Volume 5 Number 9


Madhva Prasad Sarvothaman

There are many qualities that define a good doctor, and medical training should aim to inculcate all of these in medical trainees. The first few years of the medical career- the undergraduate and the postgraduate training period are the most important formative years. Academic improvement, obtaining of knowledge and skill enhancement are the main areas which are taught in medical school curricula. However, conscious efforts that impart attitudes and behavioral improvement to budding doctors are also part of an ideal teaching program. The complex matter of evolving medical education in Obstetrics and Gynecology (Ob/Gyn) is discussed here.  
Knowledge of the subject and assimilation of principles and facts are not the only things to be learnt in residency. Apart from factual accuracy, being vocally articulate is also a very important characteristic. Stohl et al demonstrated this using fetal heart rate parameters as the conversation point. They showed that it is important for residents to read (and have knowledge about) what they are supposed to see, to see what they are supposed to see and say what they see. Most importantly, they showed that this can be taught.

Resident doctors treat patients round the clock. Many a time, they are faced with a situation of having to choose between patients, especially in an obstetric emergency room. Actively or passively, the concept of prioritisation is eventually learnt. Whether a formal obstetric triage system should be taught to Ob/Gyn residents has been pondered over. One such contemporary obstetric triage teaching, highlighted by Sandy et al, attempts this. The doctors have to answer two simple questions “Sick or not sick”, “In labor or not in labor”, as a guide to performing obstetric triage. Learning to prioritise activities in patient care, in the wake of reduced resources and time, is best learnt during residency.
Even the Millenium Development Goals have now been transformed to Sustainable Development Goals. Even at the medical professional level, sustainability is the key. Being an obstetrician-gynecologist is stressful. Naturally, residency in the same can also be stressful.
Job satisfaction, burn out and depression among Ob/Gyn residents have been rarely tested formally. In one study in the USA by Govardhan et al, it was found that a mere 13% were fully satisfied with their current status. More than 50% demonstrated high level of depersonalisation and emotional exhaustion, indicating “burn out” issues.

Owing to these and probably many other reasons, there have been some major changes in the amount of time spent by resident doctors in training. In the west, there is a restriction in the number of duty hours for resident doctors, and what kind of impact this change has caused, is still being determined. In this context, Occhino et al performed a two-institution comparison between the amount of operative experience among resident doctors, before and after duty restrictions were implemented for resident doctors. It was concluded that though there were change in number of procedures performed, overall experience appeared to be the same.
The millennials are a new crop of youngsters who are very different from the previous generation. Virtual learning, machine-based learning, interactive learning have all created a disruptive environment and clinical teaching is transforming rapidly. Mobile applications have now become the order of the day. Attempts at standardization and encouragement of applications that are accurate and acceptable; and addressing possible issues regarding inauthentic and inaccurate applications by resident doctors should be considered. Simulated obstetric teaching also forms an important part of modern medical curricula. Newer paradigms like competency based curricula are also being developed and evaluated.

Despite, all these advances, the operating room remains one of the most important places where Ob/Gyn residents gain knowledge and skill. Trainees invariably model their behaviour based on what they observe and the importance of consultants to show them the correct methods, attitudes and behaviour has been emphasized. Similarly, they can be given the responsibility of being a good role model for their juniors. This has been formally tested and positive effects have been demonstrated by Sobbing et al.

While the actual technical details of what and how things are to be taught is not being touched upon here, some issues that teaching consultants should attempt to impart are discussed below. Cost consciousness is important value that has to be picked up by resident doctors. One study showed that there could be a gap between the quality of “being aware” of costs, and actual performance of the acts of cost reduction. In medical parlance, “debriefing” is the concept wherein a teaching consultant systematically revisits or reviews how a resident doctor performed a particular procedure or technique, giving step by step comments and improvements. The concept should be popularized, especially in the context of adverse clinical events.  Inclusion of formal ethics teaching also appears to be an important consideration. Consultants should also ensure that there is no gender bias among Ob/Gyn trainees especially at junior levels.

In one study which asked consultants about what attitudes they look forward to impart to medical trainees, the four main responses were “ability to be caring”, “respect to everyone around”, “efficient and correct communication” and “integrity”. 

The emotional make-up of a doctor also appears to be a determinant of the kind of care provided to patients and the nature of response by each doctor. These have been analysed by various psychological methods. The “DISC” profile (Dominance, Influence, Submission and Conscientiousness) of resident doctors was analysed in a study by Ogunyemi et al. Doctors who showed a profile more suggestive of dominance and conscientiousness appeared to have better patient outcomes. The authors concluded that methods to improve emotional intelligence among resident doctors can be a useful tool to improve patient outcomes. The same set of investigators had done a prior analysis of emotional quotient among doctors using an instrument which tests the parameters of Self-Awareness, Self-Management, Social Awareness, and Relationship Management. They had come to a conclusion that emotional quotient can be improved with training. In this context, it should be appreciated that there are departments in the country which take an active part in resident development by offering courses on stress management, time management, communication skills and anger management. 

Notwithstanding the technological advances that have taken place, and the millennial disruptions that have occurred, bedside clinical teaching continues to be the most valuable resource for mentoring a medical trainee. This time-tested fact is validated even by recent studies on the matter. This will never go out of fashion, and will always form the pillar of medical training, or so it is hoped.
The transition from being a resident doctor to a consultant is a complex phenomenon. Very few studies have identified how to make residency more complete and how to make medical trainees more prepared for this transition. Readers are encouraged to refer to Westerman et al. for further understanding of this subject.

With this we bring to you the journal’s September issue

Mesosalpingeal Leiomyoma

Author Information

Bijapur ST*, Valvi D*, Parulekar SV***.
(* Third Year Resident, ** Assistant Professor, *** Professor and Head, Department of Obstetrics and Gynecology, Seth G S Medical College & K E M Hospital, Mumbai, India.)


Broad ligament leiomyomas are the most common extra uterine leiomyomas,  but the incidence is very low. They pose significant diagnostic and surgical difficulties. A case of a mesosalpingeal  leiomyoma in a nulliparous woman is presented here.


Leiomyoma is the most common tumor of the uterus and female pelvis.[1] Among extrauterine leiomyomas, a broad ligament leiomyoma is the most common to occur;[2] although the incidence is very low (<1%).[3] Broad ligament leiomyomas pose diagnostic and surgical difficulties. These tumors are usually asymptomatic, but may result in chronic pelvic pain, compression of the ureter, bladder and the bowel with resultant dysfunction. We present a case of a mesosalpingeal  leiomyoma. This is the first case of this type reported in the world literature.
Case Report
A 37 year old woman, married since 3 years, nulligravida, presented with a complaint of pain in lower abdomen for one year. The pain was dull aching, gradually increasing in intensity and decreased on taking non steroidal antiinflammatory agents. She had irregular menstrual cycles every 20 - 30 days, the flow lasting for 3 days, moderate and painless. There was no history of bowel and bladder disturbances. Her general and systemic examination revealed no abnormality. Abdominal examination show no tenderness, guarding or rigidity. Bimanual pelvic examination showed a 6-7 cm diameter, firm, nontender mass in right fornix  in continuity with the retroverted uterus. Ultrasonography showed a right broad ligament leiomyoma measuring 3.8x3.5 cm and a right ovarian simple cyst measuring 3.5x1.5 cm. She followed up for surgery after 6 months, and a repeat scan done now showed an 8.5x9.1 cm sized right broad ligament leiomyoma with significant increase in size as compared to previous scan and a right ovarian simple cyst of 2.7x1.7 cm.
Her investigations for fitness for anesthesia showed normal results. An exploratory laparotomy was performed with a plan to do a myomectomy and chromopertubation. During laparotomy, a large mesosalpingeal leiomyoma measuring 10x12 cm was found on the left side, with left utero-ovarian ligament stretched posteriorly and left fallopian tube stretched anteriorly over it (figure 1). The ureter well below the mass. The uterus was  normal in size and shape. The right fallopian tube and both ovaries were normal. An incision was made parallel and above the left utero-ovarian ligament and the leiomyoma was enucleated avoiding injury to the fallopian tube. Hemostatic figure of eight sutures taken over leiomyoma bed with No. 1-0 polyglactin. Mesosalpinx was reconstructed in continuous non-interlocking suture of No. 1-0 polyglactin. Transfundal chromopertubation done with methylene blue solution. Both fallopian tubes were found to be patent. She made an uneventful recovery from the operation. Histopathological examination of the tumor removed confirmed the diagnosis of a leiomyoma.

Figure 1. Intraoperative findings, anterior aspect: U – uterus, LRL – left round ligament, LFT – left fallopian tube, L – leiomyoma.

