Volume 1 Issue 6, June 2014

Editorial
Chauhan AR
Recurrent Acute Renal Failure Due to Recurrent Pyelonephritis in Repeated Pregnancies
Patel A, Jamkhede K, Gupta AS.

Herpes Simplex Virus Infection in Pregnancy
Pandey I, Qureshi S, Gupta AS.

An Unusual Case of Endometrial Polyp
Prakash S, Parulekar SV, Sathe P.

Endometrial Stromal Tumor
Kulkarni S, Parulekar SV, Sathe P.

A Successful Cesarean Myomectomy
Bang N, Chaudhary H, Panchbudhe S, Satia MN.

Misplaced IUD In Rectosigmoid Mesentery
Poonia S, More V, Panchbuddhe S, Satia MN.

Retropubic Haematoma After Transobturator Sling Surgery
Patil A, Samant PY, Parulekar SV, Kothari K.

A New Symptom Of Uterine Leiomyoma
Parulekar SV

Editorial

Chauhan AR
Maternal infections have been associated with pregnancy since time immemorial, be it the ubiquitous throat infection or full-blown septicemia; however despite pregnancy being an “immune-compromised state”, maternal response to infections in pregnancy is usually the same as in non- pregnant adults. Some infections may be more dangerous in pregnancy and have short and long-term devastating sequel like pregnancy wastage, preterm labor, fetal death, and maternal -fetal transmission leading to lifelong stigmata.
Infections in pregnancy may be classified based on the route of infection and type of organism (viral, bacterial, protozoal). However the diagnostic approach is usually based on symptomatology, gestation age and immune status of the mother. Both humoral and cell mediated immunity have a significant role; the former tackles extracellular pathogens and the latter, intracellular pathogens. Pregnant women may be at risk, exposed to, or contract a viral fever with rash, where the management varies from simple observation and counseling to medical termination of pregnancy, for example in cases of rubella in first trimester.
Infections usually have a “vertical transmission”, a term that refers to the unique relationship between mother and fetus. Transmission may be intrauterine (transplacental), perinatal (just prior to or during delivery via hematogenous route or genital tract), or postnatal through breast milk. Viruses like rubella, cytomegalovirus (CMV), varicella zoster, HIV and parvovirus, bacteria like syphilis, and protozoans like toxoplasma and malaria are all transmitted via the placenta, while herpes simplex virus (HSV) and group B streptococcus (GBS) usually ascend through the genital tract and infect the fetus.
The exact impact on pregnancy varies widely: maternal reactions like high fever and anemia can precipitate embryonic demise; teratogenicity may occur if fetal insult occurs early in first trimester; non- specific fetal problems like IUGR, hydrops, and microcephaly may be seen later in pregnancy with a number of viral infections.
Congenital infections may be transmitted in any trimester, but in general, fetal affectation is more severe when the infection is acquired early in pregnancy, resulting in abortion, fetal loss or teratogenicity; rubella infection is a classic example with a well-defined syndrome of congenital malformations. Fortunately the risk of transmission of infections is low in early gestation. Conversely, though the rates of fetal infection are higher in later gestation, the effects are not as severe and manifest as IUGR or developmental anomalies.
Routine antenatal screening at the first prenatal visit using a battery of tests may appear ideal, but is neither feasible nor routinely possible. A viable compromise between the potential dangers of infection, resources available for testing and maternal willingness for the same should be reached; the standard minimum screen should include rubella IgG, hepatitis B surface antigen, and serological tests for syphilis and HIV.
Ideally, rubella non-immune women should be offered vaccination prior to conception, or if screened during pregnancy, they should be counseled about viral fevers and rash, especially in the first trimester. Current recommendation is to offer measles – mumps –rubella (MMR) vaccine postnatally. Infants born to hepatitis B positive mothers should be actively and passively immunized at birth to decrease the risk of development of carrier state. Syphilis is still an infection to be reckoned with; if untreated, there is an alarmingly high perinatal mortality of 40% (25% of affected pregnancies result in stillbirth and 14% in neonatal deaths). Despite WHO guidelines, syphilis screening is not done in many underdeveloped countries with disastrous fetal consequences. Penicillin remains the drug of choice.
In the absence of any intervention, the risk of transmission of HIV from mother to child is about 25- 30%; this can be reduced significantly to about 12% with treatment. National AIDS Control Organization (NACO) recommends single dose nevirapine during labor in treatment-naïve pregnant women with CD4 count >250cells/mm3. For HIV positive pregnant women already on antiretroviral therapy, their existing regimen should be continued; efavirenz however should be avoided in the first trimester due to teratogenicity.
TORCH is an acronym for congenital infections: Toxoplasmosis, Other infections (syphilis, hepatitis B, Coxsackie virus, Epstein-Barr virus, varicella-zoster virus, and human parvovirus), Rubella, CMV and HSV. TORCH infections are usually the cause of isolated fetal loss and not recurrent losses, as is mistakenly believed. Routine screening is not recommended except for rubella IgG, and CMV screening for women who work in neonatal ICUs, child care facilities or dialysis units.
Diagnosis of TORCH and other infections is based on maternal symtomatology and serology. Flu- like symptoms with fever, myalgia and lymphadenopathy may point to primary CMV or toxoplasma infection, or listeriosis, if associated with diarrhea. Listeriosis is an uncommon foodborne illness which can be prevented with simple advice like meticulous washing of raw food, adequate cooking, and hand washing. Presence of maculopapular rash along with fever and arthralgia should raise the suspicion of rubella or parvovirus infection. Parvovirus infection causes erythema infectiosum, and is responsible for fetal loss and hydrops; intrauterine transfusion greatly improves the fetal outcome. Varicella rash is usually a typical vesicular rash and the diagnosis is clinical. Urinary tract infection, HSV, gonorrhea and Chlamydia should be ruled out when patients present with genitourinary symptoms, loin pain, fever, genital ulcers and vaginal discharge. Varicella and herpes infection in pregnancy may warrant treatment with acyclovir, which though not routinely recommended in pregnancy, may be used to reduce maternal morbidity. Patients with HSV infection at term should be delivered through cesarean section to avoid the risk of neonatal sepsis and encephalitis, which may be fatal.  Fetal diagnosis of infection may be confirmed with chorion villous sampling or amniocentesis in select cases.
Malaria is endemic in many parts of India and pregnancy with malaria is associated with an increased parasite density and severity of disease, especially in the first part of pregnancy. Prophylactic antimalarials and insecticide –treated nets are recommended in endemic areas.
The vicious cycle between maternal infection and preterm labor, as both cause and result, has been well documented. Infections like bacterial vaginosis, gonorrhea and chlamydia increase the risks of preterm labor and premature rupture of membranes. Treatment with antimicrobials may improve fetal outcome by decreasing chances of chorioamnionitis and hence neonatal sepsis and NICU admission.
Infections of the urinary and reproductive tracts during pregnancy are likely to be underplayed by both the patient and her obstetrician. UTI, bacterial vaginosis and asymptomatic bacteriuria may have far- reaching consequences for both mother and fetus, ranging from mild fever and  discomfort to pyelonephritis,  higher incidence of PROM and subsequent chorioamnionitis, and neonatal septicemia. During delivery, GBS infection of the reproductive tract can transmit and manifest as neonatal sepsis. Hence adequate antibiotic prophylaxis and treatment are indicated.
Maternal periodontal disease is emerging as a new preventable infection associated with preterm deliveries and low birth weight babies; however evidence is conflicting. Improvement in standards of periodontal care and treatment during pregnancy may help combat this trend.
Other emerging infectious diseases include the not so recent scare of SARS (severe acute respiratory syndrome), viral hemorrhagic fevers like Lassa fever and Ebola which are more severe in pregnancy, and Psittacosis, a flu-like illness with fever, headache, and atypical pneumonia. Pneumocystis jiroveci, previously known as Pneumocystis carinii, responsible for pneumonia in immune-compromised patients, may be more severe in pregnancy and vertically transmitted by HIV-positive patients to their offspring.
It is these emerging infections against which we need to be well informed and vigilant, so as to provide adequate protection to our expectant mothers and their unborn babies. It gives me great pleasure to present to you the June issue of our Journal, which features an interesting case of HSV in pregnancy.

