Nama SH, Kima SC, Kima DY. Experience with meconium peritonitis. J Pediatr Surg 2007; 42(11):1822–1825.
  5. Valladares E, Rodriguez D, Vela A, Cabre S, Lailla JM. Meconium pseudocyst secondary to ileum volvulus perforation without peritoneal calcification: a case report. Journal of Medical Case Reports 2010;4:292–296. 
  6. Wanga C, Changa S, Chaoa A, Wanga T, Tsenga L, Changa Y. Meconium Peritonitis In Utero—the Value of Prenatal Diagnosis in Determining Neonatal Outcome. Taiwanese Journal of Obstetrics and Gynecology 2008;47:391–396.
  7. Miyake H, Urushihara N, Fukumoto K, Sugiyama A, Fukuzawa H, Watanabe K, et al. Primary anastomosis for meconium peritonitis: first choice of treatment. J Pediatr Surg 2011; 46: 2327–2331.
  8. Pelizzo G, Codrich D, Zennaro F, Dell'oste C, Maso G, D'Ottavio G, Schleef J. Prenatal detection of the cystic form of meconium peritonitis: no issues for delayed postnatal surgery. Pediatr Surg Int. 2008 Sep;24(9):1061-5.
  9. Zerhouni S, Mayer C, Skarsgard ED. Can we select fetuses with intra-abdominal calcification for delivery in neonatal surgical centres? J Pediatr Surg 2013;48(5):946-50.
  10. Herschkowitz S, Mizrahi S, Sujov P. Meconium peritonitis, a benign course in a premature infant. Am J Perinatol 1990;7:31-2.
  11. Saxena P, Dabral A, Arora R, Minocha B. Meconium Peritonitis – Two case reports. J Obstet Gynaecol India 2009; 59 (5): 475-476.

Jain P, Tiwari N, Goel A, Chauhan AR. Spontaneous Resolution Of Meconium Peritonitis. JPGO 2015. Volume 2 No.6. Available from: http://www.jpgo.org/2015/06/spontaneous-resolution-of-meconium.html

Vaginal Sinus Due To Rupture Of Posterior Vaginal Wall Cyst

Author Information

Parulekar SV
(Professor and Head of Department of Obstetrics and Gynecology, Seth G.S. Medical College and K.E.M Hospital, Mumbai, India.)


Vaginal wall cyst is a not very common condition. It may be developmental (of mullerian or wolffian duct origin), dermoid, or due to inclusion, as after an episiotomy or perineal tear. A 69 year old menopausal woman, presented with a complaint of intermittent mucoid vaginal discharge for one year. She gave a history of a cystic swelling in the vagina in the past. She had four normal vaginal deliveries. She was found to have a 2 mm diameter opening in the center of the posterior vagina, which was continuous with a 3x3x2 cm cavity under the mucosa. A diagnosis of a sinus due to spontaneous rupture of a posterior vaginal wall cyst was made. Ultrasonograpy (USG) revealed a smooth walled cavity under the posterior vaginal mucosa, with no solid component. The patient opted not to have surgical excision of the lesion. This is the first case of a vaginal sinus due to spontaneous rupture of a vaginal wall cyst in the world literature.


Vaginal wall cyst is a not very common condition. It is usually diagnosed incidentally while the woman is examined for some other condition. Large cysts located in the lower vagina may present with a complaint of something coming out per vaginaum. Vaginal cysts may be developmental, as from mullerian duct or wolffian duct remnants. A dermoid cyst (mature cystic teratoma may be found in the midline posteriorly.[1] An inclusion cyst may develop due to trauma like an episiotomy or a perineal tear. The cysts are benign, and need removal when large or symptomatic. Spontaneous rupture of a cyst and formation of a sinus is so far unknown. We present the first case of a vaginal sinus due to spontaneous rupture of a vaginal wall cyst in the world literature.

