Volume 5 Number 7

Editorial

Parulekar SV

Non-steroidal anti-inflammatory drugs (NSAIDs) like such as ibuprofen, naproxen, diclofenac and celecoxib are commonly used in pregnancy for treating fever and pain. The proportion of self medication is probably higher than that of prescribed medication. One study reported presence of NSAIDs in meconium in nearly 50% newborns. Of these, 22.8% had ibuprofen, 18.8% had naproxen, 7.9% had indomethacin, and 43.6% had aspirin. Presence of at least one NSAID in meconium, particularly aspirin, ibuprofen, or naproxen was associated with primary pulmonary hypertension (PPHN) of newborn.

The NSAIDs readily cross the placenta and can cause adverse effects on the embryo, fetus and neonate. NSAIDs block the synthesis of prostaglandins and thromboxane. The prostaglandins  are required for successful implantation of the embryo. Thus their deficiency can cause an early abortion. The odds ratios of women who develop a miscarriage is 6.99 when an NSAID is taken in the week preceding a miscarriage and 2.69 when it is taken 7 to 9 weeks before miscarriage. After correction for other factors which can increase the risk of a miscarriage, use of NSAIDS is associated with a 59 percent greater risk of miscarriage than women who took no medication and 45 percent greater risk than women who took acetaminophen. The risk is greater when the medication is taken for at least 2 weeks than when it is taken for shorter period. The risk increases directly proportional to the dosage of the drug. Women with lower body mass index (BMI) are more vulnerable as compared to those with greater BMI.

The prostaglandins and thromboxane are required to keep the fetal ductus arterious open. NSAIDs can cause its closure and oligohydramnios. Its early closure causes neonatal persistent pulmonary hypertension, as when the drug is used to control preterm labor after 30 weeks of gestation. The effect depends on the gestational age, the dose and duration of treatment, and the interval between the administration and time of delivery.

It is found from animal studies that nonselective NSAIDs (which inhibit both cyclooxegenase-1 and -2) like aspirin, ibuprofen, and naproxen might cause congenital malformations like midline defects, diaphragmatic hernia, and ventricular septal defects. The use of specific NSAIDs might cause a small to moderate increase in risk of congenital anomalies like eye defects, oral clefts, neural tube defects, limb or body wall defects, pulmonary valvular stenosis.

Use of NSAIDs has not been reported to cause fetal growth restriction, stillbirth or preterm delivery.

If severe and persistent pain is not treated effectively during pregnancy, the gravida may develop anxiety, depression, and hypertension. The patient may be on NSAID medication for chronic painful conditions like arthritis, when she gets pregnant. In such cases exposure to the drug during the early first trimester is unavoidable. It is difficult to strike a balance between treating the patient adequately for her pain and not treating her out of fear of effects of the drug on the fetus. NSAIDs should be used in pregnancy only if the maternal benefits outweigh the fetal risks. Furthermore the lowest effective dose should be used, for the shortest duration required. Counseling of gravidas should be done about risks associated with the use of NSAIDs, before prescribing the drugs. Self medication should be discouraged. It is found that the product insert is not present when strips of tablets are sold. If it is present, the print is so small that a normal person may not be able to read the contents without the use of a magnifying lens. Such practices by pharmaceuticals should be banned.

Co-existence pf Reactive NST and Variable Decelerations Of FHR

Author Information

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

Abstract

Assessment of fetal heart rate has been considered to be the gold standard of assessment of fetal well being. It was by intermittent auscultation in the past. With the advent of electronic fetal heart rate and fetal electrocardiogram monitoring, the science has made a great advance. Analysis of the baseline fetal heart rate and changes in fetal heart rate with fetal movements and uterine contractions have been used extensively to check fetal well being. Co-existence of good and bad patterns creates a diagnostic dilemma. A case of co-existence of a reactive nonstress test and variable decelerations is presented.

Introduction

Fetal well being is conventionally evaluated by assessment of fetal heart rate (FHR) patterns. A nonstress test (NST) is a noninvasive and commonest cardiotocographic method of assessment of fetal well being  antenatally. FHR is recorded electronically after 26-28 weeks of gestation, with the mother at physical and mental rest. The test is said to be reactive and the fetus is said to be well if there are at least two FHR accelerations of at least 15 beats per minute (bpm) lasting for at least 15 seconds in a 20-minute period. Variable and late FHR decelerations are suggestive of fetal compromise. When a reactive NST and FHR decelerations are found in the same FHR recording, interpretation becomes difficult. A case of co-existence of a reactive nonstress test and variable decelerations is presented.

Case Report

A 24 year old primigravida presented at term. Her due date was 4 days away. Her past medical and surgical history was not contributory. Her general and systemic examination showed normal findings. Obstetric examination showed a single intrauterine fetus of 36 weeks' size in vertex presentation. The amount of liquor was adequate. Her pelvis was adequate. Her Bishop score was 4. A nonstress test was obtained. It showed one acceleration (green arrow) with fetal movement in 20 minutes and repetitive variable decelerations (white arrows) as seen in figure 1. An ultrasonographic scan (USG) was obtained. It showed a single intrauterine fetus of 36 weeks' size in vertex presentation. Her amniotic fluid index was 6. No abnormalities of the umbilical cord were seen, such as cord presentation, loops around the fetus or true knots. Her hematological and biochemical tests for fitness for anesthesia showed normal results. Tests for syphilis, HIV, hepatitis B and C were negative. In view of mild fetal growth restriction and presence of  repetitive variable decelerations, a No. 16 Foley's catheter was inserted into the cervix, its fully inflated balloon placed just above the internal os, in order to ripen the cervix for induction of labor. The catheter was expelled spontaneously after 6 hours. The cervix was 3 cm dilated and 30% effaced at that time. Artificial low rupture of membranes was done. The amniotic fluid was scanty and thickly meconium stained. Fetal cardiotocography showed repetitive variable decelerations and no acceleration of FHR. An emergency cesarean section was done. A male child weighing 2300 g was born, with an Apgar score of 8/10 at one minute and 9/10 at 5 minutes. The mother made an uneventful recovery postoperatively. Mother and baby were well at the time of discharge after 5 days, and at first follow-up after two weeks.


Figure 1. FHR monitoring strip. It shows one acceleration of FHR (green arrow) with fetal movement and repetitive variable decelerations (white arrows).

Discussion

Accelerations of FHR are often associated with fetal movements, due to stimulation of peripheral proprioceptors, increased release of catecholamines and sympathetic stimulation of the fetal heart. Spontaneous accelerations of FHR are also seen in labor. Presence of FHR accelerations is believed to indicate an absence of fetal hypoxia and fetal metabolic acidosis.[1-3]  A variable deceleration is due to transient compression of the umbilical cord which may be due to umbilical cord presentation or prolapse, tight loops of cord around the fetal neck, true knots in the umbilical cord, or oligo- or anhydramnios.[4,5]  There is an initial acceleration due to occlusion of the umbilical vein, which decreases fetal venous return and triggers a baroreceptor-mediated reflex. Continued compression causes an occlusion of the umbilical arteries, which causes, through action on baroreceptors, an increase in parasympathetic activity and a decrease in FHR by increasing fetal peripheral resistance and blood pressure. An acceleration follows due to a decrease in umbilical arterial compression as compression of the umbilical cord is relieved.

Co-existence of FHR accelerations and variable decelerations is not clear. The rate of operative delivery is increased in the patients who show such a pattern of FHR.[6-11] While the FHR acceleration indicates that the fetal autonomic system is responding to proprioceptive stimulation and fetal heart is capable for responding to resultant sympathetic stimulation, variable deceleration of FHR indicates that there is umbilical cord compression. Such compression over a prolonged period compromises fetal well being and can result in fetal death. It is not clear when FHR accelerations would disappear in this process. But it is likely to be a late process, as hypoxia has to be severe enough to cause such a loss of accelerations, while hypoxia due to umbilical cord compression is intermittent, and the fetus is well in between such decelerations. The presence of umbilical cord copmression which is not treatable is an indication for emergency delivery of the fetus to avoid further compromise of its well being. False positive variable decelerations of FHR do not occur. Thus their presence should be considered an ominous sign, the gravity of which cannot be negated by the presence of FHR accelerations. In the case presnted, additional evidence of meconium in the amniotic fluid was the deciding factor for immediate delivery of the fetus.

Acknowledgment

I thank Dr. Kaviya .S for providing the image of fetal heart rate tracing.

