Volume 6 Number 8

Editorial
Gupta AS

Striae Distensae Development After Ectopic Pregnancy Removal
Parulekar SV

Hysteroscopic Lateral Myometrial Resection – A Procedure To Be Shunned?
Parulekar SV

Human Vestigial Tail –An Interesting Case Report
Madhura P, Vaidya A, Gupta AS.

Basal Cell Carcinoma Of The Vulva
Mahanti S, More V, Chaudhari HK.

A Rare Case Of Uterine Rupture In An Unscarred Uterus
Saxena A, Bhandari P, Gupta AS.

A Successful Pregnancy Outcome following Uterine Artery Embolization for Fibroids
Shilotri M, Fonseca MN, Kapote D.

Pregnancy with Chronic Kidney Disease
Choksi K, Chaudhari HK.

Remembering Past Greats: Munro Kerr
Prasad M, Venkatesh S.

Cesarean Scar Endometriosis
Thakurdesai A, Tiwari N, Chaudhari H.

Intestinal Perforation Misdiagnosed As A Case Of Abruption
Pradhan M, Vaidya A, Gupta AS.

Spontaneous Fallopian Tubal Recanalization After Sterilization
Parulekar SV

Coexisting Chronic Fourth Degree Perineal tear and Rectal Mucosal Prolapse
Parulekar SV

Unusually Large Tubal Ectopic gestation
Parulekar SV

Hemihematometra Or Leiomyoma?
Parulekar SV

Cervix within cervix?
Parulekar SV

Posterior Reversible Encephalopathy Syndrome (PRES) Associated With Eclampsia And HELLP Syndrome
Kulkarni S, Mali K, Warke H.

Mucinous Borderline Ovarian Cystadenoma Misdiagnosed As Tuberculous Adnexal Abscess In A Patient With Disseminated Koch’s Disease
Modi A, Pardeshi S, Gupta AS.

Spontaneous Posterior Wall Full Length Rupture Of A Uterus With Intact Previous Cesarean Scar During Labor
Srinivasan N, Hatkar PA.

Editorial

Gupta AS

Gynecology has few surgical procedures that are done more by the tactile senses rather than under direct vision. These procedures are D&C, suction evacuation for termination of pregnancy, uterine manipulation during laparoscopic evaluation for infertility, insertion of the Veres’ needle or trocar cannula for primary port placement during a laparoscopy. Almost all intrauterine procedures can result in uterine injuries. Some of these injuries can have serious immediate complications, some have serious late sequlae and some of them may go unnoticed.

It is actually difficult to know the true incidence of uterine perforations as most of these are self reported and as mentioned earlier since some of the procedures are blind and only dependent on tactile sensation they can be missed unless there is a high degree of suspicion which is then followed through by diagnostic laparoscopy to confirm presence or absence of a uterine perforation.

Perforations that occur by a uterine sound, a curette with no suction connected, a dilator usually do not have immediate or acute presentations unless the lateral uterine wall involving the uterine vessels is injured. In such a case signs of acute blood loss would be the clinical presentation. Perforations that occur during a suction evacuation of a pregnant uterus or when instruments like ovum forceps are used that can avulse tissues they need to be evaluated carefully immediately as they can result in not only uterine injuries but also injury to hollow viscus like the bowel and bladder with disastrous life threatening morbidity and mortality.

Confirmation of a uterine perforation is done by laparoscopy and if perforation is present then it can be repaired by laparoscopy depending on the expertise of the surgeon or by laparotomy. Procedure like evacuation of a pregnancy is completed under laparoscopic guidance. When there is injury during suction evacuation or by an ovum forceps then the entire bowel and its mesentery should be minutely evaluated to detect and then repair the trauma.

Injuries that occur in a uterus heal by various degrees of fibrosis and the scar in a small non gravid uterus would be negligible or insignificant. However, when these women conceive, some unique problems can develop. First of all the placenta that forms may develop morbid adhesions focally on this scar tissue due to defect in the decidual basalis and its Nitabuch layer. This allows the trophoblast to penetrate beneath the decidua and attach to the myometrium or the serosa or also go beyond the serosa resulting in placenta accreta, increta or percreta respectively. Pregnancy with morbid adhered placenta is high risk with serious consequences to the mother and the child. Scar tissue does not have the elasticity and the distensibility of the normal myometrium. As the pregnancy grows the scar tissue stretches and thins out and can rupture. Old uterine injuries in the upper segment will be more likely to get disrupted then injuries and scars in the lower segment and these upper segment scars may give way in the antenatal rather than intrapartum period. Almost 40 % of the times the placenta will implant on the anterior wall of the upper segment and anterior perforations being the commonest can result in morbidly adhered placenta or rupture uterus or both.

In this issue of our esteemed journal we bring one such case who presented with uterine rupture and had a placenta percreta at the site of the rupture that we suspect occurred due to an occult remote uterine injury. Unfortunately her uterus had to be removed and her reproductive career got curtailed.

The august issue of our journal is now in your hand and I hope that you enjoy the collection of cases that we have presented in this issue.

Striae Distensae Development After Ectopic Pregnancy Removal

Author Information

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

Abstract

Striae distensae is a condition characterized by scarring of the dermis seen as violaceous, erythematous or hypopigmented linear striations on the skin. It is called as striae gravidarum when it occurs secondary to a pregnancy. A curious case of striae distensae of the abdomen which developed 15 days after surgical removal of a first trimester tubal ectopic pregnancy is presented.

Introduction

Striae distensae can develop in relation to a pregnancy, as well as with other conditions like Cushing’s disease, obesity and augmentation breast surgery. [1] They are violaceous to erythematous initially, and become hypopigmented and atrophic later, especially after the pregnancy in case they have developed with the pregnancy. They are called striae gravidarum when they develop in relation with a pregnancy. A curious case is presented, who developed hypertrophic striae on left side of the lower abdomen 15 days after surgical removal of a first trimester tubal ectopic pregnancy, which responded to topical steroids and did not recur in a subsequent pregnancy. They are rarely hypertrophic. A curious case of striae distensae of the abdomen which developed 15 days after surgical removal of a first trimester tubal ectopic pregnancy is presented. This is the first case of this type in the world literature.

Case Report

A 23 years old woman, gravida 2 para 1, presented with 1.5 months of amenorrhea and acute pain in  left iliac fossa for 2 hours. She past menstrual cycles had been regular, every 28-30 days, with flow for 3-4 days. She had a normal vaginal delivery. Her past medical and surgical history were not contributory. Her vital parameters were within normal limits. There was no abnormality on her general and systemic examination. Abdominal examination showed no scars or striae. Mild tenderness was present in the left iliac fossa. Speculum examination showed normal vagina and cervix. Bimanual pelvic examination showed tenderness in left fornix and on transverse movement of the cervix to the left. The uterus was retroverted, normal sized, smooth firm and mobile. No pelvic masses was palpable. A pregnancy test on her urine was positive. A pelvic ultrasonography showed an empty uterus and a 2 cm diameter mass with mixed echoes in the left adnexa. There was no free fluid in the abdomen or pelvis. A diagnosis of an unruptured left tubal ectopic pregnancy was made. A laparotomy was performed and an unruptured left tubal ectopic pregnancy was removed by partial salpingectomy. She made an uneventful recovery. Histopathological examination of the mass confirmed the diagnosis of a tubal ectopic pregnancy.
She presented after 15 days with a complaint of hypertrophic striae much more on the left side of the lower abdomen than on the right side. There was no itching sensation over the striae. Examination of the abdomen showed hypertrophic reddish-white striae on the left side of the midline below the umbilicus, up to the left flank. She had not ingested any glucocorticoids. She had not put on any weight. There was no family history of such striae. There was no clinical or laboratory evidence of Cushing’s disease. She had not participated in any exercise program, which could have lead to muscular hypertrophy. A dermatologic reference was done. A diagnosis of hypertrophic striae distensae was made, and confirmed by a biopsy. She was given topical steroid cream for local application, with which the striae disappeared in 2 months. She became pregnant without any treatment after 2 more months. Her antenatal course was uneventful. She did not develop any abdominal striae in that pregnancy. She delivered uneventfully at term and had a normal puerperium, without appearance of any striae at any time during the pregnancy and puerperium.

Figure 1. Hypertrophic striae distensae.

Discussion

Up to 90% of gravidas develop striae gravidarum.[2] Striae gravidarum usually appear after 24th week of pregnancy. They are most commonly found on the abdomen, and less often on breasts, buttocks, and thighs. They may be due to a mechanical stretching of the skin due to weight gain of pregnancy and abdominal distension by the gravid uterus, along with hormonal changes. [2,3,4,5] Risk factors for development of severe striae gravidarum include ethnicity (more often in non-Caucasian women), family history, and young maternal age. There is an increased expression of glucocorticoid and androgen receptors and decreased expression of estrogen receptors in the dermis.[6, 7] An elevation in serum cortisol levels increases protein catabolism and alters collagen and elastic fibers.[8,9] Lower levels of serum relaxin may cause development of striae.[10] Differential diagnosis of striae distensae includes linear focal elastosis and anetoderma.[11,12] These conditions were ruled out by performing a biopsy of the skin lesions in the case presented.

The case presented here was unique in many respects. The patient had no family and past history of development of striae gravidarum. She did not develop striae even when she had a pregnancy in the fallopian tube. The striae developed 15 days after the ectopic pregnancy was removed surgically, at which time the hormonal influences would have been lost. Even if one considers the possibility that the hormonal changes due to the ectopic pregnancy caused the appearance of the striae, the gestational age was much less than 24 weeks after which the striae usually develop. Furthermore, development of striae has not been reported with first trimester ectopic pregnancy in the world literature. The striae were not bilateral and symmetrical, but much more on the left side than the right side. The striae responded to topical glucocorticoids. The patient did not develop any striae throughout her subsequent intrauterine pregnancy.