Recurrent Acute Renal Failure Due to Recurrent Pyelonephritis in Repeated Pregnancies

Author Information

Patel Amit*, Kshitij Jamdade**, Gupta AS***
(*First Year Resident, ** Assistant Professor, *** Professor. Department of Obstetrics and Gynecology, Seth GS Medical College and KEM Hospital, Mumbai, India.)

Abstract

Recurrent pyelonephritis is a very common complication in pregnancy. Our patient presented with acute renal failure and recurrent preterm labor due to recurrent episodes of pyelonephritis in the index pregnancy and previous pregnancy. She was managed with  antimicrobial therapy leading to good maternal and fetal outcome.

Introduction

Acute pyelonephritis complicates approximately 1-2% of pregnancies, and is one of the foremost indications of non-obstetric antepartum hospitalization [1, 2]. Earlier the incidence was as high as 10% [3], but with improved antenatal surveillance, the incidence of acute pyelonephritis has decreased in current times. Asymptomatic bacteriuria is the most significant factor associated with acute pyelonephritis. It is commonly acquired prior to conception. Invasion of renal parenchyma by coliforms is the cause of acute pyelonephritis.  Escherichia coli (E. Coli) is the commonest pathogen followed by Klebsiella and Proteus.[4]
Approximately 20 to 30% of pregnant patients with pyelonephritis develop recurrent infections later in pregnancy. It can lead to renal failure or even acute renal shut down and pre-term labor. Appropriate broad spectrum or specific antibiotic therapy according to the culture sensitivity can avoid its complications like renal dysfunction and pre-term labor.[5,6]

Case report

A 22 year Gravida 2 Para 1 and FSB 1 at 22 weeks of gestation was treated conservatively by a physician  in view of vomiting, hypotension and ultrasonography (USG) features of medical renal disease. Patient presented to us  at 33 weeks of gestation with preterm labor, pyuria, fever, decrease urine output and pre-term labor. Patient had a past history of acute pyelonephritis leading to acute renal failure, preterm labor and fresh still birth in her first pregnancy in October 2012.  On review of her 1st pregnancy case records it was seen that she had an acute episode of vomiting and reduced urine output for 4 days. Her serum creatinine levels were 4.7mg%, her urine routine and microscopy should pyuria with 40-50   pus cells per high power field (hpf), 5-7 RBC's/hpf, and field full of bacteria. There were calcium oxalate/triple phosphate amorphous crystals in the urine. Her 24 hour urine protein was 0.048gm%. Her Blood urea nitrogen was 38.34 mg% and her blood urea was 82.10 mg%. Serum calcium was 7.2 mg/dl, uric acid was 6.3mg/dl, parathyroid hormone was elevated to 115 pg/ml.Her renal USG of the right kidney size as 9.6 x 4.1 cm and left kidney size as 7.6 x 3.6 cm. Cortical echogenecity of both kidneys was elevated. Pelvicalyceal systems of both the kidneys were full. Findings were suggestive of Grade II bilateral medical renal disease. Her urine culture report had shown E. Coli organism in significant numbers sensitive to the antimicrobial Nitrofurantoin. She was treated for a month with the same.
In the present pregnancy on admission  her renal parameter was deranged. Serum creatinine was  5.2mg/dl and urine routine microscopy showed 45-50 pus cells/hpf. Patient was admitted under the physician. She was empirically started on parenteral Piperacillin Tazobactum combination (4.5gm ) 12 hourly. Her urine was sent for culture sensitivity. She was treated with tocolytics for preterm labor.  Nephrologist advised catheterization, adequate hydration, renal diet and continuation of the above antibiotic for 14 days given.  Her urine showed no growth probably due to the use of the antibiotic Piperacillin.  It was continued for 14 days. Her preterm labor was controlled and her serum creatinine reduced to 1.1mg/dl by the end of 2 weeks. She was discharged with advise of regular follow up.  Later fetus showed clinical and USG evidence of growth restriction and Doppler studies indicated uteroplacental insufficiency. She spontaneously delivered a SGA fetus  at 37 weeks of gestation vaginally. Neonate weighed 1.9kg.  Post-delivery urine routine microscopy showed pyuria with 30-40 pus cells/hpf and bacteria. Urine culture was sent. It grew gram positive Enterococci that was sensitive to amoxicillin. Her serum creatinine again increased to 1.8mg/dl. Tablet amoxicillin 500mg  three times a day was given for 14 days. Patient improved symptomatically. Her serum creatinine levels decreased to 1.0mg/dl.  She was discharged and educated about risk of recurrence of urinary tract infection and need for repeated urine examinations.