Figure 2. Intraoperative findings, posterior aspect : LFT – left fallopian tube, LO – left ovary, L – leiomyoma.

Figure 3. Stage of surgery almost near the point of removal of the leiomyoma: LO – left ovary, LUOL – left utero-ovarian ligament, L – leiomyoma, LFT – left fallopian tube.

Figure 4. Stage of surgery after removal of the leiomyoma: MS - mesosalpinx, LB – leiomyoma bed, LFT – left fallopian tube, LO – left ovary.

Figure 5. End result of the operation: LFT – left fallopian tube, LO – left ovary, LUOL – left utero-ovarian ligament, U – uterus, SL – suture line of closure of mesosalpinx.


Leiomyomas are benign tumors of myometrium. Extra-uterine leiomyomas are rare, broad ligament leiomyomas  being the most common among them, though their overall incidence is less than 1%.[1]  Broad ligament leiomyomas are of two types- false and true. True broad ligament leiomyomas arise from the muscle fibers normally found in the mesometrium, like the round ligament, utero-ovarian ligament and connective tissue surrounding the ovarian and the uterine vessels. These do not have a pseudocapsule and are associated with a greater risk of injury to the ureter, as it can lie medial, lateral, above or below the leiomyoma. False broad ligament leiomyomas originate mostly from the lateral walls of the uterus or cervix and bulge outward between the layers of the broad ligament. A false broad ligament leiomyoma usually lies above the uterine vessels, and hence the ureter lies below and lateral to it.[4] A leiomyoma in the mesosalpinx has not been described before. It can be confused for a true or false broad ligament leiomyoma during a laparotomy. It can be diagnosed by presence of the fallopian tube stretched over its upper part, the utero-ovarian ligament and ovary posterior to but separate from it, and a normal broad ligament below it. There is not much risk of an injury to the ureter during removal of such a leiomyoma because it is not closely related to it. The fallopian tube can be injured during its removal, and caution is necessary to avoid such an injury. Hemorrhage is possible during its removal, from the branches of the uterine and ovarian vessels anastomosing in the mesosalpinx. Digital compression of these vessels in the mesosalpinx during the operation minimizes the blood loss.


We thank Dr Neha Mathews for taking operative photographs.

  1. Te Linde’s Operative Gynecology 10th edition,Surgery for Benign Gynecological condition.
  2. Bhatta N. Tumours of the corpus uteri. Jeffcoats Principles of Gynaecology. 6th ed. London: Arnold Printers; 2001. p. 470.
  3. Parker WH. Uterine myomas: An overview of development, clinical features, and management. Obstet Gynecol 2005;105:216-7.
  4. Parulekar SV. Practical Gynecology and Obstetrics. 5th ed. Mumbai: Vora Medical Publications; 2011. p 348.

Bijapur ST, Valvi D, Parulekar SV. Mesosalpingeal Leiomyoma. JPGO. 2018 Vol 5 No. 9. Available from: http://www.jpgo.org/2018/09/mesosalpingeal-leiomyoma.html

Traumatic Periurethral Tear And Posterior Dislocation Of External Urinary Meatus

Author Information

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

We present a case of a periurethral tear due to trauma secondary to a fall which dislocated the urethra posteriorly, thus making it difficult for a patient to pass urine. The patient was a primigravida with 20 weeks of gestation, had a history of fall in a ditch and presented to the emergency room with complaints of bleeding per vaginum, pain and inability to pass urine.

Injuries to vulva are common and most commonly occur secondary to birth trauma & less commonly due to any other trauma secondary to fall astride a hard object, a road traffic accident or sexual violence. Periurethral injuries may occur due to obstetric trauma, by misdirection of expulsive forces. Correct anatomical orientation of structures is very important in identifying the injury and for its correct anatomical repair to avoid any future symptoms related to urinary stream or urethral strictures. We present an unusual case in which there was injury to epithelium all around the urethra extending to labia minora laterally resulting in posterior dislocation of the distal urethra and external urethral meatus.

Case Report

A 21 years old, gravida 2 para 1 living 1 with previous full term normal delivery, with 24 weeks of gestation, presented to the emergency room with history of fall in the ditch and complaints of bleeding per vaginum, pain over the perineum, and inability to pass urine. She had no history of pain in abdomen or any injury anywhere else over the body. She had no history of any high risk medical or surgical illness. On examination her vital parameters were normal. General and systemic examination revealed no abnormality. Per abdominally  the uterus was relaxed and corresponding with her gestational age. Fetal heart rate was normal on auscultation. On local vulvar examination there was a bleeding laceration around 3 cm extending from external urethral meatus anteriorly to the clitoris and 4 cm laterally to labia minora which led to posterior dislocation of the urethra. On per speculum examination, there was no injury to the vaginal mucosa or cervix. There was no active bleeding from the cervical os. Anal sphincters were intact. An obstetric ultrasonographic scan was done. It showed normal fetal cardiac activity and no evidence of placental abruption. The patient was taken to operation theater for repair of the tear. A saddle block anesthesia was given. Urinary bladder catherized with 14 French silicone catheter. There was no evidence of hematuria. The tear was sutured from urethral meatus anteriorly to clitoris and laterally to labia minora in simple inturrupted manner with polyglactin 3-0 on round body needle, after occlusion of all dead space underneath and achieving hemostasis. A continuous metronidazole and gentamycin irrigation was continued throughout the procedure to decrease the chance of wound breakdown postoperatively secondary to infection. Postoperatively a course of antibiotic was completed and urinary catheter was kept in situ for 21 days. The patient recovered well.

Figure 1. The appearance of the injured vulva. A Foley’s catheter (F) has been passed through the urethra. Original position of the external urinary meatus is pointed out by the tip of dissecting forceps (arrow).

Figure 2. The appearance of the injured vulva after repair of the injury. The suture line is pointed out by arrows.


The lower two third part of the urethra lies immediately above the anterior vaginal wall opening into external urethral meatus which lies in the midline of the vestibule, 1 to 1.5 cm below the public arch just below the clitoris and just above the vaginal opening.[1] Injury to the vagina and perineum are classified as first to fourth degree perineal tears. First degree includes laceration involiving the fourchette, perineal skin and vaginal mucosa . Periurethral tears are also included in first degree tears. Second degree includes laceration involving, in addition, fascia and perineal body muscles. Third degree extends to anal sphincters and a fourth degree involves the rectal mucosa.[1] Risk factors for perineal tear may include nulliparity, Asian race, second stage arrest of labor, operative vaginal delivery including forceps and ventouse delivery and use of local anaesthetics.[2] Timing of episiotomy is also important, if performed too late, lacerations will not be prevented. An episiotomy has to be given with crowning of the presenting part.[1] Tears of the labia and around the urethra are more common in women when episiotomy is not given when required.[1] According to Carrolli and Mignini, the incidence of injury to anterior perineam was lower in the routine-use episiotomy group.[3] Such tears also occur when there is premature extension of the fetal head during childbirth. Hence modified Ritgen’s maneuver is performed to prevent this premature extension of fetal head.[1] Positioning of parturient’s legs during labor is also important. Legs should not be separated too widely or one leg should not be higher than the other. This uneven positioning of the legs exerts pulling forces on the perineum which may increase the chances of perineal injury.[1] Laine et al suggest that head should be delivered slowly while advising the laboring woman not to push, to reduce the perineal injury.[4] A case of periurethral tear of similar nature and subsequent posterior dislocation of distal urethra secondary to obstetric trauma was reported by us in the past.[5]

Apart from the obstetric trauma other trauma can also inflict similar injuries. Such injuries were witnessed in our patient antenatally at 24 weeks due to a fall. While the obstetric injury is due to a misdirection of the force of expulsion of the fetal head during childbirth, the non-obstetric injury is due to an application of a trauma directly to the local area. As there is no underlying bone in the vestibular area, direct trauma causes contused lacerated wounds, which may disrupt the attachments of this soft tissue to surrounding bone. In the case presented, the anterior pubourethral ligament was torn and hence the distal urethra was dislocated posteriorly. Identifying the anatomical defect and repairing it is very important to avoid future problems related to urinary stream or urethral strictures. Such a tear does not increase the risk of development of urinary stress incontinence, as the provimal urethra is intact, well supported and is in its normal position. Successful and accurate repair of such tears in antenatal period does not increase the chance of their recurrence during a vaginal delivery. Hence a cesarean section is not indicated solely for this purpose.[6]


We thank Dr. Girija Swaminathan for taking intraoperative photographs.