Acknowledgment

I thank Dr Sana Bijapur for taking clinical photograph.

References

1. Chang A.L., Agredano Y.Z., and Kimball A.B.: Risk factors associated with striae gravidarum. J Am Acad Dermatol 2004; 51:881-885
2. Wong R.C., and Ellis C.N.: Physiologic skin changes in pregnancy. J Am Acad Dermatol 1984; 10: 929-940.
3. Shuster S. The cause of striae distensae. Acta Derm Venereol 1979;59:161-169.
4. Thomas RGR, Liston WA. Clinical association of striae gravidarum. J Obstet Gynecol 2004;24:270-271.
5. Davey CMH.Factors associated with the occurrence of striae gravidarum. J Obstet Gynecol Br Commonwealth 1972;79:113-114.
6. Cordeiro RC, Zecchin KG, de Moraes AM. Expression of estrogen, androgen, and glucocorticoid receptors in recent striae distensae. Int J Dermatol 2010;49:30.
7. Youssef SES, El-Khateeb EA, Aly DG, Moussa MH. Striae distensae: Immunohistochemical assessment of hormone receptors in multigravida and nulligravida. J Cosmet Dermatol 2017; 16:279.
8. Simmons PS, Miles JM, Gerich JE, Haymond MW. Increased proteolysis. An effect of increases in plasma cortisol within the physiologic range. J Clin Invest 1984; 73:412.
9. Klehr N. Striae cutis atrophicae. Morphokinetic examinations in vitro. Acta Derm Venereol Suppl (Stockh) 1979;59:105.
10. Lurie S, Matas Z, Fux A, et al. Association of serum relaxin with striae gravidarum in pregnant women. Arch Gynecol Obstet 2011; 283:219.
11. Pui JC, Arroyo M, Heintz P. Linear focal elastosis: histopathologic diagnosis of an uncommon dermal elastosis. J Drugs Dermatol 2003;2:79-83.
12. Kineston DP, Xia Y, Turiansky GW. Anetoderma: a case report and review of the literature. Cutis 2008;81:501-6.

Citation

Parulekar SV. Striae Distensae Development After Ectopic Pregnancy Removal. JPGO 2019. Volume 6 No.6. Available from: https://www.jpgo.org/2019/08/striae-distensae-development-after.html

Hysteroscopic Lateral Myometrial Resection – A Procedure To Be Shunned?

Author Information

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

Abstract

Hysteroscopy has been used extensively for the management of a number of intrauterine conditions. There is a new trend towards hysteroscopic resection of the lateral endometrium and myometrium to expand the uterine cavity in cases of infertility. Two such cases with catastrophic results are presented.

Introduction

Hysteroscopy is useful in evaluation of infertility, abnormal uterine bleeding, repeated pregnancy wastage, suspected endometrial tuberculosis, endometrial carcinoma and hypomenorrhea.[1-5] It is used extensively for the management of conditions like submucosal leiomyomas, endometrial polyps, uterine septum, removal of intrauterine devices whose threads are missing, and Asherman syndrome.
[6-11] There is a new worrying trend towards hysteroscopic resection of the lateral endometrium and myometrium to expand the uterine cavity in cases of infertility. Two such cases with catastrophic results are presented.

Case Report 1

A 26 year old infertile woman presented to our outpatient clinic for evaluation of her infertility. She had been married for five years, had been cohabiting since then and had not used any contraception. Her menarche had been at the age of 12 years. Her past cycles had been every 28-30 days, regular, mildly painful and with moderate flow. She had hypomenorrhea for 1 year, from the time of her hysteroscopic surgery. She had undergone a laparoscopy plus hysteroscopy for evaluation of infertility. Her laparoscopic and hysteroscopic findings had been reported as normal. Hysteroscopic resection of the lateral endometrium and myometrium had been done at that time. She did not have any significant medical or surgical disease. Findings of her general and systemic examination were normal. Gynecological examination showed a normal sized, mobile uterus and normal vagina. There were no abdominal or pelvic masses. Her investigations like hemogram, urinalysis, plasma sugar levels (fasting and postprandial), liver function tests, renal function tests, thyroid function tests, electrocardiogram, chest radiograph and serological tests for syphilis, HIV, hepatitis B and hepatitis C yielded normal results. Follicular study showed that she was ovulating normally. Her husband’s semen analysis showed normal findings. Laparoscopy and hysteroscopy were performed. Laparoscopy showed normal uterus, fallopian tubes, ovaries, pelvic peritoneum and intraabdominal structures. Hysteroscopy showed occlusion of endometrial cavity with extensive fibrosis, such that there was a central tubular canal and non-visualization of the tubal ostia (figure 1).

Figure 1. Hysteroscopic findings of case 1.

Case Report 2

A 27 year old infertile woman presented to our outpatient clinic for evaluation of her infertility. She had been married for seven years, had been cohabiting since then and had not used any contraception except during the first year after marriage. Her menarche had been at the age of 13 years. Her past cycles had been every 30 days, regular, mildly painful and with moderate flow. She had hypomenorrhea for 2 year, from the time of her hysteroscopic surgery. She had undergone a laparoscopic myomectomy 3 years ago. She had also undergone a hysteroscopy for evaluation of infertility. Her hysterosalpingography prior to the hysteroscopy showed normal findings. Her hysteroscopic findings had been reported as normal, except the presence of a uterine septum. Hysteroscopic resection of the septum, lateral endometrium and myometrium had been done at that time. She did not have any significant medical or surgical disease. Findings of her general and systemic examination were normal. Gynecological examination showed a normal sized, mobile uterus and normal vagina. There were no abdominal or pelvic masses. Her investigations like hemogram, urinalysis, plasma sugar levels (fasting and postprandial), liver function tests, renal function tests, thyroid function tests and serological tests for syphilis, HIV, hepatitis B and hepatitis C yielded normal results. Follicular study showed that she was ovulating normally. Her husband’s semen analysis showed normal findings. Laparoscopy and hysteroscopy were performed. Hysteroscopy showed Asherman syndrome, there being fibrous bands passing across the uterine cavity, occlusion of the left one-fourth of the uterine cavity by fibrous tissue, and extensive fibrosis in the fundus and along the right uterine wall (figure 2). Laparoscopy showed a few adhesions between the back of the uterus and omentum. The fallopian tubes were thickened. The right tube was patent on chromopertubation, while the left tube was blocked. The ovaries were normal.

Figure 2. Hysteroscopic findings of case 2.

Discussion

Indications for operative hysteroscopy considered to be useful include endometrial ablation for abnormal uterine bleeding, lysis of intrauterine synechiae of Asherman syndrome, resection of uterine septum, endometrial polyps and leiomyomas. There have been reports of resection of uterine walls for the management of hypoplastic uterus and T-shaped uterine cavity, the value of which is logically questionable and has not been proved by clinical studies.[12-15] The value of such procedures has prior to in vitro fertilization has also not been proved.[16]

There has been a worrying trend towards performing lateral endometrial and myometrial resection of women undergoing evaluation for infertility and to be subjected to in vitro fertilization and embryo transfer. No studies have been published so far on these methods and their results. We encounter some women who have undergone this procedure elsewhere and have reported to us for management when they did not get pregnant. The two cases presented here presented in a span of one month, prompting us to report them.

Hysteroscopic resection of endometrium, leiomyomas and septa can cause serious complications, including Asherman syndrome.[17,18] Hence it makes sense to perform the procedure only when its value has been proved for the indication for which it is performed. It is also dangerous when it is performed when it is not warranted. Furthermore, lateral resection of the myometrium for infertility or circumferential resection of the myometrium for hypoplastic uterus reduce the myometrial thickness. Such uteri are likely to rupture should the patient manage to get pregnant and reach the third trimester.

Conclusion

Unwarranted hysteroscopic resection of the lateral endometrium and myometrium should not be performed for the management of infertility.

Acknowledgment

I thank Dr Aashlesha Kulkarni for taking operative photographs.

