Volume 6 Number 7


Parulekar SV

In vitro fertilization (IVF) is the most important achievement in the management of infertility. It has given babies to a large number of couples who could not have any before this treatment was available, and hope to many more. Owing to the relatively recent nature of this treatment and the complex processes involved, including use of drugs, manipulation of the reproductive endocrine system, and manipulation of the ovum, sperm and embryos, there is grave concern about the short and long term outcomes of IVF. During the process, the patient may experience symptoms like nausea or vomiting, reduced urinary frequency, breathlessness, faintness, severe abdominal pains and bloating and excessive weight gain (all due to ovarian hyperstimulation syndrome). Egg retrieval may cause vaginal bleeding, infection, and injury to the urinary bladder or bowel. The risk of venous thromboembolism after IVF is twice that with spontaneous pregnancies, related to ovarian hyperstimulation syndrome. This rise is in the first trimester. Obstetric problems associated with IVF include multifetal pregnancies, prematurity, intrauterine growth restriction, placenta previa, placental abruption, perinatal mortality, preeclampsia, need for cesarean delivery, and birth defects. These risks are increased not only with multiple pregnancies, but also with singleton pregnancies. It is not known as yet whether they are due to IVF or underlying causes of infertility. The rates of miscarriage are similar to those in spontaneous conceptions. The risk of ectopic pregnancy with IVF is 2-5%. There is a significant financial, physical and emotional stress on the couple. Emotional problems are common, especially when the IVF procedure is not successful. A significant rise (0.8%) is seen in sex chromosomal aberrations after intracytoplasmic sperm injection (ICSI). The risk of congenital malformations is increased after use of assisted reproductive techniques (ART) than with natural conceptions, especially of cardiovascular malformations. It is similar with IVF and ICSI. Children born with IVF are more likely to require rehabilitation than controls. Cerebral palsy tends to occur more often in IVF babies. There is a small association between IVF and cancers of early childhood, especially hepatic cancers. As the babies conceived with IVF grow, more problems may come to light. Perhaps the procedure is disrupting the genome in a non-fatal manner, with effect on specific organs which may manifest after years. Until we have all the answers, we should continue to counsel patients, screen the couple for genetic conditions, especially infertility-associated conditions, consider embryo reduction in higher order multifetal pregnancy and look for and treat complications during pregnancy.

Succenturiate Lobe Of Placenta: An Unusual Case

Author Information

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

Succenturiate lobe of placenta is an entity where one or more accessory lobe may develop in the membranes at a distance from the main placenta. These lobes have vessels that course through the membranes. It may get retained in the uterus after delivery and cause postpartum uterine atony and hemorrhage. These lesions can be identified sonographically antenatally and  grossly after childbirth. We present an unusual case of a succenturiate lobe of a placenta.

Division of placenta into two or more lobes is the most common abnormality of placental configuration. It is called bipartite when there are two or more lobes and tripartite when there are three lobes. The lobes are usually attached in the region of cord origin. They are connected by vessels, membranes and thinned portion of the placenta. A succenturiate lobe is formed by the persistence of one or more groups of villi apart from the main portion of placenta and is connected to the latter merely by vessels and membranes. It is called placenta spuria when the vascular connection is lacking.
Case Report

A 24 year old woman, married for 3 years, gravida 2 with a spontaneous abortion at 2.5 months of amenorrhea one year ago, presented with preterm labor at 32 weeks of gestation.She was a known case of gestational diabetes mellitus, under treatment with Metformin 500 mg q8h. Her blood pressure was 140/90 mm Hg, pulse rate 70/min and respiratory rate 18/min. Her general and systemic examination findings were normal. Obstetric examination showed a single fetus in vertex presentation, its size corresponding to the period of amenorrhea. She was administered betamethasone for hastening fetal lung maturity and Nifedipine to control preterm labor. Her hemogram, serum TSH, liver and renal function test results were normal, serological tests for HIV, hepatitis B and C were negative. Her obstetric ultrasonography showed a single intrauterine gestation of 31weeks and 4 days, and the placenta in right posterolateral position with a succenturiate lobe at right anterolateral position, measuring 11x10x3 cm. She went in spontaneous labor and delivered a male baby of 2.002 kg of Apgar score 9/10. Examination of the placenta showed a succenturiate lobe measuring 11x10x3 cm, attached to the main placenta by membranes, in which the vessels of the lobe ran free for a distance of 12 cm. There was no postpartum hemorrhage.

Figure 1. Succenturiate lobe (SL), main placenta (P), umbilical cord (UC) and vessels connecting the succenturiate lobe to the main placenta (V).

A succenturiate lobe is found in 15-30:10000 pregnancies. It is a structural abnormality of the placenta. It is characterized by the presence of a main placenta, and a smaller segment, the blood vessels of which run from the edge of the main placenta or from the main umbilical cord.[1] These vessels include a branch of the umbilical artery and a tributary of the umbilical vein. These vessels may branch off right before the main vessels enter the main placental mass, or they may run in the substance of the main placenta and then leave it to enter the succenturiate lobe. The former arrangement is similar to that in a bilobed placenta. The difference between a succenturiate placenta and a bilobed placenta is not defined precisely, but it is assumed that when one lobe is quite small, like a cotyledon of the placenta, it is called a succenturiate lobe. When the two lobes are approximately of the same size, it is called a bilobed placenta. When the vessels branch off from the umbilical cord before it enters the main placenta, their course inthe fetal membranes tends to be quite long, while it is shorter when they leave the main placental mass to enter the succenturiate lobe. Vasa previa is more likely to occur with the former than with the latter.

Recognition of a succenturiate lobe antenatally is important because the vessels connecting the succenturiate lobe to the main placenta may rupture during labor leading to fetal death, and if missed after delivery of the baby, the succenturiate lobe may be retained, leading to atonic postpartum hemorrhage.[2,3] Ultrasonography is the mainstay of diagnosis of this condition antenatally.[4,5,6] The case presented here had the vessels running from the edge of the main placenta to the succenturiate lobe for a distance of 12 cm, which was unusual. The succenturiate lobe was also larger than usual, measuring 11x10x3 cm,  comprising of a mass of two cotyledons instead of one. 

  1. Jeanty P, Kirkpatrick C, Verhoogen C, Struyven J. The Succenturiate Placenta. J Ultrasound Med 1983;2:9-12.
  2. Ma JS, Mei X, Niu YX, Li QG, Jiang XF. Risk Factors and Adverse Pregnancy Outcomes of Succenturiate Placenta: A Case-Control Study. J Reprod Med. 2016 Mar-Apr;61(3-4):139-44.
  3. Suzuki S1, Igarashi M. Clinical significance of pregnancies with succenturiate lobes of placenta. Arch Gynecol Obstet. 2008;277(4):299-301.
  4. Angtuaco TL, Boyd CM, Marks SR, Quirk JG, Galwas B. Sonographic diagnosis of the bilobate placenta. J Ultrasound Med 1986;5(11):672-4.
  5. Nelson LH, Fishburne JI, Stearns BR. Ultrasonographic description of succenturiate placenta. Obstet Gynecol 1977;49(1 suppl):79-80.
  6. Hata K, Hata T, Aoki S, Takamori H, Takamiya O, Kitao M.  Succenturiate placenta diagnosed by ultrasound. Gynecol Obstet Invest 1988;25(4):273-6.

Kaviya. S, Parulekar SV. Succenturiate Lobe Of Placenta: An Unusual Case. JPGO 2019. Vol 6 No. 7. Available from: https://www.jpgo.org/2019/07/succenturiate-lobe-of-placenta-unusual.html

Silent Umbilical Vein Thrombosis

Author Information

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


Umbilical cord contains two arteries and one vein. Either or both of these type of vessels can develop thrombi. There are a number of causes for umbilical vascular thrombosis, and the fetal outcome can be poor in a number of cases. A case of silent development of multiple thrombi in fetal umbilical vein without any cause and with normal fetal outcome is presented.


Thrombosis of the umbilical vein is a rare condition that may cause a high fetal mortality and serious fetal morbidity. There are a number of maternal and fetal causes for umbilical arterior and/or venous thrombosis. Presence of any of the maternal conditions should alert one to look for such thrombosis. Presence of fetal complications should also alert one in a similar manner. A case of thrombosis of the umbilical vein without any cause and with a good fetal outcome is presented.

Case Report

A 25 year old primigravida was registered with us for antenatal care. She had a normal cpurse of pregnancy. She did not have any illness. She took her iron, calcium and folic acid medication and tetanus immunization as per prescription. Her hemogram, plasma sugar levels, liver, renal and thyroid function tests showed normal results. Her serological tests for syphilis, HIV, hepatitis B and hepatitis C were negative. First trimester obstetric ultrasonography (USG) and an anomaly scan at 18 weeks showed normal results and no abnormalities. Subsequent USG scans showed normal fetal growth. She underwent an elective cesarean section for inlet pelvic contraction, and delivered a female child weighing 3.05 kg. The newborn had Apgar score of 9/10 at 1 min and 5 minutes after birth. The umbilical cord showed multiple small thrombi. The baby did not show any abnormality.

Figure 1. Umbilical vein thrombi (arrows).