Discussion

Recurrent pyelonephritis is common in pregnancy and can lead to mild renal function impairment to sever renal dysfunction or even severe oliguria or anuria. It can also lead to obstetric complications like pre-term labor and intra uterine growth retardation and fetal loss.
Thus we saw in our case that patient had acute renal failure, preterm labor  not once but twice in successive pregnancies.  Treatment of the same restored her renal function both the times but she lost her 1st child. Prompt institution of parenteral antibiotic without awaiting culture report lead to resolution of her symptoms and her 2nd pregnancy could be prolonged to term. However the intra uterine growth of the fetus was restricted. Nevertheless she took home a live neonate. Infection again raised its head in the puerperium but it was diligently sought and appropriately treated.

Conclusion

Acute pyelonephritis in pregnancy is a common medical complication and recurrence is also very common. It can lead to medical as well as obstetric complications. Obstetricians should be vigilant to its possibility especially in patients with previous history. Prompt diagnosis and vigorous treatment can not only give a good obstetric outcome but also saves the renal parenchyma from scarring and permanent damage.

References

1.                  Gilstrap LC, Ramin SM. Urinary tract infections during pregnancy. Obstet Gynecol Clin N Am 2001;28:581–591.
2.                  Otero N. P, Ricoy LF, Pérez BF , Vázquez CM, Poch MM, Díaz JLO. Pyelonephritis and pregnancy. Our experience in a general hospital. Anales de Medicina Interna, 2007;24:585-587.
3.                  Wait RB, “Urinary tract infection during pregnancy. Asymptomatic bacteriuria, acute cystitis, and acute pyelonephritis,” Postgraduate Medicine, 1984;75: 153-157.
4.                  Cunningham F. , Leveno K. , Bloom S. , Hauth J. , Gilstrap L. , and Wenstrom K. , “Renal and urinary disorders,” in Williams Obstetric,  22nd edition, McGraw-Hill, New York, NY, USA,2005;  pp. 1093-1110.
5.                  Lawn JE, Cousens S, Zupan J. 4 million neonatal deaths: When? Where? Why? Lancet.2005;365:891-900.
6.                  Smaill F. Asymptomatic bacteriuria in pregnancy. Best Pract Res Clin Obstet Gynaecol.2007;21:439-450.

Citation

Patel A, Jamkhede K, Gupta AS. Recurrent Acute Renal Failure Due To Recurrent Pyelonephritis in Repeated Pregnancies. JPGO 2014 Volume 1 Number 6 Available from: http://www.jpgo.org/2014/06/recurrent-acute-renal-failure-due-to.html

Herpes Simplex Virus Infection in Pregnancy

Author Information

Pandey Indu*, Qureshi Shabnam**, Gupta AS***
(*First Year Resident, ** Assistant Professor, *** Professor. Department of Obstetrics and Gynecology, Seth GS Medical College and KEM Hospital, Mumbai, India.)

Abstract

Herpes simplex infection is the most common sexually transmitted infection of reproductive age group. It is an important cause of intra-uterine fetal and neonatal infection. We present a case of HSV-2 infection in second trimester of pregnancy in which the patient developed an IUFD at 26 weeks of gestation.

Introduction

Herpes simplex virus (HSV) is a DNA virus. Infection is transmitted through mucosal membranes and grazed skin. It reaches the nerve tissues and rests there in a dormant state. HSV-1 and HSV-2 are the two subtypes infecting orofacial and genital area respectively. However crossover infection can happen with both the subtypes.[1] Genital herpes infection can be primary, non primary, recurrent or asymptomatic.[1] In our case, patient was infected but was asymptomatic.

Case report

A 23 years old primigravida 26 weeks of gestation was referred from a private hospital in view of intrauterine fetal death. She had no complaints. She had a ultrasonography (USG) report at 14 weeks showing a thickened placenta of 4-5 cm  in size, liquor pocket of 2-3 cm, nuchal translucency (NT) of 1.2mm (corresponding to13.5weeks). Patient was tested for TORCH infection. HSV 2 IgM antibody was detected. She was treated with tablet Acyclovir in the dose of 200mg 3 times a day for 21 days .After one month she had a repeat USG at 18 weeks of gestation. It showed placental thickness of 5-6cm.There were no congenital anomalies seen, fetal biometry was suggestive of symmetrical intrauterine growth retardation. Patient received Injection Alamine intravenously thrice a week for three weeks till 5 months of gestation. The repeat U SG done at 26 weeks showed intrauterine fetal death of 19-20 weeks of gestation, Spalding sign was also seen. There was no history of fever, of multiple sexual partners, any vaginal discharge or history of rashes around the genitalia. On examination there was no active lesion or healed lesion seen on the body. Her vital parameters were stable. Abdominally the uterus was 20 weeks in size. On speculum examination, there were no genital lesion seen, cervix and vagina were healthy. On vaginal examination, Os was closed, uneffaced. Her husband, a textile mill worker was asymptomatic. He had no history of lesions on his genitalia, or fever or multiple sexual partners. Her hemogram, DIC profile, urine examination were within normal limits. Consent to induce labor was obtained. Single dose of 200 micrograms of misoprostol tablet was administered vaginally. A macerated male abortus of 300 grams and thickened placenta of 150 grams were expelled spontaneously and completely.


Figure 1. It shows the large placenta with its fetal surface. M is the fetal membranes. Arrow indicates the umbilical cord.


Figure 2. It shows the maternal surface of the thickened placenta and the unhealthy cotyledons. C is the cotyledon. Arrow indicates the umbilical cord.

Pathological of the placenta and the umblical cord showed grossly the surface to be congested with yellowish brown discoloration at places. Cotyledons were distorted and could not be identified. On cut section the cotyledons appeared congested and autolytic. On microscopy placenta showed normal villi with sheets of trophoblastic cells, fibrinoid necrosis, hemorrhage, and presence of lymphocytes, myeloid precurssor cells with hneutrophils. No evidence of vilitis. Featrues suggestive of maternal sepsis.

