Volume 2 Issue 1, January 2015

Editorial
Parulekar SV

A Cesarean Scar Ectopic Pregnancy: Conservative Management
Desale S, Gupta AS.

Pregnancy In A Case Of Methemoglobinemia -A Rarity
Dudhe M, Khadkikar R, Saxena N, Chauhan AR.

A Leiomyoma Which Won’t Enucleate
Parulekar SV, Fernandes G.

Genitourinary Tuberculosis In Pregnancy.
Pandey I, Thakur H, Gupta AS.

Vertical transmission of Salmonella typhi
Poonia S, Satia MN, Torame VP, Natraj G.

Female Genital Tuberculosis: An unusual presentation
Chawla LJ, Mirchandani A, Mayadeo NM, Chakre S.

A Rare Case Of Complex Mullerian Anomalies With Partial Aplasia Of Pancreas
Valvi D, Parulekar SV, Kulkarni S, Hira P.

Budd Chiari Syndrome With Shunt Obstruction In Pregnancy
Kumari P, More V, Panchbudhe S, Satia MN.

Ovarian Cancer With Pus-Like Fluid
Parulekar SV, Fernandes G.

Genital Tuberculosis - Hysterosalpingography
Parulekar SV

Quiz January 2015


Editorial

JPGO has completed one year. It has been an interesting time. We did not opt for software that made all processes of publication automatic, but chose to do everything ourselves. Preparing the design and layout of the journal's website, coding to make it work, getting peer reviews, editing, uploading articles and images, and getting the journal indexed was a lot of hard work. Managing it along with our clinical, teaching and research work and meeting the deadline of the first of every month was taxing, but rewarding too. It has kindled an academic interest in resident doctors in the institute. It has improved their thought process and writing skills tremendously. It has also generated a lot of interest in the scientific community outside our institute, as is evident from the ever expanding readership of the journal. We introduced 'quiz' based on the articles published in each issue, to help assess our postgraduate students. That was a great success. From this issue, we have introduced another section on 'image'. Various interesting images will be published. The idea is based on the fact that in clinical management, one has to make rapid decisions based on what one sees. Analytical discussion of interesting images should help clinicians and students sharpen their skills further.

An ovary can be a seat of a number of conditions, both functional and organic. Its lesions can be small to large, cystic, solid or solid-cystic. Organic lesions can be neoplastic or nonneoplastic. There is a particular group formed by large cystic lesions that is of current interest. Mucinous cystadenoma, mucinous borderline tumor and mucinous cystadenocarcinoma form a part of this group. They can be quite large tumors. Serous cystadenomas and carcinomas are not so large. A benign cystic teratoma can sometimes be large, though usually it is moderate sized. Nonneoplastic cysts in the ovary include simple follicular cyst, corpus luteal cyst, hemorrhagic cyst, and endometrioma. Of these, an endometrioma can be large. A primary ovarian abscess is rare, and usually an acute condition. Sometimes a tubo-ovarian abscess heals and gets converted into a cyst. It may mimic an ovarian neoplasm at laparotomy and even during histopathological examination. Rarely an abscess may develop in an endometriotic cyst. An actinomycotic abscess can be very large. It is usually associated with the use of an intrauterine device. Chronic ovarian abscess is an uncommon presentation of ovarian tuberculosis. A hydatid cyst of the ovary is another uncommon condition. Usually differentiation of the cystic lesions of the ovary can be done by clinical examination, ultrasonography, and computed tomography in selected cases. A cystic lesion of the ovary may need magnetic resonance imaging for differentiation during pregnancy, when ultrasonography proves to be inadequate for that purpose. In this issue we have two interesting case reports. One is of a large ovarian abscess of tuberculous etiology in a young virginal girl. What is unusual in this case is that there was a slow leak of the pus from the abscess into the peritoneal cavity producing a large peritonitis, without involvement of any other organ by the disease. The other case is that of a large mucinous cystadenocarcinoma in a young virginal girl, who was asymptomatic. The tumor contained a large volume of fluid which appeared like pus, but was sterile. Such varied presentations of large ovarian cystic masses need to be known to practicing gynecologists, so that they can manage an unusual case better, should they encounter one. That is the reason we have presented these two cases in this issue.

A Cesarean Scar Ectopic Pregnancy: Conservative Management

Author Information

Desale S*, Gupta AS**.
(* Fourth Year Resident, ** Professor, department of Obstetrics and Gynecology, Seth GS Medical College & KEM Hospital, Mumbai, India)

Abstract

A case report of first-trimester Cesarean scar pregnancy treated with systemic Methotrexate (MTX) followed by oral Mifepristone therapy is presented. It is the rarest kind of ectopic pregnancy and may lead to severe life threatening complications such as uterine rupture and severe hemorrhage or may have adverse effect on future fertility. Hence it is important to have early and accurate diagnosis to avoid complications and preserve fertility.

Introduction

Ectopic pregnancy is an important cause of maternal morbidity and mortality. Of all reported pregnancies 1 to 2% are ectopic, which include the cesarean / hysterotomy scar ectopic pregnancy whose incidence is about 6.1% of all ectopic pregnancies.[1] Cesarean scar pregnancy is a rare type of ectopic pregnancy defined as a gestation completely surrounded by myometrium and fibrous tissue of previous scar, separate from endometrial and endocervical cavities. It occurs when pregnancy implants in the area of the previous cesarean scar. Presence of microscopic tracts from the scar site in the cavity into the myometrium allows the blastocyst to implant wholly within the myometrium.[2] Treatment includes surgical and medical therapy with Methotrexate, or Mifepristone.

Case Report

A 35 year old G3P1L1A1 at 5.3 weeks of gestation was referred from a private hospital with the diagnosis of cesarean scar pregnancy. At presentation the patient had no complaints of abdominal pain, vaginal bleeding, or syncopal attack. Her past obstetric history included preterm lower segment cesarean sections done 13 years back and a spontaneously abortion at 2 months of gestation 4 years back. Check curettage was not done. On examination vital parameters were stable. Abdomen was soft; there was no guarding, rigidity or tenderness on palpation. There was a Pfannenstiel scar. On speculum examination no bleeding was seen. Her serological and biochemical preoperative investigations were done.  Hemoglobin was 13.1 g/dL.  All other investigations were in their normal range. Ultrasonography (USG) revealed a gestational sac with yolk sac and peripheral ring vascularity at the previous scar site. Mean sac diameter was 9 mm corresponding to 5.5 weeks of gestation. No fetal pole was seen. Endometrial and endocervical cavities were empty and both  ovaries were normal. Endometrial thickness was 7 mm. 


Figure 1.  Transabdominal USG image of scar ectopic pregnancy; gs and thick arrow: gestational sac, ut: uterus. Thin arrow the scar of LSCS (anterior myometrium); green line posterior part of the anterior wall myometrium.


Figure 2. Transabdominal USG image of scar ectopic pregnancy; arrow mark: gestational sac.