References

1. Bradley LD. Overview of Hysteroscopy. UpToDate. Available at http://www.uptodate.com/online/content/topic.do?topicKey=gyn_surg/13448&view=print.
2. Lindelmann HJ, Mohr J. CO2 hysteroscopy: diagnosis and treatment. Am J Obstet Gynecol. 1976 Jan 15. 124(2):129-33.
3. Golan A, Ron-El R, Herman A, Soffer Y, Bukovsky I, Caspi E.Diagnostic hysteroscopy: its value in an in-vitro fertilization/embryo transfer unit. Human Reproduction. 1992;7(10):1433–1434.
4. Parasins HB, Parulekar SV. Significance of negative hysteroscopic view in abnormal uterine bleeding. J Postgrad Med. 1992;38:62-4.
5. Panda A, Parulekar SV, Gupta A. Diagnostic hysteroscopy in abnormal uterine bleeding and its histopathological correlation. J Obstet Gynecol India. 1999;175:74-6.
6. Siegler AM, Valle RF. Therapeutic Hysteroscopic Procedures. Fertil Steril 1988;50(5):685-701.
7. Vilos GA. Hysteroscopic and nonhysteroscopic endometrial ablation. Obstet Gynecol Clin North Am. 2004 Sep;31(3):687-704, xi.
8. Jeong KA, Park KH, Chung DJ, Shin JS, Bai SW, Lee BS, Cho DJ, Song CH. Hysteroscopic endometrial ablation as a treatment for abnormal uterine bleeding in patients with renal transplants. J Am Assoc Gynecol Laparosc. 2004 May;11(2):252-5.
9. Capella-Allouc S, Morsad F, Rongières-Bertrand C, Taylor S, Fernandez H.Hysteroscopic treatment of severe Asherman's syndrome and subsequent fertility. Human Reproduction, 1999;14(5)1230–1233.
10. Fayez JA. Comparison between abdominal and hysteroscopic metroplasty. Obstet Gynecol. 1986;68:399–403.
11. Shamma FN, DeCherney A. The Role of Hysteroscopy in In Vitro Fertilization-Embryo Transfer. REP 1992;2(3):132-3.
12. Barranger E, Gervaise A, Doumerc S, Fernandez H. Reproductive performance after hysteroscopic metroplasty in the hypoplastic uterus: a study of 29 cases. BJOG. 2002 Dec;109(12):1331-4.
13. Garbin O, Ohl J, Bettahar-Lebugle K, Dellenbach P. Hysteroscopic metroplasty in diethylstilboestrol-exposed and hypoplastic uterus: a report on 24 cases. Hum Reprod. 1998 Oct;13(1O):2751-5.
14. Katz Z, Ben-Arie A, Lurie S, Manor M, Insler V. Beneficial effect of hysteroscopic metroplasty on the reproductive outcome in a 'T-shaped' uterus. Gynecol Obstet Invest. 1996;41(1):41-3.
15. Nagel TC, Malo JW. Hysteroscopic metroplasty in the diethylstilbestrol-exposed uterus and similar nonfusion anomalies: effects on subsequent reproductive performance; a preliminary report. Fertil Steril. 1993 Mar;59(3):502-6.
16. Carneiro MM. What Is the Role of Hysteroscopic Surgery in the Management of Female Infertility? A Review of the Literature. Surgery Research and Practice. vol. 2014, Article ID 105412, 6 pages, 2014. https://doi.org/10.1155/2014/105412.
17. Cooper JM, Brady RM. Late complications of operative hysteroscopy. Obstet Gynecol Clin North Am. 2000;27(2):367-74.
18. Jansen FW, Vredevoogd CB, van Ulzen K, Hermans J, Trimbos JB, Trimbos-Kemper TC. Complications of hysteroscopy: a prospective, multicenter study. Obstet Gynecol. 2000 Aug. 96(2):266-70.

Citation

Parulekar SV. Hysteroscopic Lateral Myometrial Resection – A Procedure To Be Shunned? JPGO 2019. Volume 5 Number 8. Available from: https://www.jpgo.org/2019/08/hysteroscopic-lateral-myometrial.html

Human Vestigial Tail –An Interesting Case Report

Author Information

Madhura P*,  Vaidya A**,  Gupta AS***.
(* Junior resident, ** Senior resident, *** Professor, Department of Obstetrics & Gynecology, Seth G S Medical College and K E M Hospital, Mumbai, India).

Abstract

The appendix, auricular muscles, wisdom teeth, the caudal bone and the semilunar fold are few of the many putative vestigial structures as described by the famous biologist Charles Darwin in literature. The human tail is usually considered as a marker of underlying pathology of occult spinal dysraphism. It is also associated with medical and social implications that require timely intervention and holistic approach for treatment.

Introduction

There are only 40 cases of true human tails reported in the medical literature.[1] We report an interesting case of a vestigial tail detected after birth in a newborn and its management. Interestingly the antenatal malformation scan revealed no structural abnormality and in the post natal period baby did not have any neurological abnormality or externally visible spinal cord defect but the radiological imaging was suggestive of a probable lipomeningcoele.

Case Report

We report a case of a gravid 3 para 2 living 2 with no antenatal high risk factors. She had a normal malformation ultrasound scan.  She had a full term normal vaginal delivery and delivered a male child of 3 kg. Neonate had a 3 x 3 cm midline swelling in the sacral region of the spinal cord. It was soft compressible with normal overlying skin. There was no evidence of hair tufts or dimpling or nevus [ Figure 1 and 2]. Baby was conscious, playful, and was moving all four limbs. There were no neurological abnormalities. Ultrasound done on day 5 of life was suggestive of 2.4 x 1.3 x 1.7 cm lesion in the sacral region. Lesion was filled with fat and fluid and it had a communication with the spinal cord. The most likely diagnosis was that of a lipomeningocele extending into the spinal canal with tethered and thickened filum terminale. Baby was evaluated by the neurosurgeons and was operated on day 10 postnatally where the lesion was excised and tethered cord was released and baby was observed for 10 days and was discharged. The histopathology report was also suggestive of a lipomeningcoele.

 Figure 1. Midline tail.

Figure 2. Tail lifted up.

Discussion

Human tail is an idiosyncratic entity with a cosmetic issue that presents as an adjunct structure in the lumbosacral region. They are usually classified as true tails and pseudo tails. Spinal dysraphism is a common anomaly associated with the tails. Embryological study reveals that the human tail which is present at 5th week of gestation disappears by the 8th week of intrauterine life and is formed on 11-12 vertebrae. The most distal remnant of the embryonic tail gives origin to the true human tail. Connective tissue, striated muscles, adipose tissue and blood vessels are the chief histological components of the true tail. It is deficient in notochord, spinal cord, bone and cartilage. A true human tail is easily removed surgically without any residual disease. Pseudo tails superficially resemble true tails. Human tails most commonly arise in the lumbosacral region.[2]
Lipomeningocele is a type of closed neural tube defect with adverse neurological sequele secondary to an inherent tethered spinal cord. Around 0.3 and 0.6 per 10,000 live births is the prevalence of lipomeningocele and lipomeningomyelocele in the general population respectively.[3] Lipomyelomeningocele is characterized by a subcutaneous lipoma located in the lumbar or sacral region. The most common symptom is a clinically apparent fatty mass positioned in the midline or off the midline in the lumbosacral region.The lumboscaral fascial defect restricts the axial growth of conus medullaris leading to tethered spinal cord causing neurological and urinary functional deficits.[4] It may be difficult to detect lipomyelomeningocele by ultrasonography if the spine lies adjacent to the uterus.  Magnetic resonance imaging is useful in identifying fatty mass and presence of spinal cord tethering. Additional specialized testing such as urodynamic function studies and neurophysiological monitoring may be beneficial in evaluation of these patients to assist with timing of surgical intervention. Surgical management of the human tail depends on the presence or absence of associated anomalies on the MRI. A true human tail is considered as a failure of regression in fetal life and can be treated by simple excision whereas a pseudo tail is associated with an underlying anomaly thus requiring an extensive surgery which involves the excision of the lesion with correction of the anomaly leading to the tethered cord. In our case, it was a pseudo tail as it had anomalous communication with the spinal cord. If the neurological symptoms allow, surgery can be withheld for 3 months or until the baby has reached 5 kg weight.[5] The cardinal steps in lipomyelomeningocele repair involve resection of the adipose mass, defect identification in the lumbosacral fascia, release of the filum terminale with the aim to preserve the neural elements. Further care should be taken to prevent the tethering of the spinal cord. Lipomeningomyelocele is a form of closed neural tube defect with the risk of worsening neurological and urological function secondary to tethered spinal cord and hence requires timely intervention.

References

1. Kansal R, Agrawal N, Khare S, Khare A, Jain S, Singhal BM. Newborn with a tail – A genetic throwback. Peoples J Sci Res 2010;3:15-7. 
2. Mukhopadhyay B, Shukla RM, Mukhopadhyay M, Mandal KC, Haldar P, et al. Spectrum of human tails: A report of six cases. Journal of Indian Association of Pediatric Surgeons. 2012;17(1):23-5.
3. Agopian AJ, Canfield MA, Olney RS, Lupo PJ, Ramadhani T, Mitchell LE et al.  Spina bifida subtypes and sub‐phenotypes by maternal race/ethnicity in the National Birth Defects Prevention Study, American Journal of Medical Genetics Part A. 2011;158A(1):109-15.
4. Huang S-L, Shi W, Zhang L-G. Surgical treatment for lipomyelomeningocele in children. World Journal of Pediatrics. 2010;6(4):361-5.
5. Giri PJ, Chavan VS. Human tail: A benign condition hidden out of social stigma and shame in young adult – A case report and review. Asian J Neurosurg 2019;14:1-4.

Citation

Madhura P, Vaidya A, Gupta AS. Human Vestigial Tail –An Interesting Case Report. JPGO 2019. Vol 6 No. 8. Available from:  https://www.jpgo.org/2019/08/human-vestigial-tail-interesting-case.html

Basal Cell Carcinoma Of The Vulva

Author Information

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

Abstract

Basal cell carcinoma of the vulva is very rare. This entity in gynecological and dermatological oncology presents a diagnostic challenge in view of the late presentation of the patients, who are usually elderly. Here we have a case of a 72 year old woman, who presented to our outpatient department with complains of itching and irregular swelling in the genital area.

Case Report

A 72 year old, postmenopausal woman presented to the gynecological outpatient department with complains of swelling and discoloration in the genital area for 1 month. She had no complaints of pain over the area, bleeding or associated abdominal pain. History of itching over the lesion was present. On examination, her vital parameters and systemic examination were stable and normal. On local examination, a 2x2 cm, dark pigmented, ulcerative lesion was noted over the superior aspect of the right labia majora, around 2 cm lateral to the midline. The margins of the lesion were irregular but there was no associated involvement of the clitoris, urethral orifice, labia minora. There was no palpable inguinal lymphadenopathy. On per abdomen examination, all quadrants were soft and non-tender and on per speculum examination, cervix and vagina appeared atrophic but healthy. On per vaginal examination, uterus was atrophic and fornices were free and not tender. Differential diagnosis at this stage included lichen sclerosus or lichen simplex atrophicus. She was referred to the dermatological outpatient department (OPD) for their expert opinion

Figure 1. Gross morphological appearance of basal cell carcinoma of vulva.