References
  1. Macones GA, Hankins GD, Spong CY, et al. The 2008 National Institute of Child Health and Human Development workshop report on electronic fetal monitoring: update on definitions, interpretation, and research guidelines. Obstet Gynecol 2008; 112:661.
  2. Clark SL, Nageotte MP, Garite TJ, et al. Intrapartum management of category II fetal heart rate tracings: towards standardization of care. Am J Obstet Gynecol 2013; 209:89.
  3. Executive summary: Neonatal encephalopathy and neurologic outcome, second edition. Report of the American College of Obstetricians and Gynecologists' Task Force on Neonatal Encephalopathy. Obstet Gynecol 2014; 123:896.
  4. Itskovitz J, LaGamma EF, Rudolph AM. The effect of reducing umbilical blood flow on fetal oxygenation. Am J Obstet Gynecol 1983; 145:813.
  5. Itskovitz J, LaGamma EF, Rudolph AM. Heart rate and blood pressure responses to umbilical cord compression in fetal lambs with special reference to the mechanism of variable deceleration. Am J Obstet Gynecol 1983; 147:451.
  6. Hoskins IA, Frieden FJ, Young BK. Variable decelerations in reactive nonstress tests with decreased amniotic fluid index predict fetal compromise. Am J Obstet Gynecol 1991; 165:1094.
  7. Begum F, Buckshee K. Foetal compromise by spontaneous foetal heart rate deceleration in reactive non-stress test and decreased amniotic fluid index. Bangladesh Med Res Counc Bull 1998; 24:60.
  8. Glantz C, D'Amico ML. Lack of relationship between variable decelerations during reactive nonstress tests and oligohydramnios. Am J Perinatol 2001; 18:129.
  9. Judge NE, Mann LI, Lupe P, Amini S. Clinical associations of variable decelerations during reactive nonstress tests. Obstet Gynecol 1989; 74:351.
  10. Phelan JP, Lewis PE Jr. Fetal heart rate decelerations during a nonstress test. Obstet Gynecol 1981; 57:228.
  11. Bruce SL, Petrie RH, Davison J. Prediction of abnormal umbilical cord position and intrapartum cord problems from the nonstress test. Diagn Gynecol Obstet 1980; 2:47.
Citation

Parulekar SV. Co-existence pf Reactive NST and Variable Decelerations Of FHR. JPGO. 2018 Vol 5 No. 7. Available from: http://www.jpgo.org/2018/07/co-existence-pf-reactive-nst-and.html

Peritoneal Inclusion Cyst

Author Information

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

Abstract

Cysts in the female are a not uncommon condition. Most of the cysts are ovarian, and most of those are functional. Other cysts in the ovary are non-neoplastic or neoplastic – benign or malignant. There are a large number of other sources of cystic lesions in the pelvis. We present an unusual case of a peritoneal inclusion cyst which developed in a woman who had undergone a hysterectomy in the past.

Introduction

Finding a cystic lesion in the female pelvis is a not uncommon occurrence in gynecological practice. Most of them are detected clinically in symptomatic and sometimes asymptomatic women. Some of them are detected during pelvic ultrasonography (USG). These cysts are either in the ovary or are extraovarian in origin. Ovarian cysts are functional, non-neoplastic (such as endometriotic) or neoplastic – benign or malignant. Pelvic cysts not of ovarian origin can be paraovarian cyst, peritoneal inclusion cyst, hydro- or pyosalpinx, sigmoid mesocolon cyst, colonic duplication cyst, cystic degeneration of a leiomyoma or adenomyosis, hydatid cyst, lymphocele, pelvic hematoma, pelvic abscess, lymphangioleiomyomatosis, lymph nodes with cystic degeneration,  spinal meningeal cyst,  retrorectal developmental cyst, cystic lymphangioma or hemangioma. An unusual case of peritoneal inclusion cyst  is presented here.

Case Report

A 38year old woman, married for 22 years, presented with mild chronic pain in left part of lower abdomen for 3 months. She had 3 normal deliveries in past, the last delivery being 15 years ago. She had undergone a puerperal tubal ligation operation 18 eyars ago, and an abdominal hysterectomy 8 years ago for abnormal uterine bleeding at another hospital. She gave a history of epilepsy, cerebrovascular accident hypertension and bronchial asthma. These conditions were well controlled. Her general and systemic examination revealed no abnormality. Abdominal examination showed an infraumbilical midline scar of a previous laparotomy and an infraumbilical transverse scar of puerperal tubal ligation. There was no tenderness, guarding or rigidity. Speculum examination of the vagina showed no abnormality. Bimanual pelvic examination showed a 4-5 cm diameter nontender cyst in the left fornix.

Pelvic ultrasonography showed a 6.9x5x7.8 cm diameter cystic, unilocular mass above the vaginal vault. There were no solid areas within it. The ovary was separate from the mass. Abdominal ultrasonography showed no abnormality. Her CA125 level was 16.4 U/ml. Her chest radiograph, electrocardiogram, and biochemical investigations for fitness for anesthesia showed normal findings. An exploratory laparotomy was performed. A 5 cm diameter cyst was found between the left ovary and fallopian tube on one side and the sigmoid mesocolon on the other side. It was dissected away from the sigmoid mesocolon. It was firmly adherent to the left broad ligament. The ureter was found to be medial to its lower part. The top of the cyst was opened and clear fluid was drained. The lining epithelium was smooth. There were no nodules or solid areas in its wall. The top of the cyst was excised and hemostatic sutures were placed in its edges. The patient made an uneventful recovery. Histopathological examination of the cyst wall showed mainly collagenous tissue bundles, loose connective tissue and a few blood vessels. There was no epithelial lining found on the inner surface of the cyst.
Figure 1. Inside of the cyst.
Figure 2. Relation of the cyst (C) to the left ureter (white arrows) and left ovary(O).

Discussion

A cystic lesion in the female pelvis is most commonly an ovarian cyst. Usually the diagnosis clinically evident, but it not possible to differentiate it from other cystic adnexal structures like a paroophoron cyst, hydrosalpinx and chronic pyosalpinx. A hydrosalpinx or a pyosalpinx is usually small or moderate in size, while ovarian cysts can be small, medium or large. Functional ovarian cysts are small. Neoplastic cysts can be very large, such as mucinous cystadenoma. A small cyst is lateral to the uterus, a moderate cyst displaces the uterus to one side and usually forward. A dermoid cyst has a long pedicle and can be found anterior to the uterus. A large cyst lies on top of the uterus and its side cannot be made out on clinical examination. Imaging techniques like USG, computed tomography and magnetic resonance imaging are quite useful in making the diagnosis. CT and MRI show the cyst to be close to, but separate from the ovary. MRI shows a homogenous structure with low signal intensity on T1-weighted images and high signal intensity on T2-wieghted images. A torsion may cause  a high signal intensity on T1-weighted images.
A peritoneal inclusion cyst is a mesothelial lesion which islocated around the ovary, but separate from it. It is usually associated with abdominal or pelvic surgeries or inflammation. It is usually small (up to 1 cm in diameter), but sometimes it can be larger (up to 30 cm in diameter). It contains clear or yellow fluid. It is lined by flat epithelium in single or multiple layers.

An ovarian mass should first be excluded before giving an interpretation of a mass as a peritoneal inclusion cyst. The imager should look carefully for a normal ovary (either within or at the edge of the mass) when presented with a septated cystic adnexal mass. If a normal ovary is not visualized, an ovarian neoplasm is considered the most likely diagnosis.

A hematoma and a pyosalpinx are acute conditions and are associated with acute pain. The former has features of predisposing conditions and pallor. The latter is associated with fever and tenderness on palpation. A chronic pyosalpinx may be asymptomatic. USG shows a hydrosalpinx as a tubular or corkscrew-like thin-walled structure separate from the ovary. It may look like a cogwheel on transverse image. A pyosalpinx looks similar, but its walled are thick.

Acute cystic degeneration of a leiomyoma is a painful condition. The leiomyoma is usually intramyometrial, causing tenderness and cystic feel of the uterus on bimanual pelvic examination.  A pedunculated leiomyoma with cystic degeneration can be distinguished from an adnexal cyst only on imaging.[1] An adenomyoma is associated with abnormal uterine bleeding, severe secondary dysmenorrhea, and a tender and cystic feel of the uterus.[2]

Peritoneal inclusion cysts develop in response to peritoneal injury due to endometriosis, infection or surgery.[3]  They are small to medium in size, thin walled, and anechoic on USG. There may low-resistance flow within the septations on color Doppler USG.  CT and MRI show uni- or bilateral cystic lesions with attenuation.

A cyst in the sigmoid mesocolon accounts for about 25% cases of mesenteric cysts.[4]  It is believed to be a very rare condition, there being only 4 cases reported so far.[5] However we have enountered three cases in last 2 years, all following past hysterectomies for benign conditions (unpublished data). So it is probably not a such a rare condition as believed. The cyst in this case was believed to be either a left ovarian cyst on opening the abdomen. When its close proximity to the lateral aspect of the sigmoid mesocolon was noted, a differential diagnosis of sigmoid mesocolon cyst was considered. However it was connected to it only by loose connective tissue and hence it was not in the sigmoid mesocolon.

Colonic duplication cysts constitute about 7% of gastrointestinal duplication cysts.[6] Their  histopathlogical examination shows colonic mucosa, heterotopic gastric mucosa, layers of smooth muscle with attachment  to the colon , inflammatory cells, necrosis and calcification. Colonic cysts can also contain multiple layers of the bowel wall including mucosa, submucosa, and muscularis propria. They can contain at least one outer muscular layer with an inner gastrointestinal mucosal lining. Colonic duplication cysts can also contain well-organized.[7] The cyst in our case was initially suspected to be a colonic duplication cyst during the operation owing to it close proximity to the sigmoid colon and being away from the adnexal structures and broad ligament. But it was not a  colonic duplication cyst because there was no connection to the sigmoid colon except by loose connective tossie and its histopathology did not show any features of a  colonic duplication cyst.

Retroperitoneal cystic lesions are uncommon in the pelvis. They displace structures forward, both clinically and on imaging. These lesions include  spinal meningeal cyst and  retrorectal developmental cyst. CT and MRI are useful in making their diagnosis.[8,9]

The cyst in the case presented was close to the ovary and was not arising from the fallopian tube. Thus it could be called a paraovarian cyst. Byt paraovarian cysts arising from the epoophoron or paroophoron are in the mesosalpinx while this was outside the broad ligament. It was closely related to the outer surface of the posterior leaf of the broad ligament and external surface of the sigmoid mesocolon. But it was not originating from the sigmoid mesocolon. It did not have any epithelium lining its inside. Since it did not have intestinal mucosa and smooth muscle, it was not a duplication cyst of the colon. After exclusion of all the other types of cysts, the cyst in the case presented was diagnosed as peritoneal inclusion cyst. [10,11] It developed after a hysterectomy. There were pelvic adhesions as are found with an inclusion cyst. However it did not have any epithelium lining it, while an inclision cyst is lined bya flat epithelium. Absence of epithelium cannot be explained. The cyst possibly had a lining epithelium, which underwent atrophy due to pressure of the fluid inside the cyst.