Case Report

A 69 year old woman presented with a complaint of intermittent mucoid vaginal discharge for one year, occurring at intervals of 1 to 2 months. The discharge would be copious and would last for a few hours every time. She had a history of a swelling in the vagina a few years ago, which ceased to be symptomatic about one year ago. She was postmenopausal for twenty years. She had four normal deliveries. She had an episiotomy during her first delivery There was no history of any dyspareunia. She had undergone puerperal sterilization operation after her last delivery 39 years ago. She was under treatment for hypertension for 15 years. She had undergone some abdominal operation in childhood, the details of which were not known to her. She also had undergone surgical treatment for a cervical rib many years ago. Her general and systemic examination showed no abnormality. A speculum examination showed a 2 mm diameter opening in the center of the posterior vagina, which was continuous with a cavity under the mucosa. Palpation of the posterior vaginal wall around the opening between a finger in the vagina and another in the rectum showed thickening in that area and sliding movement between the two fingers, suggesting the presence of smooth walled and lubricated opposing walls between them. A hemostat was passed through the opening. It passed into a space measuring 3x3x2 cm, suggesting the presence of a cavity of that size (figure 1). A diagnosis of a vaginal wall sinus following spontaneous rupture of a posterior vaginal wall cyst was made. Ultrasonograpy (USG) revealed a smooth walled cavity under the posterior vaginal mucosa, with no solid component. The patient opted not to have surgical excision of the lesion, in view of her age, four deliveries and three operations in the past, and chronic hypertension.

Figure 1. Posterior vaginal wall cyst with an opening into the vagina (arrow).

Figure 2. Posterior vagina showing an opening, through which a hemostat has been passed and its blades have been opened to demonstrate the extent of the underlying space.


A mucous cyst is variously located in the vagina.[2,3,4] It is unilocular and measures 0.5 to 7 cm in diameter. It is lined by a single layer of columnar mucous cells, though ciliated cells and squamous metaplasia may be seen focally.[2] A Gartner duct (mesonephric) cyst is small, single, and found along the lateral or anterolateral vaginal wall. It is lined by a single layer of cuboid, nonmucinous cells. A basement membrane and smooth muscle fibers in the surrounding stroma are not always present.[2] An epidermal inclusion cyst is small, located in the anterior or posterior vaginal wall. Vaginal adenosis is seen as multiple small cysts. An ectopic ureter may drain into a Gartner duct cyst, producing a large cyst.[5] Vaginal endometriotic cysts are found along the posterior vaginal fornix, or in areas of trauma.[6] They produce tender, small to medium sized lesions with fibrosis around them. A dermoid cyst is low down under the posterior vagina. It is small to medium sized. Its contents are sebaceous, though derivatives of all the germ layers can be found in it.[7]

Vaginal wall cysts should not be mistaken for vaginal wall prolapse. Vaginal wall prolapse shows an expansile impulse on Valsalva's maneuver, while a cyst does not do so.

The cyst in the case presented was a mucous cyst. These cysts often have very thin walls which appear to be likely to rupture any time. They often rupture during surgical dissection. However spontaneous rupture of a vaginal wall cyst has not been reported in the world literature so far. The site of rupture is usually small. If it does not heal, it would result in formation of a small permanent opening. The size of the cyst is much larger than the opening, and hence a chronically discharging sinus would form. After collection of mucus in it over a period of some time (dependent onthe initial size of the cyst), the contents would empty into the vagina, only to fill again. This is what happened in our patient. She had undergone four deliveries and three operations in the past, was elderly and had chronic hypertension. In view of all this, the benign nature of the lesion, and her age, she opted not to undergo any operative treatment. If an operative treatment is required for a ruptured vaginal wall cyst, it would be best to wait until it fills again, and then excise it.[8] Marsupialization of the cyst is another therapeutic option. The opening created is quite large and the contents drain out readily. After some time, the lining epithelium undergoes metaplasia and assumes characteristics of adult vaginal epithelium.[8]


Spontaneous rupture of a vaginal wall cyst is a possibility. If it occurs, one should wait for it to fill up again before attempting to operate on it.


I thank Dr Manjarekar V for taking the two photographs included in the case report.

  1. Kurman RJ, Prabha AC. Thyroid and parathyroid glands in the vaginal wall: report of a case. Am J Clin Pathol 1973;59:503-507.
  2. Deppisch LM. Cysts of the vagina. Classification and clinical correlations. Obstet Gynecol 1975;45:632-637.
  3. Pradhan S, Tobon H. Vaginal cysts: a clinicopathological study of 41 cases. Int J Gynecol Pathol 1986;5:35-46.
  4. Sahnidt WN. Pathology of the vagina – Vaginal cysts. In: Fox H, Wella M, editors. , eds. Haines and Taylor Obstetrical and Gynecological Pathology. Vol. 1, Fifth edition New York, NY: Churchill Livingstone; 2003:180–3.
  5. Kjaeldgaard A, Fianu S. Classification and embryological aspects of ectopic ureters communicating with Gartner's cysts. Diagn Gynecol Obstet 1982;4:269-273.
  6. Gardner HL. Cervical and vaginal endometriosis. Clin Obstet Gynecol 1966;9:358-372.
  7. Kondi-Pafiti A, Grapsa D, Papakonstantinou K, et al. Vaginal cysts: A common pathological entity revisited. Clin Exp Obstet Gynecol 2008;35:41–4.
  8. Parulekar SV. Practical Gynecology and Obstetrics. 5th ed. Mumbai: Vora Medical Publications; 2011.