  1. Mikolajczyk RT, Zhang J, Troendle J, Chan L. Risk Factors for Birth Canal Lacerations in Primiparous Women. Am J Perinatol. 2008 May; 25(5): 259–264.
  2. Combs CA, Robertson PA, Laros RK Jr. Risk factors for third degree and fourth degree perineal lacerations in forceps and vacuum delivery. Am J Obstet Gynecol. 1990 Jul;163(1 Pt 1):100-4.
  3. Carroli G, Mignini L: Episiotomy for vaginal birth. Cochrane Database Syst Rev 1:CD000081,  2009.
  4. Laine K, Pirhonen T, Rolland R, Pirhonen J. Decreasing the incidence of anal sphincter tears during delivery. Obstet Gynecol 2008 May;111(5):1053-7.
  5. Pednekar R, Valvi D, Warke HS. Traumatic Posterior Dislocation Of Urethra. JPGO 2017. Volume 4 No. 5.
  6. RCOG Green-Top Guideline no:29, Management of Third- and Fourth- Degree Perineal tears. Available from: https://www.rcog.org.uk/en/guidelines-research-services/guidelines/gtg29/

Pednekar R, Parulekar SV. Traumatic Periurethral Tear And Posterior Dislocation Of External Urinary Meatus. JPGO. 2018 Vol 5 No. 9. Available from:  http://www.jpgo.org/2018/09/traumatic-periurethral-tear-and.html

Pregnancy In A Case Of Pyruvate Kinase Deficiency

Author Information

Kumar M*, Mali K**, Warke HS***.
(* Junior Resident, ** Assistant Professor, *** Associate Professor, Department of Gynecology and Obstetrics, Seth G S Medical College and K E M Hospital, Mumbai, India.)


There is a wide variety of congenital disorders which can affect pregnancy. One such rare condition is pyruvate kinase deficiency. It can result in hemolytic anemia of varying severity. A case of pyruvate kinase deficiency and its outcome in pregnancy is presented here.


Pyruvate kinase deficiency (PKD) is the second most common heredity hemolytic anemia. Inheritence is mainly autosomal recessive. Pyruvate kinase is the rate limiting enzyme of Embden Meyeroff glycolytic pathway. Its deficiency results in build up of the intermediates of this pathway making erythrocytes susceptible to hypoxic injury. Homozygote carriers for PKD experience multiple episodes of hemolysis requiring multiple transfusions and sometimes splenectomy. Heterozygous carriers are usually less affected but may experience hemolysis under stressful conditions.[1]

Case Report

A 30 year old gravida 5 with 4 prior spontaneous abortions at 35 weeks of gestation presented to the emergency with epigastric discomfort, and episodes of vomiting along with yellow discolouration of eyes and urine. She had these symptoms from 2 months of gestation with minimal improvement, but had not consulted any physician for the same. She had no complaints of pain in abdomen or itching. On admission her total bilirubin was 21 mg/ dl of which indirect bilirubin was 10 mg/ dl. Her haemoglobin was 8.5 gm%, leukocyte count of 11400 cu/ mm, and platelet count was 2 lakhs/ cu mm. Hematology advice was taken regarding increased indirect bilirubin. Complete hemogram was normal. Both DCT and ICT were negative, but serum LDH levels were high (2251units). ANA, anti dsDNA, aCLA, and anti beta-2 glycoprotein 1 IgM and IgG were negative. Viral markers were negative. She was monitored as a case of Coombs negative hemolytic anaemia. Over ten days, total bilirubin dropped down to 5.6 mg/ dl with indirect bilirubin 3.5 mg/ dl, but never normalized. Her hemoglobin was always in the range of 7-8.0 gm %. In view of persistent hemolysis in the absence of autoimmune abnormality, hematologists advised red blood corpuscle enzyme studies (done using enzyme assay in the hematology laboratory of our institute).  This revealed a normal G6PD enzyme activity, but surprisingly, revealed a pyruvate kinase deficiency. This confirmed the underlying pathology.
Two units packed cell transfusion was given in the antenatal period as she was approaching term. Liver function test and complete blood count were monitored every other day. Biweekly non-stress test was done which was reactive. Obstetric Doppler showed normal flow studies. Her predelivery hemoglobin was 8.5 gm %. At 37 weeks of gestation she went into spontaneous labor. Amniotic fluid was meconium stained and intrapartum monitoring was non-reassuring, for which a lower segment cesarean section was performed. She delivered a healthy male child of 2.8 kg with of Apgar score of 9/10. On third post-operative day, she experienced two episodes of fever following which injection amoxicillin-clavulanate was converted to injection piperacillin-tazobactum, which resulted in fever resolution. She was discharged uneventfully on day 15. She was advised to follow up with hematologists regularly.


Pyruvate kinase deficiency causing hemolytic anaemia is an uncommon disease and is rare in pregnancy. In humans, the pyruvate kinase gene is found at chromosome 1q212.[2] Deficiency or dysfunction of the enzyme results in hemolysis. Most common complication of hemolytic anaemia in pregnancy is fetal growth restriction. However, it was not seen in this pregnancy. Heterozygous carriers are usually not affected but may experience hemolysis under stress conditions. Hence our patient was never diagnosed prior. She underwent investigations and diagnosis for the first time at 30 years of age and in her 5th pregnancy. Apart from pregnancy itself, there appeared to be no other stress factor.
Pre-pregnancy counseling is essential in patients with known pyruvate kinase deficiency for boosting immunity to encapsulated microorganisms and maternal screening for hepatitis B, C, HIV and CMV. Our patient did not have any of these infections. Cardiac investigations include echocardiography and MRI to exclude cardiac siderosis, due to iron overload. The carrier status of the partner should be determined to allow proper prenatal counseling.[3] Our patient was herself diagnosed late in pregnancy, and hence prenatal counseling was not a possibility.
Antenatal folic acid therapy is required to alleviate folate deficiency due to chronic hemolysis. Increased risk of impaired fetal growth is common in these patients and necessitate the need of regular fetal monitoring.[4,5] Our patient was on bi-weekly non-stress tests.  Placental dysfunction may also increase the risk of hypertensive disorders. Uterine artery Doppler may be used as a screening tool to identify risk of preeclampsia.[6] However, our patient was also normotensive.
In established cases of severe pyruvate kinase deficiency, splenectomy is indicated in patients with severe anaemia. However, in our patient, who did not have severe anemia, the hematologists had decided to follow up the patient and assess for further management after the completion of puerperal period. Although there is no research to confirm, breastfeeding is safe when patient has pyruvate kinase deficiency.


The occurrence of hyperbilirubinemia in pregnancy could be the first presentation of rare conditions such as RBC enzyme disorders. A successful pregnancy outcome with pyruvate kinase deficiency in the mother is presented. Close coordination with hematologists helped in improving outcomes.
  1. Luzzatto L. Hemolytic Anemias and Anemia Due to Acute Blood Loss: Introduction. In Longo DL, Kasper DL, Jameson JL, Fauci AS, Hauser SL, Loscalzo J, editors. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGrawHill 2012; pp. 487.
  2. Lenzer C, Nurnberg P, Jacobasch G, Gerth C, Thiele BJ. Molecular analysis of twenty-nine pyruvate kinase deficient patient from Central Europe with hereditary hemolytic anemia. Blood 1997; 89(5):1793-9.
  3. Baroniciani L, Beutler E. Prenatal diagnosis of pyruvate kinase deficiency. Blood 1994; 84(7): 2354-6.
  4. Fanning J, Hinkle RS. Pyruvate kinase deficiency hemolytic anaemia: two successful pregnancy outcomes. Am J Obstet Gynecol 1985; 153(3): 313-4.
  5. Dolan LM, Ryan M, Moohan J. Pyruvate kinase deficiency in pregnancy complicated by iron overload. BJOG 2002; 109(7):844-6.
  6. Amankwah KS, Dick BW, Dodge S. Hemolytic anaemia and pyruvate kinase deficiency in pregnancy. Obstet Gynecol 1980; 55(3 suppl):42S-45S.

Kumar M, Mali K, Warke HS. Pregnancy In A Case Of Pyruvate Kinase Deficiency. JPGO 2018. Volume 5 No.9. Available from: http://www.jpgo.org/2018/09/pregnancy-in-case-of-pyruvate-kinase.html

Adherent Placenta In First Trimester Pregnancy

Author Information

Thakare R*, Prasad M**, Gupta AS***.
(* Junior Resident, ** Assistant Professor, *** Professor. Department of Obstetrics and Gynecology, Seth G S Medical College and K E M Hospital, Mumbai, India.)


Adherent placenta diagnosed in the first trimester is a rare occurrence. Most of the cases are detected later in pregnancy. A case of morbidly adherent placenta at 13 weeks of gestation is presented here. The surgical management consisting of laparotomy, removal of retained products of conception (RPOCs) and uterine repair is presented.