Acknowledgment

I thank Dr Sreshthha Mahanti for taking operative pictures.

References
  1. Low SC, Chong CL. A case of cystic leiomyoma mimicking an ovarian malignancy. Ann Acad Med Singapore 2004;33(3):371–374.
  2. Tamai K, Togashi K, Ito T, Morisawa N, Fujiwara T, Koyama T. MR imaging findings of adenomyosis: correlation with histopathologic features and diagnostic pitfalls. RadioGraphics 2005;25(1):21–40.
  3. Levy AD, Arnaiz J, Shaw JC, Sobin LH. Primary peritoneal tumors: imaging features with pathologic correlation. RadioGraphics 2008;28(2):583–607.
  4. Kurtz R.J., Heimann T.M., Beck A.R. Mesenteric and retroperitoneal cysts. Ann Surg. 1986;203:109–112.
  5. Kumar A, Jakhmola CK, Arora NC, Chauhan SS. Mesenteric cyst in sigmoid mesocolon – A rare location and its laparoscopic excision. Medical Journal, Armed Forces India. 2015;71(Suppl 2):S425-S428. doi:10.1016/j.mjafi.2014.11.005.
  6. Puligandla PS, Nguyen LT, St-Vil D, Flageole H, Bensoussan AL, Nguyen VH, Laberge JM. Gastrointestinal duplications. J Pediatr Surg. 2003 May;38(5):740-4.
  7. Mourra N, Chafai N, Bessoud B, Reveri V, Werbrouck A, Tiret E. Colorectal duplication in adults: report of seven cases and review of the literature. J Clin Pathol. 2010 Dec; 63(12):1080-3.
  8. Foshager MC, Hood LL, Walsh JW. Masses simulating gynecologic diseases at CT and MR imaging. RadioGraphics 1996;16(5):1085–1099.
  9. Dahan H, Arrivé L, Wendum D, Docou le Pointe H, Djouhri H, Tubiana JM. Retrorectal developmental cysts in adults: clinical and radiologic-histopathologic review, differential diagnosis, and treatment. RadioGraphics 2001;21(3):575–584.
  10. Kim JS, Lee HJ, Woo SK, Lee TS. Peritoneal inclusion cysts and their relationship to the ovaries: evaluation with sonography. Radiology 1997; 204:481.
  11. Hoffer FA, Kozakewich H, Colodny A, Goldstein DP. Peritoneal inclusion cysts: ovarian fluid in peritoneal adhesions. Radiology 1988; 169:189.
Citation

Parulekar SV. Peritoneal Inclusion Cyst. JPGO. 2018 Vol 5 No. 7. Available from: http://www.jpgo.org/2018/07/peritoneal-inclusion-cyst.html

Vault Granulation Tissue In A Post-Hysterectomy Patient

Author Information

Bora A*, Joshi A**, Gupta AS***
(* Third year Resident, ** Senior Resident, *** Professor, Department of Obstetrics and Gynecology, Seth GS Medical College and KEM Hospital, Mumbai, India.)

Abstract

Hysterectomy is the most frequently performed major gynecological surgery. A case of post hysterectomy vault granulation tissue with persistent spotting and pain, undiagnosed for a period of two years, is discussed below.

Introduction

The rate of hysterectomy in India varies from 4-6 % in contrast to other countries where it varies from 10-20 %. The most common indications for a hysterectomy in India are menorrhagia, uterine prolapse and fibroid uterus. Post hysterectomy, bleeding at the vault site is an early post-operative period complication. However, delayed spotting or bleeding may arise due to multiple causes, among which vault granulation tissue amounts to 34 %. [1]

Case Report

A 40 year old, P4L4 with history of vaginal hysterectomy with anterior colporrhaphy and posterior colpoperineorrhaphy done at a private hospital in 2016 presented to us with intermittent spotting per vaginum since 2 years. She had followed up after the operation in the same hospital with complaints of pain and spotting per vagina. Examination done at that time was suggestive of an intact vault with minimal slough. She was advised vaginal douching, and to keep povidone iodine vaginal pessaries. However, she was not completely relieved of her symptoms and had multiple follow up visits for the same. During each of these visits, she was given the same symptomatic treatment.
She later presented to us with similar complaints. On examination, general condition was fair, vital parameters were normal. On systemic examination, abdomen was soft with scar of mini-laparotomy tubal ligation. On speculum examination, large fragile granulation tissue of about 2x2 cm size was seen at the vault. Two bunches of linen sutures were seen in the right angle of the vault and these were removed. The fragile granulation tissue was sent for histopathology (figure 1).
The histopathology report was suggestive of inflammatory granulation tissue. She was advised to follow up if symptoms persisted or increased. She visited us again after 15 days with similar complaints. Electrocauterization of the granulation tissue was done.
She was advised to follow up after fifteen days. She did not follow up, presumably because she got relieved of her symptoms.

Figure 1. Image showing granulation tissue (arrow 2) and linen sutures (arrow 1) in per speculum examination.


Figure 2. Image showing linen sutures (arrow) removed from the vault.

Discussion

Hysterectomy is one of the most widely done gynecological surgeries. Like any other surgery, it has its own set of post-operative complications. In our case, the patient had undergone a vaginal hysterectomy with anterior colporrhaphy and posterior colpoperineorrhaphy for uterine vaginal prolapse, following which she had persistent spotting and pain not responding to conservative management. The differential diagnosis for this is based on the clinical examination and time of presentation.


The causes of vaginal bleeding in a post hysterectomy patient could be either immediate or delayed. The most common cause of immediate bleeding from the vault is a hematoma. Other causes are fimbrial prolapse, endometriosis, granuloma, etc. The delayed complications of bleeding from the vault are usually granulation tissue at the vault or a fimbrial prolapse. Fimbrial prolapse is a rare complication. In a study by Pozzi in 1902 two cases of fimbrial prolapse were described after vaginal hysterectomy. In a study by Fan et al, the incidence is found to be 0.1%.[4] These patients present with vaginal bleeding. Grossly, it appears as a red hemorrhagic granular mass, which can be confused with a vault granulation tissue, both microscopically and macroscopically. Clinically, it can be diagnosed by a traction test, in which the tissue if originating from the fimbria will cause pain on traction unlike in a case of granulation tissue which will be painless. A vault biopsy should be done to avoid misdiagnosis in such cases.[5] Vault granulation tissue is a frequently encountered entity. It is seen approximately in one third of the patients who have undergone hysterectomy.[3] The incidence of vault granulation tissue has been found to be 34%, making it more common than a fimbrial prolapse.[2] In a case published by Cha Hien Choi et al, a similar case is discussed, where a patient had presented with bleeding per vaginum after 13 months of hysterectomy and she was diagnosed with vault endometriosis on biopsy, with no prior history of endometriosis.[2] In a study conducted by Manyoda IT et al, the influence of different suture materials on vaginal vault granulation tissue was studied. it showed that, polygalactide, a synthetic polymer, has fewer associations with vaginal vault granulations as compared to chromic catgut.[6] In this case, the suture material seen and removed from the vault angle was linen, which is a non-absorbable, braided multifilament suture material. Traditional linen threads have the most intense histological reaction, leading to cicatrization. The fibrosis forming role of the mastocytes, fibroblasts and histiocytes are seen to dominate with use of linen.[7] Granulation tissue basically replaces all dead, dying and necrotic tissue and replaces it with living mesenchyme. It invades the tissues which are devitalized by ischemia, hence the higher correlation with linen suture material.[8] In this case, as her surgery was a vaginal hysterectomy, the use of non-absorbable sutures is not recommended. Previously, linen sutures were used for trans fixation of upper pedicles, but not for vault closure.

In this case, electro-cauterization of the granulation tissue was chosen as the modality of treatment due to persistent symptoms. Benjamin J et al have discussed a case where carbon di oxide laser has been used as a method of treatment for persistent granulation tissue.[9] In lesions which are small (≤5 mm), it would be advisable to leave them alone as spontaneous regression was seen in such small lesions.[2] In our case, the size was around 2x2 cm, so electrocautery was done.

References
  1. Singh A, Arora AK. Why Hysterectomy Rate are Lower in India. Indian J Community. 2008;33(3):196–7.
  2. Choi CH, Kim JJ, Kim WY, Min KW, Kim DH. A rare case of post-hysterectomy vault site iatrogenic endometriosis. Obstet Gynecol Sci. 2015;58(4):319–22.
  3. Saropala N, Ingsirorat C. Conservative treatment of vaginal vault granulation tissue following total abdominal hysterectomy. Int J Gynecol Obstet. 1998;62(1):55–8.
  4. Ouldamer L, Caille A, Body G. Fallopian Tube Prolapse after Hysterectomy: A Systematic Review. PLoS One.2013;8(10):e76543.
  5. Song YS, Kang JS, Park MH. Fallopian tube prolapse misdiagnosed as vault granulation tissue: A report of three cases. Pathol Res Pract. 2005;201(12):819–22.
  6. Manyonda IT, Welch CR, McWhinney NA, Ross LD. The influence of suture material on vaginal vault granulations following abdominal hysterectomy. Br J Obstet Gynaecol. 1990;97(7):608–12
  7. Salamon A, Kádas L, Sarang I, Vidó S, Ihász M, Németh L. [Histological reactions caused by various types of suturing threads]. Acta Chir Acad Sci Hung. 1980;21(1):31–42.
  8. Hadfield G. GRANULATION TISSUE. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2238602/pdf/annrcse00054-0053.pdf
  9. Steinberg BJ, Mapp T, Mama S, Echols KT. Surgical treatment of persistent vaginal granulation tissue using CO(2) laser vaporization under colposcopic and laparoscopic guidance. J Soc Laparoendosc Surg. 2012;16(3):488–91.
Citation
Bora A, Joshi A, Gupta AS. Vault Granulation Tissue In A Post-Hysterectomy Patient. JPGO 2018. Volume 5 No.7. Available from: http://www.jpgo.org/2018/07/vault-granulation-tissue-in-post.html

Association Of Preeclampsia And Peripartum Cardiomyopathy

Author Information

Thakare R*, Joshi A**, Gupta AS***
(* Third Year Resident, ** Senior Resident, *** Professor, Department of Obstetrics and Gynecology, Seth GS Medical College and KEM Hospital, Mumbai, India.)