The serum level of ß-HCG on day 0 was 4309 mIU/mL. Since the patient was stable option for medical treatment was taken. Injection Methotrexate 0.5mg/m2 , total dose of 80 mg was given intramuscularly. The patient was followed up on day 9 with serum β HCG. The serum β HCG increased to 18,223 mIU/mL. USG on day 11 showed gestational sac diameter had increased to  1 cm corresponding to 6.2 weeks and yolk sac was present. In view of increase in serum βhCG level and USG finding, tablet Mifepristone 200 mg was given orally. The patient further followed up on day 15 with serum βhCG which was 12,168 mIU/mL and on day 30 was 2264 mIU/mL. She had her normal menstrual cycle on day 34. On day 54 serum βhCG was 387 mIU/mL. USG reported increase in gestational sac diameter to 31 mm , irregular and without any yolk sac or fetal pole in anterior myometrium as seen in Figure 3. The patient remained hemodynamically stable throughout follow up.


Figure 3. Post treatment transvaginal USG. gs: irregular gestational sac; b: empty bladder; A is  myometrium anterior to sac and P is  myometrium posterior to gestational sac


Figure 4. The decreasing trend of serum β HCG after Methotrexate followed by Mifepristone treatment.

Discussion

Cesarean scar ectopic pregnancy is very rare condition with increasing trend of incidence.[3] This is because of increasing rate of cesarean section and newer advances of diagnostic technology. As the cesarean scar ectopic pregnancy is very rare, there are no ideal management options available. The treatment options depend on the  patient’s hemodynamic condition, severity of vaginal bleeding, gestational age, βhCG levels, demonstration of fetal cardiac activity, need for future childbearing, and the available infrastructure and expertise. A patient with uncontrolled bleeding and/or uterine rupture usually requires surgical management. Surgical management includes conservative and radical procedures. The conservative procedures include evacuation of the pregnancy or trophoblastic tissue, wedge resection and repair of the scar either by laparotomy or laparoscopy; bilateral ligation of anterior division of iliac artery and dilatation and curettage.[3] A radical procedure like hysterectomy is done in patients with uterine rupture not willing for conservation of uterus or having  uncontrolled bleeding. Medical management is done in patients with stable vital parameters and minimal or no bleeding. Medical management includes local or systemic injection of Methotrexate. The medical management requires long duration follow up. Complications in medical management like bleeding, failure of resorption or persistence of ectopic pregnancy, morbid adherence of placenta in future pregnancy may later require surgical management.[4] Also there is a possibility of long term complications like scar dehiscence, scar rupture, and repeat cesarean scar ectopic pregnancy. The surgical repair of the scar is recommended before the next conception following Methotrexate treatment.[1] The success of Methotrexate depends on serum βhCG level, size of ectopic pregnancy and cardiac activity. High success rate is found if serum βhCG level is less than 3000 IU/L. Patient’s with serum βhCG levels more than 3000 IU/L can have good outcome, but require long follow up, repeat doses of Methotrexate and higher medical cost.[1,5] The presence of fetal cardiac activity on USG has poor success with medical management.[5] The local injection of Methotrexate into the gestational sac is a satisfactory form of treatment of cesarean scar pregnancy.[4]  The follow up of medical management is done by serum βhCG which is marker of trophoblastic viability. Other parameters used for monitoring are gestational sac volume and degree of vascularity.[6]  In our case, as the patient was having stable vital parameters with minimal bleeding,  medical treatment with Methotrexate was given. The 15% drop between two βhCG levels at an interval of a week  is expected with Methotrexate treatment. In our case the serum βhCG rose by 425%. As our patient did not develop any bleeding, 200 mg of Mifepristone was given for further treatment. Mifepristone is an antiprogesterone drug used in medical termination of pregnancy in the first  trimester. The anti-progesterone activity of Mifepristone helps to destroy and detach the chorionic villi, thus making Methotrexate more effective. With use of Mifepristone there was a 33% fall seen in serum βhCG level within one week. The fall continued on further follow up. USG showed an increase in the size of the gestation sac when quantitative βhCG level was 387 mIU/mL probably due to bleeding that occurred due to detachment of the chorionic villi.  A meta-analysis has reported the more effective use of  combination therapy of Methotrexate and Mifipristone over Methotrexate alone [7].  

Conclusion

Combination therapy of Methotrexate and Mifepristone is found to be effective with less requirement of repeated dose of Methotrexate avoiding its side effects. Further studies are required for evaluation of combination therapy of Methotrexate and Mifepristone or Mifepristone alone in management of cesarean scar ectopic pregnancy.

References

1.      Seow K.M, Huang L.W, Lin Y.H, Lin. M. Y., Tsai Y.L and  Hwang J.L, Cesarean scar pregnancy: issues in management. Ultrasound Obstet Gynecol 2004; 23: 247–253.
2.   Godin P. A, Bassil S, and Donnez J, “An ectopic pregnancy developing in a previous caesarian section scar,” Fertility and Sterility, 1997; 67(2):398–400.
3.   Rotas MA, Haberman S, Levgur M: Cesarean scar ectopic pregnancies: etiology, diagnosis, and management. Obstet Gynecol 2006, 107:1373-1381.
4.  Hasegawa J, Ichizuka K, Matsuoka R, Otsuki K, Sekizawa A, and Okai T, “Limitations of conservative treatment for repeat Cesarean scar pregnancy,” Ultrasound in Obstetrics and Gynecology, 2005; 25(3): 310–311.
5.      RCOG, The Management Of Tubal Pregnancy. Green top Guideline No. 21, May 2004, Reviewed 2010; 3-4.
6.   Timor-Tritsch IE, Monteagudo A, Santos R, Tsymbal T, Pineda G,  Arslan A A. The diagnosis, treatment, and follow-up of cesarean scar pregnancy. Am J Obstet Gynecol 2012; 207:44.1-13.
7.  Gazvani M.R, Baruah D.N, Alfirevic Z and Emery S.J. Mifepristone in combination with Methotrexate for the medical treatment of tubal pregnancy: a randomized, controlled trial Human Reproduction1998 ;13(7) 1987–1990.

Citation

Desale S, Gupta AS. A Cesarean Scar Ectopic Pregnancy: Conservative Management. JPGO 2015. Volume 2 No. 1. Available from: http://www.jpgo.org/2015/01/a-cesarean-scar-ectopic-pregnancy.html

Pregnancy In A Case Of Methemoglobinemia

Author Information

Dudhe M*, Khadkikar R**, Saxena N*, Chauhan AR***
(* Third Year Resident, ** Assistant Professor, *** Additional Professor. department of Obstetrics and Gynecology, Seth GS Medical College & KEM Hospital, Mumbai, India)

Abstract

Methemoglobin is an oxidized form of hemoglobin with iron in the ferric form instead of the usual ferrous form, which results in decreased availability of oxygen to the tissues. Methemoglobinemia occurs when red blood cells contain methemoglobin higher than 1%. It is a well-known but frequently forgotten cause of hypoxia and respiratory distress in patients of all ages. [1] As most patients are asymptomatic, congenital form may be diagnosed for the first time during pregnancy. We report a primigravida with congenital methemoglobinemia who was treated with injection methylene blue prior to emergency lower segment cesarean section (LSCS) for abruptio placentae.