In the dermatological OPD, the above clinical findings were noted and confirmed. Dermascopy that was performed was highly suggestive of basal cell carcinoma and hence biopsy of the lesion was advised. Punch biopsy was performed and histopathology report confirmed the diagnosis of basal cell carcinoma of the vulva. She was referred to onco-surgeon for further management of the same. They performed a wide local excision. She is presently following up with the oncosurgeons.

Discussion

Basal cell carcinoma is one of the commonest malignancies involving the skin. But the predilection is for the sites exposed to sun, including the head and neck in view of role of ultraviolet rays in the pathogenesis of the same. Hence basal cell carcinoma of the vulva is an extremely rare entity accounting for less than 5 percent of all vulvar malignancies and less than 1 percent of all basal cell carcinomas.[1]
Although the exact etio-pathogenesis is not known, exposure to ultraviolet radiation, chronic irritation of the vulvar region and exposure to arsenic are identified risk factors.[2] Apart from these, genetic conditions such as xeroderma pigmentosum, nevoid basal cell carcinoma and mutations in p53 genes are also known to predispose to basal cell carcinoma of the vulva.
The diagnosis is often delayed because of the morphological similarity of the lesions to Paget’s disease of the vulva and lichen simplex atrophicus which are benign lesions. It is therefore recommended to perform incisional biopsies of all suspicious vulvar lesions especially in patients in the postmenopausal age group. Basal cell carcinoma diagnosis is often delayed in view of its similarity to other dermatological diagnosis such as eczema, psoriasis, seborrheic dermatitis and angiokeratoma.[3]
Even though slow growing, the lesion should be examined with high clinical suspicion for malignancy especially in the elderly, for early diagnosis and timely treatment.[4]
Treatment is fairly direct in the form of wide local excision of the lesion or Moh’s micrographic excision.[5] A margin of 1cm around the lesion is usually considered adequate for excision of the lesion. In view of the slow growing and indolent course of the disease, wide local excision of the lesion is usually considered sufficient treatment. However, in some large invasive tumors with large lymph node involvement, selective lymphadenectomy maybe performed. Reconstruction of the excision site can be done with advancement of skin flaps. Patients who are considered surgically unfit may undergo radiotherapy.[6]

Conclusion

Although extremely rare, basal cell carcinoma is a recognized entity in gynecological oncology with an indolent course and fairly direct mode of management. Clinical suspicion for malignancies should be especially high in vulvar lesions in the postmenopausal age group.

References

1. Mulayim N, Foster SD, Tolgay OI, Babalola E. Vulvar basal cell carcinoma: two unusual presentations and review of the literature. Gynecol Oncol. 2002;85(3):532–7.
2. Finan MA, Barre G. Bartholin's gland carcinoma, malignant melanoma and other rare tumours of the vulva. Best Pract Res Clin Obstet Gynecol. 2003;17(4):609–33.
3. de Giorgi V, Salvini C, Massi D, Raspollini MR, Carli P. Vulvar basal cell carcinoma: retrospective study and review of literature. Gynecol Oncol. 2005;97(1):192–4.
4. Yaghoobi R, Razi T, Feily A. Clinical image : an unusual pigmented basal cell carcinoma arising from vulva. Acta Dermatovenereol Alp Panonica Adriat 2011;20(2):81-2.
5. Benedet JL, Miller DM, Ehlen TG, Bertrand MA. Basal cell carcinoma of the vulva: clinical features and treatment results in 28 patients. Obstet Gynecol. 1997;90(5):765–8.
6. Miller ES, Fairley JA, Neuburg M. Vulvar basal cell carcinoma. Dermatol Surg. 1997;23(3):207–9.

Citation

Mahanti S, More V, Chaudhari HK. Basal Cell Carcinoma Of The Vulva. JPGO 2019. Vol 6 No. 8. Available from: https://www.jpgo.org/2019/08/basal-cell-carcinoma-of-vulva.html

A Rare Case Of Uterine Rupture In An Unscarred Uterus

Author Information

Saxena A*,  Bhandari P**,  Gupta AS***.
(* Junior resident, ** Senior resident, *** Professor, Department of Obstetrics & Gynecology, Seth G S Medical College and K E M Hospital, Mumbai, India.)

Abstract

Uterine rupture is an uncommon entity in a scarred uterus and is rare in an unscarred one. Here we are presenting a case of uterine rupture in a 28 year old patient with 36 weeks of gestation with past history of an ectopic pregnancy and a spontaneous incomplete abortion for which check curettage was done.

Introduction

Uterine rupture in pregnancy is not very common. It significantly raises maternal and fetal morbidity and mortality.[1] The most important risk factor for a uterine rupture is the scarred uterus.[2] Uterine rupture during labor in women undergoing trial of labor, with a previous cesarean section, ranges from 325 to 468 per 1,00,000 women.[3,4] Less data is available for uterine rupture in women with no previous history of cesarean section.[5]

Case Report

A 28 year old, gravida 3, ectopic pregnancy 1 and spontaneous abortion 1 with 36 weeks of gestation had come to our emergency room with complaint of acute pain in abdomen and distention since 4 hours. She had past history of a check curettage which was done for spontaneous incomplete abortion 4 years ago and a right salpingectomy was done for an ectopic pregnancy 2 years ago. She was in immense pain, her peripheral pulsations were not palpable, carotid pulse rate was 120 bpm and blood pressure was 80/60 mm of Hg. On per abdomen examination, the uterine size and contour could not be made out and fetal heart sounds could not be heard. Abdomen was guarded and tender. On vaginal examination, cervical os was 1.5 cm dilated, 20-30 % effaced, and presenting part was not felt. There was no evidence of bleeding. On investigations, her hemoglobin, which was 12 gm% 4 weeks ago, had dropped down to 7.5 gm%, white blood cell count was 28,000/mm3 and platelet count was 2,00,000/mm3. She was immediately shifted to the operation theater for exploratory laparotomy with the clinical diagnosis of uterine rupture with hemoperitoneum and hemorrhagic shock. Intraoperatively, hemoperitoneum of 1.5 litres was drained and blood clots of approximately 900 gm were evacuated. A 2x2 cm rent in the fundus of the uterus was seen, close to the right cornua.[Figure 1] The placenta could be seen coming out through the rent. Baby was delivered by taking lower uterine transverse curvilinear incision. Unfortunately, it was a still birth of 3 kg. A drip of 20 IU oxytocin was started but the placenta was completely adherent to the anterior wall of the uterine cavity and could not be separated.[Figure 2] So, an emergency subtotal hysterectomy was done. She received 5 units of whole blood, 4 units of fresh frozen plasma and 8 units of platelets. Postoperatively, she was kept in ICCU for one day for monitoring and then shifted to the general ward. She was stable and was discharged on day 6. Histopathology examination report of the specimen was suggestive of placenta percreta. Suture removal was done on postoperative day 14 and wound was healthy.

Figure 1. Uterine fundal rupture.

Figure 2. Completely adherent placenta at rupture site.

Discussion

Uterine rupture causes significant morbidity and mortality in the mother and the fetus. There are various causes for such an event in an unscarred uterus such as obstructed labor, morbidly adherent placenta specially placenta percreta, injudicious use of oxytocin or prostaglandins and rarely intrauterine manipulations such as internal podalic version and breech extraction.[6]
In our case, the cause of rupture was placenta percreta which could have been because of overzealous curetting of the uterine cavity during previous check curettage. Vernekar and her coworker have published a case series of 13 cases of uterine ruptures in unscarred uteruses and found only one case in which uterine rupture was due to placenta percreta. Similar ruptures secondary to placenta percreta have been reported by Imseis et al and Esmans et al.[7,8] Esman et al reported a case of 14th week of pregnancy with previous history of manual extraction of the placenta  followed by a check curettage, came with complaints of severe abdominal pain. On performing a laparotomy a hemoperitoneum of 2500 ml and a fundal uterine defect of 4 cm with placental tissue penetrating through the uterine serosa was found which required a hysterectomy. In this case, just like ours, no placental morbidities were diagnosed on repeated antenatal ultrasound examinations. With increasing rates of curettages, morbid adhesions of the placenta should be ruled out by the sonologists to prevent such catastrophies in patients with previous history of check curettage.
Heemskerk and her team reviewed 13 cases of uterine rupture, where 8 cases had a past history of dilatation and curettage which had led to perforations and later to uterine rupture in subsequent pregnancies. It is possible that in our case also an undiagnosed perforation led to a scar and a defect. This defect on healing must have had deficient decidua which eventually led to placenta percreta and rupture at the onset of labor.[9]
Our patient also had right salpingectomy done a few years ago, but it is unlikely to be the cause of this rupture as there was a band of normal tissue between the right cornua and the rent. This rupture may have also occurred by the morbidly adherent placenta which reached the serosa and mimicked a rupture. A subtotal hysterectomy had to be performed in our case though in other cases conservative measures have been described.[10] However, considering that these conservative treatments are associated with a four-fold mortality rate as compared to hysterectomy, the latter is usually preferred in such a situation.[11] Also, besides prompt surgical management, effective fluid management and blood replacement is the key to good outcomes.