Parulekar SV. Vaginal Sinus Due To Rupture Of Posterior Vaginal Wall Cyst. JPGO 2015 Volume 2 Number 6. Available from: http://www.jpgo.org/2015/06/vaginal-sinus-due-to-rupture-of.html

Anesthesia Management In A Patient Of Eisenmenger’s Syndrome For Cesarean Section

Author Information

Patil YS*, Wajekar AS**, Garasia MB***.
(* Associate Professor, ** Assistant Professor, *** Professor and Head, Department of Anaesthesiology, Seth GS Medical College & KEM Hospital, Mumbai, India.)


Eisenmenger's syndrome is a cyanotic heart disease characterized by pulmonary hypertension with reversed or bidirectional shunt associated with septal defects or patent ductus arteriosus (PDA). Pregnancy associated decreased systemic vascular resistance increases the degree of right to left shunting, thereby increasing substantially both the maternal mortality and fetal wastage which  is reported to be as high as 30–70%. We present a case of a 20 year old primigravida with Eisenmenger's syndrome who gave birth at 34 weeks of gestation via cesarean section to a live baby under combined spinal and epidural anaesthesia. On the second post-operative day, the patient had a fall in oxygen saturation despite supplemental oxygen, managed conservatively. We describe the successful  anesthetic management for caesarean section and its complications in a patient with Eisenmenger's syndrome.


Eisenmenger’s syndrome is characterised by pulmonary hypertension with reversed or bidirectional shunt associated with septal defects or patent ductus arteriosus (PDA).[1] Pregnancy can worsen Eisenmenger’s syndrome due to fall in systemic vascular resistance resulting in high maternal mortality and fetal wastage ranging from 30 to 70%.[1,2] Generally an anesthesiologist comes into picture for providing anesthesia for delivery of the fetus by vaginal or cesarean route.[3] We present the anesthesia management of elective cesarean section in a patient with Eisenmenger’s syndrome.

Case Report

A 20 year old unregistered primigravida, with 34 weeks of gestation, recently diagnosed with Eisenmenger’s syndrome, on oral sildenafil and furosemide since one week, presented for elective cesarean section in view of cephalopelvic disproportion. Her pulse was 72/min, blood pressure 120/72 mm Hg with room air saturation 98%. She had no cyanosis or clubbing. She had grade IV ejection systolic murmur at apex. Her haemoglobin was 12g% with hematocrit of 32. Electrocardiogram revealed right ventricular hypertrophy. Chest radiograph revealed cardiomegaly, prominent pulmonary conus and pulmonary vascular congestion. All other routine investigations were normal. Echocardiography revealed severe pulmonary artery hypertension (55-65 mm Hg), mildly dilated and thickened right ventricle (RV), normal RV systolic function and bidirectional shunt due to a large ventricular septal defect (VSD). Her arterial blood gases were normal.
Preoperative aspiration prophylaxis and infective endocarditis prophylaxis were given.
In the operating room, difficult intubation cart with necessary cardiac drugs was kept ready. Standard monitoring including electrocardiography, automated blood pressure, pulse oximetry and endtidal CO2 was instituted. De-airing of all the lines was done. Left radial artery and right internal jugular vein (IJV) were cannulated for invasive monitoring. Her central venous pressure (CVP) was 4-6 cm of water. The patient was preloaded with 300 ml Ringer’s lactate. Epidural and spinal anesthesia were performed in the L2-3 and L3-4 space respectively in sitting position. 25 mcg fentanyl was given intrathecally. Then she was made supine. Left uterine displacement was maintained throughout the perioperative period. T6 level of anesthesia was achieved using a titrated dose of 2% lignocaine in incremental doses over 20 minutes (Total 12 ml) with steady hemodynamic monitoring. There was a fall in systolic pressure up to 80 mm of Hg once, treated with phenylephrine 50 mcg. Oxygenation was instituted with face mask at 5 l/min.
A male child of 2 kg with good Apgar scores was delivered. Oxytocin infusion was started. Intraoperative period was uneventful. Total 1000 ml Ringer's lactate was administered intraoperatively to maintain a CVP of 6-8 cm of water. She had an episode of desaturation (SPO2 92%) on day 2 postoperatively which was treated with oxygenation, nebulizations and antibiotics. Furosemide and sildenafil were continued. Postoperative epidural analgesia with tramadol was continued. She was shifted to ward on day 7 and discharged after 15 days.