Introduction

Methemoglobin, along with carboxyhemoglobin and sulfhemoglobin, are types of dyshemoglobin   i.e. a type of haemoglobin that does not bind with oxygen. [2]
Tissue hypoxia is due to reduction in levels of free haemoglobin and hence difficulty in release of oxygen. Congenital methemoglobinemia is a rare genetic abnormality in which patient is mostly asymptomatic and only presents with cyanosis which may be present since birth. [3] During pregnancy, it may lead to uteroplacental insufficiency causing intrauterine growth retardation, oligohydramnios, severe preeclampsia and abruption. [4]

Case Report

A 23 year old primigravida,  known case of  congenital methemoglobinemia was admitted in our tertiary care hospital at 34 weeks’ of gestation for evaluation of pedal edema. Significant finding at this time was methemoglobin level of 25%. Hematologist opinion was sought; no active treatment was advised except to continue tablet vitamin C twice daily. Obstetric evaluation and other investigations were normal hence patient was discharged.
On past history, patient had mild cyanosis since birth but was diagnosed with congenital methemoglobinemia only 4 years ago, when she presented with breathlessness not responding to oxygen along with slate grey cyanosis. At that time, cardiovascular and respiratory system examination were normal and all routine investigations were normal. G6PD enzyme activity was normal. However, methemoglobin levels were significantly elevated (44%), and nicotinamide adenine dinucleotide (NADH) cytochrome b5 reductase activity was decreased. She was started on tablet vitamin C and multivitamin twice a day. At 38 weeks of gestation, patient was readmitted in early labour. On examination, she had cyanosis, her pulse was 92/ min, blood pressure was 130/ 90 mm of Hg, urine albumin was 2+. Blood drawn for investigations was chocolate brown in colour. ABG showed oxygen saturation of 92 %. In view of foetal distress and signs of abruption, decision for emergency LSCS was taken. Urgent haematology opinion was sought; repeat urgent methemoglobin levels were not possible hence based on recent report of methemoglobin 25 %, patient was given intravenous 1 mg/ kg (50 mg) methylene blue in 500 ml normal saline over 30 minutes prior to commencement of LSCS. Patient underwent emergency LSCS in view of abruptio placenta under general anaesthesia, with high doses of oxygen. LSCS was uneventful; she delivered a male child of 2.6 kg with Apgar score of 9/10. Repeat methemoglobin level postoperatively was 3.3%. Patient was stable and was discharged on day 7.  

Discussion
Hemoglobin can transport oxygen only when the iron is in ferrous form. When hemoglobin loses an electron, the iron atom is converted to the ferric state, forming methemoglobin. This causes leftward shift of the oxygen-hemoglobin dissociation curve, hence decreased release of oxygen to the tissues, and hence clinical manifestations.
Normally, the methemoglobin level is < 1 %; this low level is maintained by 2 mechanisms. The first is the hexose-monophosphate shunt pathway within the erythrocyte, where oxidizing agents are reduced by glutathione. The second mechanism requires NADH and nicotinamide adenine dinucleotide phosphate (NADPH) to reduce methemoglobin to its original ferrous state. Methemoglobinemia results from a redox imbalance, either due to decrease in the activity of reducing enzymes (congenital form) or excessive oxidization of haemoglobin (acquired form).
Congenital methemoglobinemia is very rare and is of two types: one due to NADH methemoglobin reductase enzyme deficiency, which is autosomal recessive and the other due to an abnormal oxygen affinity hemoglobin termed hemoglobin M, which is autosomal dominant; our patient had the former deficiency.[1]
Acquired form is more common, and may occur when erythrocytes are affected by oxidizing agents like acetaminophen, anticonvulsants, nitrofurantoin, sulphonamides, valproic acid, dapsone, nitroglycerin, topical anaesthetic agents like benzocaine, and volatile organic compounds.[2] Occasionally it may occur secondary to pathologic conditions like sepsis, sickle cell crisis, and gastrointestinal infections in children.[2]

Presence of cyanosis without any cardiopulmonary disorder or decrease in oxygen saturation, and an appearance of “more blue than sick” are diagnostic.[1] Symptoms depend upon percentage of methemoglobin in blood:

<3%
asymptomatic
3 – 15 %
grayish skin color
15 - 30 %
cyanosis and chocolate brown blood
30 – 50 %
dyspnea, headache, fatigue, dizziness, syncope, with oxygen saturation as low as 80 %, as seen in our case
50 – 70 %
tachypnea, metabolic acidosis, cardiac arrhythmias, seizures, CNS depression and coma [2]

Organs with high oxygen demands i.e. central nervous system and cardiovascular system are usually the first to manifest toxicity. Main symptoms include central cyanosis not responding to oxygen, and in severe cases altered mental status, convulsions and coma leading to death when level rises to 70%.
Most common complications during pregnancy include anemia, threatened abortion, preterm labor, pregnancy induced hypertension, IUGR, and placental abruption. [4] These changes may be a result of hypoxia, excessive production of free radicals, resultant oxidative damage to cellular membranes and DNA.  Monitoring of methemoglobin concentrations in maternal blood is a reliable indicator of effects of free radicals and oxidative states. Our patient presented with pregnancy induced hypertension and placental abruption for which emergency LSCS was performed. Environmental toxins like nitrogen oxides, sulphur dioxide and their metabolites over longer periods, cause maternal vascular endothelial dysfunction from early pregnancy. There is no definitive treatment for hereditary methemoglobinemia which is a chronic and mild condition. Treatment depends upon symptoms and level of methemoglobin. Chronic mild forms are given ascorbic acid (which acts as reducing agent), riboflavin and N-acetylcystine to reduce oxidative damage.
Primary emergency treatment includes administration of intravenous methylene blue in symptomatic cases. It is a thiazine dye with dose-dependent antiseptic and oxidizing properties.  Methylene blue activates NADPH methemoglobin reductase, resulting in reduction of  methylene blue to methylene leucoblue, which transforms methemoglobin into normal hemoglobin by a non-enzymatic mechanism. Methylene blue restores the iron in hemoglobin to its normal oxygen-carrying state by providing an artificial electron acceptor for NADPH methemoglobin reductase. Methemoglobin level falls significantly 30 to 60 minutes after the first dose; in our case we commenced LSCS within 30 minutes of methylene blue. [2] Rapid intravenous administration or higher doses can cause thoracic pain, dyspnoea, hypertension, diaphoresis and haemolysis. It should be administered carefully in patients with renal failure; it is slowly excreted by the kidneys and the urine has a bluish tint.
Exchange transfusion or hyperbaric oxygen is suggested treatment options in resistant cases and in G6PD deficient individuals in whom methylene blue is contraindicated. Combined efforts of hematologist, obstetrician and anesthetist contributed towards effective management of this case.