Conclusion

Uterine rupture in an unscarred uterus is uncommon and very often not an anticipated complication and therefore, it is important to spread awareness regarding its occurrence, risk factors and management amongst health care providers. Maternal and perinatal outcome can be optimized by awareness of risk factors, recognition by clinical symptoms, signs and prompt surgical intervention.

References

1. Guise JM, McDonagh M, Osterweil P, Nygren P, Chan BK, Helfand M. Systematic review of the incidence and consequences of uterine rupture in women with previous caesarean section. British Medical Journal. 2004;329(7456):19–25. 

2. Cantwell R, Clutton-Brock T, Cooper G, Dawson A, Drife J, Garrod D, et al. Saving mothers’ lives: reviewing maternal deaths to make motherhood safer: 2006–2008. BJOG. 2011;118(S-1):1–203. 

3. Signore C, Spong CY. Vaginal Birth After Cesarean: New Insights Manuscripts from a National Institutes of Health Consensus Development Conference, March 8-10, 2010. Seminars in Perinatology 2010;34(4):235-236.
4. Guise JM, Denman MA, Emeis C, Marshall N, Walker M, Fu R, et al. Vaginal birth after cesarean: new insights on maternal and neonatal outcomes. Obstetrics and Gynecology 2010 Jun;115(6):1267-78.
5. Turner MJ. Uterine rupture. Best Practice and Research Clinical Obstetrics and Gynaecology 2002;16(1):69–79. 

6. Vernekar M, Rajib R. Unscarred Uterine Rupture: A Retrospective Analysis. The Journal of Obstetrics and Gynecology of India. 2016;66(S1):51–54.
7. Imseis HM, Murtha AP, Alexander KA, Barnett BD. Spontaneous rupture of a primigravid uterus secondary to placenta percreta. A case report. Journal of Reproductive Medicine. 1998;43(3):233–6.
8. Esmans A, Gerris J, Corthout E, Verdonk E, Declercq S. Placenta percreta causing rupture of an unscarred uterus at the end of the first trimester of pregnancy: case report. Human Reproduction. 2004;19(10):2401–3.
9. Heemskerk S, Eikelder MLGT, Janssen CAH. Uterine rupture in pregnancy after an intervention complicated by uterine perforation: Case report and systematic review of literature. Sexual & Reproductive Healthcare. 2019;19:9–14.
10. Wang LM, Wang PH, Chen CL, Au HK, Yen YK, Liu WM. Uterine preservation in a woman with spontaneous uterine rupture secondary to placenta percreta on the posterior wall: a case report. Journal of Obstetrics and Gynaecology Research. 2009;35(2):379-84.
11. Moriya M, Kusaka H, Shimizu K, Toyoda N. Spontaneous rupture of the uterus caused by placenta percreta at 28 weeks of gestation: a case report. Journal of Obstetrics and Gynaecology Research 1998;24(3):211-214.

Citation

Saxena A, Bhandari P, Gupta AS. A Rare Case Of Uterine Rupture In An Unscarred Uterus. JPGO 2019. Vol 6 No. 8. Available from: https://www.jpgo.org/2019/08/a-rare-case-of-uterine-rupture-in.html

A Successful Pregnancy Outcome following Uterine Artery Embolization for Fibroids

Author Information

Shilotri M*, Fonseca MN**, Kapote D***.
(* Senior Resident, ** Professor and Head of Unit, *** Assistant Professor, Department of Obstetrics and Gynecology, Lokmanya Tilak Municipal Medical College and General Hospital, Mumbai, India.)

Abstract

The use of uterine artery embolization (UAE) in women who wish to retain their fertility is a controversy. There are concerns that premature ovarian failure and impaired decidual blood supply supposedly caused by UAE contribute to infertility and recurrent pregnancy loss. We report a case of a nulligravida with UAE done for fibroids that not only alleviated her symptoms but also resulted in a successful live birth.

Introduction

UAE has been used successfully since three decades for the treatment of symptomatic uterine fibroids. However, its effects on the child bearing function have not been satisfactorily examined and need further evaluation.

Case Report

A 27 year old recently married nulligravida had visited our outpatient department with complaints of heavy menstrual bleeding and dysmenorrhea since one year. On examination, she was markedly pale and there was a 20 weeks gestation size firm mass arising from the pelvis. She was admitted in view of hemoglobin of 3.6 gm% and the anemia was corrected by blood transfusion and parenteral iron. She was prescribed tranexamic acid with ethamsylate during menses to limit her blood loss. The ultrasound was suggestive of multiple small uterine fibroids and a large submucosal anterior wall fibroid. A computed tomography of abdomen and pelvis done for fibroid mapping was suggestive of a bulky uterus (volume of 400.5cc) with a 4.5 x 4.2 x 4 cm (volume 39.3cc) submucosal, left lateral fibroid and a conglomerate of multiple small fibroids throughout the uterus. In view of the severity of menorrhagia, multiple number and the scattered location of the fibroids she was offered myomectomy or uterine artery embolization as treatment options. She was counseled regarding the uncertain effects of UAE on reproductive function and the associated risks of both myomectomy and UAE. She opted for UAE. She underwent bilateral uterine artery embolization using polyvinyl alcohol particles of 300-350µm under fluoroscopic guidance until near complete stasis of blood flow. She had an uneventful post-procedure course with no history of fever, bleeding or discharge vaginally. Her heavy menstrual bleeding and dysmenorrhea gradually reduced 2 months post procedure and were eventually completely relieved. At the monthly follow-up ultrasounds the fibroid size remained the same up to three months post-procedure. By nine months post UAE the uterine volume had reduced by 83.7% to 65cc and the largest fibroid volume had reduced by 94.3% to 2.2cc. She conceived spontaneously two years after UAE and registered at our hospital antenatally at 10 weeks of gestation. She had an uneventful antenatal course. However, at 31 weeks she was diagnosed to have grade 2 anterior placenta previa. At 34 weeks gestation she developed bleeding per vaginum with fetal distress. Hence, an emergency lower segment cesarean section was undertaken. She delivered a 2.2 kg male child with an Apgar score of 9/10. Intra-operatively, the placenta was extensive, spreading from the fundus into the lower segment up to 2 cm from the internal os. It was unhealthy, calcified and ragged and had to be delivered out piecemeal. Fortunately, there was no bleeding from the placental bed, no postpartum hemorrhage and she did not require blood transfusion. The uterus was larger than a normal postpartum uterus (24 weeks size) probably due to small intramural fibroids. A small seedling fibroid on the posterior wall was noted. Uterine cavity was regular and there were no areas of myometrial thinning. Her post-operative period was uneventful and she was discharged on day 7.

Fig. 1: Ragged, unhealthy placenta.

Discussion

Uterine artery embolization for treatment of symptomatic fibroids was first reported by Ravina et al in 1995.[1] Today it is an established treatment option in women who do not want to undergo surgery. Relief of symptoms in 80-90% of women along with a reduction in the fibroid volume of 40-70% is seen at the end of one year.[2] In this case there was a stupendous response with complete relief of symptoms and a reduction in fibroid volume by 94.3%. While there is no dilemma for women who have completed their families, experts deem it prudent to be cautious while offering this procedure to women who want to conceive in the future. The primary concern was UAE causing premature ovarian failure and hence infertility as suggested by earlier reports.[3] However, a better designed study refuted these claims and showed that ovarian function remained unaltered, especially in women younger than 40 years of age.[4] Indeed, there are several reports of successful pregnancies, most of them spontaneously conceived, as was seen in this case.[5-7] There is limited evidence on comparative fertility outcomes post myomectomy and UAE. In a randomized controlled trial, Mara et al have reported a comparable pregnancy rate in both groups.[8]There are concerns regarding compromised decidual blood supply which may result in adverse pregnancy events such as implantation failure, miscarriage and intrauterine growth restriction. The miscarriage rate in the UAE group was significantly higher than the myomectomy group.[8] However, these complications are also primarily associated with fibroids in pregnancy and hence to attribute them entirely to UAE may be erroneous. As in this case, pregnancy continued into the third trimester without hormonal support and delivered an appropriate for gestational age baby. An increased incidence of placenta previa and adherent placenta in pregnancies after UAE has been reported.[7] This may be due to denudation of the endometrium as reported in a study that visualized the uterine cavity hysteroscopically post UAE.[9] This case had grade 2 anterior placenta previa without adherence. Another anticipated complication is the risk of uterine rupture during pregnancy due to myometrial ischemia. However, there have been no such reported cases and this may be one of the advantages of UAE over myomectomy. In this case, integrity of the uterus was maintained and there were no areas of myometrial thinning as seen intra operatively. There are no definitive guidelines regarding the appropriate time to wait until conception so that healing occurs after UAE. It is generally recommended to wait for 3-6 months after myomectomy.

Conclusion

UAE is a promising modality of treatment for women with symptomatic fibroids who wish to retain their fertility. However, until more robust studies prove its safety for pregnancy, women should be cautioned regarding the risks of miscarriage and abnormal placentation. It may be a viable option for young women with multiple, scattered fibroids, small and large, where myomectomy may be difficult and could potentially end up in a hysterectomy or massive blood loss as in this case. Thus, careful patient selection is the key.