Discussion

Prevalence of HSV infection increases with age. Factors that facilitate risk of infection are related to number of sexual partners. HSV has a greater propensity for the female gender.[2,3]  Perinatal transmission of HSV infection can occur at three periods. One as a vertical transmission transplacentally or as an ascending infection from the cervix in the intrauterine period, during labor from the infected birth canal or after birth due to breast feeding or if the neonate comes in contact with the infected lesions of the parent. Risk of neonatal infection is in the range of 30%-50%, when HSV infection is acquired in the last trimester, whereas risk is only 1% when it is acquired in early pregnancy. Late in pregnancy the body does not have adequate time to develop antibodies against HSV. Viral load increases as the replication cannot be stopped prior to onset of labor. Affect of genital herpes on pregnancy is spontaneous abortion, intrauterine growth retardation, preterm labor and congenital herpes infection [4,5]. Congenital herpes is a catastrophic infection that affects the CNS in 50% of neonates. Our patient had no risk factors for HSV-2 infection; she did not have any active lesion. Yet, she had an acute HSV-2 infection which infected the fetus gravely resulting in intrauterine fetal death. In our case obviously the infection was intrauterine in origin most likely transplacental as seen by the thickened placental membranes, cotyledons and the thickened cord and increased placental weight. Placenta weighed half that of the fetus. It is most likely that our patient had a primary type of the HSV infection as the incidence of vertical transmissions from primary infection is to the tune of 40 to 50 % against 5 % in the recurrent HSV infections.[6] In primary infections there is increased maternal viral load and hence greater transplacental transfer of the virus and severe infection to the fetus in utero leading to its demise as seen in our patient.

Conclusion:

Primary Herpes Simplex Virus infection during pregnancy leads to grave intrauterine consequences for the fetus. Hence it is important to educate about sexually transmitted diseases and identify pregnant women at risk to prevent the vertical transmission or congenital herpes infection.

References

1.      Gupta R, Warren T, Wald A. Genital herpes. Lancet, 2007;370(9605):2127-2137.
2.      Smith JS, Robinson NJ. Age-Specific prevalence of infection with herpes simplex virus types 2 and 1: a global view. Journal of Infectious Diseases. 2002:186(supplement 1):S3-S28.
3.      Suligoi B, Cusan M , Santopadre P , Palu G , Catania S , Girelli G , Pala S , and  Vullo V; HSV-2 specific seroprevalence among various populations in Rome, Italy. Sex Transm Infect 2000;76:213-214.
4.      Arvaja M, Lehtinen M, Koskela P, Lappalainen M, Paavonen J, Vesikri T. Serological evaluation of herpes simplex virus type 1 and type 2 infections in pregnancy. Sexully Transmitted Infections , 1999:75(3):168-171.
5.      Brown ZA, Selke S, Zeh J, Kopelman J, Maslow A, Ashley RL, et al.The acquisition of herpes simplex virus during pregnancy. N Engl J Med. 1997;337(8):509-15.
6.      Katharine H Barefoot AB, George A Little MD and Kim T Ornvold MD. Fetal Demise Due to Herpes Simplex Virus: An Illustrated Case Report. J. Perinatol 2002;22:86-88.

Citation

Pandey I, Qureshi S, Gupta AS. Herpes Simplex Virus Infection in Pregnancy. JPGO 2014 Volume 1 Number 6 Available from: http://www.jpgo.org/2014/06/herpes-simplex-virus-infection-in.html

An Unusual Case of Endometrial Polyp

Author Information

Swati Prakash*, Parulekar SV**, Pragati Sathe***
(*Third Year Resident, ** Professor and Head of Department. Department of Obstetrics and Gynecology, *** Assistant Professor, Department of Pathology, Seth GS Medical College and KEM Hospital, Mumbai, India.)

Abstract

A 57 year old woman, married for 27 years, para 2 abortion 1, menopausal for 14 years, presented with a complaint of post-menopausal vaginal spotting. She had had 2 such episodes in the preceding 2 months. She had undergone colpohysteroscopy with dilatation & curettage in just prior to menopausal 2 years ago, for abnormal uterine bleeding. Pelvic ultrasonography (USG) done prior to the procedure had shown hypertrophied endometrium. Histopathology report though, was not available. On per speculum examination; she had a 2x1x.3cm irregular polyp protruding from external os. Polypectomy with fractional curettage was done. A 6×2×1 cm polyp was removed. The polyp had a 1 mm diameter pedicle. Histopathology report showed a benign polyp with endocervical dysplasia.

Introduction

An endometrial polyps is a localized overgrowth of endometrial tissue. It may be pedunculated or sessile, single or multiple. Pedunculated polyps are more common than sessile ones.[1] Endometrium grows in response to circulating estrogen, and localized growth results in formation of polyps. Formation of new polyps should be unusual after menopause, because estrogen production by the ovaries is low or absent. Similarly old polyps should not grow after menopause. Uterine contractions may cause elongation of the pedicle of a polyp, trying to extrude it from the uterine cavity. If the pedicle finally necroses, the polyp may be expelled spontaneously. We present a case in which a polyp grew after menopause and one which had a pedicle measuring 1 mm in diameter, attaching it to the endometrial surface.

Case Report

A 57 year old woman, married for 27 years, para 2 abortion 1, presented with a complaint of post-menopausal vaginal spotting. She had 2 such episodes. She had been menopausal for 14 years. She had had 2 such episodes in the preceding 2 months, for which she had not taken any treatment. She had undergone colpohysteroscopy with dilatation & curettage in just prior to menopausal 2 years ago, for abnormal uterine bleeding. Pelvic ultrasonography (USG) done prior to the procedure had shown hypertrophied endometrium. Histopathology report was not available, though the patient stated that there had been no cancer. On per speculum examination; she had a 2x1x0.3cm irregular, soft polyp protruding from external os which did not bleed on touch. It was free from cervix all around. Polypectomy with fractional curettage was done, keeping in mind her post-menopausal status. The polyp was held with sponge holding forceps and it came off very easily on mild traction. It was soft, flat, and easured 6x2x0.3 cm (figure 1). It was attached to the endometrial surface with a pedicle 1 mm in diameter. The patient made an uneventful post-operative recovery. Histopathology report showed a benign polyp. Endometrium could not be commented upon.


Figure 1- Gross appearance of the polyp. Arrow indicated the broken pedicle, 1 cm from the upper end.


Figure 2. Microscopic appearance of the polyp. A. Low power; B. High power; C. Oil immersion.