Incidence of umbilical vascular thrombosis varies from 1:1300 to 1:1500 deliveries and is found in 1:1000 perinatal necropsies.[1,2] The thrombosis can be of the umbilical vein alone, umbilical vein and artery(ies) both, or umbilical artery alone
in 70, 20, and 10% of cases respectively.[3] The fetal male/female ratio is 1.5:1. Though an umbilical artery has two ateries and only one vein, umbilical arterial thrombosis has a worse fetal prognosis than venous thrombosis.[2]

Umbilical vascular thrombosis may occur due to stasis in the vessels, as seen with true knots in the cord, stretching of the cord due to its shortness.[4,5]
Hypercoiling of the cord, oligohydramnios, velamentous insertion of the cord, fetal vascular ectasia and amniotic bands can also cause umbilical vascular stasis and thrombosis.[6,7] There may be hypercoagulability of the fetal blood, as in case of thrombophilia. There may be endothelial damage due to funisitis or meconium induced vascular necrosis. Maternal conditions like diabetes mellitus and preeclampsia predispose to umbilical vascular thrombosis.[6,8] The mechanisms of action of maternal diabetes may be increased levels of of α 2-antiplasmin and decreased fibrinolysin in fetal blood. There is also an imbalance between vasoconstriction and vasodilatation factors leading to platelet aggregation and vasoconstriction. Fetal hemolysis, massive fetomaternal hemorrhage and hydrops fetalis increase risk of umbilical vascular thrombosis.[1,2]

Complete occlusion of the umbilical vessels can cause fetal death.[6,7,9.] Less than complete occlusion can cause fetal growth restriction.[1] Migration of smaller thrombi in the fetal circulation can cause renal  or cerebral infarcts, and amputation of the digits.[3,6] Hyrtl’s anastomosis is anastomosis between two umbilical arteries. It is found in 90% placentas normally. It protects from development of placental hypoxia and infarction in cases of umbilical arterial thrombosis.[6,8] Such anastomosis was seen in the case presented.

The umbilical vascular thrombosis may be detected accidentally during routine obstetric USG. It may be detected when such thrombosis is looked for in presence of predisposing factors or fetal growth restriction. USG including Doppler study is the best of making a diagnosis of such thrombosis.[10,11]

The outcome was good in the case presented because there were small scattered umbilical venous thrombi without complete occlucion of the vein. The importance of detecting such thrombi in the absence of any fetal effect is to make the obstetrician and neonatologist alert to the possibility of presence of the predisposing conditions, so that appropriate investigations can be done and conditions not detected so far can be diagnosed early and then treated appropriately. Neonatal clinical evaluation investigations did not reveal any neonatal morbid conditions and predisposing factors in the case presented.

  1. Schröcksnadel H, Holböck E, Mitterschiffthaler G, Tötsch M, Dapunt O. Thrombotic occlusion of an umbilical vein varix causing fetal death. Arch Gynecol Obstet 1991;248:213–215.
  2. Heinfetz SA. Thrombosis of the umbilical cord: analysis of 52 cases and literature review. Pediatr Pathol 1988;8:37–54.
  3. Sato Y, Benirschke K. Umbilical arterial thrombosis with vascular wall necrosis: Clinicopathologic findings of 11 cases. Placenta. 2006;6–7:715–18.
  4. Devlieger H, Moerman P, Lauweryns J, de Prins F, van Assche A, Eggermont E et al. Thrombosis of the right umbilical artery, presumely related to shortness of the umbilical cord: an unusual case of fetal distress. Eur J Obstet Gynecol Reprod Biol 1983;16:123–127.
  5. Hasaart TH, Delarue MW, de Bruine AP. Intra-partum fetal death due to thrombosis of the ductus venosus: a clinicopathological case report. Eur. J. Obstet. Gynecol. Reprod. Biol. 1994;56:201–203.
  6. Avagliano L, Marconi AM, Candiani M, Barbera A, Bulfamante G. Thrombosis of the umbilical vessels revisited. An observational study of 317 consecutive autopsies at a single institution. Hum Pathol. 2010;7:971–79.
  7. Hasegawa J, Matsuoka R, Ichizuka K, Otsuki K, Sekizawa A, Farina A, et al. Ultrasound diagnosis and management of umbilical cord abnormalities. Taiwan J Obstet Gynecol. 2009;1:23–27.
  8. Klaritsch P, Haeusler M, Karpf E, Schlembach D, Lang U. Spontaneous intrauterine umbilical artery thrombosis leading to severe fetal growth restriction. Placenta. 2008;4:374–77.
  9. Dussaux C, Picone O, Chambon G, Tassin M, Martinovic J, Benachi A et al. Umbilical vein thrombosis: To deliver or not to deliver at the time of diagnosis. Clin Case Rep. 2014;6:271–73.
  10. Allen SL, Bagnall C, Roberts AB, Teele RL. Thrombosing umbilical vein varix. J. Ultrasound Med. 1998;17:189–192.
  11. Viora E, Sciarrone A, Bastonero S, Errante G, Campogrande M. Thrombosis of umbilical vein varix. Ultrasound Obstet. Gynecol. 2002;19:212–213.

Parulekar SV. Silent Umbilical Vein Thrombosis. JPGO Volume 5 Numbar 7. Available from: https://www.jpgo.org/2019/07/silent-umbilical-vein-thrombosis.html

A Case Report Of Broad Ligament Endometriotic Cyst

Author Information

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


Endometriosis is a common benign gynecological disease in women. Here we are presenting a rare case of broad ligament endometriotic cyst.


The broad ligament is a rare site for endometriosis. The most common site for endometriosis is the ovaries which usually present as a chocolate cyst. The prevalence of this disease increases up to 30 % in patients with infertility and up to 45 % in patients with chronic pelvic pain.[1] Depending upon the site of implantation, endometriosis can be either endopelvic or extrapelvic. Extrapelvic endometriosis is rare but it can occur. These sites include gastrointestinal, urinary tracts, the upper and lower respiratory system, the diaphragm, the pleura, the pericardium, and abdominal scars.

Case Report

A 32 year old multigravida, married for 13 years presented in the gynecology OPD with complaint of dysmenorrhea since 4 years. She was infertile for 4 years. She was relatively asymptomatic 4 years back when she started having dysmenorrhea, increasing pain with each cycle. Pain would appear 4-5 days before menses and subsided when menses stopped. Pain was severe in intensity, not relieved by medication. She tried some non allopathic treatment too however she had no symptomatic relief. Previous menstrual cycle was normal of 30 days and painless. On general examination she was moderately built and had mild pallor. On per abdominal examination, abdomen was soft, had no guarding, tenderness, or  rigidity. Per speculum examination showed cervical erosion, vagina was otherwise healthy. On per vaginal examination uterus was of normal size deviated to the left with restricted mobility. Right fornix was ill-defined, pulled up and tender
She had an ultrasound done that was suggestive of right ovarian chocolate cyst of size 4.1×4.4×3.4 cm, about 31 cc in volume with normal vascularity on color Doppler. Tubular cystic mass of 3.9×1.9 cm was seen in the right adnexa suggestive of a hematosalpinx. Left ovary was normal. Except for Hb of 8.9 gm% all other hematological parameters including LFT’s, RFT’s were normal. PAP smear was inflammatory. A diagnostic hystero-laparoscopy was performed under general anesthesia. Hysteroscopic examination was normal. On laparoscopic examination uterus appeared bulky with restricted mobility. Right sided fallopian tube and ovary could not be visualized. There was an adnexal mass of about 4×4 cms size on the right side. Left fallopian tube and ovary too could not be visualized as a fold of omentum was covering the left adnexa. Posterior uterine wall was densely adherent to the sigmoid colon. Decision for exploratory laparotomy was taken.  Intraoperatively uterus could not be delivered out as it was densely adherent to the sigmoid colon and a 5×5 cm right broad ligament cyst was noted (figure 1). The right adnexal anatomy was also distorted, and the right ovary was adhered to the posterior uterine wall and the posterior surface of broad ligament on the right side. Right fallopian tube was dilated and convoluted with agglutination of the fimbrial end.   
Prior to excision of the cyst, the cyst was aspirated and endometriotic fluid aspirate was confirmed. Cyst was then dissected from between the leaves of the broad ligament but it ruptured inadvertently punctured. Chocolate colored endometrotic fluid drained out (figure 2). Cyst wall was peeled off and sent for histopathological examination. Base of the cyst cauterized. Right ovary was densely adherent to the posterior uterine wall on its right side and hence could not be separated. Broad ligament was reconstructed.

Adhesiolysis between sigmoid colon and posterior surface of the uterus was attempted; however in view of excessive bleeding during dissection and significant risk of injury to the sigmoid colon further dissection was abandoned. Abdomen was irrigated and then closed in layers.  She tolerated the procedure well. Post operatively she was administered injection luprolide 3.75mg monthly for 3 months. Histopathology report of the cyst wall was confirmed an endometriotic cyst.

Figure 1. Babcock forceps has held the round ligament. Arrow points to the broad ligament endometrioma.

Figure 2. Aspiration of the endometrioma.