The diagnosis of morbidly adherent placenta in early pregnancy is rare. There is an increase in the incidence of morbidly adherent placenta due to increased rates of prior uterine surgeries especially cesarean section.[1] Among the adherent placentas, placenta accreta contributes to 75 % of such cases.[2] However, majority are diagnosed in late pregnancy.[3] Here, a case of adherent placenta managed in early pregnancy is discussed.

Case Report

A 27 year old woman G3P1L1MTP1 at 13 weeks and 2 days of gestation by menstrual dates presented with complaints of vaginal bleeding since 2 months. She was referred from a primary private center with ultrasonography (USG) suggestive of 10 weeks gestation and with an impression of missed abortion. A differential diagnosis of invasive mole was also mentioned. She reported vaginal bleeding since 2 months that had increased over the last few days. She denied history of passing grape like masses per vagina. She gave history of taking oral contraceptive pills as prescribed by private practitioner. In her first pregnancy, a lower segment cesarean section was done in view of placenta previa, two years prior. This was followed by a surgical termination of pregnancy by dilatation and curettage, in view of failure of contraception. She denied undergoing any other uterine procedures. On examination, she was stable, well oriented and afebrile, pale but with no tachycardia, with blood pressure 110/70 mm of Hg, and unremarkable cardiovascular and respiratory system examination. Abdomen was soft and non-tender, and showed healthy well healed Pfannenstiel scar. Uterus was just palpable. Speculum examination revealed a healthy cervix and vagina with minimal bleeding, and no passage of clots. On vaginal examination internal cervical os was closed and the uterine size was 14-16 weeks. β HCG was 601 mIU/ml and the value repeated after 48 hours was 430 mIU/ ml. Serum TSH (1.5 µUL/ml), chest x ray and electrocardiogram were normal. Ultrasonography was advised and it showed retained products of conception with suspicion of myometrial invasion at lower uterine segment, approximately at the site of the previous cesarean scar. For confirmation, magnetic resonance imaging was done, and it showed similar findings with adherence at the scar site, most likely to be placenta percreta (figure 1).

Figure 1. MRI image showing retained products of conception (yellow arrow), uterine wall (blue arrow), intrauterine blood (purple arrow), suspected area of adherence (green arrow) and bladder (red arrow). 

Decision of exploratory laparotomy was made, and possibility of hysterectomy was explained, and appropriate consent was taken. Intra-operatively dense adhesions between lower uterine segment and bladder were released by sharp dissection, and upon opening uterovesical layer of the visceral peritoneum, placenta was seen just beneath the thinned out uterine serosa. Transverse incision was taken after sufficient mobilisation of bladder.  Placenta and retained products of conception, amounting to almost 300 ml were removed and sent for histopathological examination, which confirmed RPOCs. Lower part of the anterior uterine wall was thinned out, friable and multiple button holes formed. In the process of sharp dissection from the thinned out anterior uterine wall from the bladder, inadvertent injury to the bladder serosa occurred, involving the posterior wall of bladder (3 cm in length). It was also noted that the bladder serosa was densely stuck to the uterus. Urologist who were called repaired the bladder without tension in two water tight layers.(Figure 2). The thinned out button hole part of the uterine wall was excised and then the healthy part of the uterine lower segment that was identified after further dissecting the urinary bladder by the urologist was closed in a single layer with ployglactin No 1-0 suture material.

Figure 2. Intraoperative image showing RPOCs’ (yellow arrow), thinned out serosa (green arrow) and bladder ( blue arrow).

A 12 F suprapubic catheter was inserted and 20 FR per urethral catheter was inserted, and left in situ for 21 days.  She was given 1 unit of blood transfusion intraoperatively. Intra-peritoneal drain was also inserted.  Post operative period was uneventful. Intravenous antibiotics were continued for two weeks and an anti-spasmodic tablet Solefenacin 5 mg twice a day was given till catheter removal. Urine culture showed no growth. Renal function tests were monitored and were within normal limits. Ultrasonography on day 7 postoperative showed no collection. Tablet Nitrofurantoin modified release 100 mg twice a day was started as catheter prophylaxis. Skin sutures were removed on day 15. There were no postoperative febrile episodes and overall post operative recovery was uneventful. Intraperitoneal drain was removed on postoperative day 3. Before removal of urinary catheter, cystoscopy that was done showed integrity of bladder. Per urethral catheter was removed after 3 weeks. After resumption of normal voiding function, suprapubic catheter was removed. 


Adherent placenta is mainly a problem of late gestation. However, it can occur in early pregnancy also. There is considerable overlap in the pathogenesis of cesarean scar pregnancy and placental adherence in early pregnancies.[4] The risk factors of adherent placentae include previous uterine surgery and curettage.[5] Our patient also had these risk factors (one prior LSCS and one curettage). Termination of pregnancy, including by hysterotomy, has been reported as early as 19th week of gestation. Our patient was in her 13th week of gestation at the time of the procedure. However, it was already an abortion, and she required evacuation of the retained products of conception, through an abdominal approach. In this context, it is interesting to note that most of the adherent placentas diagnosed in early pregnancy are done so after the pregnancy has been terminated. This has been reported in a 31 case series by Yu et al.[6] However, in our case, the diagnosis was achieved prior to the termination of pregnancy, during evaluation for persistent vaginal bleeding. In our case, the patient had been referred to us with a differential diagnosis of vesicular mole. This was because in the ultrasonograpy the features were that of intrauterine hypoechoic contents with vascularity. However, the β hCG was in the range of less than 1000 IU/ ml. Hence, the diagnosis of vesicular mole was ruled out.  The ultrasonography findings not only diagnosed retained products of conception but also diagnosed the possibility of placenta accreta. The confirmation was done by magnetic resonance imaging. While  MRI is an established clinical tool for adherent placenta, whether it should be used as a first line modality is doubtful.[7] Hysteroscopic procedure for evacuation of retained products of conception, following which diagnosis of accreta was attained has also been reported by Guarino et al.[8] However, we preferred an abdominal approach. Intraoperative difficulties encountered were an extremely thinned out lower uterine segment, and a densely adherent bladder. A similar case report by Gupta et al had also described identical difficulties.[9]  In our patient, inadvertent bladder injury occurred. Checking for bladder integrity is recommended, whenever sharp dissection of the lower uterine segment from a densely adherent bladder is done.[9] However, postoperative recovery was uneventful and she regained good voiding function and was voiding normally at 2 months follow-up. Usually, in such cases massive blood transfusion is required.[10] However, our patient required only one unit blood transfusion.


Here we have discussed a case with adherent placenta being diagnosed and managed in the first trimester of pregnancy. Abdominal approach was opted for the removal of retained products of conception and the post operative period was uneventful. With timely diagnosis and appropriate management of such cases, one can have a favorable outcome despite the dreaded complications associated with this condition.


  1. Shaamash AH, Houshimi WM, El-Kanzi EM, Zakaria AE. Abortion hysterectomy at 11 weeks' gestation due to undiagnosed placenta accreta (PA): A case report and a mini review of literatures. Middle East Fertility Society Journal. 2014;19(3):147–152.
  2. Buetow MP. Sonography of placenta percreta during the first trimester. American Journal of Roentgenology. 2002; 179(2): 535-535
  3. Rac MW, Wells CE, Twickler DM, Moschos E, McIntire DD, Dashe JS. Placenta accreta and vaginal bleeding according to gestational age at delivery. Obstet Gynecol. 2015; 125(4):808–13.
  4. Timor-Tritsch IE, Monteagudo A, Cali G, Palacios-Jaraquemada JM, Maymon R, Arslan AA, et al. Cesarean scar pregnancy and early placenta accreta share common histology. Ultrasound Obstet Gynecol. 2014; 43(4):383–95.
  5. Findeklee S, Costa SD. Placenta Accreta and Total Placenta Previa in the 19th Week of Pregnancy. Geburtshilfe Frauenheilkd. 2015 Aug; 75(8):839–43.
  6. Yu M, Liu XY, Dai Q, Cui QC, Jin ZY, Lang JH. [Diagnosis and treatment of placenta accreta in the second trimester of pregnancy]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2010; 32(5): 501–4.
  7. Einerson BD, Rodriguez CE, Kennedy AM, Woodward PJ, Donnelly MA, Silver RM. Magnetic resonance imaging is often misleading when used as an adjunct to ultrasound in the management of placenta accreta spectrum disorders. Am J Obstet Gynecol. 2018; 218(6):618.e1-618.e7.
  8. Guarino A, Di Benedetto L, Assorgi C, Rocca A, Donatella C. Conservative and timely treatment in retained products of conception: a case report of placenta accreta ritention. Int J Clin Exp Pathol. 2015; 8(10):13625–9.
  9. Gupta N, Gupta A, Green M, Kang HS, Blankstein J. Placenta percreta at 17 weeks with consecutive hysterectomy: a case report and review of the literature. Case Rep Obstet Gynecol. 2012; 2012:734834.
  10. Matsuzaki S, Matsuzaki S, Ueda Y, Tanaka Y, Kakuda M, Kanagawa T, et al. A Case Report and Literature Review of Midtrimester Termination of Pregnancy Complicated by Placenta Previa and Placenta Accreta. AJP Rep. 2015; 5(1):e6–11.