Discussion

An endometrial polyp ranges in size from a few millimeters to many centimeters. Its prevalence rate ranges from 10% to 40% in women with abnormal uterine bleeding.[2] Polyps may be found in up to 12% of asymptomatic women in routine examinations.[3] Malignancy is found in endometrial in 0.8% to 8% cases.[4] Lee et al reported in a metaanalysis the prevalence rate of premalignancy and malignancy in endometrial polyps of 3.57%.[5] Larger polyps are associated with a higher risk of malignancy.[6] Owing to low rates of malignancy, there is trend towards not removing such polyps if asymptomatic. However all polyps must be removed if symptomatic, or if a malignancy is considered likely. Polyps associated with endometrial hyperplasia should also be removed. Polyps which are recurrent, or which appear or grow after menopause should also be removed. In the case presented, the polyp possibly appeared and grew after menopause. The endometrium lining the uterine cavity did not show hyperplasia or malignancy, suggesting that the polyp possibly had existed at the time of the first curettage, and had been missed. Another unusual thing about the polyp was the size and location of its pedicle. It measured just 1 mm in diameter, and was attached to the polyp 1 cm from its upper end. It was very fragile and possibly would have broken by itself some time. Whether the postmenopausal uterus would have been able to expel it was doubtful. But would have necrosed after breaking of its pedicle, got infected, and would have necessitated its removal eventually.

References

1.      Sternberg SS.; Mills SE, Carter D. Sternberg's Diagnostic Surgical Pathology. Lippincott Williams & Wilkins; 2004. p. 2460.
2.      Anastasiadis PG, Koutlaki NG, Skaphida PG, Galazios GC, Tsikouras PN, Liberis VA. Endometrial polyps: prevalence, detection, and malignant potential in women with abnormal uterine bleeding. Eur J Gynaecol Oncol 2000;21:180–183.
3.      Dreisler E, Stampe SS, Ibsen PH, Lose G. Prevalence of endometrial polyps and abnormal uterine bleeding in a Danish population aged 20–74 years. Ultrasound Obstet Gynecol 2009;33:102–108.
4.      Savelli L, De Iacco P, Santini D, et al.. Histopathologic features and risk factors for benignity, hyperplasia, and cancer in endometrial polyps. Am J Obstet Gynecol 2003;188:927–931.
5.      Lee SC, Kaunitz AM, Ramos LS, Rhatigan RM. The oncogenic potential of endometrial polyps. A systematic review and meta-analysis. Obstet Gynecol 2010;116:1197–1205.
6.      Rahimi S, Marani C, Renzi C, Natale ME, Giovannini P, Zeloni R. Endometrial polyps and the risk of atypical hyperplasia on biopsies of unremarkable endometrium: a study on 694 patients with benign endometrial polyps. Int J Gynecol Pathol 2009;28:522–528.

Citation

Prakash S, Parulekar SV, Sathe P. An Unusual Case of Endometrial Polyp. JPGO 2014 Volume 1 Number 6 Available from: http://www.jpgo.org/2014/06/an-unusual-case-of-endometrial-polyp.html

Endometrial Stromal Tumor

Author Information

Shruti Kulkarni*, Parulekar SV**, Pragati Sathe***
(*Third Year Resident, ** Professor and Head of Department. Department of Obstetrics and Gynecology, *** Assistant Professor, Department of Pathology Seth GS Medical College and KEM Hospital, Mumbai, India.)


Abstract
A 60 years old postmenopausal woman presented with a complaint of postmenopausal bleeding for 6 months. She was a known diabetic on insulin. She had a small 1x1 cm polyp protruding from os. Ultrasonography (USG) showed a 3x3 cm hourglass shaped polyp extending from within the uterine cavity to external os. A fractional curettage with polypectomy was done. While histopathology report was still awaited she came back with complaints of heavy bleeding per vaginam in 2 weeks’ time, She was found to have a polyp at the os. Histopathology report of curettage specimen was suggestive of endometrial stromal tumor (EST). Immunohistochemistry showed CD10 positive cells suggestive of endometrial stromal tumor. A total abdominal hysterectomy with bilateral salpingo-oophorectomy was done. Histopathology revealed a benign endometrial stromal nodule (ESN).

Introduction

Endometrial stromal tumors comprise of 0.2% of all uterine malignancies. They account for less than 10% of all such tumours.[1] They usually present as peri- and postmenopausal menorrhagia or postmenopausal vaginal bleeding. Very rarely they can be present in young women with puberty menorrhagia. By WHO classification they are divided into three groups - benign endometrial stromal nodule (ESN), low grade endometrial stromal sarcoma (ESS), and undifferentiated endometrial sarcoma (UES). We present here an unusual case of ESN treated by abdominal hysterectomy.

Case Report

A 60 year old with four full term normal deliveries in the past presented with complaints of postmenopausal bleeding for 6 months. She was a known diabetic for 18 years. She had undergone tubal ligation 25 years ago. General and abdominal examination showed no abnormality. On per speculum examination there was a 1x1cm soft to firm polyp protruding from os, bleeding on touch. Ultrasonography (USG) showed an hourglass shaped mass measuring 3x3 cm, extending from within uterine cavity to protrude from the external os. Her blood sugars were controlled with insulin therapy Polypectomy and fractional curettage were performed. While the histopathology and immunohistochemistry report was still awaited patient came after 2 weeks with heavy bleeding per vaginum with soakage of 6-7 pads per day, with passage of clots. She was examined and was diagnosed to have a polyp protruding from external os, bleeds to touch. USG showed a large polypoidal lesion arising from left posterolateral wall of uterus. Histopathology report of curettage specimen was suggestive of endometrial stromal tumor. Immunohistochemistry revealed CD10 positive cells. A total abdominal hysterectomy with Bilateral Salpingo-oophorectomy was performed. Histopathology of specimen revealed endometrial stromal nodule.


Figure 50.1. histology of fractional curettage specimen showing well defined non-infiltrative margin suggestive of benign endometrial stromal tumor.


Figure 50.2. Immunohistochemistry showing CD10 positive cells.


Figure 50.3. cut surface of uterus showing endometrial stromal nodule within uterine cavity with well defined margins.