Endometriosis is defined as the presence of functional endometrial glands and stroma outside the uterine cavity. Its prevalence is 5 % with peak age between 25 to 35 years. As endometriosis is an estrogen dependent condition, it mainly affects female of reproductive age group.[2] The most common site is the ovaries followed by fossa ovarica, uterosacral ligaments, and pouch of Douglas.
In our case the endometriosis collection was between the leaves of the right broad ligament. We postulate that the right ovary which had dense adhesions to the posterior surface of the right broad ligament was the site of an endometrioma which must have ruptured through the posterior leaf of the right broad ligament and an endometriotic collection.
Etiology and pathogenesis of endometriosis is still unclear. The mechanism most widely accepted for the peritoneal endometriotic lesions is via retrograde menstruation. Menstrual debris are found in peritoneal fluid in perimenstrual period in 90 % of women with patent fallopian tubes. Development of pelvis endometriosis depends on the balance between retrograde flow of menses and their clearance by the immune mechanism.[3] Patients with mullerian anomaly and active endometrium causing hematometra have increased incidence of endometriosis.[4] Another theory is celomic hyperplasia suggested by Grunewald in 1942 which can explain endometriosis in amenorrheic women and extrapelvic site endometriosis like pleural cavity, diaphragm, brain and others. According to this theory, mesothelial cells under the influence of steroid hormones or exogenous factors differentiate into functional endometrial cells.[5] Cytokine imbalance in the form of increased pro-inflammatory mediators such as TNF alpha, IL 4 & 6 and decreased production of INF gamma leads to defective cytotoxicity by T cell and NK cell. It may be the reasons for local proliferation of ectopic endometrial tissue.[6] Endometriosis can be diagnosed by laparoscopy and biopsy of lesions.[2] Blood diagnostic test such as CA 125 cannot be used for diagnosis because of lack of sensitivity and specificity.[7] Combined oral contraceptive pills can be used empirically for pain relief as it decreases menstrual flow and causes decidualization of ectopic endometrium. It reduces cell proliferation and causes apoptosis.[8] Progesterone administered as depot medroxy progesterone acetate (DMPA) or norethisterone acetate (NETA) also cause pseudo pregnancy state, decidualization and atrophy of the endometrial implants. It also decreases matrix metallo-proteinase that is required for implantation and growth of the endometrial implant. LNG IUD is also effective for pain relief in patient who does not want to conceive. It decreases menstrual flow and reduces future recurrence.[9] GnRH agonists bind to pituitary receptors resulting in a shutdown of pituitary hormone secretion which in turn down regulates the ovarian production of estrogen. This down-regulation is constant and results in a hypoestrogenic state much like menopause.[10]  Combined use of laparoscopy surgery and GnRH analogous decreases recurrence rate compared to surgery used alone.

  1. Mehedintu C, Plotogea MN, Ionescu S, Antonovici M. Endometriosis still a challenge. Journal of medicine and life. 2014;7(3):349-57.
  2. Vercellini P, Viganò P, Somigliana E, Fedele L. Endometriosis: pathogenesis and treatment. Nat Rev Endocrinol. 2014 May;10(5):261-75.
  3. Olive DL, Henderson DY. Endometriosis and mullerian anomalies. Obstet Gynecol. 1987;69(3 Pt 1):412-5.
  4. Halme J, Hammond MG, Hulka JF, Raj SG, Talbert LM. Retrograde menstruation in healthy women and in patients with endometriosis. Obstet Gynecol. 1984 Aug;64(2):151-4.
  5. Gruenwald P. Origin of endometriosis form the mesenchyme of the celomic walls. Am J Obstet Gynecol. 1942; 44(3):470-474.
  6. Szyllo K, Tchorzewski H, Banasik M, Glowacka E, Lewkowicz P, Kamer-Bartosinska A. The involvement of T lymphocytes in the pathogenesis of endometriotic tissues overgrowth in women with endometriosis. Mediators Inflamm. 2003; 12(3): 131–138.
  7. Agic A, Djalali S, Wolfler MM, Halis G, Diedrich K, Hornung D. Combination of CCR1 mRNA, MCP1, and CA125 measurements in peripheral blood as a diagnostic test for endometriosis. Reproductive Sciences. 2008;15(9):906-911.
  8. Meresman GF, Auge L, Baranao RI, Lombardi E, Tesone M, Sueldo C. Oral contraceptives suppress cell proliferation and enhance apoptosis of eutopic endometrial tissue from patients with endometriosis. Fertil Steril.2002;77(6):1141–7.
  9. Petta CA, Ferriani RA, Abrao MS, Hassan D, E Silva RJC, Podgaec S et al. Randomized clinical trial of a levonorgestrel-releasing intrauterine system and a depot GnRH analogue for the treatment of chronic pelvic pain in women with endometriosis. Hum Reprod. 2005;20(7):1993–8.
  10. Wilson AC, Meethal SV, Bowen RL, Atwood CS. Leuprolide acetate: a drug of diverse clinical applications. J Expert Opinion on Investigational Drugs. 2007;16(11):1851-1863.

Modi A, Pardeshi S, Gupta AS. A Case Report Of Broad Ligament Endometriotic Cyst. JPGO 2019. Vol 6 No. 6. Available from: https://www.jpgo.org/2019/07/a-case-report-of-broad-ligament.html

Seven (7) Twists Of Fallopian Tube With Parasitic Blood Supply

Author Information

Shah N*, Paranjpe SH**, Jindal N***.
(*Consulting Gynecologist/Obstetrician, Hon. Endosopic Surgeon Wadia Hospital & Railway Hospital, Byculla, **Director Velankar Hospital & Paranjpe Maternity Home, Chembur, ***Consultant Anesthesiologist, Mumbai, India.)


Isolated Fallopian tube torsion is a rare gynecological cause of chronic or acute lower abdominal pain. There are no specific investigations like imaging, or blood workup. Very rarely, a diagnosis is made before the operation. In this case, we present a case of a 46 year old female undergoing a hysterectomy. She had an incidental finding of a twisted fallopian tube with 7 turns and a blood supply from the bowel.


Fallopian tube torsion without ovarian torsion is a rare identity. Its incidence in the reproductive age group is 1 in 1.5 million.[1]  Presentation is usually similar to that of an ovarian torsion, but pain may be chronic dull aching and vague as compared to ovarian torsion.[2]

Case Report

A 46 year old multiparus woman with previous 2 normal deliveries came to our OPD with chronic dull aching lower abdominal pain since 1 year. She had symptoms of irregular menses with menorrhagia. She had no other symptoms like fever, nausea, vomiting or vaginal discharge. On physical examination, there was no focal tenderness. On pelvic examination, right ovarian tenderness was noted, but no cervical motion tenderness could be elicited. All routine blood and urine tests were within normal limits.
Ultrasonography showed a bulky uterus with 2 small intramural fibroids. Both ovaries were normal and no free fluid was seen in the pelvis.  She was posted for a total Laparoscopic Hysterectomy for abnormal uterine bleeding.  During laparoscopy, the uterus was bulky but normal in appearance. Both ovaries were normal. Right sided tube was dilated with mild hydrosalpinx with isolated 7 twists of the fallopian tube. Another unique feature that was found, was that the tubal end had a parasitic blood supply from the bowel. The adhesion was coagulated and cut and then the untwisting was done 7 times to finally completely untwist the fallopian tube.  Bilateral salpingectomy was performed after the hysterectomy.  Diagnosis of torsion and hydrosalpinx was established on histopathology.

Figure 1. Normal ovary with 7 twists of fallopian tube seen.

Figure 2: Twist, 1st.

Figure 3. Twist, 2nd.

Figure 4. Twist, 3rd.
Figure 5. Twist, 4th.
Figure 6.  Twist, 5th.
Figure 7.  Twist, 6th.

Figure 8 . Parasitic blood supply from bowel.


The exact mechanism of isolated fallopian tube torsion is not well understood. Various documented causative factors include, prior surgery such as tubal ligation, hematosalpinx, hydrosalpinx, or other tubal neoplasms. There are also various physiological factors which can cause torsion which include hyper motility of the fallopian tube, or tubal spasm or increased peristalsis. Other congenital pathologies have also been mentioned which include long tubal size, excessive spiral nature of the tube, incomplete mesosalpinx, and large cysts of morgagni. Extrinsic factors for tubal torsion may include ovarian or para ovarian cyst, tubal adhesions, uterine enlargement due to any tumor or pregnancy.[3] Besides these, the Sellheim theory states that tubal torsion can occur due to sudden body position changes, or trauma or venous congestion in the mesosalpingeal area.[4] An undiagnosed torsion may undergo alternate states of torsion and detorsion which may finally lead to chronic nature of the torsion.
Clinical presentation of an isolated fallopian tube torsion is quite nonspecific. Pain may be  specific but is usually vague dull aching generalized lower abdominal pain. Nausea vomiting may accompany. Pelvic examination does not reveal much as hydrosalpinx is not always palpable. Ultrasonography may pick up hydrosalpinx but can be easily missed as in this case. Laboratory findings are also nonspecific. Leukocytosis may be present if necrosis has occurred. CRP may be raised.[4] Many reports have also suggested that torsion of fallopian tube is more likely to occur on the right side. This is because of the partial immobilization of the left tube because of the sigmoid and mesocolon of the left side. Also it is more likely for patients to get operated for right lower abdominal pain due to suspicion of appendicitis.[5]
Complications of tubal torsion include local necrosis leading to gangrenous transformation and super infection.[6] This did not occur in our case even after 7 twists as it had obtained a parasitic blood supply from the bowel.


Thus, although a rare entity, differential for tubal torsion must be kept in mind if ultrasonography shows both normal ovaries and a hydrosalpinx. Delay in diagnosis may lead to increased morbidity.