Abstract

Peripartum cardiomyopathy (PPCM) is a rare occurrence, preeclampsia being one of the associated high risk factors. We had a 27 year old primigravida with preeclampsia admitted at 31 weeks and 5 days of gestation for evaluation. She had an intrauterine fetal demise for which an induction of labor was done. She delivered vaginally. Immediate post delivery she went into cardiac failure with left ventricular ejection fraction of 20%. Diagnosis of peripartum cardiomyopathy was made by exclusion. She was managed in cardiac intensive care unit. She responded to the treatment well and was discharged subsequently.

Introduction

Pre-eclampsia is a common complication in later months of pregnancy and has a wide spectrum of symptoms. Peripartum cardiomyopathy is a rare but dreadful complication of pregnancy. The diagnosis is by exclusion of other causes of cardiomyopathy. An association has been noted between peripartum cardiomyopathy and pre-eclampsia. Its diagnosis requires left ventricular ejection fraction (LVEF) of less than 45% diagnosed for the first time either in the later month of pregnancy or in the first 5 weeks post-partum. Unless the LV systolic function is normalized, this condition has a high recurrence rate.

Case Report

A 27 year old primigravida was admitted at 31 weeks and 5 days of gestation in view of newly diagnosed pre eclampsia with intrauterine growth restriction for evaluation. She was antenatally registered at 18 weeks of gestation, had regular antenatal visits, received 3 doses of injection tetanus toxoid, hematinics and calcium. She came to outpatient department at 31.5 weeks of gestation with a high BP reading of 150/90 mm of Hg and urine albumin of +4; detected for the first time. She was admitted for further evaluation.
On admission, she was afebrile, pulse was 80 beats per minute regular with good volume, blood pressure was 140/80 mm of Hg. Systemic examination was normal. No premonitory symptoms were reported, bilateral knee jerks were normal and urine albumin was +2. Per abdomen, uterus was relaxed, 28-30 weeks by fundal height and fetus was with a vertex presentation. Fetal heart sounds (FHS) were 140 bpm regular. On per vaginum examination cervical os was closed and uneffaced. PIH profile was sent (Hemoglobin was 13.1gm%, platelet count was 1.8 lac/cmm, BUN was 12.0 mg/dl, creatinine was 1.0 mg/dl, SGOT and SGPT were 24 U/L and 18U/L respectively) and all serological and biochemical parameters were within normal limits. She was started on T. Aspirin 75 mg OD and C. Nifedepin 5 mg QID. Blood pressure was controlled and monitoring was continued. On day 6 of admission fetal heart sounds were not heard and intrauterine fetal demise was confirmed on ultrasound. At that time, her general condition was fair, afebrile, pulse was regular and had good volume, blood pressure was 140/90 mm of Hg. Systemic examination was normal. Premonitory symptoms were present with brisk knee jerks, urine albumin was +2. Per abdomen uterus was 28 -30 weeks, vertex presentation, relaxed. FHS were absent. On vaginal examination external os admitted one finger, internal os closed. Repeat PIH profile was also normal (Hemoglobin 11.3 gm%, platelet count 1.7 lacs/cu.mm, BUN 12.2 mg%, creatinine 0.9 mg%, SGOT 21U/L, SGPT 29U/L). Inj. Magnesium sulphate by Zuspan’s regimen was started and pre induction cervical ripening was done with dinoprostone gel method. She was monitored throughout the labor. Labor augmentation was done with oxytocin. On per abdominal examination, uterus was tonically contracted. In view of clinical suspicion of (concealed) abruption and to prevent further increase in abruption, artificial rupture of membranes was done and liquor was found to be clear. Symphysio-fundal height and abdominal girth monitoring was done and one unit of blood was transfused. Duration of first stage of labor was around 12 hours and that of second stage was 1 hour. She delivered vaginally. Retroplacental clot of approximately 350 cc was expelled out. Active management of third stage of labor was done but fluid overload was avoided. Immediately post delivery she had tachycardia 118/ min, saturation was 99% on oxygen (O2) by mask and in propped up position. One more unit of blood transfusion was transfused slowly. One hour later she continued to have tachycardia 120 beats/ min, tachypnea of 30 breaths/ min and she started bringing out pink frothy sputum. Magnesium sulphate administration was stopped, intravenous frusemide 40 mg was given and physician was called urgently. DIC profile was sent, D-dimer value was raised and rest of the coagulation profile was within normal limits. Fresh PIH profile was sent and total leucocyte count was found to be raised. Physician evaluated her and she was admitted in the medical ICU for suspected pulmonary edema for further management. Considering pulmonary embolus as a possible diagnosis a computed tomography pulmonary angiogram (CTPA) was done which showed no evidence of pulmonary embolism. Urgent 2D echocardiogram done showed an ejection fraction of 20%, mild MR and mild TR. Autoimmune profile was done and was found to be negative. Diagnosis of sepsis with peripartum cardiomyopathy was made and she was shifted to cardiac ICCU and kept on O2 and inotropic support. She was started on diuretics, beta blockers, ACE inhibitors and higher antibiotics. She had repeated fever spikes in post partum period (from day 5-7) which settled on intravenous antibiotics (piperacillin and tazobactum, metronidazole). Fever profile was negative. She responded to the management. Repeat 2D echo was done 10 days later and it showed EF of 30%. She was observed for any signs of decompensation. No further fever spikes were noted and patient was discharged 2 weeks later on lactation suppression. On discharge she was counselled regarding the possible consequences and need of pre-conceptional cardiology evaluation and if necessary a repeat 2D echocardiography before planning her next pregnancy. She followed up after discharge and was asymptomatic and well.

Discussion

Preeclampsia is known to be a common condition associated with pregnancy which can prove fatal. PPCM is a rare but dreaded complication of pregnancy with an incidence of 1:4000 deliveries.[1] The echocardiographic criteria to diagnose PPCM consists of a left ventricular ejection fraction (LVEF) below 45%, left ventricular fractional shortening below 28% and a left ventricular end diastolic dimension greater than 5.5 cm or greater than 2.7 cm/m2.[2] It is a myocardial disorder of unknown cause, characterized by left ventricular systolic dysfunction. The heart failure usually develops towards end of the pregnancy or in the first few months postpartum in women without prior history of heart disease and in absence of an identifiable cause for heart failure.[2,3] Pregnancy induced hypertension is one of the risk factors others being inflammatory changes, viral myocarditis and immune mediated, though the etiology is not completely understood. PPCM can be considered as a part of  the spectrum of hypertensive heart failure of pregnancy which is characterized by the heart failure associated with any type of hypertension in pregnancy (either chronic hypertension, gestational hypertension, preeclampsia, eclampsia or preeclampsia superimposed on chronic hypertension) occurring in peripatum period in the absence of any identifiable cause and pre existing heart disease. Hull and Hidden first described an association between postpartum heart failure and hypertension in 1938 when > 85% of cases of “toxic’ postpartal” heart disease were associated with hypertension.[4] While describing PPCM, Demakis and Rahimtoola have reported that “toxemia,” (term for preeclampsia) was detected in 22% of the study subjects.[5] The anti-angiogenic factors which are elevated in pre-eclampsia may cause an angiogenic imbalance in susceptible patients and may trigger the development of peripartum cardiomyopathy. These patients present with symptoms of congestive cardiac failure (pulmonary edema, basal crepts, pedal edema, raised jugular venous pressure) or with pulmonary symptoms (tachypnea, dyspnea and cough). Association of PPCM with pre eclampsia can be considered responsible for the extremes of low ejection fractions resulting from the increased workload placed on an already failing ventricle. For the same reason, there is a rapid improvement in left ventricular function once pre-eclampsia starts to resolve post delivery.
The management of PPCM is same as of other types of non-ischaemic dilated cardiomyopathy, drugs safe in pregnancy and lactation should be selected. Approximately 30–50 % of the patients recover completely with normal LV systolic function at rest.[6] However, the risk of recurrence of PPCM is high.[6] If the disease persists after 6 months, it indicates irreversible cardiomyopathy with poor prognosis.[7]

Conclusion

When symptoms and signs of heart failure appear in a pre eclamptic woman, peripartum cardiomyopathy should be considered as a differential diagnosis. This condition requires high degree of suspicion, prompt diagnosis and multi disciplinary approach for successful outcome. Preconceptional counselling and assessment of cardiac function prior to next pregnancy is also very important.