References

1. Ravina JH, Ciraru-Vigneron N, Bouret JM, Herbreteau D, Houdart E, Aymard A, et al. Arterial embolisation to treat uterine myomata. Lancet 1995 Sep;346(8976):671-2.
2. Royal College of Obstetricians and Gynaecologists. Clinical recommendations on the use of uterine artery embolisation (UAE) in the management of fibroids. 3rd ed. London: 2013.
3. Tulandi T, Sammour A, Valenti D, Child TJ, Seti L, Tan SL. Ovarian reserve after uterine artery embolization for leiomyomata. Fertil Steril. 2002 Jul;78(1):197-8.
4. Tropeano G, Di Stasi C, Amoroso S, Gualano MR, Bonomo L, Scambia G. Long-term effects of uterine fibroid embolization on ovarian study: a prospective cohort study. Fertil Steril. 2010 Nov;94(6):2296-300.
5. Ravina JH, Vigneron NC, Aymard A, Le Dref O, Merland JJ. Pregnancy after embolization of uterine myoma: report of 12 cases. Fertil Steril. 2000 Jun;73(6):1241-3.
6. McLucas B, Goodwin S, Adler L, Rappaport A, Reed R, Perrella R. Pregnancy following uterine fibroid embolization. Int J Gynaecol Obstet. 2001 Jul;74(1):1
7. Pron G, Mocarski E, Bennett J, Vilos G, Common A, Vanderburgh L; Ontario UFE Collaborative Group. Pregnancy after uterine artery embolization for leiomyomata: the Ontario multicenter trial. Obstet Gynecol. 2005 Jan;105(1):67-76.
8. Mara M, Maskova J, Fucikova Z, Kuzel D, Belsan T, Sosna O. Midterm clinical and first reproductive results of a randomized controlled trial comparing uterine fibroid embolization and myomectomy. Cardiovasc Intervent Radiol. 2008 Jan-Feb;31(1):73-85.
9. Tropeano G, Litwicka K, Di Stasi C, Romano D, Mancuso S. Permanent amenorrhea associated with endometrial atrophy after uterine artery embolization for symptomatic uterine fibroids. Fertil Steril. 2003 Jan;79(1):132-5.

Citation

Shilotri M, Fonseca MN, Kapote D. A Successful Pregnancy Outcome following Uterine Artery Embolization for Fibroids. JPGO 2019. Vol.6 No.8. Available from: https://www.jpgo.org/2019/08/a-successful-pregnancy-outcome.html

Pregnancy With Chronic Kidney Disease

Author Information

Choksi K*, Chaudhari HK**.
(*Junior Resident, **Associate Professor, Seth G S Medical College and K E M Hospital, Mumbai, India.)

Abstract

Pregnancies in women on renal replacement therapy have higher chance of maternal and fetal complications. Medical management of pregnant women with chronic kidney disease is a great challenge and requires nephrologists, gynecologists and neonatologists to work in liason. This case report gives an overall review of how successful pregnancy rates have improved in women with chronic renal disease with renal replacement therapy.

Introduction

Renal disease during pregnancy is relatively uncommon. Renal insufficiency is uncommonly associated with pregnancy because many women with significant renal insufficiency or renal failure are either beyond childbearing age or are infertile. Incomplete reporting or data collection and the fact that the incidence of mild renal disease is often not included in many of the reported series could be the other causes. Patient of renal disease have irregular menses and most of the times cannot produce healthy ovum and are infertile. Pregnancy is a challenging experience for women suffering from chronic kidney disease. Damaged kidney cannot adapt to the physiological changes of pregnancy hence, have higher chances of adverse outcome like abortion, preterm labor, preeclampsia and intrauterine fetal demise.[1] Maternal and fetal outcome have inverse relationship with baseline renal function and worsens with proteinuria. It is more challenging for patient of end stage renal disease (ESRD) on dialysis. Fetus is benefited by earlier and intensified clearance of solutes.[2] Despite the fact that mortality remains high and prematurity and low birth weight is commonly seen, the number of successful pregnancies in dialysis patients has increased over time with a gain in fetal survival. The improvement of outcomes between the nineties and now is due to an acquired expertise in dialysis schedules and technique, close monitoring of clinical, biochemical and renal parameters in a pregnant women.

Case Report

27 year old second gravida married since 9 years, 36 weeks pregnant with chronic kidney disease with anemia and chronic hypertension came with chief complaints of breathlessness on routine activity, generalized body swelling, easy fatigability and decreased urine output. She had no complaints of headache, epigastric pain or blurring of vision. She had no joint pain, rash, photosensitivity or uremic complaints. In her previous pregnancy, she developed hypertension, had a fetal demise and was diagnosed as a case of stage 4 CKD. She had received hemodialysis and was put on oral steroids. On investigations, anti nuclear antibodies were positive. In between pregnancies she was following up regularly with the nephrology department and underwent hemodialysis regularly. On examination in this pregnancy, pallor and a blood pressure of 160/100 mm of Hg was noted .On abdominal examination, uterus was 34 weeks, relaxed with a live fetus in cephalic presentation and she was not in labor. Serum creatinine was 5.7 mg% and hemoglobin was 7.6 gm%. She underwent one session of hemodialysis. She was started on oral nifedipine 10 mg, carvedilol 6.25 mg, sodium bicarbonate and aspirin 75mg. Two packed cell transfusion were given. She went into spontaneous labor and delivered vaginally a baby of 1.8 kg. She had postpartum hemorrhage and was transfused five units of packed cells then. In the post partum period, she was stable and discharged on day10. She has been following up with nephrology department for management of chronic renal disease.

Discussion

The renal plasma flow and glomerular filtration rate increase by 50% during pregnancy hence average serum urea and creatinine fall by 20-30% in comparison to non-pregnant women. Due to increase filtration, 24 hour protein excretion upto 300mg is considered normal. Baseline renal function determines pregnancy outcome. Women with primary renal disease have successful pregnancy outcome when she is not hypertensive and has low serum uric acid levels.[3] Adverse maternal outcome include gestational hypertension, preeclampsia or eclampsia, anemia, preterm delivery, need for ceserean section( 32% higher chance), postpartum hemorrhage, increased need of blood transfusion and acute renal failure. Adverse fetal outcome include fetal growth restriction, preterm birth( 52% higher chance of preterm delivery), low birth weight and neonatal morbidity. Fetal complications are primarily due intrauterine growth restriction and low birth weight due preterm termination of pregnancy in view of worsening hypertension and non-reassuring non stress test. Patient maintained on dialysis usually abort or end up in preterm delivery at around 32 weeks. Polyhydramnios is seen due to increased placental urea levels which cause fetal diuresis.[4] Women with high baseline serum creatinine are more likely to have accelerated renal damage. Renal function deteriorates in 75% women with severe renal disease and progress to end stage renal disease within one year of delivery when serum creatinine is more than 2mg/dl. Pre pregnancy counseling is a must in women with renal disease. Baseline blood pressure, renal function, urinary proteinuria and complete blood picture should be done. These women should be registered in a tertiary care hospital and should have more frequent antenatal visits. Special attention should be paid to control hypertension and avoid worsening of renal function. They should be advised to have good quality protein intake of atleast 1.2g per day and have a salt restricted diet. Women on angiotensin converting enzyme inhibitors as antihypertensive should be changed over to other anti hypertensives after first trimester as there is risk of oligohydraminos, hypocalvaria, renal failure and IUFD. Anemia should be treated aggressively with hematinics and injection erythropoietin  if required to maintain a hemoglobin of 10-11gm%. Successful correction of anemia in chronic renal disease has reduced the associated morbidity and mortality. Low dose aspirin or low molecular weight heparin should be given in women with hypertension and bad obstetric history. Uterine artery Doppler at 20-24 weeks helps to detect fetal growth restriction and surveillance to be done twice weekly depending on severity of renal impairment and hypertension.

Conclusion

Usually women on chronic dialysis do not conceive due to associated amenorrhea and irregular menstrual cycles and even if conceive they tend to abort or have preterm delivery, preeclampsia, placental abruption and still birth. Pregnant women need sessions of dialysis weekly to maintain blood urea of <50mg/dl. Successful pregnancy outcome now occur in 50% of pregnancy with improvised medical management and prompt and regular concurrent nephrology and obstetric management.

References

1. Kendrik J, Sharma S, Holmen J, Palit S, Nuccio E, Chonchol M. Kidney disease and maternal and fetal outcomes in pregnancy. American journal of kidney diseases 2015 July;66(1);55-59.
2. Shemin D. Dialysis in pregnant women with chronic kidney disease. Semin Dial. 2003 Sept-Oct;16:379–383.
3. Bar J, Ben-Rafael Z, Padoa A, Orvieto R, Boner G, Hod M. Prediction of pregnancy outcome in subgroups of women with renal disease. Clin Nephrol. 2000 Jun;53(6):437-44.
4. Bili E, Tsolakidis D, Stangou S, Tarlatzis B. Pregnancy management and outcome in women with chronic kidney disease. 2013 Apr-Jun;17(2):163–168.

Citation

Choksi K, Chaudhari HK. Pregnancy With Chronic Kidney Disease. JPGO 2019. Vol. 6. No. 8. Available from: https://www.jpgo.org/2019/08/pregnancy-with-chronic-kidney-disease.html

Remembering Past Greats: Munro Kerr

Author Information

Prasad M*, Venkatesh S**
(*Assistant Professor, **Professor, Department of Obstetrics and Gynecology, Vydehi Institute of Medical Sciences and Research Centre, Whitefield, Bengaluru-66.)