  1. Hansen OH. Isolated torsion of the Fallopian tube. Acta Obstetricia et Gynecologica Scandinavica. 1970;49(1):3–6.
  2. Casey RK, Damle LF, Gomez-Lobo V. Isolated fallopian tube torsion in pediatric and adolescent females: a retrospective review of 15 cases at a single institution. Journal of Pediatric and Adolescent Gynecology. 2013;26(3):189–192.
  3. Comerci G, Colombo FM, Stefanetti M, Grazia G. Isolated fallopian tube torsion: a rare but important event for women of reproductive age. Fertility and Sterility. 2008; 90(4):1198.e23-5.
  4. Krissi H, Shalev J, Bar-Hava I, Langer R, Herman A, Kaplan B. Fallopian tube torsion: laparoscopic evaluation and treatment of a rare gynecological entity. Journal of the American Board of Family Practice. 2001;14(4):274–277.
  5. Gross M, Blumstein SL,Chow LC. Isolated fallopian tube torsion: a rare twist on a common theme. American Journal of Roentgenology. 2005;185(6):1590–1592.
  6. Ferrera PC, Kass LE, Verdile VP. Torsion of the fallopian tube. American Journal of Emergency Medicine. 1995;13(3):312–314.

Shah N, Paranjpe SH, Jindal N. Seven (7) Twists Of Fallopian Tube With Parasitic Blood Supply. JPGO 2019. Volume 6 No.7. Available from: https://www.jpgo.org/2019/07/seven-7-twists-of-fallopian-tube-with.html

Fallopian Tube Cancer: A Rare Presentation

Author Information

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


The incidence of primary fallopian tube carcinoma is 0.1-1.8% of all malignancies of the female genital tract. This entity in gynecological oncology presents a diagnostic dilemma because in most cases it is extremely hard to have a provisional diagnosis of fallopian tube carcinoma preoperatively in view of non specific history and clinical findings. We are here presenting a case of a 52 year old postsurgical menopausal woman with primary endometrioid adenocarcinoma of the fallopian tube.


Primary fallopian tube cancer is a very uncommon entity in the gynecological oncology spectrum. However, with high clinical suspicion especially in the elderly population the condition can be diagnosed early and managed appropriately.[1] Despite high clinical suspicion, the preoperative diagnosis of fallopian tube cancer is only as common as 0-10% and is most often an incidental intraoperative finding or histopathological diagnosis as was in this case.[2]

Case Report

52 year old presented to the gynecology outdoor patient department (OPD) with complaints of lower abdominal pain. She underwent vaginal hysterectomy five years back in view of abnormal uterine bleeding. However, she did not have any medical records or operative notes to elaborate on the indication and procedure performed. She had now come to the hospital in view of lower abdominal pain that was dull aching and localized to the lower abdomen. General and systemic examination was unremarkable. On abdominal examination, all quadrants were soft and non-tender. Vault appeared healthy on speculum examination. On bimanual examination, a soft boggy mass of 3 cm diameter was felt in the anterior fornix which was tender on palpation. Ultrasonography (USG) showed a retort shaped convoluted cystic lesion of 13.5 cm diameter in the pelvis in close proximity of the right ovary with a diameter of 8 mm at the ovarian end and 20 mm on the other end. Right ovary was 2x1cm in diameter whereas left ovary could not be visualized. There was no evidence of abdominal lymphadenopathy, ascites or collection in the right iliac fossa. USG reported it as right sided hematosalpinx. On re-evaluation of the USG findings by a senior radiologist, the mass was noted to have similar dimensions however, the contents of the mass were hyperechoic and the folds of the right fallopian tube were of increased vascularity. This led to a provisional diagnosis of right sided pyosalpinx and less likely to be hematosalpinx. Patient was managed conservatively with oral antibiotics (doxycycline and metronidazole) for 2 weeks. Repeat USG showed similar findings but features were suggestive of torsion of the right adnexal lesion. She continued to have complaints of lower abdominal pain. Hence, she was admitted and posted for exploratory laparotomy with bilateral salpingo-oophorectomy. Intraoperatively, right-sided, brown irregular cystic mass involving the right fallopian tube was seen with four turns of torsion around the right infundibulopelvic ligament. Right ovary appeared normal. Left ovary and fallopian tube grossly looked normal. Left mesosalpinx showed two tubercles of 0.5 cm diameter which were isolated and sent for histopathological examination. Uterus was absent (post-vaginal hysterectomy) and there was no free fluid in the abdomen.  Curved clamp was applied across the right infundibulopelvic ligament, cut and pedicle was transfixed using polyglactin 910. Similar procedure was repeated on the left side. Specimen including bilateral ovaries, left fallopian tube and the right irregular cystic mass (pyosalpinx) was sent for histopathological examination. She tolerated the procedure and anesthesia well and was discharged on the eighth day after suture removal. On follow-up, histopathology report was suggestive of foci of endometrioid adenocarcinoma from a section of dilated right fallopian tube. There was evidence of proliferating glands, papilloid projections, tubules with complex architecture cytoplasmic vacuoles in the tubular lumen with focal invasion in the sub-epithelium.[Fig.1] There was no evidence of pre-existing endometriosis. Section from right ovary showed normal ovarian parenchyma. Left ovary and fallopian tube were unremarkable. Tubercle like tissue isolated from left mesosalpinx showed single hyalinised nodule with fibro-collagenous tissue but with no accompanying evidence of granuloma or malignancy. She was subsequently referred to a gynecological oncologist with the above report.  A contrast enhanced computerised tomography of the abdomen and pelvis was done which did not reveal any lymphadenopathy or organomegaly. There was no ascites. She was started on cycles of paclitaxel and carboplatin based chemotherapy after confirming glomerular filtration rate above 83. Till date, she has received two cycles of chemotherapy and is planned to undergo exploratory staging laparotomy (re-look surgery) after the third cycle.

Figure1. Histopathological appearance of endometrioid adenocarcinoma of fallopian tube.


Though clinically and pathologically fallopian tube cancer resembles epithelial ovarian cancer, the exact etiology has still not been isolated. It is difficult to distinguish from serous epithelial ovarian cancer or primary peritoneal serous carcinoma.[3] Unlike ovarian cancers that often present at a later stage, primary fallopian tube cancer presents earlier by virtue of the symptoms of pain abdomen in view of distension and torsion of the distended tube. All components of Latzko’s triad of symptoms of primary fallopian tube cancer including colicky abdominal pain, ‘hydrops tubae profluens’ or profuse sero-sanguineous vaginal discharge and abdominal or pelvic mass were rarely present.[4] Since our patient had already undergone vaginal hysterectomy previously, the symptom of vaginal discharge was absent and the vault smear did not describe any atypical cells. Tumor markers such as CA 125 can also lead to the clinical suspicion of epithelial tumors of the fallopian tube. Tumor markers were however not done preoperatively for our patient and neither was it advised post operatively, when histopathology report suggestive of endometrioid carcinoma was noted. The role of tumor markers such as CA 125 have been evaluated in primary fallopian tube cancer and has been found to be elevated in advanced or recurrent conditions. Its role in primary endometrioid cancer of fallopian tube has still not been studied in detail. CA 125 maybe of significance in patients where initial levels are high to predetermine prognosis of the tumor and detect recurrence.[5] Imaging modalities such as USG may show adnexal mass with solid mural nodules or complex sausage shaped lesions with cog wheel appearance. They however have poor specificity for detection of fallopian tube cancers.[6] Magnetic resonance imaging is considered superior to computed tomography to evaluate the spread of disease in the soft tissues beyond the fallopian tube. According to the diagnostic criteria for primary fallopian tube cancer established by Hu and colleagues; grossly, the main tumor is in the tube and arises from the endosalpinx, the histological pattern reproduces the epithelium of tubal mucosa and transition from benign to malignant tubal epithelium should be demonstrated and ovaries and endometrium are either normal or have a much smaller tumor volume than that of the tube.[7] Like ovarian carcinoma, fallopian tube carcinoma also has a surgical staging and the stage of the disease at initial exploration is a major determinant of the prognosis. The classification system for ovarian and fallopian tube carcinoma however is the same FIGO classification. Other determinants include volume of residual disease after initial cytoreductive surgery, presence of ascites and the histological grade of tumor.[8] The most common histological subtype of fallopian tube cancer is adenocarcinoma. Endometrioid adenocarcinoma of the fallopian tube was the subtype seen in this case. Endometrioid adenocarcinoma is often associated with a previous history of endometriosis, which was not present in our case neither in her history nor on pathology to suggest of a pre-existing endometriosis.[9] Definitive stage of the disease was not ascertained during the exploratory laparotomy since we did not have clinical suspicion regarding the condition. The re-look surgery planned after three cycles of chemotherapy could further enhance information regarding the same, even though postoperative computed tomography did not reveal any residual disease. Primary mode of management of fallopian tube cancer involves cytoreductive surgery to remove as much of the tumor as physically possible which usually includes total abdominal hysterectomy, bilateral salpingo-ovariectomy, omentectomy, selective pelvic and para-aortic lymphadenectomy for any stage of fallopian tube carcinoma. Postoperatively these patients usually receive adjuvant platinum based chemotherapy.[10] Endometrioid carcinomas of the fallopian tube are typically noninvasive or only superficially invasive. This type usually has a favorable prognosis and hence this subtype of tubal carcinoma should be differentiated from the more common neoplasms of fallopian tube i.e. serous type.[9] Rosen et al studied the 5-year survival rate for stage I and stage II cases and was 59% and for stage III and IV cases was 19% but this as not evaluated specific for the different histopathological types of carcinoma.[11] The prognosis after adequate treatment also depends on the age and the medical co-morbidities of the patient.