References
  1. Brar SS, Khan SS, Sandhu GK, Jorgensen MB, Parikh N, Hsu JW, et al. Incidence, mortality, and racial differences in peripartum cardiomyopathy. Am J Cardiol 2007;100(2): 302–304.
  2. Pearson GD, Veille JC, Rahimtoola S, Hsia J, Oakley CM, Hosenpud JD, et al. Peripartum cardiomyopathy. National Heart, Lung, and Blood Institute and Office of Rare Diseases (National Institutes of Health) Workshop Recommendations and Review. JAMA 2000; 283(9): 1183–1188.
  3. Sliwa K, Hilfiker-Kleiner D, Petrie MC, Mebazaa A, Pieske B, Buchmann E, et al. Current state of knowledge on aetiology, diagnosis, management, and therapy of peripartum cardiomyopathy: a position statement from the Heart Failure Association of the European Society of Cardiology Working Group on peripartum cardiomyopathy. Eur J Heart Fail 2010; 12(8):767–778.
  4. Hull E, Hidden E. Postpartal heart failure. Southern Med J. 1938;31(3):265–70   
  5. Demakis JG, Rahimtoola SH. Peripartum cardiomyopathy. Circulation. 1971;44:964–8.
  6. Ramaraj R, Sorrell VL. Peripartum cardiomyopathy: causes, diagnosis, and treatment. Cleveland Clinic Journal of Medicine. 2009;76(5):289–296.
  7. Mehta NJ, Mehta RN, Khan IA. Peripartum Cardiomyopathy: Clinical and Therapeutic Aspects. Angiology. 2001;52(11):759–62.
Citation

Thakare R, Joshi A, Gupta AS. Association Of Preeclampsia And Peripartum Cardiomyopathy. JPGO Volume 5 No.7. Available from: http://www.jpgo.org/2018/07/association-of-preeclampsia-and.html

Cesarean Scar Ectopic Pregnancy: A Rare Case

Author Information

Jain D*, Warke HS**.
(* Second Year Resident, ** Associate Professor. Department of Obstetrics and Gynecology, Seth G S Medical College and K E M Hospital, Mumbai, India.)
Abstract

Cesarean scar ectopic is the one of the rarest locations for an ectopic pregnancy. The incidence is increasing because of the rise in rates of cesarean section. It requires prompt diagnosis and management, in order to prevent complications like uterine rupture, massive hemorrhage and hypovolemic shock. We report a rare case of intramural pregnancy with implantation in a previous cesarean scar.
Introduction

Ectopic pregnancy is one of the leading causes of morbidity and mortality among women in child bearing age group, accounting for 9 % of pregnancy-related deaths. The diagnosis is usually made by ultrasonography and can be confirmed by MRI or during laparotomy or laparoscopy.[1,2,3]

Case Report

A 27 year old G6P2L2MTP3 with two months amenorrhea, presented to our emergency department, with chief complains of acute lower abdominal pain. She gave history of bleeding per vaginum for 3-4 days followed by spotting per vaginum for 3 days. Urine pregnancy test was positive. She underwent two lower segment cesarean sections prior, the first of which was 6 years ago for postdatism and the latter was 17 months prior in view of refusal for vaginal birth after cesarean section (VBAC). She had past history of three medical terminations of pregnancies followed by dilatation and curettage, each in view of incomplete abortion. Ultrasonography suggested early viable pregnancy with a single gestational sac of 7 weeks 4 days in the anterior wall of lower uterine segment (lower segment cesarean scar area) with decidual reaction. The uterine cavity was empty with clearly defined endometrium. Cervical canal was empty and bilateral adnexae were normal. These findings were confirmed by MRI pelvis. On MRI pelvis 18x8 mm gestational sac implanted within the anterior myometrium of the lower uterine segment in the region of previous cesarean scar was seen, with vascularity within. The anterior myometrium anterior to gestational sac was thinned out to 1-2 mm  (figure 1).


Figure 1. MRI image showing scar ectopic with yellow arrow pointing to gestational sac; green arrow pointing to empty uterine cavity and red arrow pointing to bladder.

The patient was posted for laparotomy and intraoperatively, a soft and vascular mass was seen at the site of previous cesarean scar. Incision was taken on the bulge and products of conception were evacuated gently. Uterine scar was extremely thinned out (figure 2).


Figure 2. Intraoperative picture showing thinned out uterine scar.


Figure 3. Arrow pointing to chorionic villi at the site of cesarean scar.

Products of conception were communicating with the uterine cavity; edges of scar tissue were excised and freshened. Products of conception and the cesarean scar both were sent for histopathological examination. The products of conception sent for examination showed endometrium with hyper secretory glands and Arias Stella reaction (figure 3). Extensively decidualised stroma and many chorionic villi with trophoblastic tissue were also seen. The cesarean scar sent for histopathological examination showed dilated and hypersecretory endometrial glands surrounded by decidualised stroma. Few basal glands were also seen penetrating the myometrium.(Figure 4) Patient had an uneventful postoperative course and was chose barrier method of contraception.


Figure 4. Uterine scar tissue showing endometrium in secretory phase. Yellow arrow pointing to stroma and green arrow pointing to endometrial glands.

Discussion

Ectopic pregnancy in a previous cesarean scar was first reported by Larson and Solomon in 1978. The prevalence is about 1 in 1800 to 1 in 2216 ectopic pregnancies.[4]
The documented risk factors include previous dilatation and curettage, previous placental pathology, manual removal of placenta, previous ectopic pregnancy, in vitro fertilisation, two or more previous cesarean sections, and other uterine surgeries like myomectomy, metroplasty or operative hysteroscopy. Our patient had history of three curettages and two prior cesarean sections, increasing her chances of this type of ectopic pregnancy.
It is believed that the myometrial implantation occurs through a microscopic route or a dehiscent area in the previous uterine scar, immaterial of the reason of the scar. When the blastocyst implantation takes place in the fibrotic scar, further growth occurs unpredictably. In one type, there can be an anterior progression, leading to scar ectopic pregnancy, or if worse, can cause bladder invasion and related problems. In the other type, it can progress towards the endometrial cavity, resulting in a successful pregnancy, but causing adherent placenta.
Cesarean scar ectopic can present clinically in varied forms. The most common clinical presentation is minimal, painless vaginal bleeding, mild abdominal discomfort or severe abdominal pain, substantial hemorrhage and collapse. Our patient came with a milder variety, and could wait for further evaluation before a definite procedure can be done. The sonographic criteria for diagnosis include an empty uterus, an empty cervical canal, gestational sac located in the anterior part of isthmic portion of uterus with thin layer of myometrium between the bladder and the sac, and discontinuity in anterior wall of uterus.[5,6]
MRI findings are identical to those seen on ultrasound. The implantation of gestational sac on previous cesarean scar, central myometrial defect and empty endometrial-endocervical canal. MRI imaging can be used to evaluate placental localization and degree of invasion. Our patient showed typical changes in the MRI.
The goals of treatment are termination of pregnancy, reduction of hemorrhage, prevention of uterine rupture and preservation of fertility. Observation is generally not recommended.[7]  Medical line of management is using methotrexate, which can be given intramuscularly, intravenously, or locally under image guidance. It has shown to be effective at a dose of 50 mg/ m2 when β-hCG is less than 5000 mIU/ml. Uterine artery embolization is used in conjunction with medical treatment. According to recent studies it is safe, effective and causes less morbidity.[8] Operative hysteroscopy has much lesser complication rates of 18%. It allows direct visualization of vessels at the site of implantation of gestational sac, short operative period, less blood loss and higher success rate than laparotomy or laparoscopy.[9] When cesarean scar ectopic is deeply implanted, laparoscopy is needed to exclude bladder involvement.[10] Laparotomy is an accepted method[11] required when there is high suspicion of uterine rupture and can be beneficial in preventing further cesarean scar implants by excising the old scar.

Conclusion

Cesarean scar ectopic now figures in the differential diagnosis of early pregnancy complications. The clinician should be aware of this condition. While other forms of treatment are available, laparotomy is safe and this case demonstrates the same.

Acknowledgements

We thank Dr Asha Shenoy, Professor and Dr.Pragati Sathe, Associate professor, Department of Pathology, Seth GS Medical College and KEM Hospital for the histopathology slides.

References
  1. Vial Y, Petignat P, Hohlfeld P. Pregnancy in a Cesarean scar. Ultrasound Obstet Gynecol 2000; 16(6): 592-3.
  2. Fylstra DL, Pound-Chang T, Miller MG, Cooper A, Miller KM. Ectopic pregnancy within a cesarean delivery scar: a case report. Am J Obstet Gynecol. 2002; 187(2):302- 4.
  3. Maymon R, Halperin R, Mendlovic S, Schneider D, Herman A. Ectopic pregnancies in a Cesarean scar: review of the medical approach to an iatrogenic complication. Hum Reprod 2004;10(6):515-23
  4. Larsen JV, Solomon MH. Pregnancy in a uterine scar sacculus: an unusual cause of postabortal haemorrhage. A case report. S Afr Med J. 1978;53: 142-3.
  5. Seow KM, Huang LW, Un YH, Un MY, Tsai YL, Hwang JL. A cesarean scar pregnancy: issues in management. Ultrasound Obstet Gynecol 2004; 23(3):247-53.
  6. Graesslin O, Dedecker F Jr, Quereux C, Gabriel R. Conservative treatment of ectopic pregnancy in a Cesarean scar. Obstet Gynecol 2005;105: 869-71.
  7. Marchiole P, Gorlero F, de Caro G, Podesta M, Valenzano M. Intramural pregnancy embedded in a previous Cesarean section scar treated conservatively. Ultrasound Obstet Gynecol 2004; 23:307-9.
  8. Yang M, Jeng MH. Combination of transarterial embolization of uterine arteries and conservative surgical treatment for pregnancy in a cesarean section scar. J Reprod Med 2003;48(3): 213-6.
  9. Lee CL, Wang CJ, Chao A, Yen CF, Soong YK. Laparoscopic management of an ectopic pregnancy in a previous cesarean section scar. Human Reprod 1999; 14:1234-6.
  10. Lai YM, Lee D, Lee CL, Chen TC, Soong YK. An ectopic pregnancy embedded in the myometrium of a previous cesarean section scar. Acta Obstet Gynecol Scand 1995;74(7):573-6.
  11. Mhaske NC, Jhaveri R, Prasad M, Kharat D, Fonseca MN. Conventional laparotomy for management of Caesarean scar ectopic pregnancy: a case report. Int J Reprod Contracept Obstet Gynecol 2015; 4:1581-4.
Citation