It is largely contended that the current technique of lower segment cesarean section, one of the most commonly performed operative procedures in the world, is passed on from teacher to student without delving deep into the history of the origins of the procedure. This brings us to the stalwart John Munro Kerr (1868-1960). 
He was born in Glasgow and after initial schooling, received medical education in different cities including Vienna, Dublin and Berlin. By the age of 32, he achieved the designation of faculty at the university of Glasgow and remained in the position for 40 years. One of his major areas of interest as an obstetrician was the contracted female pelvis and management options for the same. It is to be noted that he started his career in an era where the mortality attributable to cesarean section was almost 50 %.[1] The Kronig procedure (high vertical incision on the uterus) was found unacceptable to him. Though Munro Kerr was not the first to describe the low transverse incision, (Robert Wallace Johnson and Johann Osiander had suggested this in 1700’s independently), Kerr repeatedly reproduced it and perfected it, thereby popularizing it.[2] His initial case series of 107 consecutive cases with just 1 case of scar thinning as against the existing literature of 4 % scar rupture impressed most practising obstetricians of that time.[3]
One of the time-tested clinical examinations for the assessment of adequacy of pelvis is named after Munro-Kerr. While Muller introduced placement of vaginal fingers at the ischial spine to check for adequate descent of the fetal head into the pelvis, Munro-Kerr is credited to have introduced the then rather innovative method of abdominal placement of the thumb to rule out cephalopelvic disproportion at the pelvic inlet. That this test continues to be mentioned, and will always continue to be mentioned in basic textbooks of obstetrics speaks volume about the contribution of this great obstetrician.[4]
He was one of the founding fellows of the Royal College of Obstetricians and Gynecologists, of which he was also the first vice-president.[5] His book ‘Operative Midwifery’ published first in 1908, continues to be published and widely read, albeit in a different name “Munro Kerr’s Operative Obstetrics”.[6]
He retired from his hugely impactful, successful stint as Professor in the university and continued to live a long peaceful life upto the ripe age of 92 years. His career, works, books and memories will continue to inspire generations of obstetricians to come. 

References

1. Dunn PM. Professor Munro Kerr (1868-1960) of Glasgow and cesarean delivery. Arch Dis Child Fetal Neonatal Ed. 2008;93(2): F167-9.
2. Peleg D, Burke YZ, Solt I, Fisher M. The History of the Low Transverse Cesarean Section: The Pivotal Role of Munro Kerr. Isr Med Assoc J. 2018;5(20):316-319.
3. Powell JL. The Kerr Incision: John Martin Munro Kerr (1868–1960). Journal of Pelvic Surgery. 2001; 7(3): 177-8
4. Contracted Pelvis. In Konar H, editor. DC Dutta’s Textbook of Obstetrics. 9th ed. New Delhi: Jaypee 2018; pp. 330.
5. John Martin Munro Kerr. Available from https://en.wikipedia.org/wiki/John_Martin_Munro_Kerr
6. Munro Kerr. A Biography. Available from : https://universitystory.gla.ac.uk/biography/?id=WH2476&type=P

Citation

Prasad M, Venkatesh S. Remembering Past Greats: Munro Kerr. JPGO 2019. Volume 6 No.8. Available from: https://www.jpgo.org/2019/08/remembering-past-greats-munro-kerr.html

Cesarean Scar Endometriosis

Author Information

Thakurdesai A*, Tiwari N**, Chaudhari H***.
(* Final Year MBBS student, ** Assistant Professor, *** Associate Professor and Head of Unit, Department of Obstetrics and Gynecology, Seth G S Medical College and K E M Hospital, Mumbai, India.)

Abstract

The presence of functioning endometrial tissue outside the uterine cavity is known as endometriosis. Scar endometriosis is the occurrence of endometriosis at the surgical scar site. It is a rare condition and may be difficult to diagnose. It follows after any obstetrical or gynecological surgery. The clinical presentation is pain and swelling at the scar site which may or may not coincide with menstruation. A case report of a patient with a painful swelling at the scar site of cesarean section is presented. High clinical suspicion clinches the diagnosis and surgical excision with a histopathology report proves it. The pathogenesis, diagnosis and treatment of this rare condition are discussed here.

Introduction

Endometriosis is the occurrence of functioning endometrial tissue outside the uterine cavity.[1] Endometrial tissue can be found in the pelvis or in extra pelvic locations such as the abdominal wall, lungs, skin, brain, urinary tract and gastrointestinal tract.[2] Classical endometriosis characteristically presents with changes in the intensity of pain and the size of implants during menstruation.[3] The overall incidence of endometriosis is 5% to 10% in women of reproductive age. Scar endometriosis is an extremely rare clinical entity. The diagnosis is difficult and may be delayed if high clinical suspicion is not exercised.[4] The present report describes a case of scar endometriosis which was promptly diagnosed and aptly treated.

Case Report

A 24 year old lady P1L1 with previous lower segment cesarean section (LSCS) presented to the outpatient department with pain and swelling over the left side of the abdomen during menstruation for the past 6 months. The pain was well localised and relieved after menstruation. There were no other aggravating or relieving factors. She had no other complaints and no significant past medical history. She underwent a lower segment cesarean section four years back for oligohydramnios and delivered a female child. Her past menstrual cycles were regular, 30 days in length, moderately painful with bleeding for 4 days. On examination, her vital parameters were stable. On abdominal examination, the LSCS scar was healthy. An approximately 1cm well defined, tender mass was felt on the left side of the scar under the skin. Clinically, the differential diagnosis were scar endometriosis, sebaceous cyst, epidermoid cyst and incisional hernia. Ultrasonographic examination of the mass showed a hypoechoic nodule with posterior acoustic shadowing. A provisional diagnosis of scar endometriosis was thus put forth. After preoperative investigations and fitness, she was posted for excision of the scar endometrioma under spinal anesthesia. A 3cm transverse incision was taken just above the palpable swelling on the left lower abdomen. The endometriotic mass was excised completely after opening the rectus sheath with the help of a cautery (figures 1, 2). Complete hemostasis was achieved. The rectus sheath was closed and skin was approximated with Ethilon no. 1 sutures. The procedure was uneventful. The excised mass was sent for histopathology (figure 3). The diagnosis of scar endometriosis was confirmed by histopathology. She was given antibiotics and analgesics and was discharged uneventfully in the due course.

Figure 1. Endometriotic mass held with Babcock's forceps intraoperatively.

Figure 2. Site after excision of the mass.

Figure 3. The excised mass.   

Discussion

Endometriosis is a disease of women in the reproductive age group. Various theories for the etiopathogenesis of endometriosis have been suggested like vascular or lymphatic dissemination and retrograde menstruation.[5] The most plausible theory is direct mechanical transplantation of endometrial implants to the wound edge during surgery.[6] The ectopic endometrial implants attract an inflammatory response leading to pain, fibrosis and adhesions. These implants are responsive to cyclical hormonal changes and bleed and increase in size during menstruation thus giving rise to cyclical change in pain intensity. However, not all patients may complain of such characteristic changes in pain intensity. The diagnosis is made by a thorough history, clinical examination, ultrasonography (USG) and histopathology of the excised tissue. The usual clinical signs and symptoms are tenderness on palpation, a raised and hypertrophic scar or a localised swelling. On USG, a scar endometrioma may appear as a fixed solid, cystic, polycystic or a mixed nodule, depending on the amount of glandular and stromal components. A roundish heterogeneous hypoechoic area in the abdominal incision with spiculated margins and fibrotic changes and peripheral hyperechogenicity due to inflammation is a common finding.[7] Intraoperatively, endometriotic lesions grossly appear as small dark red, black or bluish cysts or nodules on the surface of peritoneal or pelvic organs. Scar endometriosis appears as a bluish or blackish swelling with tarry contents and surrounding fibrosis. Histology shows ectopic presence of endometrial glands, spindled endometrial stroma and hemosiderin deposition within macrophages or in the stroma. In many cases, such diagnostic findings are not present or the glands and stroma may be obscured by hemorrhage, hemosiderin laden macrophages or foamy cells.[3] Treatment includes hormonal suppression and surgical excision. Oral contraceptive pills, progesterone, GnRH agonists or androgenic agents may be used for hormonal suppression. The duration of treatment should be at least three months. Medical treatment however, provides only partial symptomatic relief and permanent regression is rare.[5,8] Surgical excision is the definitive treatment. Complete excision with clear margins is diagnostic as well as therapeutic. It is the preferable method to prevent recurrences.[9]

Conclusion

High clinical suspicion is the key to prompt diagnosis and treatment of scar endometriosis, a rare entity which can be difficult to diagnose. Surgical excision is the treatment of choice as it has excellent results.

References

1. Sedhain N, Dangal G, Karki A, Pradhan H, Shrestha R, Bhattachan K, et al. Caesarean scar Endometriosis. J Nepal Health Res Counc. 2018;15(3):292–294.
2. Tatli F, Gozeneli O, Uyanikoglu H, Uzunkoy A, Yalcin HC, Ozgonul A, et al. The clinical characteristics and surgical approach of scar endometriosis: A case series of 14 women. Bosn J Basic Med Sci. 2018 Aug 1;18(3):275–278.
3. Danielpour PJ, Layke JC, Durie N, Glickman LT. Scar endometriosis - a rare cause for a painful scar: A case report and review of the literature. Can J Plast Surg. 2010;18(1):19–20.
4. Gupta P, Gupta S. Scar Endometriosis: a Case Report with Literature Review. Acta Med Iran. 2015 Dec;53(12):793–95.
5. Al-Jabri K. Endometriosis at caesarian section scar. Oman Med J. 2009 Oct;24:294–95.
6. Uzunçakmak C, Güldaş A, Ozçam H, Dinç K. Scar endometriosis: a case report of this uncommon entity and review of the literature. Case Rep Obstet Gynecol. 2013;2013:386783.
7. Francica G. Reliable clinical and sonographic findings in the diagnosis of abdominal wall endometriosis near cesarean section scar. World J Radiol. 2012 Apr;4(4):135–140.
8. Sengul I, Sengul D, Kahyaoglu S, Kahyaoglu I. Incisional endometriosis: a report of 3 cases. Can J Surg. 2009 Oct;52:444–45.
9. Uçar MG, Şanlıkan F, Göçmen A. Surgical Treatment of Scar Endometriosis Following Cesarean Section, a Series of 12 Cases. Indian J Surg. 2015 Dec;77(2):682–86.