Primary fallopian tube cancer though rare should be a differential diagnosis while evaluating postmenopausal patients with adnexal mass and pain abdomen. This will help provide adequate surgical management in the primary setting. The learning points in this case was to perform tumor markers which could have possibly heightened our clinical suspicion and to perform an intra-operative frozen section histopathology of the tumor could have facilitated a more complete surgical management in the form of a surgical staging. That said, fallopian tube cancers continue to remain a primary histopathological diagnosis in a majority of early stage cases at least.


We thank Dr. Ameya from department of surgical histopathology for providing us with the histology picture.

  1. Kalampokas E, Kalampokas T, Tourountous I. Primary fallopian tube carcinoma. Eur J Obstet Gynecol Reprod Biol. 2013 Jul;169(2):155–61.
  2. Jeung IC, Lee YS, Lee HN, Park EK. Primary carcinoma of the fallopian tube: report of two cases with literature review. Cancer Res Treat. 2009 Jun;41(2):113–6.
  3. Tahiri EL, Erragad FZ, Jayi S, Hammas S, Harmouch T, Chbani L, et al. Primary adenocarcinoma of the fallopian tube: report of two cases. J Clin Case Rep. 2016 May; 6: 792.
  4. Lau HY, Chen YJ, Yen MS, Chen RF, Yeh SO, Twu NF. Primary fallopian tube carcinoma: a clinicopathologic analysis and literature review. J Chin Med Assoc. 2013 Oct;76(10):583–7.
  5. Ajithkumar TV, Minimole AL, John MM, Ashokkumar OS. Primary fallopian tube carcinoma. Obstet Gynecol Surv 2005 Apr;60:247–252.
  6. Ludovisi M, De Blasis I, Virgilio B, Fischerova D, Franchi D, Pascual MA, et al. Imaging in gynecological disease (9): clinical and ultrasound characteristics of tubal cancer. Ultrasound Obstet Gynecol. 2014 Mar;43(3):328–35.
  7. Hu CY, Taymor ML, Hertig AT. Primary carcinoma of the fallopian tube. Am J Obstet Gynecol. 1950 Jan;59(1):58–67.
  8. Hariprasad PSH, Srinivas T, Shetty KJJ. Primary bilateral fallopian tube carcinoma the report of a single case with review of the literature. Clin Diagn Res. 2013;7(5):930–2.
  9. Navani SS, Alvarado-Cabrero I, Young RH, Scully RE. Endometrioid carcinoma of the fallopian tube: a clinicopathologic analysis of 26 cases. Gynecol Oncol. 1996 Dec;63(3):371-8.
  10. Berek JS, Crum C, Friedlander M. Cancer of the ovary, fallopian tube, and peritoneum. Int J Gynaecol Obstet. 2015 Oct;131 Suppl 2:S111-22.
  11. Rosen AC, Ausch C, Hafner E, Klein M, Lahousen M, Graf AH. A-15 Year Overview of Management and prognosis in primary fallopian tube carcinoma. Austrian Cooperative Study Group for fallopian tube carcinoma. Eur J Cancer. 1998;34:1725–1729.

Mahanti S, Chaudhari HK. Fallopian Tube Cancer: A Rare Presentation. JPGO 2019. Vol.6 No. 7. Available from: https://www.jpgo.org/2019/07/fallopian-tube-cancer-rare-presentation.html

Postpartum Collapse In A Case Of Giant Ovarian Dysgerminoma In Pregnancy

Author Information

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


Ovarian dysgerminoma, the commonest malignant tumor of germ cell origin, predominantly affects young women. About 75 % of dysgerminoma’s occur between the age group of 10 - 30 years and thus can affect the fertility or may be associated with pregnancy. We present one such case of dysgerminoma associated with pregnancy.


Classification of ovarian tumors is based on their origin. These are of three types;  epithelial, germ cell and sex cord tumors. Commonest are the epithelial tumors. Only 30 % of all ovarian neoplasms and 3 % of all ovarian malignancies are germ cell tumors (GCTs).  Ovarian germ cell tumors, derived from the primordial germ cells, are further divided into subgroups based on the histological features. Mature teratoma being the commonest benign variety while dysgerminoma is the commonest malignant germ cell tumor.

Case Report

A 27 year old, gravida 3, para 2, living 2 with previous two full term normal deliveries, at 38.3 weeks of gestation was referred from a private hospital to our emergency department in view of fever and abdominal discomfort for the prior two days. On examination, she was conscious, oriented, febrile with a temperature of 1000 F, and pulse was 108/ min.. Her systemic examination was normal. On per abdomen examination uterus was full term, relaxed, and vertex was the presenting part. FHS were 146/ min., On per vaginal examination cervix was undilated, and uneffaced. She was admitted with the physician for fever. On investigation, Hemoglobin was 11 gm%, TLC was 3,000/ mm3, and platelet count was 81,000/ mm3. Dengue IgG and IgM, widal test, leptospirosis IgG & IgM were negative, malarial parasite was not detected on peripheral smear. Serum biochemistry was normal wherein BUN was 9.1 mg/dl, creatinine was 0.7 mg/dl, and electrolytes were normal, SGOT and SGPT were 329 and 39 u/l respectively. Blood sugar and thyroid profile  were  within normal limits. Next day she went into spontaneous, precipitate labor and delivered vaginally a full term female baby of 2.4 Kg with APGAR score of 6/10 and 7/10 at 1 minute and 5 minutes respectively. Neonate was kept in NICU. There was a 3rd degree prolapse . Cervix was entirely out of the introitus after delivery. After delivery, she was conscious oriented, and all her vital parameters were normal. Around 3-4 hours later she suddenly started complaining of breathlessness. Her extremities were cold, pulse was 128/ min., feeble and her systolic blood pressure was 60 mm of Hg. Chest was clear. Crystalloids and colloids were given to her but still her systolic BP remained 60 mm of Hg. Abdominal kept distending. Physician started her on two inotropes; dopamine and noradrenaline. On re-examination a hard mass of approximately 20x20 cm with irregular surface was felt in the abdomen behind the gravid, well contracted uterus. The lower end of the mass was also felt through the right and posterior fornix . Groove sign was present suggestive of a right adnexal mass. There was no active vaginal bleeding.  Her relatives then produced her early antenatal records of a private practitioner wherein an ultrasound (USG) done in 2nd trimester of pregnancy showed detection of a heterogeneous right ovarian mass of 12x8 cm at 22 weeks of gestation.  Review of subsequent USG’s was done. None of them commented about this mass. Her biochemical, hematological and serological investigations were repeated. Her  hemoglobin was 7.2 mg/dl, total leukocyte count was 9200/mm3, platelet count had dropped to 80,000/ mm3, PT test was 21.8s against a control of 13.0s. INR was 1.81, LDH was 2744 IU/L. Arterial blood gas analysis showed a pH of 7.23, pCO2 11 mm Hg, pO2 148 mm Hg, HCO3 4.6 mEq/L, and lactate levels were 10.7 mmol/L. This was suggestive of metabolic acidosis. An ultrasound that was repeated soon after delivery showed mild ascites and a septate, hyperechoic, heterogeneous mass with solid and multiple cystic components of approximately 26*22*14 cm arising from the right adnexa, extending upto the epigastrium. Ovaries could not be identified separately. She was taken for emergency exploratory laparotomy with the diagnosis of rupture or torsion of an adnexal mass. Introperatively, ascitic fuid of approximately 500 cc was aspirated and 20 cc fluid was collected and sent for cytology.  A Large, lobulated, hard, right ovarian mass of approximately 25x20x10 cm was present. No evidence of torsion of mass or breach of capsule was found. Left sided fallopian tubes, left sided ovary and the postpartum uterus appeared normal.[Figure 1]  Right ovarian mass was removed after clamping and cutting the pedicle and then pedicle was ligated. On handling of the mass the mass had a tendency of splitting up. [Figure2]  Right fallopian tube could not be removed due to high vascularity. There was no evidence of parietal peritoneal, omental and liver metastasis. Frozen section could not be done as facilities were not available during emergency hours. Intraoperatively, iliac and para-aortic lymph nodes were not palpable. Surgical staging was stage 1A. The mass weighed approximately 3.02 kgs.[Figure 3] Even though the capsule of the mass was intact it appeared very fragile and the mass split open on handling. No incision was required to open it.  Gross inner surface of the neoplasm showed predominantly solid areas with central and a few peripheral hemorrhagic area (figure 4).
Figure 1. The postpartum uterus (U) and the mass (M).
Figure 2. Mass splitting up on handling
Figure 3. Gross external appearance of the tumor.

Figure 4. Gross internal appearance of the tumor with arrow pointing towards hemorrhagic areas.

Intraoperatively, she received two units of whole blood and 4 units of fresh frozen plasma (FFP). Postoperatively, she was shifted to ICCU. She was in ICCU for 5 days. She was on the ventilator and on 2 inotropes for 3 days. Ionotropes were gradually tapered off. She was totally transfused with 2 units whole blood, 4 units of packed red blood cells, 10 units of FFP, 6 units of platelets, and 10 units of cryoprecipitate. She was weened off the ventilator after 3 days. Histopathological examination was suggestive of nested pattern with thin fibrovascular septa, large tumor  cells with pleomorphic nuclei, with many mitotic figures and large areas of necrosis. The fibrovascular septae showed presence of lymphocytes. No other germ cell component was seen. The features were consistent with dysgerminoma of the ovary. Ascitic fluid cytology was negative for malignant cells. She was stable, sutures were removed after 12 days. She was discharged and referred to a oncology centre where she was advised to follow up with abdominal CECT and tumor markers every 3 month. Baby expired on day 2 of life due to sepsis and lactic acidosis.