Jain D, Warke HS. Cesarean Scar Ectopic Pregnancy: A Rare Case. JPGO 2018. Volume 5 No.7. Available from: http://www.jpgo.org/2018/07/cesarean-scar-ectopic-pregnancy-rare.html

Pregnancy In A Case Of Takayasu Arteritis

Author Information

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

Takayasu Arteritis is a rare, chronic vasculitis of unknown etiology characterized by inflammation of the aorta or its branches. Females are more likely to be affected 8-9 times more than males. Features of the disease include pulseless upper extremities or with weak or absent pulse, leading to the name “pulseless disease”. There is not much effect of pregnancy on the evolution of the disease. However, the second and third trimesters of pregnancy warrant specific care. This case report describes one such pregnancy where prompt management led to good maternal and fetal outcome.
Introduction
Takayasu arteritis mainly affects women of childbearing age. Pregnant patients are at increase risk of cardiovascular complications including congestive heart failure and hypertension which may jeopardize both maternal and fetal outcome. Controlling the disease before pregnancy may improve chances of pregnancy success.[1]
Case Report
25 year old primigravida who was a diagnosed case of Takayasu arteritis was registered in antenatal clinic at 13 weeks of gestation. She was incidentally diagnosed with hypertension in two years prior and angiography confirmed the diagnosed. Echocardiogram was suggestive of aortoarteritis type 2 with no valve abnormalities. CT aortography was done suggestive of Takayasu arteritis Type 2B. CT Angiography abdomen was suggestive of narrowing of descending thoracic aorta and occlusion of left common carotid artery (figure 1).

Figure 1. Angiography pictures with arrows pointing to segments of arterial stenosis.

She was on tablets prednisolone, azathioprine, cyclosporine, aspirin, and nifedipine, and during pregnancy required addition of tablet labetalol. At 13 weeks of gestation, she had an episode of breathlessness, with wheezing following which she was given metred dose inhaler salbutamol. Her haemoglobin was 9.5gm %, white blood count of 10,000/ cu mm and platelet 1.46 lakh. Renal Doppler there was no evidence of renal artery stenosis All other investigations were within normal limits. Antenatal follow up was otherwise uneventful. Non-stress test done biweekly from 32 weeks of gestation was reactive. Obstetric Doppler showed symmetrical intrauterine growth restriction with oligohydramnios and normal Doppler flow studies. She was admitted in medicine department twice during antenatal period with complaints of breathlessness, giddiness and palpitations which was managed symptomatically, and discharged within 3 days. Induction of labor with dinoprostone gel was done at 38 weeks in view of IUGR with oligohydramnios. She underwent emergency LSCS in view of fetal distress in first stage of labour under general anesthesia, and delivered a healthy female child of 2.3 kg, not requiring NICU stay. Post operatively, she had accelerated hypertension with BP in right arm 190/100mmhg and left arm 140/90, and was shifted to ICU postoperatively and was aggressively monitored, requiring intravenous labetalol. At discharge she was sent on Nifedipine sustained release 20 mg given four times a day and tablet labetalol 100 mg thrice a day. Postoperative Echocardiography did not show any worsening.  Recovery was otherwise uneventful and was discharged on day 15 postoperatively.
Discussion
Takayasu arteritis leads to aortic inflammation which gradually progresses to occlusion and aneurysms of carotid, subclavian, pulmonary, renal and iliac arteries. Mean age is between 2nd and 3rd decade.[2,3] Etiology is mainly idiopathic. Autoimmunity, sex hormones and genetic factors have been linked to its etiology. Four types have been acknowledged based on the type of involvement of the arteries, of which our patient fits into type 2, described as involvement of abdominal aorta. Measurement of blood pressure in lower limbs is recommended and the need for accurate diagnosis of this disease has been emphasized.[4]

Pregnancy does not appear to interfere with the disease progression. In our patient also, the postoperative echocardiogram showed similar findings as that done during early pregnancy. However, it has implications on pregnancy like abortions, intrauterine growth restriction, intrauterine death and abruption. In our patient, though she did not have prior abortions, she did have intrauterine growth restriction. Prompt intervention prevented poor neonatal outcomes.

Presence of renal disease raises the chance of occurrence of IUGR.[2] Renal Doppler and renal function tests were also normal. Retinopathy, secondary hypertension and aneurysmal complications can occur. Hence, patient has been asked to have meticulous follow up of the disease even after pregnancy, the need for which should be emphasized. Obstetric Doppler is beneficial in the evaluation of fetal well-being in women with Takayasu arteritis, as in our case also. Pre-conceptional counseling is essential regarding timing of pregnancy and modification of dose of cytotoxic drugs in the peri-conceptional period. Conception during remission phase is preferable. Along with routine antenatal visits, serial monitoring of blood pressure, renal function, cardiac status and fetal Doppler is also imperative as per requirement.[4]

Treatment includes starting antihypertensive and antiplatelet as per need. Steroid therapy at a dose of 1-2mg/kg/body weight is suggested. Our patient was on prednisolone tablets throughout pregnancy. Use of immunomodulators like mycophenolate mofetil, infliximab, toclizumab and azathioprine is gaining popularity, however their safety in pregnancy has not been established. This case adds to the literature that use of azathioprine in pregnancy did not result in any specific adverse outcome. Vaginal delivery is the preferred mode of delivery epidural analgesia advocated for labor and delivery. In women with advanced disease, lower segment caesarean section is preferred to prevent sudden cardiac deterioration due to changes in blood volume and pressure. The overall 5-year survival rate after diagnosis is 83.1 %.[5] Death is usually due to congestive heart failure or cerebrovascular events.

Conclusion
Takayasu arteritis requires special care during pregnancy. This case highlights the fact that a meticulous multidisciplinary approach can result in good maternal and fetal outcomes.

References
  1. Assad APL, Da Silva AL, Bonfa E, Pereira ERE.  Maternal and neonatal outcomes in 89 patients with Takayasu Arteritis (TA): comparison before and after the TA diagnosis. J Rheumatol.  2015; 42 (10):1861–4.
  2. 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 Oct;90(4):1855-60.
  3. Fauci AS, Langford CA. The Vasculitis Syndromes. In Longo DL, Kasper DL, Jameson JL, Fauci AS, Hauser SL, Loscalzo J, editors Harrison’s Principles of Internal Medicine.18th Ed. New York: McGraw Hill; 2012; pp 2180-2.
  4. Parulekar SV. Takayasu Arteritis – Towards A Better Diagnosis. JPGO 2018. Volume 5 No.3. Available from: http://www.jpgo.org/2018/03/takayasu-arteritis-towards-better.html
  5. Papandony MC, Brady AR, Aw T. Vasculitis or fibromuscular dysplasia? Medical J Aust. 2-15; 202(2):100-1.
Citation

Kumar M, Mali K, Warke HS. Pregnancy In A Case Of Takayasu Arteritis. JPGO 2018. Volume 5 No.7. Available from:http://www.jpgo.org/2018/07/pregnancy-in-case-of-takayasu-arteritis.html

Large Fibroid In A Young Girl

Author Information

Venkateswaran S*, Hatkar P**.
(* Second Year Resident, ** Associate Professor, Department of Obstetrics and Gynecology, Seth G.S. Medical College and K.E.M. Hospital, Mumbai, India.)

Abstract

There can be multiple causes of vague, generalized abdominal distension in a young woman. Using clinical history, examination findings and investigations, diagnosis as to the origin of the mass can be made. In case of a uterine origin, fibroid (leiomyoma) is the commonest diagnosis. Although some cases can also be treated using other methods including medical management and minimal access surgery, major surgery is the only treatment option in most cases. Here we discuss a case of a large leiomyoma in a 21-year-old patient managed with myomectomy.

Introduction

Leiomyomata (fibroids) are benign, monoclonal proliferation of smooth muscle cells of the myometrium containing varying amounts of fibrous connective tissue. They are the most common tumors of the uterus and the female pelvis. They can also arise from smooth muscles and extrauterine sites like the broad ligament, round ligament[1]. Rare cases of abdominal wall fibroids are also reported.[2] The formation of the myomas is still not understood well, but are now thought to be linked to genetic factors and to proteins that may be responsible in stimulating their growth. We are reporting the case of a young girl with a large fibroid. 

Case Report
A 21-year-old unmarried girl presented with complaints of vague distention of abdomen and discomfort in lower abdomen for six months. She had no menstrual complaints nor any other significant past medical or surgical illness. On examination, patient was conscious oriented, vitally stable. There was uniform abdominal distension, a mass of around 32 weeks size was palpable. The consistency was firm and the mass had smooth contours. It was not ballotable from side to side. The lower end of the mass could not be reached which confirmed the pelvic origin of the mass.

All routine blood investigations, hemogram, liver and renal functions, electrolytes of the patient were within normal limits. Ultrasound of the abdomen and pelvis showed a large fibroid in the posterior wall of the uterus of 15x16x10 cm size, pushing the urinary bladder down. MRI of the abdomen was asked for, in order to delineate the course of the ureters, and also to rule out possibility of malignancy. The report confirmed a large subserous fibroid with no other remarkable findings in the remaining abdominal organs. Treatment options were reconsidered and consulted with the patient and her family, who then opted for operative intervention as advised. 