Citation

Thakurdesai A, Tiwari N, Chaudhari H. Cesarean Scar Endometriosis. JPGO 2019. Vol. 6. No. 8. Available from:https://www.jpgo.org/2019/08/cesarean-scar-endometriosis.html

Intestinal Perforation Misdiagnosed As A Case Of Abruption

Author Information

Pradhan M*, Vaidya A**, Gupta AS***.
(* Junior Resident, ** Senior Resident, *** Professor, Department of Obstetrics & Gynecology, Seth G S Medical College and K E M Hospital, Mumbai, India).

Abstract

Tuberculosis is a leading communicable disease in developing nations like India. Populations which are most prone to contract TB are those belonging to the pediatric population, seropositive status as well as immunocompromised individuals. Pregnancy is one such condition where the chance of developing TB is high. The diagnosis of extra pulmonary TB (EPTB) can often be very difficult due to the diffuse symptoms and nonspecific presentations, often mimicking inflammatory bowel disease or malignancy. We present a case of abdominal Koch’s in pregnancy, which was misdiagnosed to be a case of abruption placenta but resulted in intestinal perforation and preterm delivery. We present a case report to discuss the diagnosis of extra pulmonary TB, as well as its management in pregnancy.

Introduction

The diagnosis of EPTB can often be a tricky situation due to its nonspecific and varied presentation, as it can mimic inflammatory bowel disease or even malignancy. Immunocompromised persons are found to be more susceptible to EPTB.[1] Pregnancy is a relatively immunocompromised state and hence there is a predominance of TB in this state. Pregnancy confounds a clear diagnosis of extra pulmonary TB, as preterm labor and placental abruption which cause pain in abdomen may present a similar picture. Also, certain medical and surgical causes of abdominal pain, such as acute appendicitis, inflammatory bowel disease and acute pyelonephritis may present with a diagnostic dilemma. However, the diagnostic and treatment modalities in pregnancy are similar to those in the non-pregnant patients.

Case Report

A 24 year old married woman gravid 3, para 2, living 1, death 1 with 24 weeks of gestation had presented with complaints of fever with chills since 7 days, intermittent per vaginum bleeding since 7 days with soakage of 2 pads per day, no passage of clots and complaints of abdominal pain for 2 days. She was a recently diagnosed case of sputum positive pulmonary tuberculosis and started on Category 1 AKT in the last 10 days. She had no other antenatal high risk factors. On general examination her condition was moderate, she was febrile, her pulse rate was 120 beats/min., BP was 100/70 mm of Hg, RS was clear, CVS had no murmur, and CNS had no focal neurological abnormality. In her investigations Hb was 6.9 gm %, WBC was 6900/cubic mm, platelet was 2.6 lakh/ml, BUN was 17.2 mg/dl, creatinine was 0.6mg/dl, serum electrolytes were within normal limit, USG abdomen was suggestive of single live intrauterine gestation corresponding to 23 weeks and 2 days. She went into preterm labor and had complaints of intermittent pain in abdomen for 2 hours. On examination uterus was 24 weeks, vertex presentation, engaged, FHS were regular and 200 bpm. Uterine contraction was 2/10/20. Uterine tenderness was present and it was tonically contracted. Clinical impression was of placental abruption. On per vaginum examination os was 2.5 cm dilated, 60 % effaced, vertex was at station 0, and membranes were present. Artificial rupture of membranes was done; liquor was clear and moderate in quantity. Intrapartum blood was given and labor was augmented with oxytocin. She delivered a fresh still born female child of 678 gm. There was no evidence of retroplacental clot or postpartum hemorrhage. Day 2 post-delivery she had complaints of severe abdominal pain and 3 episodes of vomiting. Her pulse was 110/min, BP was 100/60 mm of Hg. On per abdominal examination there was generalized tenderness and guarding. Urgent ultrasonography of the abdomen and pelvis was suggestive of suprapubic collection and the provisional diagnosis was of infection or hemorrhage. No gas under the diaphragm was seen on erect x-ray of chest and abdomen. CECT abdomen and pelvis was suggestive of peritonitis with sealed off perforation of distal bowel and adjacent loculated collection with air fluid level within and necrotic mesenteric lymphadenopathy. An emergency exploratory laparotomy was performed. Intraoperative findings were suggestive of bilious fluid in the entire peritoneum. Bowel loops, liver, spleen, uterus were studded with tubercles, bowel loops were clumped up, a stercoral perforation was seen 180 cm distal to the duodenojejunal flexure, and a non-passable stricture 120 cm from duodenojejunal flexure was also seen. Ileal resection and anastomosis of stercoral perforation with proximal diverting double barrel ileostomy at the site of the non-passable stricture was done. She was started on Meropenam injection 500 mg TDS, injection Metronidazole 100 mg TDS, injection Ofloxacin 200 mg BD, injection  Streptomycin 500 mg OD and category 1 AKT was continued. Resected specimen was sent for histopathological examination.  The diagnosis of intestinal tuberculosis was confirmed. Characteristic multiple caseating granulomas and non-necrotic lymphadenopathy were seen. She was admitted in the surgical intensive care unit for 10 days for stoma care and is at present in the medicine general ward for further evaluation of extrapulmonary tuberculosis.

Figure 1. Loculated collection (arrow).

Figure 2. Clumped bowel loops (arrow).

Figure 3. Collection with air fluid level (arrow).

Discussion

Tuberculosis remains as an important cause of morbidity and mortality in the developing countries and it is often difficult to differentiate extra pulmonary TB from malignancy and Crohn’s disease. The most common site of involvement in extra pulmonary TB is the ileocecal region.[1] The reason for ileocecal involvement is the increased physiological stasis and fluid absorption and reduced digestive activity, and also the abundance of lymphoid tissue in this segment of the intestine (Peyer’s patches).[2] Symptoms of abdominal TB include abdominal distension, chronic abdominal pain fever, night sweats, loss of appetite, rapid and significant weight loss. Viscous perforation due to tuberculosis is very rare and occurs most commonly in immunocompromised individuals. In cases of intestinal perforation, the number of lesions and the depth of invasion determine the line of management. The most commonly affected areas in the intestine are the recto sigmoid colon, the appendix, the cecum and the distal ileum.[3, 4] Acute abdomen poses a great diagnostic dilemma in pregnancy as nausea, vomiting and abdominal pain are common in obstetric population and the  expanding uterus dislocates the other intra-abdominal organs. Tuberculous ulcers heal by fibrosis hence perforation leading to peritonitis is rare. Placental abruption is characterized by a triad of vaginal bleeding, abdominal and pelvic pain and uterine hypertonia. In our case, the perforation that occurred in the antenatal period remain undiagnosed, the resultant peritonitis subsequent to the perforation lead to peritoneal irritation due to which the patient presented with abdominal pain and generalized tenderness and guarding which got misdiagnosed as a case of suspected placental abruption as the gravid uterus seemed to be tonically contracted. Her fetal loss was the consequence of the perforative peritonitis. There are obstetric and non –obstetric causes of acute abdominal pain in pregnancy such as appendicitis, cholecystitis, urolithiasis, perforation, torsion, abruption and others. Laparotomy is gold standard for diagnosis of perforation but ultrasonography with an erect x-ray is sufficient to give enough clues in a pregnant state. Omental patch closure, simple closure, resection and anastomosis, loop ileostomy are the various operative interventions performed to manage perforations. Increased vigilance should be afforded to the pregnant population presenting with constitutional symptoms such as drastic weight loss, malaise and night sweats. High degree of suspicion with a broad outlook is required to identify the non-obstetric causes of acute abdomen as the diagnosis can get easily confounded by other obstetric emergencies such as abruption, preterm labor, ovarian torsion, or uterine rupture. With early multidisciplinary team involvement and holistic approach medical cure rates and prognosis is excellent in extrapulmonary tuberculosis in pregnancy.

References

1. Lwin S, Jing NLL, Suharjono H, Kipli M, Nwe TM, Yi MS. Caecal Perforation from Primary Intestinal Tuberculosis in Pregnancy. Case reports in gastrointestinal medicine. 2017; 90(1):545-547.
2. Michalopoulos A, Papadopoulos VN, Panidis S, Papavramidis TS, Chiotis A, Basdanis G. Cecal obstruction due to primary intestinal tuberculosis: A case series. Journal of Medical Case Reports. 2011;5(128). Available from:https://jmedicalcasereports.biomedcentral.com/articles/10.1186/1752-1947-5-128.
3. Tripathy SN, Tripathy SN. Tuberculosis and pregnancy. International Journal of Gynecology & Obstetrics. 2003; 80(3), 247-253.
4. Jana N, Barik S, Arora N, Singh AK. Tuberculosis in pregnancy: the challenges for South Asian countries. The Journal of Obstetrics and Gynaecology Research. 2012;38(9):1125-1136.

Citation

Pradhan M, Vaidya A, Gupta AS. Intestinal Perforation Misdiagnosed As A Case Of Abruption. JPGO 2019. Vol 6 No. 9. Available from: https://www.jpgo.org/2019/08/intestinal-perforation-misdiagnosed-as.html