References

1.      Palaniappan S, Aan GJ, Ken CC. Case report in congenital methemoglobinemia in pregnancy Research Updates in Medical Sciences (RUMeS) 2013; 1:30-32. The internet journal of obstetrics and gynecology. Available from: http://rumesjournal.com/sites/default/files/articles/pdf%20choo%20%282%29.pdf
2.   Nascimento TS, Pereira ROL and Mello HLD, Costa J. Methemoglobinemia: from Diagnosis to Treatment. The internet journal of obstetrics and gynecology. 2008; 58(6):651-664
3.      Pepper G, Weinstein HG, and Heller P. Congenital methemoglobinemia in pregnancy. The journal of American medical association. 1961; 177(5):328-330. Available from: http://jama.jamanetwork.com/article.aspx?articleid=331509
4.   Mohorovic L. The role of methemoglobinemia in early and late complicated pregnancy. Medical hypothesis. 2007;68(5):1114-1119. Available from: www.mdpi.com

Citation

Dudhe M, Khadkikar R, Saxena N, Chauhan AR. Pregnancy In A Case Of Methemoglobinemia -A Rarity. JPGO 2015. Volume 2 No. 1. Available from: http://www.jpgo.org/2015/01/pregnancy-in-case-of-methemoglobinemia.html

A Leiomyoma Which Won’t Enucleate

Author Information

Parulekar SV*, Fernandes G**.
(* Professor and Head, department of Obstetrics and Gynecology, ** Associate Professor, department of Pathology; Seth GS Medical College & KEM Hospital, Mumbai, India)

Abstract

Endometrial stromal sarcoma is a very rare malignant tumor of the uterus. Usually it is mistaken for a uterine leiomyoma clinically, and the diagnosis is usually made after surgical removal. We present a case that was suspected during myomectomy and was managed by hysterectomy. Histopathology confirmed the diagnosis.

Introduction

Endometrial stromal sarcoma (ESS) is a very rare malignant tumor of the uterus. It accounts for about 0.2% of all uterine malignancies. Usually it is an intramyometrial tumor, and cannot be diagnosed clinically. Its presence can be suspected by imaging preoperatively. We present an unusual case that presented as a submucous polyp in the uterine cavity. This diagnosis was suspected during a failed attempt at myomectomy, and was confirmed by histopathology later.

Case Report

A 42 year old woman with two term deliveries in the past presented with abnormal uterine bleeding for four months. She had prolonged and excessive blood loss during menstruation and in between menses too. Her past menstrual cycles had been regular and with moderate flow over 3 to 4 days. Her last delivery had been 10 years ago. She did not use any contraception. General examination showed moderate pallor. Her vital parameters were normal. Systemic examination showed no abnormality. Gynecological examination showed uterus enlarged to a size of about 12 weeks of gestation. The cervix was 2 cm open, 30% effaced. The vagina was normal. There were no pelvic or abdominal masses. Abdominopelvic ultrasonography (USG) showed a 6.5 cm diameter polypoid mass arising from the anterior wall of the endometrial surface of the uterus. There was no lymph node enlargement or hepatic metastasis. Her blood sugar level, hepatic and renal function tests, chest radiograph and electrocardiogram were normal. Her hemoglobin level was 6 g/dL. She was transfused 4 units of packed cells over 4 days. Polypectomy was undertaken under general anesthesia. The posterior cervical wall was cut in the midline up to the internal os, so as to enable enucleation of the polyp. The mass was spherical, more than 75% of it projecting into the uterine cavity. There was no pedicle. The mass was held with a tenaculum and a vulsellum. Its capsule was bluntly dissected by digital pressure and attempt was made to dissect and enucleate it from its bed (figure 1). That attempt failed. Its removal was attempted by holding it firmly and twisting it clockwise. However it delivered piecemeal and could not be delivered in its entirety. There was no bleeding from the mass left behind. A diagnosis of a degenerated leiomyoma or a tumor like an ESS was made, the reason being the inability to enucleate it despite ease of access. After closure of the cervicotomy, the patient started bleeding vaginally, though not from the cervical os. A uterine wall injury could not be ruled out. So an abdominal hysterectomy was done. There was no uterine injury. The bleeding was from a cut edge of the cervicotomy incision, which had not been diagnosed before. There was no spread of the disease to the omentum, bowel, parietal peritoneum, pelvic or paraaortic lymph nodes and liver. About one-third of the mass was seen to be left behind, when the uterus was opened after the hysterectomy (figure 2). The patient made an uneventful recovery.
Gross examination showed full thickness involvement of the myometrium by the tumor, but serosa was intact.Histopathology of the tumor (figures 3-6) showed sheets and tongues of neoplastic endometrial stromal cells extensively invading the full thickness of the myometrium. The serosa was intact. The tumor cells were monotonous in appearance, oval shaped, with basophilic mildly atypical nuclei and scanty cytoplasm. A prominent delicate arborising vasculature was seen throughout the tumor. The tumor cells resembled proliferative endometrium and whorling of the neoplastic cells was seen around the arterioles. 2-3 mitosis per 10 HPF were seen. No necrosis was seen. A diagnosis of low grade endometrial stromal sarcoma was made.


Figure 1. Process of attempt at enucleation of the polyp after posterior cervicotomy.


Figure 2. Uterus cut open after abdominal hysterectomy to show partially enucleated tumor.


Figure 3. Microphotograph showing tongues of bluish neoplastic endometrial stromal cells infiltrating and splaying the smooth muscle of the myometrium. (H&E x100)


Figure 4. Microphotograph showing sheets of bluish endometrial stromal cells seen extensively invading the myometrium. (H&E x100)


Figure 5. Microphotograph showing tumor with monotonous oval endometrial stromal cells with prominent delicate arborising vasculature. (H&E x100)


Figure 6. Microphotograph showing high power view of the neoplastic endometrial stromal cells resembling proliferative endometrium. Note the whorling of tumor cells around the arterioles. (H&E x400)