Ovarian germ cell tumors commonly affects girls in the age group of 15-19 years, and they are also seen in association with pregnancy. The estimated incidence of ovarian tumors is approximately 1 in 1000 pregnancies of which approximately 3–6 % are malignant.[1,2] Etiological factors for it are ill understood, few of them have found to be associated with gonadal dysgenesis and mixed gonadal dysgenesis, however 95% of females are cytogenetically normal.[3] These tumors are usually asymptomatic and are diagnosed as an adnexal mass during routine antenatal ultrasound imaging. In our case the mass was missed in the early 2nd trimester scan by the private practitioner where she registered for antenatal care. These tumors may present with pain, mass or distension of abdomen.  In our case it was clinically missed possibly because the mass hid behind the full term gravid uterus and so could not be palpated. Differentiating ovarian malignancies from functional cysts or benign ovarian tumors during pregnancy is a major challenge as standard diagnostic methods could not be applied. Few important markers of germ cell tumors are serum alpha feto protein (AFP), human chorionic gonadotropin (hCG), and lactic dehydrogenase (LDH). Some of these tumor markers are synthesized and secreted physiologically during fetal development like hCG, AFP, inhibin, thus these cannot be used for interpretation in pregnancy.[4] Imaging studies like ultrasound (USG) and MRI are the best tools at present to diagnose adnexal masses during pregnancy and differentiate between benign and malignant ones. Few characteristic ultrasound features of adnexal masses that have been associated with increased risk of malignancy include size, solid components or heterogeneous/complex appearance, excrescences/papillary structures, internal septations, bilaterality, irregular borders, increased vascularity, low resistance blood flow, and presence of ascites.[4] Among these findings our USG was suggestive of heterogeneous mass with septations and ascites, suggesting increased risk of malignancy. Ovarian masses in pregnancy are associated with increased risk of torsion, incarceration, rupture, and or hemorrhage and these can occur in the antepartum, intrapartum during vaginal delivery or in the puerperal period. The chances of torsion was less likely in our case as the tumor was big enough to extend till epigastrium, giving no space for torsion, however sudden hemorrhage could have occured due to trauma during childbirth, as shown in figure 4, which could be one of the possible cause of neurogenic shock and collapse of our patient. The risk of torsion among pregnant patients with adnexal tumors >4 cm increases. According to studies, 51 % of torsion’s occurred in tumors measuring 6–8 cm in diameter. The highest rate of torsion occurred around 15th - 16th week of gestation.[5] The natural course of pregnancy in cases of dysgerminoma is extremely difficult, due to large sizes of the tumors and collection of fluid. There was precipitate labor and 3rd degree prolapse in our case as the tumor size was big, it filled the abdomen along with the gravid uterus thus increasing the intra-abdominal pressure causing precipitate labor and pulsion prolapse. In a study conducted by Karlen JR et al among 27 pregnant women with dysgerminoma, 25% cases had fetal demise.[6] Even in our case baby died on day 2 of life, due to severe sepsis and lactic acidosis, probably due to long term asphyxiation caused by the pressure effect of the mass on the uterus and the sudden precipitate labor.  Several authors have stated that surgical intervention is required immediately in  situations where malignancy is suspected, during acute complication like torsion or rupture or if there is an increase by 30-50 % in size during pregnancy , regardless of the gestational age.[7,8,9] The ideal time for surgery is 14–22 weeks gestational age as most of the functional cysts disappear by that time, good operative field can be achieved with minimal uterine manipulation and low risk of obstetric complication.[10] The ideal time window was missed in our case, due to improper reviewing of reports and poor clinical acumen. The surgery aims at removal of the mass to avoid complications during pregnancy, to stage or to debulk the tumor if malignancy is identified.  In our case the surgery was done with the aim to debulk the tumor and to do surgical staging. Decision for surgery in an unstable patient was  difficult. However, had we deferred the surgery in view of her being hemodynamically unstable, the tumor would have broken piece meal spontaneously in the abdomen, as it was very fragile. In all cases frozen section must be done. Quirk and Natarajan have reported that approximately 75 % of women with  dysgerminoma present with clinical stage Ia disease.[11] Dysgerminoma confined to capsule of one ovary (stage 1A) is best managed by unilateral salphingoophorectomy.[12]  Staging is important, as adjuvant therapy during pregnancy is initiated only in advanced stage disease. Routine biopsy or wedge-resection of the contralateral ovary is not necessary unless it is involved. In cases of advanced stage disease cytoreduction should be undertaken.  An interval cytoreduction followed by chemotherapy in second trimester and completion of pregnancy is a reasonable approach.[13] The chemotherapeutic agents are lethal for use in first trimester causing fetal death, growth restriction or teratogenic effects. Malformation risk is 10 % with single drug and 25 % with combination chemotherapy in the first trimester. However Kim and Park in their study have documented the use of chemotherapeutic agents during the second trimester and delivery of a normal infant.[14] Recurrence of dysgerminoma’s is commonly seen in first 2–3 years after treatment. Therefore, follow-up should be scheduled at every 3–4 months for the first 3 years, every 6 months during the fourth and fifth years, and annual surveillance thereafter. CT imaging should be done during 6th and 12th month, especially if tumor markers were negative at the time of diagnosis.  Patients should be observed for up to 10 years for rarely occurring late recurrences.[16] The survival rates for dysgerminoma’s presenting at early and advanced stages are 95 and >80 %, respectively. In stage 1a dysgerminoma, after unilateral salpingo-oophorectomy  relapse rate ranged from 10 to 20%. Patients who suffer relapses and undergo chemotherapy, the survival rate is greater than 90%.[17]

  1. Rahman MS, Al-Sibai MH, Rahman J, Al‐Suleiman SA, El‐Yahia AR,  Al‐Mulhim AA et al. Ovarian carcinoma associated with pregnancy. A review of 9 cases. Acta Obstetricia et Gynecologica Scandinavica. 2002;81(3):260-264.
  2. Zhao XY, Huang HF, Lian LJ, Lang JH. Ovarian cancer in pregnancy: A clinicopathologic analysis of 22 cases and review of the literature. International Journal of Gynecological Cancer Banner. 2006;16(1):8-15.
  3. Lee-Jones L. Ovary: Germ Cell Tumors. Atlas Genet Cytogenet Oncol Haematol. 2003;7(4):282-288.
  4. Nick AM, Schmeler K. Adnexal masses in pregnancy. Perinatology. 2010;1:13-19.
  5. Yen CF, Lin SL, Murk W, Wang CJ, Lee CL, Soong YK, et al. Risk analysis of torsion and malignancy for adnexal masses during pregnancy. Fertility and Sterility. 2009;91(5):1895-1902.
  6. Karlen JR, Akbari A, Cook WA. Dysgerminoma associated with pregnancy. Obstetrics and Gynecology. 1979;53(3):330-335.
  7. Hill LM, Johnson CE, Lee RA. Ovarian surgery in pregnancy. Am J Obstet Gynecol 1975;122(5):565-569.
  8. Ballard CA. Ovarian tumors associated with pregnancy termination patients. Am J Obstet Gynecol 1984;149(4):384-387
  9. Matsuyama T, Tsukamoto N, Matsukuma K, Kamura T, Kaku T, Saito T. Malignant ovarian tumors associated with pregnancy: report of six cases. Int J Gynaecol Obstet 1989;28(1):61-66.
  10. Cavaco-Gomes J, Moreira CJ, Rocha A, Mota R, Paiva V, Costa A. Investigation and management of adnexal masses in pregnancy. Scientifica. 2016;2016(3012802): 9.
  11. Quirk JT, Natarajan N. Ovarian cancer incidence in the United States, 1992-1999. Gynecol Oncol. 2005; 97(2):519-23.
  12. Kwon YS, Mok JE, Lim KT, Lee IH, Kim TJ, Lee KH, et al. Ovarian cancer during pregnancy: clinical and pregnancy outcome. Journal of Korean Medical Science. 2010;25(2):230-234.
  13. Horowitz NS. Management of adnexal masses in pregnancy. Clin Obstet Gynecol. 2011;54(4):519-527.
  14. Kim DS, Park MI. Maternal and fetal survival following surgery and chemotherapy of endodermal sinus tumor of the ovary during pregnancy: a case report. Obstet Gynecol 1989;73(3 Pt 2):503-507.
  15. Williams S, Blessing JA, Liao SY, Ball H, Hanjani P. Adjuvant therapy of ovarian germ cell tumors with cisplatin, etoposide, and bleomycin: a trial of the Gynecologic Oncology Group. Journal of Clinical Oncology. 1994;12(4):701-706.
  16. Michener CM, Wu AY. Ovarian Dysgerminomas  Follow-Up. In: Huh WK, editor. Medscape; 2015. https://emedicine.medscape.com/article/253701-followup
  17. Ayhan A, Celik H, Taskiran C, Bozdag G, Aksu T. Oncologic and reproductive outcome after fertility-saving surgery in ovarian cancer. Eur J Gynaecol Oncol. 2003;24(3-4):223-32.