The abdomen was opened with a vertical midline incision extending above umbilicus for adequate exposure. Intraoperatively, a large (20x21 cm) fibroid was seen, one of the possibilities was a broad ligament fibroid (figure 1).
Figure 1. Intraoperative image showing bulk of fibroid laterally.

The fibroid was approached by incising the anterior leaf of the broad ligament. However, upon opening the peritoneum, it was confirmed to be arising from the lateral wall of the uterus. It was a false broad ligament fibroid with the actual origin being from the right lateral wall in the upper 1/3rd. The fallopian tube and the round ligament on the right side were stretched overlying the fibroid. The fibroid was enucleated and excised from the right lateral wall. The right lateral wall of the uterus was then sutured back with delayed absorbable sutures (figure 2).





Figure 2. Image after myomectomy.

After approximation of the two leaves of the broad ligament, hemostasis was checked and the abdomen was closed in layers. Cut section showed multiple whorls of smooth muscle fibres. Postoperative course of the patient was uneventful. The mass was then confirmed to be a leiomyoma on histopathology.
   
Discussion

Fibroids in adolescents might originate from intrinsic abnormalities in myometrium, congenitally elevated sex steroid level and from endometrial injury acquired during menstruation.[3] They are more common in women of reproductive age group however they are an important differential in adolescents with pelvic masses. Wright et al reported a case of leiomyoma in adolescent, in which a cytogenetic study performed in the resected tumor was suggestive of a translocation between chromosomes 12 and 14.[4]

The management of fibroids should be tailored to the needs of the patient and the clinical presentation. Symptom relief, reduction in size of fibroid prior to surgery, and patient willingness for management by conservation are the factors to be taken into consideration before offering medical management. Surgical treatment can be offered to patients to young patients who are symptomatic – for example, having abnormal uterine bleeding or fertility issues.
Myomectomy, though invasive, is often the most appropriate treatment as it is curative with relief of symptoms, it preserves fertility and doesn’t interfere with the hormonal milieu of the young endometrium. The recurrence rate of fibroids is low and also, they grow slowly. Ulipristal is a specific progesterone receptor modulator and is causes amenorrhea in 70-80% women, in around 4 days in most women, and has less adverse effects that GnRH analogues. Number of treatment cycles can be decided based on the size of the fibroid and clinical response.[5] In a recent Medicines and Healthcare products Regulatory Agency (MHRA) safety alert, women taking Ulipristal for treatment of fibroids are recommended to have their liver function tests checked monthly, as there are reports of serious liver damage in women undergoing the treatment.

It was an unusual occurrence in our case that the leiomyoma did not cause any pressure symptoms. Also, as it was a false broad ligament fibroid, it didn’t cause any menstrual dysfunction. The patient did not have any significant pain either. There are many challenges that can be faced during myomectomy as was with our case. Proper preoperative workup, surgical and anesthesia team preparedness, availability of blood and blood products in anticipation of massive hemorrhage hold high importance in planning surgical management. Our patient was a young unmarried girl, so the first challenge that came up was preoperative counselling of the relatives regarding need for surgery, future fertility outcomes, need for repeat intervention in case of recurrence, need to convert to hysterectomy if required and the consequences of massive blood loss were explained. Even though consent for hysterectomy was taken, the myoma was enucleated and uterus was successfully saved. Thus, we reduced the chances of potential future infertility in our patient. [6] The largest reported uterine fibroid was weighing 63.5 kgs.[7] Some large fibroids may present with life threatening complications. Apart from the usual complications of pelvic pain, menstrual abnormalities and pressure symptoms, there may be other unusual complications like acute limb edema due to iliofemoral vein compression, obstructive uropathy, hydronephrosis, urinary tract infections and voiding problems. There can also be ovarian edema due to chronic compression on ovarian stroma leading to mistaken diagnosis of ovarian tumor.

Conclusion
Leiomyomas are thus an important differential diagnosis of pelvic masses in adolescents and young women. There is no optimal treatment defined but myomectomy seems to be an unavoidable option in young unmarried women with large fibroids.

References
  1. Sharma P, Zaheer S, Yadav AK, Mandal AK. Massive Broad Ligament Cellular Leiomyoma with Cystic Change: A Diagnostic Dilemma. J Clin Diagn Res 2016 Apr;10(4): ED01-2.
  2. Yorita K, Tanaka Y, Hirano K, Kuwahara M, Nakatani K, Fukunaga M, et al. A multilocular cystic leiomyoma of the anterolateral abdominal wall, a case report and literature review. Medicine (Baltimore). 2017 Dec; 96(48): e8971.
  3. Parker W. Etiology, symptomotology and diagnosis of uterine myomas. Fert Steril. 2007; 87:725–36
  4. Wright KN, Laufer MR. Leiomyomas in adolescents. Fertil Steril. 2011;95(7): e2415–37
  5. Donnez J, Vazquez F, Tomaszewski J, Nouri K, Bouchard P, Fauser BC, et al. Long-term treatment of uterine fibroids with ulipristal acetate. Long-term treatment of uterine fibroids with ulipristal acetate. Fert Steril. 2014;101(6):1565–73.
  6. Ezugwu EC, Iyoke CA, Ezugwu FO, Ugwu G. Successful pregnancy following myomectomy for giant uterine fibroid in an infertile woman. J Reprod Infertil. 2014 Oct;15(4):233.
  7. Nezhat C Uterine fibroid tumors – http://nezhat.org/uterine-fibroid-tumors/
Citation

Venkateswaran S, Hatkar P. Large Fibroid in A Young Girl. JPGO 2018. Volume 5 No.7. Available from:http://www.jpgo.org/2018/07/large-fibroid-in-young-girl.html

Successful Pregnancy Outcome With Chronic Kidney Disease Requiring Multiple Hemodialysis

Author Information

Chaudhari HK*
(* Associate Professor. Department of Obstetrics and Gynecology, Seth GS Medical College and KEM Hospital, Mumbai, India.)

Abstract

Pregnancies in women on renal replacement therapy are associated with an increased risk of complications, both for the mother and the fetus. Medical management of pregnant women with chronic renal failure (CRF) is a great challenge and requires a close co-operation of nephrologists, transplantologists, gynecologists and neonatologists. This case report gives overall review of pregnancy outcome in a patient with CRF on renal replacement therapy.

Introduction

Renal disease during pregnancy is not very common. During the 1960s, studies showed that fetal mortality in the presence of maternal kidney disease approached 100%, and the first case reported on dialysis was considered almost a “miracle of medicine”. Although this grim outcome has improved over the last decades, recent studies still show significantly poor fetal and maternal outcomes; the overall risk of negative maternal-fetal outcomes is inversely related to renal function and increases with proteinuria.[1] In a review by Trevisan and colleagues in 2004, the prevalence of moderate chronic renal insufficiency was 6 per 10,000 births.[2] Significant renal insufficiency occurs commonly beyond childbearing age and many times the patients are infertile, leading to a lesser rate of the disease in pregnancy.[3,4] Exclusion of mild renal disease from statistics may be another reason.[5] The challenge of management of pregnancy is harder in end stage renal disease (ESRD) patients undergoing maintenance dialysis.[6] Despite all this, due to overall improvement, the number of successful pregnancies in dialysis patients has increased over time with improvement in fetal survival too.
Case Report

A 22 year old unregistered woman married since 5 year G3P3L2 with previous 2 LSCS, 26 weeks of gestation, presented with chief complaints of breathlessness on routine activity, generalized body swelling and easy fatigability. She had no other complaints such as headache, epigastric pain, blurring of vision or decreased urine output. She was diagnosed as a case of chronic kidney disease with serum creatinine of 11 mg % and anemia with hemoglobin of 5.6 gm %.  She gave no history suggestive of respiratory, cardiac or liver disorder. Her first pregnancy was a full term LSCS in view of cephalopelvic disproportion and second LSCS was in view of prior LSCS. In both pregnancies, she had pre-eclampsia. On admission, she was afebrile with a normal pulse rate and a blood pressure of 180/ 110 mm Hg, and unremarkable cardiovascular and respiratory systems. She was pale, and abdominal examination showed an infraumbilical vertical midline scar of prior cesarean sections. Uterus was 28 weeks with fetus in cephalic presentation, and fetal heart sounds were regular. External os was closed, knee jerks were brisk and urine albumin was +3. She was admitted in the nephrology ward. Ultrasonography showed a gestational age of 26 weeks with adequate amniotic fluid and estimated fetal weight of 912 g.

For anemia, she was transfused two units of packed cells. Investigations showed creatinine of 11 mg %, sodium of 130 meq/ l and potassium of 6.2 meq/ l. She was advised further investigations such as ultrasonography of the kidney and urinary bladder and parathyroid hormone (PTH) level. Ultrasonography showed grade 3 medical disease with small right kidney with hepatomegaly and fatty liver. PTH level was 314 IU/ ml, which was in the higher range than normal. Twenty four hour urine protein was 376 mg %. She was started on renal diet after taking dietician opinion. She was also given injectable erythropoietin and weekly injection of iron sucrose. She required tablet alpha methyldopa 500 four times a day, tablet nifedipine retard preparation twice a day and tablet labetalol 200 mg four times a day, and later prazosin 5 mg twice a day was added. Hemodialysis (HD), weekly parenteral erythropoietin and iron sucrose were given. Fundoscopy revealed grade 2 hypertensive retinopathy. Weekly fetal Doppler and biweekly non-stress test were done. In the entire course of seven weeks with the nephrologist, she underwent around 17 sessions of hemodialysis starting from her 25th week to 32nd week of gestation. Dialysis sessions were more intense and prolonged. She received a total of 14 injections of erythropoietin (5000 IU) also. In view of absent end diastolic flow in umbilical artery with prior two cesarean sections, elective LSCS was done at 32 weeks 3 days. Baby weight was 1.1 kg and was shifted to NICU. Apart from four units of packed cells that were given antenatally, one unit of packed red cells was transfused intraoperatively and one unit postoperatively. Sutures were removed on day 14 and her post-operative course was otherwise uneventful, and regular dialysis was continued. She went discharge against medical advice on day 28. She was advised to continue regular dialysis till renal transplant.