Discussion

Endometrial stromal sarcoma is a very rare malignant tumor of the uterus. As compared to other malignancies, it tends to occur in younger women, the mean age being 50 years.[1] About 10 to 25% cases are premenopausal. [1] The term endometrial stromal tumor is applied to tumors composed of cells that resemble endometrial stromal cells of the proliferative endometrium. The new WHO classification classifies endometrial stromal tumors into endometrial stromal nodule, low grade endometrial stromal sarcoma and undifferentiated endometrial sarcomas. ESS is said to be predisposed to by conditions like unopposed estrogen action, tamoxifen therapy and polycystic ovarian disease.[2] Though the tumor primarily is intramyometrial, it involves the endometrium in a number of cases. Endometrial curettage in such cases may help make the diagnosis.[3,4] The patients present with abnormal uterine bleeding (90%), uterine enlargement (70%), pelvic pain, and/or dysmenorrhea. About 25% cases are asymptomatic. The diagnosis of uterine leiomyoma is usually made. USG often erroneously shows features of a leiomyoma or adenomyosis, as in our case. Transvaginal color Doppler study shows low impedance flow as compared to other benign conditions of the uterus. On magnetic resonance imaging, ESS shows myometrial invasion and bands of low signal intensity in that area (due to worm-like permeation of tumor cells) and spread by contiguity to fallopian tubes, ligaments, ovaries, and along blood vessels.[5,6] However these tests are not done routinely, because the clinical diagnosis of a leiomyoma or adenomyosis, supported by USG, does not warrant these tests. If the mass appears to be a polyp, there is even less indication for these tests, as in our case. That is unfortunate, because about 50% cases have an extrauterine spread at the time of the diagnosis.[1] Luckily, our patient had to undergo an immediate hysterectomy because of incomplete removal of the mass and suspected uterine injury. We did not perform bilateral salpingooophorectomy at that stage, because we did not know it was a malignant tumor. Total hysterectomy was adequate for her stage of the disease (stage I). Obtaining a frozen section during the operation is not useful in making a diagnosis. If the condition is strongly suspected, a biopsy may be taken before definitive treatment is planned. It is easier when it is a submucosal mass that can be seen through the cervix, as in the case presented. Prolonged follow up is required in all cases, as about 30-50% cases develop recurrences in the pelvis and lower genital tract, and sometimes in lungs years later.[7]

References

1.      Tavassoli FA, Devilee P. WHO Classification of Pathology and genetics of tumours of the breast and female genital organs. In: Tavassoli FA, Devilee P, editors, Lyon, France: IARC Press; 2003. p. 233-6.
2.      Cohen I. Endometrial pathologies associated with postmenopausal tamoxifen treatment. Gynecol Oncol 2004;2:256-66.
3.      Jin Y, Pan L, Wang X, Dai Z, Huang H, Guo L, et al. Clinical characteristics of endometrial stromal sarcoma from an academic medical hospital in China. Int J Gynecol Cancer 2010;20:1535-9.
4.      Ganjoei TA, Behtash N, Shariat M, Low AM. Grade endometrial stromal sarcoma of uterine corpus: A clinicopathological and survey study in 14 cases. World J Surg Oncol 2006;4:50.
5.      Toprak U, Paaolu E, Karademir MA, Gülbay M. Sonographic, CT, and MRI findings of endometrial stromal sarcoma located in the myometrium and associated with peritoneal inclusion cyst. AJR Am J Roentgenol 2004;182:1531-3.
6.      Oliva E, Clement B, Young RH. Endometrial stromal tumours: An update on a group of tumours with a protean phenotype. Adv Anat Pathol 2000;7:257-81.
7.      Kim GY, Sung P, Han J, Park JO, Lee KS. Pulmonary metastases of uterine endometrial stormal sarcoma: Diffusemicronodular and ground glass opacities: A case report. J Korean Med Sci 2004;19:901-3.
8.      Reich O, Nogales FF, Regauer S. Gonadotropin-releasing hormone receptor expression in endometrial stromal sarcomas: An immunohistochemical study. Mod Pathol 2005;18:573-6.

Citation

Parulekar SV, Fernandes G. A Leiomyoma Which Won’t Enucleate. JPGO 2015. Volume 2 No. 1. Available from:  http://www.jpgo.org/2015/01/a-leiomyoma-which-wont-enucleate.html

Genitourinary Tuberculosis In Pregnancy

Author Information

Pandey I*, Thakur H**, Gupta AS***.
(* Second Year Resident, ** Assistant Professor, *** Professor, Department of Obstetrics and Gynecology, Seth GS Medical College & KEM Hospital, Mumbai, India)

Abstract

Tuberculosis (TB) is a systemic disease caused by Mycobacterium tuberculosis. There is physiological immunosuppression in pregnancy especially cell mediated immunity. She had repeated episodes of pyuria non responsive to antimicrobial therapy. She was suspected to have chronic urinary tract infection (UTI). Urine PCR suggested Renal TB.

Introduction

Extra Pulmonary TB accounts for 10%-27 % of all cases.[1] Incidence of extra pulmonary tuberculosis due to Genital tuberculosis is 15%-20%.[2] Genitourinary tuberculosis is not very common in pregnancy. Patient may present with vague symptoms like flank pain, burning micturition, pyuria, dysuria, increased frequency of micturition, weight reduction.

Case report

A 22 year old patient G3P1L1MTP1 registered for ANC at 8.2 weeks of gestation. She had complaints of burning micturition, dysuria, and increased frequency of micturition since three months. She was given routine ANC care, advised urine analysis, microscopy and aerobic culture and antibiotic sensitivity. It showed only 2-3 leucocytes/high power field but urine grew E.Coli (>105 colony count) sensitive to Nitrofurantoin. Patient took oral Nitrofurantoin (Modified Release) 100 mg BD for 14 days. She had no symptomatic remission. So aerobic culture and antibiotic sensitivity of urine was repeated. It grew Klebsiella pneumonae sensitive to Cefuroxime. Patient was given oral Cefuroxime bd for 14 days. Patient was then lost to follow up and she presented in Antenatal OPD at 20.2 weeks of gestation, with same complaints, so urology reference was advised for repeated urinary tract infection not responding to organisms specific antimicrobials. Patient was seen in Urology department, where repeat urine analysis and microscopy showed 100-150 pus cells/high power field and Urine culture showed no growth. USG KUB was done which showed renal abscess. The report was as follows: Left kidney had moderate degree of hydronephrosis and proximal 2/3rd ureteric dilatation. An upper pole cortical area with shaggy/irregular walls (abscess) was seen communicating with the dilated pelvicalceal system. Dense echoes (suggestive of infection) were seen within the pelvicalceal system. A non obstructing calculus (3.3 mm) was seen in the lower calyx. Right kidney showed multiple non obstructing calculi in calyces.


Figure 1. USG of the left kidney. ‘A’ shows the abscess.


Figure 2. USG of the right kidney.

The patient was admitted under the urologist at 24.5 weeks of gestation. A urinary Ziehl Neelsen staining was done. It was negative, hence urine TB PCR was done. It was positive. So the patient was started with category I anti TB therapy. She had symptomatic relief and was discharged. Patient presented with threatened preterm labor at 33.6 weeks. On examination patient had left renal angle tenderness besides having mild uterine activity. There were no cervical changes. Patient was admitted and conservative management with antenatal steroids and tocolytics was given. AKT (cat I) was continued but patient progressed to active labor and delivered uneventfully after 6 days of admission. Baby weight was 2.225 kg, Apgar scores at 1 and 5 minutes were 9/10. Post delivery patient was relieved from her symptoms of dysuria and burning micturition. There was no tenderness at the left renal angle.