Discussion

Endometrial stromal tumors (EST) constitute less than 5% of uterine tumors. Benign ESN accounts for about 25% of the EST. ESN is a solitary, well-circumscribed, round, fleshy nodule measuring 4 cm in diameter (range 0.8 to 15 cm), with a yellow to tan cut surface. It may have focal irregularities or finger-like projections into the adjacent myometrium less than 3 in number and none them exceeding 3 mm in the largest dimension.[2] It has expansile, noninfiltrative margins which compress the surrounding endometrium and myometrium. Low grade ESSs often show an irregular nodular growth in the endometrium, myometrium or both. There is varying degrees of permeation of the myometrium, worm-like plugs of tumor which distend myometrial and often parametrial veins.[3] A dumbbell shaped EST is usually not seen. This patient had a dumbbell shaped EST, one part of the dumbbell being in the endo- and myometrium, and the other projecting into the uterine cavity, a part of which had extruded out of the cervix as a polyp. It is impossible to differentiate between an ESN and a low-grade ESS on the basis of curettage specimens in most cases, and a hysterectomy is required to make the differentiation. This is not difficult in a peri- or postmenopausal woman, but may not be possible if the woman is younger and desires to retain her uterus. Low-grade EST is distinguished from high-grade EST by the resemblance of the neoplastic cells to proliferative endometrial stroma. The diagnosis of high-grade ESS is made only in cases where a component of low-grade ESS may be recognized; in the absence of which it is UES.[4] UESs are diagnosed only exclusion of smooth or skeletal muscle differentiation (high-grade leiomyosarcoma or rhabdomyosarcoma). Small foci of carcinoma admixed with the sarcomatous component suggest a malignant mixed mullerian tumor. CD10 expression is not helpful in this differentiation as high-grade ESS, leiomyosarcomas, rhabdomyosarcomas, malignant mixed mullerian tumors and highly cellular leiomyomas express CD10.[5,6] A perivascular epithelioid cell tumour (PEComa) may resemple a ESN on gross and microscopy. It differs in that it shows a predominantly nested growth often associated with a focal fascicular growth of cells arranged in a radial fashion around the vessels, with elongated nuclei as in smoothmuscle tumors. There are no areas that resemble the normal endometrial stroma with arterioles.[7]

References

1.  Moinfar F, Kremser M L, Man YG, Zatloukal K, Tavassoli FA, Denk H. Allelic imbalances in endometrial stromal neoplasms: frequent genetic alterations in the nontumorous normal‐appearing endometrial and myometrial tissues. Gynecol Oncol 2004. 95662–671.671.
2.      Dionigi A, Oliva E, Clement PB Young RH. Endometrial stromal nodules and endometrial stromal tumors with limited infiltration: a clinicopathologic analysis of 50 cases. Am J Surg Pathol 2002. 26567–581.581.
3.  Chang KL1, Crabtree GS, Lim-Tan SK, Kempson RL, Hendrickson MR. Primary uterine endometrial stromal neoplasms. A clinicopathologic study of 117 cases. Am J Surg Pathol 1990; 14415–438.
4.      Oliva E, Clement P B, Young R H. Endometrial stromal tumors: an update on a group of tumors with a protean phenotype. Adv Anat Pathol 2000. 7257–281.281.
5.    Oliva E. CD10 expression in the female genital tract: does it have useful diagnostic applications? Adv Anat Pathol 2004. 11310–315.315.
6.   Oliva E, Young RH, Amin MB, Clement PB. An immunohistochemical analysis of endometrial stromal and smooth muscle tumors of the uterus: a study of 54 cases emphasizing the crucial importance of using a panel because of overlap in immunoreactivity for individual antibodies. Am J Surg Pathol 2002. 26403–412.412.
7.      Folpe AL, Mentzel T, Lehr HA, Fisher C, Balzer BL, Weiss SW. Perivascular epithelioid cell neoplasms of soft tissue and gynecologic origin: a clinicopathologic study of 26 cases and review of the literature. Am J Surg Pathol 2005. 291558–1575.1575.

Citation

Kulkarni S, Parulekar SV, Sathe P. Endometrial Stromal Tumor-A Case Report. JPGO 2014 Volume 1 Number 6 Available from: http://www.jpgo.org/2014/06/endometrial-stromal-tumor.html

A Successful Cesarean Myomectomy

Author Information

Nidhi Bang*, Hajaram Chaudhary**, Shruti Panchbudhe***, Meena Satia****
(*Third Year Resident, **Second Year Resident, ** Assistant Professor, *** Professor. Department of Obstetrics and Gynecology, Seth GS Medical College and KEM Hospital, Mumbai, India.)

Abstract

Uterine fibroids are the commonest pelvic tumors over the age of 30 years, as more women are delaying childbearing until their late thirties which is the time for the greatest risk of myoma growth. A 7 × 6 cm submucosal fibroid was incidentally found during caesarean section after the delivery of the baby, on the inner aspect of the lower uterine segment at the incision site. In view of difficulty in suturing of the uterine incision, myomectomy was performed.

Introduction

Uterine leiomyoma are the commonest type of benign tumor of female reproductive tract during the reproductive age group with an incidence ranging from 5.4 to 7.7%.[1,2]. This is associated with increased amount of circulating estrogen.[2] The incidence of uterine myoma during pregnancy has been reported to be2%.[3]  The blood loss during caesarean myomectomy is usually severe as the size and blood supply to the myoma are increased during pregnancy. Traditionally obstetricians avoided myomectomy during cesarean section due to severe hemorrhage often necessitating hysterectomy and also it lead to increase in postoperative morbidity. In most cases it is wise to defer myomectomy until the uterus has completely involuted, preferably for 6 months. Uterine involution causes ischemia and vascular remodeling within the myometrium which cause shrinkage in the size of uterine myoma. A few previous reports have recently suggested that cesarean myomectomy is a safe surgical procedure, provided   it is performed in carefully selected patients and also improves subsequent pregnancy outcomes.

Case report

A 35 years old women, second gravida with previous lower segment caesarean section was admitted at 39 weeks 2 days of gestation in view of false labor.  Her vital parameters were stable and systemic examination revealed no abnormality. On abdominal examination uterus was full term with fetus in oblique lie with head in left iliac fossa, with minimal uterine activity and fetal heart sounds were 140 beats per minute and were regular. On vaginal examination cervix was closed, uneffaced and posterior. After two days patient went into spontaneous labor and hence decision for emergency lower segment caesarean section was taken in view of previous caesarean section with fetus in oblique lie. Baby was delivered by vertex presentation and there was no difficulty in extraction. A submucosal fibroid of size 7×6 cm was incidentally noted on the inner aspect of the lower uterine segment at the incision site, more towards the right uterine angle. In view of difficulty in approximation of upper and lower uterine segment, decision for myomectomy was taken. A plane was created between the myometrium and myoma, and it was enucleated with electrocautery in order to reduce the bleeding. Multiple hemostatic sutures were taken in the myoma bed with polyglactin910 no.1 and hemostasis achieved. This was followed by closure of the uterine incision. After the delivery of the baby, oxytocin infusion was started and was continued for 12 hours. Broad spectrum antibiotics and analgesics were given in the postoperative period. There was no significant difference observed in the intraoperative hemorrhage and postoperative pain and hospital stay in this patient and other post cesarean section patients.