Thakre R, Prasad M, Gupta AS. Adherent Placenta In First Trimester Pregnancy. JPGO 2018. Volume 5 No.9. Available from: http://www.jpgo.org/2018/09/adherent-placenta-in-first-trimester.html

Incidental Uterine Wall Defect Detected At Cesarean Delivery

Author Information

Desai GS*, Dwivedi J*, Hatkar P**.
(* Assistant Professor, ** Associate Professor. Department of Obstetrics and Gynecology, Seth G S Medical College and K E M Hospital, Mumbai, India).


Uterine defects at the scar site are commonly seen after uterine surgeries such as hysterotomies and cesarean deliveries. The authors report a case of a uterine fundal wall defect noticed during a cesarean delivery in a patient with prior history of uterine curettage. Vigorous curettage of the uterine cavity can result in removal of myometrium and a uterine wall defect as was seen in our case. Subsequently this can lead to an outpouching or diverticulum.


Uterine defects at the incision site are commonly seen after uterine surgeries such as hysterotomy and cesarean delivery.[1] Such defects include a niche, isthmocele and in some cases an out-pouching or a diverticulum.[2] Defects in the uterine wall in the fundus of the uterus in the absence of a history of uterine surgery are not documented. The authors report a case of a uterine fundal wall defect noticed during a cesarean delivery.

Case Report

A 29 year old woman with two prior spontaneous abortions came to our department at full term. Both spontaneous abortions occurred in the first trimester and were managed with curettage. She was diagnosed with gestational diabetes mellitus at 35 weeks of gestation and started on oral metformin with dietary changes. A year ago, in 2017, she was investigated for her prior obstetric history and was found to be positive for antinuclear antibodies (1:160 titres). Additionally, in the same year, she was diagnosed with thyroiditis and hyperthyroidism and treated with methimazole and propylthiouracil. Her present confinement was spontaneous and at term an obstetric examination revealed a breech presentation. Ultrasonographic examination showed anterior placentation and a full term fetus. She underwent an elective lower segment cesarean delivery for breech presentation. A male fetus weighing 3.5 kg was delivered followed by the placenta.

After the delivery of the placenta, the surgeons noticed a 2x3 cm protrusion on the anterior surface of the uterus in the region of the uterine body, approximately 4 cm from the fundus of the uterus. This protrusion was away from the uterine incision and was increasing in size as uterus contracted. Palpation from within the uterine cavity revealed the absence of about 3x4 cm area of myometrium at this site. The out-pouching or diverticulum was covered only by a flimsy layer of serosa of the uterus (figure 1). The defect was opened, uterine myometrium approximated and sutured with vicryl 1 interlocking sutures. This was undertaken in order to prevent subsequent rupture of the uterus. She tolerated the procedure well. She was advised an elective cesarean delivery at the next confinement and is doing well on follow up visits.

Figure 1. Uterine wall defect noted at the time of cesarean delivery measuring 2x3 cm.


Cesarean scar defects have been reported. These defects are caused after previous uterine surgery like hysterotomy and cesarean delivery.[1-3] A niche is a minor defect at the scar site which does not require active intervention. In some cases there may be out-pouching of the endometrium and uterine wall at the scar site leading to a uterine diverticulum. Repair of a diverticulum should be undertaken in the presence of symptoms which include intermenstrual tarry bleeding and pelvic pain.[4,5]
Reports of uterine wall defects at a site distant from the scar site and after curettage are infrequent. It is known that perforation of uterus during curettage can lead to uterine rupture in subsequent pregnancies. Vigorous curettage of the uterine cavity can result in removal of myometrium causing a defect in the uterine wall as was seen in our case. As a result this can lead to an out-pouching or diverticulum. A possible mechanism for the development of a diverticulum is increased intrauterine pressure on the weakened uterine wall. Diagnosis of the defect includes imaging with transvaginal USG, hysterosalpingography and MRI. Definitive diagnosis is made on endoscopy and laparotomy. The presence of a diverticulum at surgery warrants repair if the defect is expansive as a result of increased intrauterine pressure. A repair is done in order to avoid rupture of the uterus in the future. The patient with a repaired uterine wall defect should undergo an elective cesarean delivery in subsequent pregnancies.

  1. Erickson SS, Van Voorhis BJ. Intermenstrual bleeding secondary to cesarean scar diverticuli: report of three cases. Obstet Gynecol. 1999;93(5 Pt 2):802-805.
  2. Tulandi T, Cohen A. Emerging Manifestations of Cesarean Scar Defect in Reproductive-aged Women. J Minim Invasive Gynecol. 2016;23(6):893-902.
  3. Fischer RJ. Symptomatic cesarean scar diverticulum: a case report. J Reprod Med. 2006;51(9):742-744.
  4. Zhang Y. A Comparative Study of Transvaginal Repair and Laparoscopic Repair in the Management of Patients With Previous Cesarean Scar Defect. J Minim Invasive Gynecol. 2016;23(4):535-541.
  5. Luo L, Niu G, Wang Q, Xie HZ, Yao SZ. Vaginal repair of cesarean section scar diverticula. J Minim Invasive Gynecol. 2012;19(4):454-458.

Desai GS, Dwivedi J, Hatkar P. Incidental Uterine Wall Defect Detected At Cesarean Delivery. JPGO 2018. Volume 5 No.9. Available from: http://www.jpgo.org/2018/09/incidental-uterine-wall-defect-detected.html

Aortoarteritis In Pregnancy: Two Cases

Author Information

Kumbhar P*, Honavar P**,  Samant PY***
(* Junior Resident, ** Assistant professor, *** Additional Professor, Department of Obstetrics and Gynecology, Seth G S Medical College and KEM hospital, Mumbai, India.)


Takayasu arteritis (TA) affects aorta and its branches, sometimes coronary and pulmonary arteries. TA is a chronic process progressive in nature with underlying inflammation of affected arteries. We report two cases with this multivessel arteritis, one of them with a valvular involvement; and their management in pregnancy.


TA is a large vessel vasculitis, primarily involving aorta and branches in the head, neck, upper and lower limbs. As the disease is more common in women of child-bearing age, adverse pregnancy outcome is a common phenomenon. Hence such pregnancies need    multidisciplinary management. Here are two cases with aortoarteritis with successful antepartum and intrapartum management.

Case Reports

Case 1.

A thirty year old primigravida came for antenatal registration in late first trimester. She was a known case of aortoarteritis, which was diagnosed 15 years ago when she had acute left sided chest pain and was detected to have high blood pressure of 160/100 mm of Hg. Computerized tomographic aortogram at that time showed left subclavian and renal artery stenosis, and left coronary artery disease. (Figure 1) She was advised coronary artery bypass grafting, but opted for medical management, and was discharged on prednisolone, atenolol, prazosin and aspirin. She took the medications for one month and stopped. Since her symptoms never recurred, she never followed up with the physicians.

Figure 1. CT Angiogram with arrows showing areas of arterial narrowing.

On examination, her vital parameters were normal except blood pressure of 140/90 mm Hg in the left upper arm and 120/80 mmHg in the right. All pulsations were well felt. In sitting positon, left sided neck pulsations were prominent. Her obstetric examination revealed uterine size corresponding to the period of gestation. Hemoglobin was 11 gm % and urine albumin was absent.   Her    aCLA IgG/IgM, anti- β 2 glycoprotein antibodies, ANA and anti-ds DNA were all negative. C Reactive Protein, Erythrocyte Sedimentation Rate and C3/C4 levels were all normal.
Echocardiography showed ejection fraction of 60% with trivial mitral regurgitation. Subclavian artery doppler showed narrowing of left subclavian artery, but normal flow in all four limbs.  She was then started on tablet prednisone 30 mg once a day with tapering doses, tablet labetalol 100 mg twice a day and nifedipine 20 mg once a day in consultation with cardiologist and rheumatologist. Blood pressure in left limb remained in the range of 150 to 140 / 90 mm Hg and in right limb 130 to 120/ 80 mm Hg.  Her antenatal course was uneventful. At term, weekly non-stress tests were done and were reactive. Anesthetic review was done for epidural analgesia. In view of her stable condition, vaginal delivery was planned after counseling of the patient and her relatives. However, at term she went into spontaneous labor but cesarean section had to be done for brow presentation under epidural and spinal anesthesia. Postoperative course was uneventful, and anti-hypertensives were continued post-delivery. She was discharged on the fifth day, and she chose barrier method of contraception. She was asked to follow up with cardiologists and rheumatologists regularly.

