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Volume 1, Number 2

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An IJCP Group Publication Corporate Panel Dr Sanjiv Chopra Prof. of Medicine and Faculty Dean Harvard Medical School Group Consultant Editor Dr Deepak Chopra Chief Editorial Advisor Padma Shri and Dr BC Roy National Awardee Dr KK Aggarwal Group Editor-in-Chief Dr Veena Aggarwal MD, Group Executive Editor

CONTENTS FROM THE ISSUE EDITOR Dr Alka Kriplani

FROM THE DESK OF GROUP EDITOR-IN-CHIEF

Role of Folate or Folic Acid in Cancer Prevention

Dr (Mrs) Prabha Arora (Delhi) Dr Hema Divakar (Bangalore) Dr Kamini A Rao (Bangalore) Dr Deepti Goswami (Delhi) Dr Neerja Bhatla (Delhi) Dr Bhawna Malhotra (Delhi) Dr Biswas Nicholas (Australia) Dr Sudhaa Sharma (Jammu) Dr Jaibhagwan Sharma (Delhi) Dr Veena Mathur (Agra) Dr Garima Kachhawa

Editorial Board Obstetrics and Gynaecology Dr Alka Kriplani Dr Thankam Verma Dr Kamala Selvaraj

ENT Dr Jasveer Singh

Cardiology Dr Praveen Chandra Dr SK Parashar

Gastroenterology Dr Ajay Kumar

Paediatrics Dr Swati Y Bhave Diabetology Dr CR Anand Moses Dr Sidhartha Das Dr A Ramachandran Dr Samith A Shetty

Dentistry Dr KMK Masthan Dr Rajesh Chandna

Dermatology Dr Hasmukh J Shroff Neurology Dr V Nagarajan Journal of Applied Medicine and Surgery Dr SM Rajendran Dr Jayakar Thomas

Anand Gopal Bhatnagar Editorial Anchor Advisory Body Heart Care Foundation of India Non-Resident Indians Chamber of Commerce and Industry World Fellowship of Religions

Dr KK Aggarwal

AJOG Specialty Panel

Dr Alka Kriplani Editor Consultant Editor Dr Urmil Sharma Assistant Editors Dr Nutan Agarwal (Delhi) Dr Neera Aggarwal (Delhi) Dr A Biswas (Singapore) Dr CS Dawn (Kolkata) Dr Gauri (Delhi) Dr Suneeta Mittal (Delhi) Dr S Mehra (Delhi) Dr Prashant Mangeshikar (Mumbai) Dr Prakash Trivedi (Mumbai) Dr Gita Ganguly Mukherjee (Kolkata)

REVIEW ARTICLE

Abdominal Pregnancy in Broad Ligament Resulting in Live Birth 8 Kamal Samarina, Chakraborty Shobha

CLINICAL STUDY

Mammoth Myoma - challenges in Management

Radha V, Palaniappan N, Diviya nanchil Kumaranl

A Comparative Study to Analyse the Association of Metabolic Syndrome in Females with Polycystic Ovarian Syndrome 15 Richa S, Saroj S, Poonam Y, Harpreet K

Prophylactic Preoperative use of Rectal Misoprostol vs Intravenous Oxytocin Infusion During Cesarean section to Reduce Intraoperative and Postoperative Blood Loss 18 Rekha R, Shikha S, Saroj S, Urvashi V, Ruchika G, Rachana A, Latica

Bilateral PSOAS Abscess in Surgery

Puneet Malik

CASE REPORT

Progesterone and Prevention of Preterm Labour Ruchika Garg, Urvashi Verma, Rajni Rawat, Somya Shrivastava, Renu Rajvanshi

Asian Journal of Volume 1, Number 2

CONTENTS

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A rare case of spinal muscular dystrophy/atrophy 27

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ORIGINAL ARTICLE

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Iron Deficiency Anemia Evaluation and Management 29 Matthew w. Short

JOURNAL SCAN

Research Review

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FROM THE ISSUE EDITOR

Women above 65 to Take Extra Care Of Their Health

Dr Alka Kriplani Professor and Head of Unit II Dept. of Obstetrics and Gynecology AIIMS, New Delhi E-mail: kriplanialka@gmail.com

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Women aged 65 and above should take low dose aspirin routinely to prevent heart attack and paralysis. All women are urged to exercise a minimum of 30 minutes per day, but women who need to lose weight or maintain weight loss are now advised to engage in 60 to 90 minutes of moderate-intensity activity on most, or preferably all, days of the week. A heart-healthy diet should be rich in fruits, whole grains and fiber foods with a limited intake of alcohol and sodium. Saturated fat should be reduced to less than 7 percent of calories. Women at very high risk for heart disease should try to lower their LDL ("bad") cholesterol to less than 70 mg/dL. Women aged 65 and over should consider taking low-dose aspirin on a routine basis, regardless of their risk. Aspirin has been shown to prevent both heart attacks and stroke in this age group. The upper dose of aspirin for high-risk women is 325 mg per day. Hormone replacement therapy, selective estrogen receptor modulators or antioxidant supplements such as vitamins C and E should be used to prevent heart disease. Folic acid should also not be used to prevent cardiovascular disease. Women should eat oily fish or some other source of omega-3 fatty acids at least twice a week. Women should not only quit smoking but should use counseling, nicotine replacement or other forms of smoking cessation therapy.

Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

FROM THE DESK OF THE GROUP EDITOR-IN-CHIEF

Role of Folate or Folic Acid in Cancer Prevention Dr KK Aggarwal

Padma Shri, Dr BC Roy National & DST National Science Communication Awardee Sr. Physician and Cardiologist, Moolchand Medcity President, Heart Care Foundation of India Group Editor-in-Chief, IJCP Group and eMedinewS National Senior Vice President, IMA Member, Ethics Committee, MCI Chairman, Ethics Committee, Delhi Medical Council Director, IMA AKN Sinha Institute (08-09) Hony. Finance Secretary, IMA (07-08) Chairman, IMA AMS (06-07) President, Delhi Medical Association (05-06) emedinews@gmail.com http://twitter.com/DrKKAggarwal Krishan Kumar Aggarwal (Facebook)

Several large observational studies have shown a decrease in risk of colorectal and other cancers with dietary folate, while other randomized trials of folic acid supplementation have raised the possibility of increased cancer risk from folic acid supplementation. In the largest meta-analysis of individual patient data from randomized trials of folic acid for the prevention of cardiovascular disease (10 trials, n = 49,969) and colorectal adenoma (3 trials, n = 2652), during an average of 5.2 years of treatment, there was no significant difference in overall cancer incidence for patients assigned to folic acid or placebo. There was also no significant effect on the incidence of specific cancers, including cancers of the large intestine, prostate, lung, or breast. (Lancet 2013;381:1029) Fish oil and cardiovascular mortality The Risk and Prevention Study enrolled patients with multiple cardiovascular risk factors or known vascular disease and, after a median follow-up of five years, found no reduction in coronary heart disease death with n-3 polyunsaturated fatty acid supplementation compared with placebo. (N Engl J Med 2013;368:1800) Breastfeeding and obesity There is increasing evidence that breastfeeding does not reduce the risk of obesity in the offspring. A follow-up study from a cluster-randomized trial of over 17,000 breastfeeding mother-infant pairs reported on outcomes of children at 11.5 years of age, and confirmed findings from 5 years earlier that there were no differences in the body mass index or rates of obesity and overweight. Population strategies to increase the duration and exclusivity of breastfeeding are unlikely to impact the obesity epidemic. Âś

Source:: JAMA 2013;309:1005.

Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

REVIEW ARTICLE

Abdominal Pregnancy in Broad Ligament Resulting in Live Birth *Kamal Samarina, †Chakraborty Shobha

ABSTRACT Abdominal pregnancy is an extremely rare form of extra uterine gestation. Broad ligament pregnancy is a rare type of secondary abdominal pregnancy accounting for about 1% of ectopic pregnancy1. Newer advances like use of MRI compliment ultrasound in the diagnosis of abdominal pregnancy. Its management is one of laparotomy with varying complications including poor perinatal outcome and increased maternal morbidity and mortality. There is no accepted consensus for the complete removal of the placenta at laparotomy. This case report is special in two manners – one is the live birth of a normal baby girl and second one being complete removal of placenta. Key words: Abdominal Pregnancy, ectopic gestation

bdominal pregnancy has historically been defined as an implantation in the peritoneal cavity exclusive of tubal and ovarian implantation. It is a rare form of ectopic pregnancy with an incidence of 1 in 8099 hospital deliveries2 and accounts for 1-4% of all ectopic gestations. It has been observed that it can occur at any age and is usually diagnosed in advanced stage of pregnancy. It can occur in any part of the abdomen – pouch of Douglas is the commonest. The placenta can be attached to the uterine wall, bowel, mesentery, liver, spleen, bladder and ligaments. Abdominal pregnancy can be primary where the fertilized ovum implants itself on an abdominal organ but majority are secondary where fertilized ovum first implants in the uterus, ovary or fallopian tube, then subsequently implants on a peritoneal surface following tubal abortion or uterine scar rupture.

low with the perinatal mortality rate being 40-95%. Here we present a case of term abdominal ectopic pregnancy with a live fetus.