Discussion

Pregnancy is an immunosuppressive state. Cell mediated immunity suppresses during pregnancy which plays a dominant role in pathogenesis of TB. Genitourinary TB is a reactivation of TB from period of dormancy.[3] Extrapulmonary tuberculosis is a rare form of TB, constitutes only 10%-27% and it is often rare during pregnancy. Genitourinary tuberculosis is a common form of extra pulmonary tuberculosis and it constitutes almost 20-73% of all cases.[4] The diagnosis of this condition may be delayed because of its variable presentation. About 20% patients may remain asymptomatic or may present with atypical symptoms [5]. It is also difficult to diagnose even with the imaging techniques as well as the bacteriological analysis. In many patients urine is generally sterile and contains leukocytes, though in 20% cases it may not have leukocytes [3]. So it is important to consider the diagnosis of genitourinary tuberculosis in a patient presenting with chronic non specific recurrent urinary complaints. The genitourinary tuberculosis may cause frequent hospitalization during pregnancy, increased incidences of maternal disabilities, preterm labor, prematurity, small for gestational age, low birth weight (< 2500 g) and delivery of neonates with low Apgar score.[6] ‘Short course chemotherapy’ is advised for the treatment of genitourinary tuberculosis. According to WHO, the anti tuberculosis drug regimen includes initial two months of intensive phase with four drugs (Isoniazide, Rifampicin, Ethambutol and Pyrazinamide) followed by four months of continuation phase with two drugs (Rifampicin and Isoniazid).[7] The 1st three drugs have no reported teratogenic effect during pregnancy; however, teratogenic data of Pyrazinamide is not adequate [8]. The same regimen was started in our patient. As our patient had a sterile pyuria, presentation of nonspecific recurrent urinary tract infection a diagnosis of urinary tuberculosis was suspected and detected early after evaluation. She had superimposed secondary infection probably due to changes in the urinary tract related to pregnancy.  Early diagnosis and timely treatment of genitourinary TB leads to better health of patient and good fetal outcome and restricts damage to the kidney.

Conclusion

Tuberculosis is a major public health problem. Most important step in management of genitourinary tuberculosis in pregnancy is awareness, early diagnosis and timely beginning of proper treatment.

References
  1. Jana N, Vasishta K, Saha SC, Ghosh K. Obstetrical outcomes among women with extra pulmonary tuberculosis. N Engl J Med. 1999; 341(9):645-649.
  2. Patel A, Qureshi S, Gupta AS. Periabortal Abdominal Tuberculosis. JPGO 2014, Vol 1(7). Available from http://www.jpgo.org/2014/07/ periabortal- abdominal- tuberculosis.html
  3. Figueiredo AA, Lucon AM. Urogenital Tuberculosis: Update and Review of 8961 Cases from the World Literature. Rev Urol. 2008; 10(3): 207-217.
  4. Cek M, Lenk S, Naber KG, Bishop MC, Johnsen TEB,Botto H,et al. EAU guidelines for the management of genitourinary tuberculosis. Eur Urol. 2005;48:353-362.
  5. Llewelyn M, Cropley I, Wilkinson RJ, Davidson RN. Tuberculosis diagnosed during pregnancy: a prospective study from London. Thorax. 2000;55(2):129-132.
  6. Snider DE Jr, Layde PM, Johnson MW, Lyle MA. Treatment of tuberculosis during pregnancy. Am Rev Respir Dis. 1980; 12:265-79.
  7. World Health Organization. Treatment of tuberculosis: Guidelines for national programmes, 3rd ed. WHO/CDS/TB/2003.313. World Health Organization. Geneva, Switzerland 2003.
  8. Friedman LN, Tanoue LT. Tuberculosis in pregnancy.UpToDate.2014. Available from http://www.uptodate.com/contents/ tuberculosis- in-pregnancy.
Citation

Pandey I, Thakur H, Gupta AS. Genitourinary Tuberculosis In Pregnancy. JPGO 2015. Volume 2 No. 1. Available from: http://www.jpgo.org/2015/01/genitourinary-tuberculosis-in-pregnancy.html

Vertical Transmission of Salmonella typhi

Author Information

Poonia S*, Satia MN**, Torame VP***, Natraj G****.
(* Third Year Resident, ** Prodessor, Department of Obstetrics and Gynecology; *** Assistant Professor, **** Professor, Department of Microbiology; Seth GS Medical College & KEM Hospital, Mumbai, India.)

Abstract

A case of typhoid fever in second trimester of pregnancy with vertical transmission leading to intrauterine fetal death at 14 weeks of gestation has generated curiosity about organisms that cross placenta in pregnancy. Salmonella typhi was isolated in the retained products of conception which were sent for culture and sensitivity as patient presented with symptoms and signs of pelvic infection.

Introduction

Typhoid fever is a major health problem in developing countries. Cases of vertical transmission have been reported from India.[1][2]Pregnant women are susceptible to food  borne infections like typhoid owing to hormonal changes that suppress immunity.[3]Salmonella typhi can cross the placenta and cause miscarriage, still births and preterm labor. We report a case where a Para 1 Living 1 with history of fever and inevitable abortion grew Salmonella typhi on her retained products of conception.

Case Report

A 22 year old Gravida 2 Para 1 Living 1 woman with 14 weeks of gestation came with pain in abdomen and spotting per vaginum since one day. She had history of fever off and on one week back, for which she had taken antibiotics from a private practitioner, the details of which were not available. She had registered at 6 weeks of gestation and pregnancy was confirmed by ultrasonography. She had a fever spike of 380 C after admission. Her vital parameters were stable.  On abdominal examination, her uterus was corresponding to 14 weeks of gestation. Bimanual pelvic examination showed the uterus to be corresponding to 14 weeks, cervical os was open and products of conception felt were through it. Vagina was warm and uterus was tender. Based on history, clinical findings, and geographical endemicity of acute onset fever pathogens, her blood samples were sent. Her hemoglobin was 9.4 g/dL, white blood cell count 7300/cmm, and platelets of 0.66/cmm. Her urine culture was sterile. Widal titre was positive up to dilution of 1: 240 for both Salmonella typhi ‘O’ (somatic) and Salmonella typhi’ H’ (flagella). Rapid test for malaria, dengue and leptospirosis were negative. Liver and renal function parameters were within normal limits. Blood sugars and thyroid profile were normal. A curettage was done for inevitable and septic abortion under antibiotic cover (ceftriaxone and metronidazole). Products of conception were sent for culture and sensitivity. Salmonella typhi was isolated from products of conception and further confirmed by Salmonella polyvalent antisera.
Salmonella typhi was sensitive to ceftriaxone, carbapenems, other third generation cephalosporins, cotrimoxazole and chloramphenicol. The isolate was a nalidixic acid resistant Salmonella Typhi (NARST) which was also resistant to ciprofloxacin. Her blood culture and stool culture sent on day 3 of admission, did not reveal any Salmonella growth. She was treated with same antibiotics for 5 days and was discharged on day 5 of procedure.
In the absence of any other likely cause of spontaneous miscarriage in this case, Salmonella typhi was presumed to be the most likely cause.