Case 2.

A twenty four year old primigravida, a diagnosed case of aortoarteritis, came for antenatal           registration at 10 weeks of gestation. She was on regular follow up with nephrologist after being diagnosed with renal hypertension a year before. She had no history of chest pain, limb claudication or syncopal attacks. Systolic blood pressure difference in right and left arm was 20 mmHg. Systolic murmur was heard, and echocardiography showed rheumatic heart disease with moderate mitral regurgitation, mild tricuspid regurgitation, mild pulmonary hypertension and good biventricular function. Her hemoglobin was 12 gm % and urine albumin was absent. Liver and renal functions were normal with creatinine of 1.1 mg/ dl, 24 hr urine protein 267 mg, C3 and C4 were 95.6 and 26.7 respectively. Her aCLA, beta 2 gycoprotein, ANA and ds DNA were negative. However, lupus anticoagulant was weakly positive. Angiography done in non-pregnant state had shown infraceliac abdominal aortic narrowing upto infrarenal aorta, 5 cm in extent. Left renal artery was narrow with multiple tortuous collaterals.  Rest of the aorta (aortic root, arch of aorta, thoracic aorta and infrarenal aorta) was normal.
She was started on tab metaprolol 50 mg once a day, tablet aspirin 75 mg once a day and tablet labetalol 100 mg thrice a day. Later tablet alpha methyl dopa 250 mg thrice a day was added as the diastolic BP of both upper limbs rose to 110 mm Hg. Renal doppler study showed parvus tardus waveform in segmental and hilar renal arteries confirming bilateral renal artery stenosis.
Her TSH was 15.86 U/ ml, for which tablet levothyroxine 75 mcg per day was started. Her antepartum course was uneventful. Obstetric sonography showed normal fetal growth with normal uterine artery doppler flow. Weekly non-stress tests were done and were reactive. She went into spontaneous labor at 39 weeks. Cesarean section was performed for breech presentation under epidural anesthesia. She delivered a female child of 2.67 kg with Apgar score of 9/10. Her postnatal period was uneventful. She was discharged on the sixth day with oral medications. She also chose barrier method of contraception and was asked to follow up with nephrologists regularly.


Takayasu’s arteritis is an early onset granulomatous aortoarteritis with aortic inflammation also known as 'pulseless disease'. It leads to proximal occlusion and/ or aneurysms of aorta, carotid, subclavian, pulmonary, iliac, and renal arteries.[1] Here, one patient had subclavian artery involvement and the other patient had renal artery involvement. Women in their second and third decades of life are predominantly affected. It is more common in the southeast Asian and Indian subcontinent regions than in the western population.[2] The disease is characterized by an early inflammatory phase, in which there may be fever, arthralgias, weight loss, and a late occlusive or a pulseless phase. Its etiology remains primarily idiopathic. However, both our patients presented at a time when the diagnosis had been achieved prior. 
The first patient in this report was labeled as type V TA and the second as type IV TA as per the angiographic classification of Takayasu Arteritis. As proposed by Ishikawa et al, the disease can be classified into groups on basis of complications such as hypertension, retinopathy, aneurysms, and aortic insufficiency.[1,2] According to this classification, the first  patient belonged to group II a and the 2nd to group III. Pregnancy may not affect disease progression but TA affects pregnancy in several ways like preterm labor, preeclampsia, intrauterine fetal growth restriction/ demise, and abruption. In a study by Gatto et al, 51.7% fetal growth restriction was reported.[3] Other complications of TA are retinopathy, secondary hypertension, aortic regurgitation, and aneurysms.[4] The disease process also causes reduction in elasticity and narrows arteries, impairs aortic and carotid baroreceptors function. Though diagnosis is based on clinical findings like decreased or absent pulses, unequal limb blood pressure and bruits, magnetic resonance angiography and fluoro-deoxy-glucose positron    emission tomography can detect TA activity before the development of vascular compromise.[5]
In our second patient, TA was associated with rheumatic heart disease (RHD). Association of RHD and TA is rare. Though aortic valve involvement is more common, mitral and tricuspid valves may be involved in upto 20% without thickening.[6] In a large autopsy study, there were very few cases on mitral involvement. Aortic valve involvement was more common.[7] Management of TA involves a multidisciplinary approach aimed at mitigation of inflammation,  treatment of complications, correction of stenotic lesions or even angioplasty when required.[8]
Preconceptional counseling includes dose adjustment or stopping cytotoxic drugs, and starting folic acid. Ideal time of pregnancy is during remission. Both our patients were in remission during conception. Early registration in tertiary care centre, regular antenatal visits with blood pressure monitoring, renal and cardiac monitoring and preeclampsia screening are vital in these patients. In our two cases, renal and cardiac involvement were present, and regular follow up with the specialists helped.
Fetal surveillance is as crucial as tests for maternal well being.[9] Our patients were monitored for fetal well being regularly using NST and obstetric sonography, which were normal at all stages. Though the preferred mode of delivery is vaginal, in stages IIb and III, cesarean section is preferred to avoid cardiac decompensation due to increased blood volume and blood pressure.[10] Neuraxial blockade is preferred for analgesia in labor. Both our patients underwent cesarean section, for obstetric indications.


Pregnancy with TA presents a challenge. Successful pregnancy outcome is possible with meticulous interdisciplinary management.

  1. Ishikawa K, Maetani S. Long-term outcome for 120 Japanese patients with Takayasu's disease: clinical and statistical analyses of related prognostic factors. Circulation. 1994; 90(4): 1855–60.                                        
  2. Johnston S, Lock R, Gompels MM. Takasayu arteritis: a review. J Clin Pathol. 2002; 55(7): 481–6.
  3. Gatto M, Iaccarino L, Canova M, Zen M, Nalotto L, Ramonda R, et al.  Pregnancy and vasculitis: a systematic review of the literature. Autoimmun Rev. 2012 May;11(6-7): A447-59.
  4. Leal P, Silveira F, Sadatsune E, Clivatti J, Yamashita A. Takayasus’s Arteritis in Pregnancy. Case Report and Literature Review. Revista Brasileira de Anestesiologia. 2011; 61(4): 479-85.
  5. Andrews J, Al-Nahhas A, Pennell DJ, Hossain MS, Davies KA, Haskard DO. Non-invasive imaging in the diagnosis and management of Takayasu’s arteritis. Ann Rheum Dis 2004; 63(8): 995–1000.
  6. Gormezano N, Dos Santos M, Okuda E, Catani, L Sacchetti S. Association between rheumatic fever and Takayasu’s arteritis. Revista Brasileira de Reumatologia. 2016; 56(2): 178-80
  7. Kinare SG. Cardiac lesions in non-specific aorto-arteritis. An autopsy study. Indian Heart J. 1994; 46(2): 65-9.
  8. Marwah S, Rajput M, Mohindra R, Gaikwad HS, Sharma M, Topden SR. Takayasu’s Arteritis in Pregnancy: A Rare Case Report from a Tertiary Care Infirmary in India. Case Reports in Obstetrics and Gynecology. 2017:2403451. doi: 10.1155/2017/2403451.
  9. Papandony M, Brady S, Aw T. Vasculitis or fibromuscular dysplasia? Medical Journal of Australia, 2015; 202(2):100-1.
  10. Henderson K, Fludder P.  Epidural anaesthesia for caesarean section in a patient with severe takayasu’s disease. Br J Anaesth, 1999; 83:956-9.

Kumbhar P, Honavar P, Samant PY. Aortoarteritis In Pregnancy: Two Cases. JPGO 2018. Volume 5 No.9. Available from: http://www.jpgo.org/2018/09/aortoarteritis-in-pregnancy-two-cases.html

An Interesting Case Of Fetal Lower Urinary Tract Obstruction

Author Information

Bhatt Bela
(Consultant, Rainbow Women’s Hospital, Mumbai, India.)


Fetal lower urinary tract obstruction (LUTO) can cause fetal morbidity and when severe, mortality also. The typical ultrasonographic presentation of this condition is that of an enlarged bladder and obstructive uropathy bilaterally. Milder presentation of the disease results in less severe effects on the fetus. When the problem is actually severe, it can lead to oligohydramnios, dysplastic fetal kidneys with eventual pulmonary hypoplasia. This case is being presented to bring about awareness that timely antenatal diagnosis can improve the neonatal outcome.