Singhania N, Bhandari P, Gupta AS. Postpartum Collapse In A Case Of Giant Ovarian Dysgerminoma In Pregnancy. JPGO 2019. Vol 6 No. 7. Available  from:  https://www.jpgo.org/2019/07/postpartum-collapse-in-case-of-giant.html

Intrapartum Chemical Burns Of The Fetus

Author Information

Mahanti S*, Samant PY**, Parulekar SV***.
(* Senior resident, **Academic Professor, *** Professor and Head, Department of Obstetrics & Gynecology, Seth G S Medical College and KEM Hospital, Mumbai, India.)


Chlorhexidine gluconate-cetrimide solution has been recommended for usage in under-resourced settings for vaginal examinations. Chlorhexidine has antiseptic as well as disinfectant properties in varying concentrations. However, it has been associated with a number of complications, such as anaphylaxis when used on mucous membranes and dermatitis. The present case is that of a neonate with first degree burns of the buttocks due to use of solution of chlorhexidine gluconate- cetrimide before vaginal examination. 


An aqueous solution containing cetrimide solution BP equivalent to cetrimide IP of 15.0% w/v and chlorhexidine gluconate solution IP 7.5% v/v equivalent to chlorhexidine gluconate 1.5% w/v should be used at a recommended dilution of 20 ml solution with 1000 ml of water for aqueous preparation or 35 ml solution with 200 ml water made up to 1 liter with spirit for the purpose of preoperative skin disinfectant and other invasive procedures.[1] It is known to develop idiosyncratic skin reactions including irritant contact dermatitis. Irritant contact dermatitis is a localized inflammatory skin response. It results from the direct cytotoxic effect of irritants, both chemical and physical. The clinical manifestations of irritant contact dermatitis range from mild skin dryness and erythema to acute eczematous dermatitis and even skin necrosis (chemical burn).[2]

Case Report

A twenty-year-old, primigravida with 37 weeks pregnancy was referred to our institute from a private hospital in view of eclampsia with history of 6-7 episodes of seizures at home. She had received loading dose of magnesium sulphate and was referred to our hospital. She was in a postictal phase and blood pressure was 170/100 mm of Hg. After initial stabilization and sending routine laboratory investigations, magnesium sulphate was continued by Zuspan’s regimen and tablet labetalol 200 mg BID was started in addition to α methyldopa QID and capsule nifedipine 10 mg QID. On abdominal examination, fetus seemed to have longitudinal lie and vertex presentation and hence pre-induction cervical ripening with intravaginal dinoprostone gel was done. She went into active labor, progressed rapidly and became fully dilated in 5 hours. Spontaneous rupture of membranes occurred. Per vaginal examination at this point revealed breech presentation and hence she was taken up for emergency cesarean section in view of breech presentation in labor.
On immediate examination of the neonate, there were no areas of hyperemia noted on the buttocks. The vital parameters and systemic examination of the neonate was within normal limits. However, after a few hours of birth, the mother noticed areas of mild hyperemia on the gluteal area of the baby, which soon became denuded as seen in the image.

Figure 1. Superficial burns on the gluteal region of the neonate.

There were no other skin lesions. These were diagnosed as superficial chemical burns due to undiluted chlorhexidine solution. The burns were treated with local antibiotic cream and healed soon without scarring. There were neither maternal complaints of vaginal burning or irritation nor remarkable findings suggestive of vaginal burns.


The image shows superficial chemical burns associated with area of erythema and superficial blistering over both buttocks of the infant. Skin irritation is the most common reported adverse event after chlorhexidine-cetrimide exposure. Preterm infants have immature skin with ineffective epidermal barrier as compared to that of term infants and hence they are susceptible to skin damage and absorption of potentially harmful substances.[3] There have also been reports of skin burns and skin irritation in preterm infants less than 48 hours of age after exposure to aqueous-based as well as alcohol based chlorhexidine gluconate-cetrimide solutions. Hence saline rinsing after antisepsis is recommended to avoid the same.[4]
Chlorhexidine gluconate-cetrimide used in appropriate dilution can be safe for per vaginal examinations barring idiosyncratic skin reactions. In fact, it was considered standard of practice to use manual swabs with chlorhexidine solution 0.25 % for every vaginal examination before delivery and babies born during the intervention were also wiped with chlorhexidine wipes. This intervention was found to reduce the early neonatal and maternal post-partum infectious morbidities.[5] Vaginal chlorhexidine-cetrimide mechanical wipes resulted in statistically significant reduction of colonization of neonates with gram positive beta hemolytic streptococcus.[6] In under-resourced settings, chlorhexidine-cetrimide solution can be used to prevent maternal peripartum and neonatal infections from the normal vaginal flora.[7]
However, as per the latest recommendations routine vaginal cleansing with chlorhexidine during labor for the purpose of preventing postpartum infections of the mother and the neonate is no longer recommended even in women with Group B streptococcus infection or colonization. Moderate quality evidence supports the use of vaginal cleansing with povidone iodine immediately before cesarean section to reduce incidence of post-cesarean endometritis alone. The guideline development group suggested the use of manual swabs with diluted povidone iodine (1-10% w/v) for a contact time of 30 seconds in the vagina, immediately after urinary bladder catheterization. The neonatal implication of the above intervention was a transient increase in neonatal iodine levels as observed in neonatal thyroid screening.[8]

In light of recent evidence and guidelines, the use of inexpensive and readily available povidone iodine solution is replacing chlorhexidine cetrimide solution for vaginal swabbing.

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  4. Chapman AK, Aucott SW, Gilmore MM, Advani S, Clarke W, Milstone AM. Absorption and tolerability of aqueous chlorhexidine gluconate used for skin antisepsis prior to catheter insertion in preterm neonates. J Perinatol. 2013;33(10):768-71.
  5. Taha TE, Biggar RJ, Broadhead RL, Mtimavalye LA, Justesen AB, Liomba GN, et al. Effect of cleansing the birth canal with antiseptic solution on maternal and newborn morbidity and mortality in Malawi: clinical trial BMJ 1997;315(7102):216-9.
  6. Stade B, Shah V, Ohlsson A. Vaginal chlorhexidine during labour to prevent early-onset neonatal group B streptococcal infection. Cochrane Database Syst Rev. 2004;(3):CD003520.
  7. Lumbiganon P, Thinkhamrop J, Thinkhamrop B, Tolosa JE. Vaginal chlorhexidine during labour for preventing maternal and neonatal infections (excluding Group B Streptococcal and HIV). Cochrane Database of Systematic Reviews 2014;9:CD004070.
  8. WHO Recommendations for Prevention and Treatment of Maternal Peripartum Infections. Geneva: World Health Organization.2015; pp32. Available at www.who.int/reproductivehealth/publications/maternal_perinatal_health/peripartum-infections-guidelines.

Mahanti S, Samant PY, Parulekar SV. Intrapartum Chemical Burns Of The Fetus. JPGO 2019. Vol 6 No. 7. Available from: https://www.jpgo.org/2019/07/intrapartum-chemical-burns-of-fetus.html

Management of Multifactorial Warfarin Toxicity

Author Information

Uppal M*, Samant PY**, Honavar PU***.
(* Junior Resident, ** Associate Professor, *** Assistant Professor, Department of Obstetrics and Gynecology, Seth G S Medical College and K E M Hospital, Mumbai, India.)


We present a rare case of warfarin toxicity leading to hemoperitoneum in a postpartum woman with mitral valve replacement, who incidentally underwent manual removal of placenta. Genetic studies for gene mutation confirmed wild genotype for CYP2C9 and heterozygous mutant for VKORC1. Aggravating factors like possible causal association of antibiotic interaction with warfarin, effect on the gut flora and management dilemma in a case of uterine perforation diagnosed on imaging are discussed.


Warfarin is used in the prevention and treatment of thromboembolism and in patients with mechanical heart valves. With a narrow therapeutic range, warfarin requires close monitoring.  Concomitant therapy with antibiotics may induce life threatening bleeding due to antibiotic and warfarin interaction.[1] Such bleeding may be considered as an obstetric pathology in pregnant and postpartum women. In some cases, even moderate amount of doses may cause toxicity due to gene mutation and severe bleeding.
Spontaneous hemoperitoneum is one such complication. Bleeding can also occur in extraperitoneal space. In such a state, even ordinary tissue handling may cause hematomas and unwarranted surgical intervention may be undertaken.[2] We report a case of warfarin induced hemoperitoneum, in whom clinical and radiological features were suggestive of uterine perforation.