Discussion

Incidence of infection with Salmonella in pregnant patients is similar to general population (0.2%).[4] Typhoid is caused by Salmonella enterica serotype typhi. The most common route of transmission is feco-oral route. In humans young, old, pregnant, HIV infected and patients who have undergone transplant are at higher risk for Salmonella infection.[5] Vertical transmission of Salmonella occurs via transplacental spread or because of the bacteraemia during labor or due to inadvertent fecal contamination of birth canal. Incidence of fetal loss in untreated typhoid can be as high as 80%.[4] Salmonella typhi has been associated with abortions in animals like sheep, cattle and horses.[6]
Salmonella typhi is an intracellular bacterium that resides within the modified phagosomes of Antigen Presenting cells (APCs). Innate immunity is important in curtailing infection during the first week of infection and CD4 T-cells response to Salmonella typhi is detectable only after 7 days of infection whereas CD8 T-cells response is delayed until second week post infection.[7] Overall, Salmonella typhi has evolved many mechanisms to evade the host immune system. In pregnancy, there is a shift in immune status from type 1 (cell mediated immunity) to type 2 (humoral immunity).This shift in immune system though is more pronounced at the maternal fetal interface and may also affect systemic immunity.[8]
Various organism other than TORCH (Toxoplasma gondii, Rubella virus, Cytomegalovirus, Herpes Simplex virus) that infect human placenta have been reported in literature.[9] These organisms are intracellular for a portion of their lifetime and infect placenta via hematogenous spread. Salmonella being an intracellular organism are recruited at the fetal implantation site early in illness before treatment or during an episode of bacteremia. The extravillous trophoblast with immune modifications are juxtaposed near these maternal decidual cells. Due to various invasive and evasive strategies Salmonella typhi may cause significant damage to mother and fetus.
As per reports by Hick’s and French, Salmonella typhi may cross placenta and cause miscarriage (65-80%), stillbirths and preterm labour.[10] Transplacental transmission usually presents as spontaneous second trimester abortion without premature rupture of membranes. Neonates born to mother with Salmonellosis are more prone to severe complications like septicaemia and meningitis.[11]
Ampicillin or amoxicillin are considered as first line drugs during pregnancy. Ceftriaxone is the preferred drug in nalidixic acid resistant Salmonella typhi (NARST), also resistant to ciprofloxacin.[12] Typhoid vaccines (both polysaccharide and live vaccine) are category C drugs during pregnancy.
Salmonellosis is usually not included in the differential diagnosis of miscarriage, stillbirth or neonatal sepsis that occur during pregnancy. However it should be considered to prevent fetal and mother morbidity.

References
  1. Raveendran R, Wattal C, Sharma A, Kler N, Garg P, Gujral K, et al. Vertical transmission of Salmonella paratyphi A. Indian J Pediatr 2007; 74:784-6.
  2. Mohanty S, Gaind R, Sehgal R , Chellani H, Deb M. Neonatal sepsis due to Salmonella Typhi and Paratyphi A. J Infect Dev ctries. 2009; 3: 633-638.
  3. Smith JL. Foodborne infections during pregnancy. J Food Prot. 1999; 62:818 – 29.
  4. Gyang A, Saunders M. Salmonella Mississippi: a rare cause of second trimester miscarriage. Arch Gynecol Obstet 2008;277:437-8.
  5. Doffinger, R., S.Patel, and D.S.Kumararatne.Human immunodeficiency that predispose to intracellular bacterial infections. Curr. Opin.Rheumatol.2005;17:440-446.
  6. Coughlin LB, McGuigan J, Haddad NG, Mannion P. Salmonella sepsis and miscarriage. Clin Microbio Infect 2003;9:866-8.
  7. Ravindran R., S.J. McSorley5.Tracking the dynamics of T-cell activation in response to Salmonella infection. Immunology. 2005; 114:450-458.
  8. Chaouat G.Innately moving away from the Th1/Th2 paradigm in pregnancy. Clin. Exp.Immuno.2003; 131: 393-395.
  9. V. B. Zeldovich and A. I. Bakardjiev, “Host defense and tolerance: unique challenges in the placenta,” PLos Pathogens, vol. 8 no. 8, Article ID e 1002804, 2012.
  10. Hick’s HT, French H. Typhoid fever and pregnancy with special reference to foetal infection. Lancet 1905;1:1491-3.
  11. Dharsandia M, Milan R, Soni Sumeeta T, Vegad Mahendra M. Salmonella Paratyphi B meningitis, isolated from CSF.NJIRM.2010; 1:55-56.
  12. Wain J, Hoe NT, Chinh NT, et al. Quinolone-resistant Salmonella typhi in Vietnam: molecular basis of resistance and clinical response to treatment. Clin Infect Dis. 1997; 25: 1404-1410. 
Citation

Poonia S, Satia MN, Torame VP, Natraj G. Vertical transmission of Salmonella typhi. JPGO 2015. Volume 2 No. 1. Available from: http://www.jpgo.org/2015/01/vertical-transmission-of-salmonella.html

Female Genital Tuberculosis: An unusual presentation

Author Information

Chawla LJ*, Mirchandani A**, Mayadeo NM***, Chakre S**.
(* Senior Registrar, ** Assistant Professor, *** Professor. Department of Obstetrics and Gynecology, Seth GS Medical College & KEM Hospital, Mumbai, India)

Abstract
Genital tuberculosis is the most baffling of all genital disorders, especially because of its various presentations. Usually considered to have a chronic course, it can present as an acute emergency as in our case. Radiological diagnosis can often be unreliable and cause diagnostic dilemmas in an atypical clinical scenario. Our case is one such example of how a young unmarried female with an acute abdomen and radiology suggestive of hemorrhagic ovarian cyst with hemoperitoneum turned out to be a case of active genital tuberculosis.