Figure 50.1. Intraoperative finding showing 7×6 cm submucosal myoma situated at the inner aspect of the lower uterine segment at the incision site near the left angle.


Figure 50.2. Myoma enucleated with electrocautery by creating a plane between myoma and the uterine myometrium.


Figure 50.3. Complete enucleation by electrocautery.


Figure 50.4. Enucleated myoma.


Figure 50.5. Myoma bed after removal of myoma.


Figure 50.6. Uterine closure after caesarean myomectomy.

Discussion

Myomectomy is rarely performed during an ongoing pregnancy because of the risk of uncontrolled hemorrhage which may require hysterectomy. Although the majority of pregnant women with fibroids are usually asymptomatic, and most affected pregnancies will be uneventful, serious complications can occur during pregnancy leading to poor outcomes.  Complications are reported in only 10% of the pregnant women.[4] Pregnancy with coexisting fibroids is associated with  increased incidence of first trimester abortions, pressure symptoms, pain due to red or carneous degeneration , torsion of a pedunculated fibroid, malpresentations, dysfunctional labor, preterm labor, preterm rupture of membranes, placental abruption, obstructed labor from a cervical or lower segment fibroid ,retained placenta, subinvolution of the uterus and postpartum hemorrhage.[5] Less common complications like urinary retention in the first trimester, fetal limb anomalies and head deformities due to compression , hypercalcemia, uterine inversion and acute renal failure have also been reported in the literature.[5] The gold standard for initial management has traditionally been conservative treatment for pain symptoms. The treatment options during pregnancy depends on multiple factors like size of the myoma, location and position of the tumor relative to the lower uterine segment, proximity to vessels, severity of symptoms and patients desire for nonconservative treatment. Myomas near the fundus and ostia of the tubes should be avoided to prevent adhesions and future fertility problems.
Myomectomy during caesarean section cannot be avoided during varied presentation of the myoma such as  severe abdominal pain due to torsion of pedunculated subserous myomas, red degeneration not responding to medical treatment, unusual intraoperative appearance of the tumor and pedunculated uterine fibroids due to increase risk of torsion in future. Other indications are patients in whom fibroids are obstructing the lower uterine segment causing difficulty in baby delivery and with uterine incision closure as was seen in our case.[6,7] The various techniques described to reduce bleeding during caesarean myomectomy includes tourniquet application through avascular area of broad ligament to compress both uterine arteries, bilateral uterine artery ligation, pericervical tourniquet application,  electrocautery and oxytocin infusion after the delivery of the baby.[8]
Myomectomy done in properly selected patients, during caesarean deliveries, prevents the added morbidity of a separate procedure either laparotomy or laparoscopy for removal of fibroids in future, adhesion formation, justifies the cost effectiveness and also prevents complications related to anesthesia.
In conclusion, we do not always recommend myomectomy during cesarean section, but may be performed in unavoidable conditions like in our present case. With proper patient selection, adequate experience, and effective haemostatic measures, the procedure does not appear as hazardous as was initially thought.

References

1.      Lippma SA, Warner M, Samuels S, Olive D, Vercellini P, Eskenazi B. Uterine fibroids and gynecologic pain symptomsin a population based study. Fertil Steril 2003;80:1488-1494.
2.    Flake GP, Andersen J, Dixon D. Etiology and Pathogenesis of uterine leiomyomas: A review. Environ Health Perspect 2003; 111:1037-1054.
3.   Katz VL, Dotters DJ, Droegemeuller W. Complications of uterine leiomyomas in pregnancy. Obstet Gynecol 1989 ;73:593-6.
4.      Phelan JP. Myomas and pregnancy. Obstet Gynecol clin North Am 1995;22:801-805.
5.      Rice JP, Kay HH, Mahony BS. The clinical significance of uterine leiomyomas in pregnancy. Am J Obstet Gynecol 1989;160:1212-1216,  .
6.      Bhatla N, Dash BB, Kriplani A, Agarwal N. Myomectomy during pregnancy: a feasible option. J Obstet Gynaecol Res 2009;35:173–175.
7.    Owolabi AT, Loto MO, Kuti O, Ehinmitan RR, Ibrahim AY. Unavoidable caesarean myomectomy: a case report. Nepal Journal of Obstetrics and Gynaecology 2007;2:81-83.
8.   Kongnyuy EJ, Wiysonge CS. Interventions to reduce hemorrhage during myomectomy for fibroids Cochrane Database of Systematic Reviews, no. 3, Article ID CD005355, 2009:44-47.

Citation

Bang N, Chaudhary H, Panchbudhe S, Satia MN. A Successful Cesarean Myomectomy. JPGO 2014 Volume 1 Number 6 Available from: http://www.jpgo.org/2014/06/a-successful-cesarean-myomectomy.html

Misplaced IUD In Rectosigmoid Mesentery

Author Information
Supriya Poonia*, Vibha More**, Shruti Panchbuddhe**, M. N. Satia ***
(*Third Year Resident, ** Assistant Professor, *** Professor. Department of Obstetrics and Gynecology, Seth GS Medical College and KEM Hospital, Mumbai, India.)

Abstract

Intrauterine devices (IUD) are amongst the most commonly used methods of contraception. Perforation of the uterus and migration into the peritoneal cavity is one of its rare  but serious complication. Here is a case with IUD migration into recto-sigmoid mesentery with removal by laparotomy.

Introduction

IUD has been in vogue since 1965 for contraception.[1]  Its increase in use is due to their efficacy, easy reversibility, patient satisfaction and minimal systemic side effects.[2, 3]  Perforation occurs rarely with migration into the organs intimately related to the uterus such as urinary bladder, rectum, colon, peritoneum, ovary, appendix and wall of iliac veins. IUD is often the method for lactating mothers as it does not affect the quality and composition of milk. Removal of IUD may be done by hysteroscopy, laparoscopy or laparotomy.