Conception is discouraged or early termination of pregnancy is advised in patients with Eisenmenger’s syndrome since the fall in systemic vascular resistance seen in pregnancy can worsen Eisenmengerization with a very high rate of mortality reaching 30-70%.[1] Maternal mortality is higher when associated with VSD in such patients as compared to atrial septal defects or PDA.[3] In spite of this, there are a few case reports of successful maternal and fetal outcomes. Sildenafil therapy produces better maternal outcome.[4]
Meticulous de-airing of all the lines for prevention of paradoxical air embolism is of utmost importance. There exists a risk of introducing infection or air during IJV line catheterisation. But fluid therapy guided by CVP is essential in prevention of right heart failure. Infective endocarditis prophylaxis has been advised in all patients of cyanotic heart diseases.[5]
The choice of anaesthesia either regional or general is guided by current pathophysiology, severity of disease, maintenance of haemodynamics, thromboprophylaxis and postoperative analgesia. Our aim was prevention of fall in SVR to avoid increase in right to left shunt.
Intermittent positive pressure ventilation can increase the PVR due to increase in intrathoracic pressure and resultant fall in venous return.[1] Also the risk of failed intubation, aspiration and postoperative hypoxia is increased with general anesthesia. Single shot spinal anesthesia can produce a precipitous fall in blood pressure. Intrathecal administration of an opioid like morphine or fentanyl is not associated with hypotension.[6] Titrated epidural anesthesia prevents hypotension. But only epidural anesthesia produces segmental action and may provide inadequate anesthesia with need to convert into general anesthesia. In this scenario, combination of intrathecal opioid and titrated epidural local anaesthetics helps to increase the safety and reliability of the neuraxial block. Also, postoperative epidural analgesia helps to reduce pulmonary hypertension. Early postoperative mobilization also helps to reduce other complications.
Polycythemia can be common in these patients secondary to chronic hypoxia.[3] Our patient did not have any signs of hypoxia and polycythemia. This can be attributed to the bidirectional nature of the shunt and sildenafil. Hence thrombo-prophylaxis was not essential making neuraxial anaesthesia an attractive choice.
Oxytocin was used as slow infusion as a bolus dose can cause precipitous fall in SVR.
Postoperative cardiac complications can be common from day 2 up to day 30.[1] Our patient had desaturation on day 2 which was managed conservatively.
We conclude that carefully titrated combined spinal epidural anesthesia is safe, appropriate  and effective for patients with Eisenmenger's syndrome for cesarean section.

  1. Cole PJ, Cross MH, Dresner M. Incremental spinal anaesthesia for elective Caesarean section in a patient with Eisenmenger’s syndrome. Br J Anaesth [Internet] 2001 [cited 2015 Apr 13];86(5):723–6. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11575352
  2. Gurumurthy T, Hegde R, Mohandas B. Anaesthesia for a patient with Eisenmenger’s syndrome undergoing caesarean section. Indian J Anaesth [Internet] 2012 [cited 2015 Apr 13];56(3):291–4. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3425292&tool=pmcentrez&rendertype=abstract
  3. Rathod S SS. Successful Pregnancy Outcome in A Case of Eisenmenger Syndrome: A Rare Case Report. J Clin Diagnostic Res 2014;8(10):OD08–OD09.
  4. Cartago RS, Alan PA BJ. Pregnancy outcomes in patients with severe pulmonary hypertension and Eisenmenger syndrome treated with Sildenafil monotherapy. Chest 2012;142(4):999.
  5. Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, et al. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Co. Circulation [Internet] 2007 [cited 2015 Feb 20];116(15):1736–54. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17446442
  6. Abboud TK, Raya J, Noueihed R, Daniel J. Intrathecal morphine for relief of labor pain in a parturient with severe pulmonary hypertension. Anesthesiology [Internet] 1983 [cited 2015 Apr 13];59(5):477–9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/6638561

Patil YS, Wajekar AS, Garasia MB. Anaesthesia Management In A Patient Of Eisenmenger’s Syndrome For Caesarean Section. JPGO 2015. Volume 2 No. 6. Available from: http://www.jpgo.org/2015/06/anesthesia-management-in-patient-of.html