Discussion

Available data suggest that the degree of renal function impairment is the major determinant of pregnancy outcome. Besides the severity of CKD, clinical features such as hypertension and heavy proteinuria also figure as important prognostic factors. The risk of accelerated progression to ESRD is highest when serum creatinine is greater than 1.9 mg/dl at the beginning of the pregnancy.[7] The creatinine level in our patient was much higher, 11 mg/ dl.
Prematurity is seen in 80% of pregnancies. The mean age of pregnancy at delivery is 32 weeks and birth-weights of the infants are usually less than 2,000 g. In our patient also, delivery was required at gestation age of 32 weeks, and the birth weight was only 1.1 kg.  Previously, many pregnancies ended up as spontaneous abortions. However, improvement in outcomes recently reflects aggressive management of antenatal women with ESRD.
The aggressive management for such patients includes more intensive dialysis schedule to maintain blood urea nitrogen (BUN) levels <16–18 mmol/L. Increasing the frequency of hemodialysis, giving over prolonged duration at night and reducing the volume of dialysis fluid to 800 ml are options for HD. Continuous uterine and fetal monitoring during dialysis, such as fetal heart rate assessment is important.  Measures to prevent dialysis-induced hypotension should be considered. Maternal haemodynamic instability may compromise uteroplacental circulation and precipitate preterm contractions.[8]
In this case, serum creatinine level at the time of conception was not available nor history of hypertension. At the time of presentation, that is, in the second trimester, serum creatinine was 11 mg%. Total of seventeen HD sittings were done which were more intense and prolonged. Postpartum requirement of hemodialysis was less frequent.
Anemia in CKD is caused by several factors, of which the most important is relative deficiency of the glycoprotein hormone erythropoietin. This is due to reduction in the endocrine function of the kidney. Anemia is very likely to develop when creatinine clearance is less than 30 ml/min. The most important component of the treatment of the anemia of kidney disease is replacement of erythropoietin by administering an erythropoiesis-stimulating agent.[9] Our patient required 14 injections of erythropoietin. Supplementation with red blood cell transfusion was required despite the use of erythropoietin. The first pregnancy with a successful outcome in patient on HD was described in 1971 by Confortini et al.[10] Many advances have occurred since then. This case is being presented to highlight the successful pregnancy outcome despite the very high number of dialysis episodes required.

Conclusion

Pregnancy in dialysis patients, though uncommon needs special care for successful outcome. Maternal complications like preeclampsia and hydramnios are common. The incidence of prematurity and growth retardation is high. In view of the need for increased frequency of dialysis for successful outcome and high chances of complications, early diagnosis of pregnancy in patients on dialysis is essential.

References
  1. Piccoli GB, Attini R, Vasario E, Conijn A, Biolcati M, D'Amico F. Pregnancy and Chronic Kidney Disease: A Challenge in All CKD Stages. Clin J Am Soc Nephrol. 2010 May; 5(5): 844–55.
  2. Trevisan G, Ramos JC, Martins-Costa S, Barros EJ. Pregnancy in patients with chronic renal insuffiency at Hospital de Clinicas of Porto Alegre, Brazil. Ren Fail. 2004; 26(1):29–34.
  3. Fisher MJ, Lehnerz SD, Hebert JR, Parikh CR. Kidney disease is an independent risk factor for adverse fetal and maternal outcomes in pregnancy. Am J Kidney Dis. 2004; 43(3):415–23.
  4. Bar J, Orvieto R, Shalev Y, Peled Y, Pardo Y, Gafter U. Pregnancy outcome in women with primary renal disease. Isr Med Assoc J. 2000;2(2):178–81.
  5. Shemin D. Dialysis in pregnant women with chronic kidney disease. Smin Dial. 2003; 16(5):379–83.
  6. Piccoli GB, Conijn A, Consiglio V, Vasario E, Attini R, Deagostini MC. Pregnancy in Dialysis Patients: Is the Evidence Strong Enough to Lead Us to Change Our Counseling Policy. Clin J Am Soc Nephrol 2010;5(1):62-71.
  7. Bili E, Tsolakidis D, Stangou S, Tarlatzis B. Pregnancy management and outcome in women with chronic kidney disease. 2013;17(2):163–8.
  8. Manisco G, Poti M, Maggiulli G, Di Tullio M, Losappio V, Vernaglione L. Pregnancy in end-stage renal disease patients on dialysis: how to achieve a successful delivery. Clin Kidney J. 2015 Jun;8(3):293–299.
  9. Provatopoulou ST, Ziroyiannis PN. Clinical use of erythropoietin in chronic kidney disease: outcomes and future prospects. Hippokratia. 2011 Apr-Jun;15(2):109–115.
  10. Confortini P, Galanti G, Ancona G, Giongo A, Bruschi E, Lorenzini E. Full term pregnancy and successful delivery in a patient on chronic haemodialysis. Proc Eur Dial Transplant Assoc 1971;8:74–80.
Citation

Chaudhari HK. Successful Pregnancy Outcome With Chronic Kidney Disease Requiring Multiple Hemodialysis. JPGO. 2018 Vol 5 No. 7. Available from: http://www.jpgo.org/2018/07/successful-pregnancy-outcome-with.html

Remembering past greats: Isidor Clinton Rubin

Author Information

Prasad M*
(*Assistant Professor, Department of Obstetrics and Gynecology, Seth GS Medical College and KEM Hospital, Mumbai, India.)

Isidor Rubin (1883-1958) is mainly remembered in gynecology for the “Rubin’s test”. However, his contributions are more than this.

Born in Austria in 1883, he received medical education in New York and worked in the Mount Sinai hospital for many years. He worked with Ernest Wertheim, making improvements in malignancy surgery, and developed a keen interest in gynecologic onco-pathology. His initial descriptions of carcinoma cervix-in-situ, though not very popular, appear to have been prior to that of Papanicalou.[1]

Long before the advent of imaging techniques, he proposed anatomic-histological criteria for the cervical ectopic pregnancy, which is known as the “Rubi'ns criteria”. 
The “Rubin’s cannula” designed by him was used for evaluation of infertility. The “Rubin’s test” involved suprapubic auscultation of sound made by the air which escaped the fallopian tube into the peritoneal cavity, when injected through the cannula. Though now outdated, the cannula designed by Rubin and his test was pathbreaking and in vogue for a long time.[2] His work involving demonstration of fallopian tube patency using gas and dyes, was regarded as one of the most important advances in female infertility management of the 20th century. For all this, he was widely regarded as a leading figure in modern female infertility management.

It is a matter of pride for clinical gynecologists that Rubin’s contribution came close to winning the Nobel prize in medicine. Many of his memorabilia are preserved in the Icahn Mount Sinai Medical University, USA.[3]

Rubin served as the president of the American Gynecological Society in 1955. He traveled widely and was well regarded by clinicians all over the world. In Europe, here received an honorary fellowship of the Royal College of Obstetricians and gynaecologists in England, and was also awarded the “officer of the French Legion of honour” for his outstanding contributions.
The then Professor in Calcutta University, Green-Armytage, recalled about how he hosted Rubin in Calcutta in 1925. The visiting stalwart lectured and demonstrated his test, winning the respect of many orthodox Indian clinicians. In an obituary column later, Professor Armytage quoted Rubin as having said “Adventure on, for the littlest cue. The next to lighten all men, may be you”.[4]
The sixtieth death anniversary of this inspirational gynecologist is celebrated on 10th July 2018. May his memory inspire many generations to come!

References
  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. Instruments. In Parulekar SV. Practical Gynecology and Obstetrics. 5th ed. Mumbai: Vora Medical Publications; 2011. pp 30.
  3. Archives and record management. Mount Sinai Medical Centre. Available from: http://icahn.mssm.edu/about/ait/archives/collection/isidore-rubin
  4. Obituary. Br Med J. 1958 Jul 19; 2(5089): 168. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2025904/?page=2
Citation

Prasad M. Remembering past greats: Isidor Clinton Rubin. JPGO 2018. Volume 5 No.7. Available from: http://www.jpgo.org/2018/07/remembering-past-greats-isidor-clinton.html

Volume 5 Number 6

Editorial
Madhva Prasad Sarvothaman

Spontaneous Cervical Perforation
Kaviya .S, Parulekar SV.

Pregnancy With Chronic Renal Anemia
Khadke B, Prasad M, Gupta AS.

Transverse Lie And Dystocia Due To Asherman Syndrome
Desai A, Parulekar SV.

A Case Of Pregnancy With Coexisting Systemic Sclerosis And Paucibacillary Leprosy
Nasare P, Prasad M, Gupta AS.

Chronic Nonpuerperal Inversion Of Uterus Secondary To Submucous Myoma
Jain N, Chaudhari H, More V.

Giant Sacrococcygeal Teratoma
Parihar A, Warke HS.

Cesarean Myomectomy
Malani K, Jagtap S, Swaminathan G, Samant PY.

Scar Endometriosis
Nebhani M, Shah R, Warke HS.

Remembering Past Greats: James Marion Sims
Pai K.