Case Report

A 26-year-old Para 2 Live issue 2 with previous cesarean section, six months postpartum was brought to emergency department from peripheral maternity hospital with ultrasonography showing a  misplaced copper –T in intraperitoneal cavity on the right side. Patient had copper T (Cu- T 380-A) inserted at peripheral hospital by an auxiliary nurse midwife on day-5 of menses during lactation period. She complained of agonizing abdominal pain. The threads were not felt the next day. Uterine perforation was suspected and hence patient was referred to tertiary care center. Clinical examination revealed stable vital parameters and a soft abdomen. Bowel sounds were present. On speculum examination copper –T threads could not be seen.  No tenderness was elicited on vaginal examination. Radiography with intrauterine sound  showed  IUD towards right side in the uterine cavity. Ultrasonography of the abdomen and pelvis showed Copper-T in the right adnexa, close to the right ovary. In view of discrepancy between X-Ray( lateral film was not available) and ultrasonography a computed tomography (CT) scan of the abdomen and pelvis was done. It revealed the copper-T lying partially outside the uterus in pouch of Douglas and one arm appeared embedded in the uterine wall, abutting the rectosigmoid colon. No air or free fluid was seen in the peritoneal cavity. A hysteroscopy was performed, which did not any copper-T, but it was felt in the left uterine wall. However, it could not be removed. In view of suspected adhesions and bowel involvement exploratory laparotomy was done. Copper-T was seen in pouch of Douglas on left side embedded in mesentery of rectosigmoid colon It was removed and a small mesentery tear was sutured with polyglactin 910 no 2-0. Bowel was inspected. No bowel injury was seen. A small sealed 2 mm uterine perforation was seen on the fundus of uterus near right cornua which was left untouched. Post procedure period was uneventful. Patient was discharged on the 7th postoperative day.


Figure 1. Anteroposterior radiograph of abdomen and pelvis with uterine sound in situ.  IUD is seen towards right side, probably in the uterine cavity.


Figure 2. CT scan abdomen and pelvis showing IUD (arrows) between uterus and rectosigmoid colon.


Figure 3. Copper-T (arrow) is seen lying in the recto sigmoid mesentery on laparotomy.

Discussion

Since the introduction in 1965, IUD is commonly used as effective, safe and economic method of contraception. Incidence of migrated IUD is 0.5-1%/1000 IUD insertions. [2]  Incidence of misplaced IUD is influenced by several factors such as parity, insertion time, previous abortions, type and method(push out insertion technique) of insertion technique, operator experience and position of uterus. IUD can be used in lactating mothers as they do not effect milk composition. Thinning of uterine wall due to hypoestrogenic state could be the cause of perforation as seen in the lactation period. Sharp pain at the time of insertion, disappearance of IUD thread and post procedure bleeding are suggestive of perforation
Perforation may be complete where IUD migrate into peritoneal cavity or embed in nearby structures or partial where part of it is retained in uterine cavity or wall. Perforation mostly occurs during insertion especially owing to wrong push out insertion technique. Less commonly perforation is due to chronic inflammatory reaction caused by cytokines release, degradation of extracellular matrix by matrix metalloproteinase resulting in gradual erosion of the uterine wall. Translocated IUD induces a dense fibro elastic reaction necessitating a laparotomy for its removal due to suspected adhesions.
Uterine perforation by IUD may remain asymptomatic in 85% cases. It may present as sharp pain at insertion time, disappearance of IUD at the time of insertion,  post coital bleeding. Misplaced IUD may  invade its neighboring organs such as the adnexa, broad ligament, pouch of Douglas, intestine(obstruction, stricture, adhesions), urinary bladder(vesical calculi), peritoneum(omental mass or intraperitoneal bleed or abscess), appendix ( perforation mimicking appendicitis) rectum or recto-sigmoid mesentery as in our case.[2,3,4,5,6,7]  Often these complications are due to faulty technique of IUD insertion which is push out technique.
A plain radiograph of the abdomen was previously the initial investigation of choice, for verifying the presence of an IUD in the pelvis but now a days often forgotten due to easy availability of  imaging modalities like ultrasound and CT scan. In our case only anteroposterior X-Ray image was available and the lateral image was misplaced.  So an ultrasound examination was done. It shows the location of the IUD in  relation to the uterus without the need for an intrauterine sound which is used to identify the uterine cavity in a radiograph.. CT Scan is indicated when when there is discrepancy  between ultrasound and radiograph or when bowel involvement is suspected. In our case anteroposterior radiograph was not sufficient to comment on IUD location  and ultrasonography showed it to be lying outside the uterus hence the need of the CT scan. Although X-Ray and ultrasonography done revealed the copper-T on the right side; CT images and direct visualization intraoperatively showed the IUD  location on the left side. This can be due to intraperitoneal migration of IUD which though rare is not uncommon. The treatment of the misplaced IUCD is surgical, laparoscopy or laparotomy. In view of suspected adhesions laparoscopic removal was not attempted and IUD was removed by laparotomy. Withdrawal of the migrated IUD is advisable even if its migration is asymptomatic, so that further complications like a bowel and bladder perforation or a fistula formation may be prevented.[8]

References

1.      Zakin D, Stern WZ, Rosenblatt R. Complete and partial uterine perforation and embedding following insertion of intrauterine devices. Obstet Gynaecol Surg.1981;36:335–53.
2.      Key TC, Kreutner AK. Gastrointestinal complications of modern intrauterine contraceptive device. Obstet Gynecol. 1980;55:239-44.
3.      Singh I. Intravesical cu-T emigration: an atypical and infrequent cause of vesical calculus. Int Urol Nephrol. 2007;39(2):457-59.
4.      Kriplani A, Garg P, Sharma M, Agarwal N. Laparoscopic removal of extrauterine IUCD using fluoroscopy guidance: a case report. J of Gynaecol Surg. 2005;21(1):29-30.
5.      Carson SA, Gatlin A, Mazur M. Appendiceal perforation by copper-7 intrauterine contraceptive device. Am J Obstet Gynecol. Nov 1, 1981;141(5):586–87.
6.      Maru L, Jharvade H, Lall PR. An unusual case of copper-T in rectum. J Obstet Gynecol India. 2005;55(1):79-80.
7.      Heartwell S, Schlesselman S. Risk of uterine perforation among users of intrauterine devices. Obstet Gynecol. 1983;61:31-36.
8.      Treisser A, Colau JC. Causes, diagnosis and treatment of uterine perforations by intrauterine devices. J Gynecol Obstet Biol Reprod. 1978;7:837-47.

Citation

Poonia S, More V, Panchbuddhe S, Satia MN. Misplaced IUD In Rectosigmoid Mesentery. JPGO 2014 Volume 1 Number 6 Available from: http://www.jpgo.org/2014/06/misplaced-iud-in-rectosigmoid-mesentery.html