Fetal lower urinary tract obstruction (LUTO) is a condition in which there is obstruction in the lower urinary tract preventing flow of urine from bladder into the amniotic cavity leading to oligohydramnios. It can give rise to enlarged bladder with bilateral obstructive uropathy, and ultimately result in secondary pulmonary hypoplasia which can lead to fetal death.[1] The occurrence of this condition has been reported to be around 22 per 100,000 births.  The condition is recognized when ultrasonography is performed during the late first or early second trimester of pregnancy.[2-5] A case of  LUTO in the fetus diagnosed antenatally and managed successfully is presented here.

Case Report

A primigravida presented at pregnancy 29 weeks 5 days. Anomaly scan done at 19 weeks was normal. Growth scan done (by this author) at 29 weeks 5 days showed a fetus having bilateral hydronephrosis and hydroureter with ‘key hole bladder’ suggestive of LUTO with normal liquor. She and her husband were counseled and pediatric surgeon was consulted. At 30 weeks 5 days rescan was done, mainly to assess liquor and predictably the liquor amount had reduced. Amniotic fluid index (AFI) reduced to 7.2 cm, from 11 cm one week prior. Injectable steroids were given. The images confirming LUTO are shown below (figures 1,2,3).
Figure 1. Hydronephrosis (longitudinal section).
Figure 2. Hydronephrosis (axial section).
Figure 3. Key hole Bladder: Diagnostic of LUTO

At 31 weeks 5 days, she came with reduced fetal movements and a further reduction of AFI from 7.2 cm to 4.5 cm was noted. To summarize, in a span of 15 days, AFI reduced from 11 cm to 4.5 cm, which implied a significant reduction of the liquor volume. At 32 weeks, 1.5 kg male baby was delivered by lower segment cesarean section in view of worsening oligohydramnios. The neonate was attended to by a pediatric surgeon, who performed urethral catheterization with difficulty and the neonate was shifted to intensive care unit. Considering a very narrow urethra and chances of damage to the urethra in case of an attempt to fulgurate the urethral valve, a cystostomy was done on 6th day of life. Baby was discharged in good condition from NICU after 1 month care. Fulguration of posterior urethral value was done at 3 months of age. At that time, the weight of the infant was 3.6 kg, and growth of the baby was satisfactory post procedure also.

Presence of posterior urethral valves, urethral atresia or stenosis can give rise to LUTO.[6] Complete bladder outlet obstruction (severe LUTO) is associated with high perinatal mortality due to pulmonary hypoplasia and decreased fetal renal function.[6] The main objective of prenatal diagnosis and management is to detect those anomalies which need early postnatal evaluation and management.[7]
This case was successfully managed by following up through ultrasonography for liquor amount, terminating pregnancy at the right time and salvaging the neonate who underwent corrective surgery on time. The fetus may have otherwise succumbed to oligohydramnios leading to hypoplastic lungs and intrauterine fetal demise. LUTO is one of the late evolving anomalies. In such cases, late 2nd trimester & 3rd trimester scan is of great importance for identification. Timely detection, planning of remaining pregnancy, deciding about mode and place of delivery, keeping necessary specialist present at the time of delivery were all factors that led to good overall outcome of the fetus.


LUTO is a late appearing anomaly.  So, apart from growth, late evolving anomalies in late 2nd and 3rd trimester scans should be looked for. Multidisciplinary management improves neonatal outcomes.

  1. Haeri S. Fetal Lower Urinary Tract Obstruction (LUTO): a practical review for providers. Matern Health Neonatol Perinatol. 2015; 1: 26. doi:  10.1186/s40748-015-0026-1
  2. Clayton DB, Brock JW. Lower urinary tract obstruction in the fetus and neonate. Clin Perinatol. 2014; 41(3):643-59
  3. Tonni G, Vito I, Ventura A, Grisolia G, De Felice C. Fetal lower urinary tract obstruction and its management. Arch Gynecol Obstet 2013; 287: 187–94.
  4. Wu S, Johnson MP. Fetal lower urinary tract obstruction. Clin Perinatol. 2009; 36(2): 377-90.
  5. Lissauer D, Morris RK, Kilby MD. Fetal lower urinary tract obstruction. Semin Fetal Neonatal Med 2007; 12: 464–70.
  6. Ruano R, Sananes N, Wilson C, Au J, Koh CJ, Gargollo P, et al. Fetal lower urinary tract obstruction: proposal for standardized multidisciplinary prenatal management based on disease severity. Ultrasound Obstet Gynecol. 2016 Oct;48(4):476-82
  7. Hindryckx A, De Catte L. Prenatal diagnosis of congenital renal and urinary tract malformations. Facts Views Vis Obgyn. 2011; 3(3):165-74.

Bhatt B. An Interesting Case Of Fetal Lower Urinary Tract Obstruction. JPGO 2018. Volume 5 No.9. Available from: http://www.jpgo.org/2018/09/an-interesting-case-of-fetal-lower.html

Pyometra And Spontaneous Uterine Rupture Due To A Forgotten Copper T

 Author Information

Jain N*, Tiwari N**, Chaudhari HK***
(* Junior Resident, ** Assistant Professor, ***  Associate Professor. Department of Obstetrics and Gynecology, Seth G S Medical College and K E M Hospital, Mumbai, India).


Pyometra is a rare condition generally seen in postmenopausal women. Pyometra rarely  leads to spontaneous perforation. Here we are presenting a case of a 61 year old postmenopausal woman who had got an intrauterine contraceptive device (IUCD) inserted and had then totally forgotten about its existence. She developed a pyometra that subsequently lead to uterine perforation which resulted in her presenting to us as a case of peritonitis. Imaging was suggestive of uterine perforation. It was managed by exploratory laparotomy with subtotal abdominal hysterectomy and intraoperative vaginal removal of the IUCD.


Pyometra is defined as the build up of purulent fluid in the uterine cavity secondary to infective or degenerative processes. Spontaneous perforation is a very rare complication of pyometra, but it must be considered in the differential diagnosis of peritonitis in elderly women. Its incidence among gynecological condition is 0.03-0.11 %.[1] Incidence increases to 0.2 % in postmenopausal elderly women. Various etiological factors of pyometra are uterine or cervical benign and malignant tumors like endometrial polyp, leiomyoma, cervical and endometrial carcinoma, radiation cervicitis, senile cervicitis, forgotten intrauterine contraceptive device and cervical occlusion after surgery.[2,3,4,5] Forgotten IUCD is an important predisposing factor for pyometra in postmenopausal patients.  In a study done by W.C. Lien, 28.6% of pyometra cases were associated with forgotten IUCD.[6] 

Case Report

A 61 year old postmenopausal woman, married since 40 years para 4, living children 3 came with complaints of severe pain in abdomen since 6 days. She also had distension of lower abdomen since 5-6 days with fever on and off. She also gave history of constipation since 4 to 5 days. She gave history of IUCD insertion 25 years ago which she forgot to remove. She attained menopausal about 20 years ago. On examination she was thin built, vitally stable. On examination, abdomen was distended especially the lower abdomen. Tenderness and guarding were elicited. On per vaginal examination, IUCD thread was felt and there was tenderness in all fornices. Sonography was suggestive of peritonitis. CT scan showed an endometrial abscess with rupture of the anterior wall of the uterus of approximate size of 0.5-1 cm. An IUCD in situ with pneumoperitonium, gross ascites and pelvic collection were also detected. All blood investigations were within normal limits.
An emergency exploratory laparotomy under spinal and epidural anesthesia was done. Intraoperative 1-1.5 liter seropurulent fluid was drained. It was sent for culture sensitivity which subsequently showed the growth of E.coli bacilli. There was a thickened omentum covering the bowel loops. Bowel loops were adherent to each other and edematous. Uterine fundus was necrotic and a perforation of approximate 0.5 to 1 cm was present in the anterior uterine wall.(Figure 1) A greenish colored foul smelling discharge suggestive of pyometra was seen coming out from the uterine perforation.(Figure 2) IUCD was removed vaginally by pulling out the threads and then a subtotal abdominal hysterectomy was performed. As the entire pelvis and abdomen was contaminated with purulent fluid and the bladder was densely adherent to the cervix a subtotal hysterectomy was done. However, care was taken to see that the entire necrotic part of the uterus was excised and the incision went through the healthy tissue only.

Figure 1.White arrow shows rupture below the uterine fundus.

Figure 2. White arrow shows uterine cavity filled with purulent discharge.

Figure 3. Specimen after sub total hysterectomy. Hemostat is passed through rent in the anterior wall of the uterus .

Intraabdominal drain was kept. Post operative parenteral antibiotics injection piperacillin/tazobactum were given as per culture sensitivity report. Postoperative patient was stable. She had no fever spikes and she tolerated oral intake well. On post operative day 7 wound check was done. It showed an adherent burst abdomen. Wound culture grew E.coli organism that was again sensitive to piperaciline/tazobactum and this antibiotic was given for total of 2 weeks. Daily compression dressing was done. Repeat wound swab was sent for culture and sensitivity after completion of antibiotic course. It was suggestive of no growth. Secondary suturing was done on day 20 of surgery. She recovered and was discharged after suture removal. Histopathology report was suggestive of acute inflammatory pathology.