Introduction

Female pelvic tuberculosis (TB) is one of the most under diagnosed conditions in gynecology. An increase in extra pulmonary tuberculosis is being reported in young women worldwide and is an important cause of significant morbidity, both short and long term, especially in the reproductive age group.[1] High risk factors include a history of previous pulmonary TB infection, low socioeconomic background and residence in high prevalence areas such as India, were present in our case. Immunocompromised status as in drug abusers, HIV positive status and contact with pulmonary TB sufferer are other risk factors.[2] High degree of suspicion, good history taking, thorough clinical examination and judicious use of investigations may help in early diagnosis and timely treatment preventing infertility and other sequelae. [1]

Case Report

A 26 years old, unmarried female presented with a complaint of sudden onset, acute abdominal pain associated with severe nausea. She had regular menstrual cycles and gave no history of sexual contact. She had no preceding complaints and was apparently asymptomatic prior to this episode. Her only significant past history was that of pulmonary tuberculosis, diagnosed 3 years back, for which she had taken AKT for 6 months. She also underwent appendicectomy 2 months back. On examination, moderate pallor was present and pulse was 96/min. The other vital parameters were normal. On per abdomen examination, tenderness and guarding were noted over the entire abdomen with moderate ascites. Pelvic ultrasound (USG) revealed a heterogeneous, predominantly hypoechoeic 6.1x 4.5x 5.2 cm right sided ovarian cyst with peripheral vascularity, suggestive of a hemorrhagic cyst. Minimal free fluid was seen  in the pouch of Douglas with internal echoes suggesting pelvic hematoma and hemoperitoneum.Tumor markers (CA 125, CEA, β-HCG, AFP) were within normal limits. Magnetic resonance imaging (MRI) showed a right adnexal hematoma with adjacent intramuscular extension due to a ruptured hemorrhagic cyst or ruptured ectopic gestation. There was no evidence of a gestational sac. Urgent exploratory laparotomy was done which revealed foul smelling pyoperitoneum. Around one liter pus was drained and pus sample was sent for microbiologic study. The uterus was normal size; both fallopian tubes were hyperemic and edematous and separate from the ovaries (figure 1).


Figure 1: Uterus with bilateral congested fallopian tubes and right ovarian cyst that drained pus. Pus flakes are seen adherent to all the pelvic structures.

A right sided ovarian cyst 7x8 cm was seen adherent to the pouch of Douglas. No apparent pelvic cause of pyoperitoneum was seen. Surgical opinion was taken and bowel tracing was done to determine its source. Bowel exploration was negative. Right ovarian cyst wall was punctured and it drained pus, hence ovarian cystectomy was done and the cyst wall was sent for histopathological examination. In the postoperative period, the patient was started on broad spectrum antibiotics. She developed paralytic ileus on day 3 which was managed conservatively. Histopathology report showed granulomatous necrosis with neutrophilic infiltrate suggestive of tuberculous abscess with secondary infection. Pus culture grew Escherichia coli in significant number which was sensitive to piperacillin and tazobactum. After diagnosis of TB on histopathology report, chest medicine opinion was taken. A high resolution computed tomography (CT) of the chest was done which was suggestive of reactivation of old tubercular pulmonary focus. Category 2 AKT was started and patient had a speedy recovery.

Discussion

In India, genital TB is found in 0.75 to 1% of all gynecological admissions. Although genital TB can occur in any age group, the majority of the patients are in the reproductive age group, 75% being in the 20–45 years age bracket, like our patient who was 26 years old. Postmenopausal women account for 7–11% of cases of genital TB.[2]
Genital TB almost always occurs secondary to pulmonary tuberculosis, commonly by the hematogenous route in a manner similar to spread to other extrapulmonary sites. In our case of genital TB in a young girl who was not sexually active, reactivation of pulmonary focus of infection lead to pelvic TB.  However, primary genital TB can rarely occur by direct inoculation of tubercle bacilli over vulva or vagina during sexual intercourse with a partner suffering from active tuberculous lesions of genitalia.[3]
Most cases of female genitourinary tuberculosis are difficult to ascertain as the disease may be asymptomatic (11%).[4] Or it may masquerade as other gynecological conditions and can go unrecognized, like in this case.  The clinical presentation varies from patient to patient, symptoms like infertility (almost in 60% cases), abdominal and pelvic pain, menstrual disorders like scanty menstruation or amenorrhea are the usual presentations.[5] Pelvic TB has also been reported in literature where it has presented as an adnexal mass with raised levels of CA 125 masquerading as ovarian cancer necessitating unnecessary surgical intervention.[6] In our case, the acute presentation of the disease with deteriorating condition of the patient made it imperative for us to intervene early and the in situ findings were unexpected.
The pickup rate of tuberculosis on ultrasound is 100% for ascites / loculated fluid and 93 % for an adnexal mass.[4] CT and MRI are also useful in the diagnosis.[1]Awareness of these features may improve diagnostic accuracy and avoid misdiagnosis and unnecessary surgical intervention like in this case where these features of TB were misinterpreted as those of a hemorrhagic cyst and hemoperitoneum.
The final diagnosis in this case was made only on the basis of histopathological examination as at laparotomy, classical features of tubercular pelvic infection, like miliary granulomas, tubercles over the fallopian tubes and uterus, hydrosalpinx and adhesions, were absent.[4] As Mycobacterium tuberculosis might not be demonstrated in every case, newer investigations like ELISA and PCR are being used. But in our set up, their use is restricted due to high cost and nonavailability.[4]

Conclusion

 Pelvic tuberculosis should always be kept in mind for the differential diagnosis of a patient with adnexal mass and ascites, especially in those at high-risk. The presence of effective antitubercular therapy significantly reduces the morbidity and mortality of the patient, but further research is required to help early establishment of diagnosis, and for interventions leading to preservation of reproductive capability of the affected individual.

References

1.      Sharma JB. “Tuberculosis in Obstetric and Gynecological Practice”. John Studd, Seang Lin Tan, Frank A. Chervenak. Current Progress in Obstetrics and Gynecology. TreeLife Media. Vol 1 (2012): 305-327.
2.      Arora, V. K., Gupta R, Arora R. Female genital tuberculosis-Need for more research. Indian Journal of Tuberculosis 2003;50:9-12.
3.  Gatongi DK, Gitau G, Kay V, Ngwenya S, Lafong C, Hasan A. Female genital tuberculosis. The Obstetrician & Gynaecologist 2005;7:75-79.
4.   Chhabra, S., K. Saharan, and D. Pohane. "Pelvic Tuberculosis continues to be a disease of dilemma-Case series". Indian Journal of Tuberculosis, 2010; Volume 57:90-94. Available from: http://medind.nic.in/ibr/t10/i2/ibrt10i2p90.pdf.
5.  Qureshi RN, Samad S, Hamid R, Lakha SF. Female genital tuberculosis revisited. JOURNAL-PAKISTAN MEDICAL ASSOCIATION, 2001;51:16-18.
6.    I˙lhan AH, Durmus¸og˘lu F. Case report of a pelvic-peritoneal tuberculosis presenting as an adnexial mass and mimicking ovarian cancer, and a review of the literature." Infectious diseases in obstetrics and gynecology 2004;12:87-89.

Citation

Chawla LJ, Mirchandani A, Mayadeo NM, Chakre S. Female Genital Tuberculosis: An unusual presentation. JPGO 2015. Volume 2 No. 1. Available from: http://www.jpgo.org/2015/01/female-genital-tuberculosis-unusual.html