Case Report

A 27 years old primipara, a known case of rheumatic heart disease with mitral valve replacement on warfarin prophylaxis presented to the casualty with pain in abdomen and abdominal distension since 7 days. There was no vaginal bleeding, vomiting or fever. Twenty days this presentation, intrauterine fetal demise (IUFD) at 29.6 weeks was diagnosed in a rural hospital where she was taking antenatal care. She was referred to the nearest district hospital. As per the history, after omitting warfarin and starting heparin, labor was induced with misoprostol for IUFD. She underwent manual removal of the retained placenta (MROP) under general anesthesia. Amoxycillin clavulinic acid and metronidazole were given to her. She was discharged after heparin to warfarin conversion and on tablet warfarin 8mg OD. As per the records, her international normalized ratio (INR) was 1.6 at discharge. After 3 weeks, she was taken to the district hospital for abdominal distension and pain of a week’s duration.  There her INR was more than 8.  Her warfarin was omitted. The relatives declined admission there and came to our center the next day. On presenting to casualty, the patient was conscious with cold clammy extremities. Her pulse rate was 100/ min with a blood pressure on 90/50 mm of Hg. She was started on inotropic support and was given one unit of whole blood and four units of fresh frozen plasma. On gynecological referral, abdominal examination showed no evidence of bruising. Abdomen was distended, soft with no guarding, rigidity or tenderness. There was evidence of free fluid on percussion. On speculum examination, there was no bleeding and cervix, vagina were healthy. Vaginal examination was indicative of an anteverted, well-involuted uterus and non-tender fornices with mild fullness. Her investigation revealed hemoglobin of 6.8 gm%, leucocyte count of 8000 /cm3, platelet count of 1,56,000/ cm3, Activated partial thromboplastin time (APTT) was normal. INR was 1.8 (after nearly 48 hours of omission of warfarin). Her renal and liver function tests were normal. Ultrasonography (USG) revealed a linear uterine wall defect measuring 11mm in length with an overlying organized hematoma measuring 4x2.4x6 cm around the fundus  suggestive of rupture and small hemorrhagic cysts in both adnexae. Computerized tomography (CT) confirmed the findings. The peritoneal covering seemed to contain the hematoma. In absence of other abdominal signs, the patient was managed conservatively. Periodic USG showed a gradual decrease in hemoperitoneum. Cardiology and hematology opinions were taken and heparin was restarted. Further investigations of the patient revealed a wild genotype for CYP2C9 (*1/*1) and heterozygous mutant for VKORC1 gene (AG). Heparin to warfarin conversion was done over a period of 3 weeks.  After close monitoring, the patient was discharged on tablet warfarin 7.5 mg daily and was advised to maintain INR in the therapeutic range by regular INR testing and cardiological monitoring. She was seen in the outpatient department two weeks after discharge and was doing well. Barrier contraception for at least 1 year, followed by USG for uterine scar of perforation was advised before planning next pregnancy.


Manual removal of placenta may rarely cause either incomplete rupture with intramyometrial and then vaginal bleeding or complete rupture with hemoperitoneum. Conservative approach or surgical intervention is decided upon depending on the presentation.[3] In this case,manual removal causing the reported rupture occurred nearly three weeks before the presentation. It must have caused minor trauma. There was no alarming vaginal bleeding probably because of the well controlled coagulation factor levels at the time of delivery and MROP. In this duration, the patient was asymptomatic and her bowel function was normal. Once under observation, the periuterine hematoma did not grow in size and her hemoglobin level was maintained. Hence, conservation in an otherwise high risk patient was thought to be the safest strategy. Amoxycillin clavulinic acid and metronidazole were given in this case as prophylaxis for infective endocarditis and intrauterine intervention primarily. There is a routine practice of giving an anaerobic cover with metronidazole in obstetric surgeries.  Antibiotics destroy gut flora that produce vitamin K. Amoxycillin-clavulinic acid is also found to cause warfarin toxicity.[4] Metronidazole and warfarin co-administration is found to be responsible for derangement of INR and studies have demonstrated that in patients on concomitant warfarin and metronidazole therapy, preemptive reduction by about 30% in warfarin dose helps maintain INR in therapeutic range.[5] As the drugs were stopped, INR probably reverted soon, hence it was not in toxic levels at presentation. The type of mutation and wild genotype of this case would require warfarin dose in the range of 5 to 7 mg [6] and our patient was on 8 mg warfarin. There is a possibility that all these factors were possible for the presentation of hemoperitoneum and subserosal hematoma.


Warfarin is a double-edged sword and while co administering antibiotics, possible drug interaction has to be taken into account. It is also advisable to know the CYP2C9 genotype of the patient requiring long-term warfarin therapy. Newer anticoagulants like dabigatran lower the bleeding risk and may be offered, but the price may be prohibitive.

  1. Baillargeon J, Holmes HM, Lin YL, Raji MA, Sharma  G, Kuo YF. Concurrent use of warfarin and antibiotics and the risk of bleeding in older adults. Am J Med. 2012 Feb;125(2):183–9.
  2. Anuhya V, Madhystha S, Nayak V, Soundarrajan G, Acharya R. Need of the hour: Warfarin-induced massive intraperitoneal bleed. J Pharmacol Pharmacother 2018;9(1):49-51.
  3. Barden G, Corkhill V, Rajagopalan C. Conservative management of uterine perforation following manual removal of placenta. Archives of Disease in Childhood - Fetal and Neonatal Edition 2010; 95(1):Fa86.
  4. Larsen TR, Gelaye A, Durando C. Acute warfarin toxicity: An unanticipated consequence of amoxicillin/clavulanate administration. Am J Case Rep. 2014;15:45–48. Published 2014;15:45-8.
  5. Holt KK, Anderson EA, Cantrell MA, Shaw RF, Egge JA. Preemptive dose reduction of warfarin in patients initiating metronidazole. Drug Metabol Drug Interact. 2010;25(1-4):35-9.
  6. Dean L. Warfarin Therapy and VKORC1 and CYP Genotype. 2012 Mar 8 [Updated 2018 Jun 11]. In: Pratt V, McLeod H, Rubinstein W, Dean L, Kattman B, Malheiro A, editors. Medical Genetics Summaries [Internet]. Bethesda (MD): National Center for Biotechnology Information (US); 2012. Available from: https://www.ncbi.nlm.nih.gov/books/NBK84174

Uppal M, Samant PY, Honavar PU. Management of Multifactorial Warfarin Toxicity. JPGO 2019. Vol. 6 No. 7. Available from: https://www.jpgo.org/2019/07/management-of-multifactorial-warfarin.html

Remembering Past Greats: Lorenzo Sazie

Author Information

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

Lorenzo Sazie was born in Asson, France on 16 July 1807.  Though his parents wished that he take up a clergy-related career, he had an excellent academic inclination. He first earned a Bachelor in humanities. His achievements were unstoppable and he went on to complete his medical degree in November 1833, at an age much lesser than his peers. It is notable that great medical pioneers were his teachers. These included Laennec, Velpeau, Dubois and Dupuytren. Destiny brought him to the South American country of Chile where he began practice as professor of obstetrics. It is to be noted that he may have been one of the first to use a stethoscope and use surgical instruments like forceps in the country. He is also credited to have been the first doctor to give general anesthesia for surgery.[1] Just like the multiple instances in history, Sazie was also met with resistance and viewed with suspicion when he brought a large armamentarium of medical equipment along with him. However, he learnt the local language quickly and gained the confidence of his patients and his peers.
He founded the Midwifery school for obstetricians in 1834, thereby establishing the first course of obstetrics in the country. The autonomy he envisaged to this school was quite forward for those times.[2] He was an inspiring personality and brought many people to cooperate with him by his influential speeches and write-ups. The speech he gave to future midwives during the inauguration of the course is particularly well documented.[3]

He was a French citizen all along, and the government conferred on him Chilean nationality honoring the yeoman contribution given to the advancement of medicine and surgery, and specifically to obstetrics. Such was his contribution that he was also ordered the knighthood and legion of honor from the French government.

The national medical system of the country, and development of a medical care in the relatively backward country was pioneered by Sazie and Andres Bello. They also put together a standardization of foreign medical degrees to suit local needs and also publicized the status of the country’s medical status to the world. Dr Sazie and his peer, Dr Blest were instrumental in shaping the medical school in Chile. A number of future stalwarts were mentored by these two.[4] He was the first dean of the Faculty of Medicine of the University of Chile between 1843 and 1851, his second term as Dean was exercised between 1855 and 1863. There were many improvements which occurred in the medical, political and cultural atmosphere in Chile during his second period as the Dean of Faculty of medicine. It was during this period that he passed away from typhoid fever which he acquired while tending to patients during the epidemics in Santiago which struck in 1865.[5]

The University of Atacama holds an award for the highest distinction for midwives bearing the name “Lorenzo Sazie Award” to appreciate outstanding contribution to the profession.
The only son of Lorenzo with Rosario Heredia was Carlos Sazié Heredia who went onto become a prominent psychiatrist/neurologist.[6]

This 3rd week of July we celebrate the birthday of a stalwart in Obstetrics and Gynecology, whose career and achievements will continue to inspire many generations of students; past, present and future.

  1. Lorenzo Sazie. Available from: https://es.wikipedia.org/wiki/Lorenzo_Sazi.
  2. Lorenzo sazie. Available from: http://www.icarito.cl/2009/12/lorenzo-sazie-in.shtml/
  3. Costa C. [The speech of Dr. Lorenzo Sazie at the inauguration of the course in obstetrics (1835)]. [Article in Spanish] Rev Med Chil. 1984;112(3):297-300.         
  4. Pérez-Olea J. [The school of Blest and Sazie]. [Article in Spanish] Rev Med Chil. 1993;121(11):1332-9.
  5. Pérez-Olea J. [Lorenzo Sazie. His 2nd and 3rd deanships]. [Article in Spanish] Rev Med Chil. 1992;120(4):457-63.
  6. Doctor Lorenzo Sazie. Availeble from: https://www.sellos.uchile.cl/egregios3.html.

Prasad M, Venkatesh S. Remembering Past Greats: Lorenzo Sazie. JPGO 2019. Volume 6 No.7. Available from: https://www.jpgo.org/2019/07/remembering-past-greats-lorenzo-sazie.html