Pyometra is commonly seen in postmenopausal women. Forgotten IUCD is important predisposing factor for pyometra in postmenopausal patients with incidence of 28.6%.[6] Patients may present with  abdominal pain, purulent vaginal discharge, and postmenopausal bleeding. More than 50% cases are asymptomatic.[7] Forgotten IUCD can lead to severe infection. This may present as pyometra, endometritis, pelvic inflammatory disease or tubo-ovarian abscess.[2] Degenerative or necrotic processes in uterine wall and stenosis in cervical canal lead to spontaneous perforation if there is any IUCD. This results in diffuse peritonitis.  After rupture symptoms of acute abdomen are seen.[8] However, other causes of acute surgical abdomen should be ruled out. Diagnosis of pyometra is made by ultrasonography and CT scan. It will reveal an IUCD in the uterine cavity in case of a forgotten IUCD.

Best management for ruptured pyometra is exploratory laparotomy, irrigation of the peritoneal cavity followed by hysterectomy. In case of unruptured pyometra, cervical dilatation and drainage should be done. In case of a young patient who wants to preserve fertility irrigation of the abdominal cavity and evacuation of the uterine cavity followed by repair of the uterine perforation should be considered.[9] Etiological organisms isolated from the cultures are usually Escherichia coli, Bacteriodes fragile, peptococcus and streptococcus species. About 8–17% of the cultures are sterile.[10]


Spontaneous perforation of pyometra is a rare condition and difficult to diagnose preoperatively therefore possibility of perforated pyometra should be considered as one of the differential diagnosis in elderly women who present with acute abdomen. One of causes of pyometra in postmenopausal women is forgotten IUCD. Removal of IUCD and exploratory laparotomy with hysterectomy is best choice of treatment.


We would like to thank our junior resident Dr Shalila Chandorkar for the intraoperative images of the case.

  1. Muram D, Drouin P, Thompson FE, Oxorn H. Pyometra. Can Med Assoc J,1981;125(6):589-592.
  2. Li CH, Chang WC. Spontaneous perforated pyometra with an intrauterine device in menopause: a case report. Japanese Journal of Infectious Diseases. 2008;61(6):477–478.
  3. Vyas S, Kumar A, Prakash M, Kapoor R, Kumar P, Khandelwal N. Spontaneous perforation of pyometra in a cervical cancer patient: a case report and literature review. Cancer Imaging. 2009;9:12–14.
  4. Lee SL, Huang LW, Seow KM, Hwang JL. Spontaneous perforation of a pyometra in a postmenopausal woman with untreated cervical cancer and "forgotten" intrauterine device. Taiwanese Journal of Obstetrics and Gynecology. 2007;46(4):439-441.
  5. Chen P.-H., Hsien-Liu, Lee S.-L., Chang C.-Y., Chang C.-C. Pneumoperitoneum caused by perforation of pyometra associated with a lost intrauterine device and perforated malignancy of the sigmoid colon. Taiwanese Journal of Obstetrics & Gynecology. 2011;50(1):124–125.
  6. Lien WC, Ong AW, Sun JT, Tsai MT, Lai TI, Liu YP,et al. Pyometra: a potentially lethal differential diagnosis in older women. Am J Emerg Med. 2010;28(1):103-57.C.J.
  7. Chuang C-J, Hung Y-C, Hsieh M-C, Hsu C-S. Huge asymptomatic pyometra with an intrauterine device. Taiwanese Journal of Obstetrics and Gynecology. 2013;52(3):426-427.
  8. Nuamah N. M., Hamaloglu E., Konan A. Spontaneous uterine perforation due to pyometra presenting as acute abdomen. International Journal of Gynecology and Obstetrics. 2006;92(2):145–146.
  9. Zeferino TM, Banuelos FJ. [Secondary peritonitis due to rupture of pyometra in cervical cancer]. Ginecol Obstet Mex. 2005;73(11):618–21.
  10. Tsanadis G, Kalantaridou SN, Kaponis A, Paraskevaidis E, Zikopoulos K, Gesouli E, et al. Bacteriological cultures of removed intrauterine devices and pelvic inflammatory disease. Contraception. 2002;65(5):339-42.

Jain N, Tiwari N, Chaudhari HK. Pyometra And Spontaneous Uterine Rupture Due To A Forgotten Copper T. JPGO 2018. Volume 5 No.9. Available from: http://www.jpgo.org/2018/09/pyometra-and-spontaneous-uterine.html

Remembering Past Greats: William Smellie

Author Information

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

William Smellie was a Scottish Obstetrician who lived between 1697 and 1763. While he is commonly remembered for the famous Mauriceau-Smellie-Veit technique for vaginal breech delivery, this contribution of his to Obstetrics, is just a small fraction. He was a pioneer in teaching obstetrics. One of the first pictorial essays of obstetric anatomy, “Atlas of the Gravid Uterus” is attributed to Smellie and his contemporary William Hunter. This included detailed drawings of the internal dissections of expired women with a gravid uterus.

The book he authored in 1752 is hailed as a pioneering and important book in Obstetrics. The book was received so well, that an updated edition, with an extensive elaboration of his principles and techniques, was required to be published by him in the same year.
He was the first to describe the bony pelvis, its dimensions and its variants. He was the first to describe the diagonal conjugate. He was the first to elucidate rotational forceps in an occiput placed posteriorly. He was the first to apply forceps for the after-coming head in a breech delivery. He had designed many types of forceps, and had uniquely used wood as the material, rather than metal.[1] However, some commentators have falsely accused him of being “instrument-happy”, due to his apparently excessive usage of instrumental delivery. Though the neonatal obstetric palsies are attributed to Erb, Duchenne and Klumpke, these were described in detail only between 1870 and 1885. Though the number of cases were lesser, Smellie had already described these obstetric palsies way back in the 1740s.[2]
A recent article has reproduced selected passages of his original book.[3] Barring a few years in France (where he collaborated with Mauriceau and Levret), he predominantly practiced in London and his home town, Lanark, in Scotland. Despite this, his influence spread far and wide. A recent article has also covered how he had a long and significant impact on medical practitioners in Japan, which lasted more than a century.[4]

Nevertheless, some recent medical historians have pointed accusatory fingers on Smellie regarding involvement in unethical activities to obtain bodies to perform dissection, and accusations of murder had been raised.[5] However, such controversies have been put to rest, and befitting replies have been given to such accusations, by experts.[6]
Recently, retrospective historical analysis of maternal mortality rates at various eras have been undertaken. It was found that along with few other pathbreaking midwives, Smellie stood out as an obstetrician with a much lesser mortality rate, compared to prevailing estimates.  It was further elucidated that Smellie’s choice of obstetric maneuvers and instrumental deliveries (which resulted in significant morbidity in that era) only in carefully selected patients, was probably the main foundation for reduction in maternal mortality rates.[7]
To sum up, William Smellie was an obstetrician par excellence. We must not forget to acknowledge his contributions, which we obstetricians rely upon, ubiquitously.

  1. Biographies. In O’Dowd MJ, Philipp EE, editors. The History of Obstetrics and Gynecology. 1st ed. Lancs: Parthenon Publishing Group 2000; pp. 644-5
  2. Collado-Vazquez S, Jimenez-Antona C, Carrillo JM. [Obstetric brachial palsy, a historical review]. Rev Neurol. 2012; 55(10):619–25.
  3. Woods R. Dr Smellie’s prescriptions for pregnant women. Med Hist. 2008;52(2):257–76.
  4. van der Weiden RM, D’Orlando A, Uhlenbeck GC. The continuing influence of William Smellie (1697–1763) in Japan during the early Meiji Period (1868–1880s). J Med Biogr. 2013; 21(3):193–5.
  5. Shelton DC. Man-midwifery history: 1730–1930. J Obstet Gynaecol. 2012;32(8):718–23.
  6. Roberts ADG, Baskett TF, Calder AA, Arulkumaran S. William Smellie and William Hunter: two great obstetricians and anatomists. J R Soc Med. 2010;103(5):205–6.
  7. Løkke A. Mrs Stone and Dr Smellie: British eighteenth-century birth attendance and long-run levels and trends in maternal mortality discussed in a north European context. Population Studies. 2018 Jan; 72(1):123–36.

Prasad M. Remembering Past Greats: William Smellie. JPGO 2018. Volume 5 No.9. Available from: http://www.jpgo.org/2018/09/remembering-past-greats-william-smellie.html