Case History A 27 years old G2P1L1 was referred to our hospital with pain abdomen and bleeding per vaginum. She was 37 weeks 4 days period of gestation by dates and her 2nd trimester scan was also corresponding. Her routine investigations and ultrasound done in 2nd trimester were normal. She complained that she had dull aching pain throughout her gestation and she had mild bleeding pervaginum since 2 days. Her pulse rate was 90/minute, blood pressure was 130/80 mm kg. Per abdomen examination revealed a size of around 34 weeks. Fetal heart rate was 130/mt

Maternal mortality is 7.7 times higher than tubal ectopic pregnancy and 90 times higher than the intrauterine pregnancy due to catastrophic haemorrhage from placental separation3. The chance of survival of a newborn are very *Consultant Dept. of Obstetrics and Gynaecology, Alam Hospital & Research Centre Senior Consultant Dept. of Obstetrics and Gynaecology, Agarwal Nursing Home, Ranchi

†

Address for correspondence Dr Samrina Kamal Dept. of Obstetrics and Gynaecology, Alam Hospital & Research Centre Bariatu, Booty Road, Ranchi - 834009 E-mail: drsamrinakamal@gmail.com

Figure 1. Uterus displaced to the left and abdominal pregnancy is seen to the right.

Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

REVIEW ARTICLE

Figure 2. Gestational sac seen in the right sided broad ligament.

Figure 5. Note the adhesions to the mesentery. The space seen after delivery of the fetus and placenta going right up to the pouch of Douglas.

Figure 3. Fetal delivery by breech. Note that the head still inside in the pouch of Douglas

Figure 6. USG diagnosis of abdominal pregnancy with empty uterine cavity and fetal head lying outside.

Figure 3. Membranes seen in the right broad ligament.

Figure 7. MRI showing fetus outside uterus.

and presentation appeared to be cephalic. There was a distinct suprappubic bulge around 16-18 wks size. On pervaginum examination, we found that the cervix was long, closed, uneffaced. There was mild bloody discharge. A remarkable finding was the fetal head was felt in posterior fornix.

Ultrasound examination in our outpatient department revealed a single live fetus of gestational age of about 36 weeks. Placenta appeared to be mature with signs of calcification. Liquor pockets were almost absent. The uterus was seen to be separate and big in size. The fetus and and placenta were lying outside the uterus but since

Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

REVIEW ARTICLE fetal heart was seen and the patient’s vitals were stable, rupture uterus was ruled out and the diagnosis was made to be abdominal pregnancy. Now, the patient was sent to a senior radiologist where it was confirmed by ultrasound and MRI to be abdominal pregnancy.Routine investigations were done which were normal. Since the fetus was almost 37 weeks and was live, there was no point waiting for fetal maturity, so the patient was put up for laparotomy after bringing 2 pints of blood transfusion and keeping 2 more pints of blood arranged. A senior anaesthesist and a surgeon were called. The abdominal was opened by midline vertical incision. A 20 weeks size uterus was seen displaced to the left and a gestational sac formed by the layers of right broad ligament and extending to the pouch of Douglas were seen. Incision was given on the gestational sac and a live term female baby smeared with thick meconeum was delivered by breech and handed over to the paediatrician. The baby cried after resuscitation and weighed 2.4 kg. The baby was admitted to NICU for 48 hours, then handed over to the mother. Now the pelvic anatomy was carefully examined. There were some adhesions to omentum and mesentery, so adhesiolysis was done. Luckily the placenta was not adherent to any vital structures like mesentery, gut, liver etc but it was deriving its blood supply from the omentum. So infracolic omentectomy was done thus removing the placenta in toto. Some portion of membranes were left behind as it was densely adherent to the rectum. Haemostasis was checked, then the abdomen was closed after giving an intraperitoneal drain. Postoperative period was uneventful and the patient was discharged on 10th post operative day.

Discussion Abdominal pregnancy beyond 20 weeks gestation and with a viable fetus is a rare condition. In primary abdominal pregnancy, the fallopian tubes and ovaries are intact. There were only 24 cases of primary abdominal pregnancy reported up to 20074. In contrast, secondary abdominal pregnancy accounts for most cases of advanced extra uterine pregnancy and there is evidence of tubal or ovarian damage. In our case the tubes and ovaries were found to be normal, so the possibility that it was a primary abdominal pregnancy can’t be ruled out. The diagnosis of primary abdominal pregnancy was confirmed according to studdiford’s5 criteria.

• Normal tubes and ovaries • Absence of uteroplacental fistula • Attachment exclusively to a peritoneal surface early enough in gestation to eliminate the likelihood of secondary implantation. Documented risk factors such as previous ectopic pregnancy, tubal corrective surgery, IUCD, progesterone only pills usage, pelvic inflammatory disease, endometriosis, assisted reproductive technology, history of secondary infertility, sexually transmitted disease, prior caesarean delivery, smoking, cocaine abuse was not associated with our patient. The presentation of patients with an abdominal pregnancy varies and depends on gestational age. In first trimester, symptoms mimic those of ectopic pregnancy though a dull lower abdominal pain goes more in favour of broad ligament ectopic. In advanced cases, the patients complain of painful fetal movement, sudden cessation of fetal movement and perception of fetal movement high in the abdomen. Physical examination will reveal easy palpation of fetal parts, palpation of uterus separate from the gestational sac, persistent abnormal fetal positioning, abdominal tenderness and a displaced uterine cervix6,7. There should be a high index of suspicion if there is perception on the part of the mother or the physician that ‘something is not right’. There can also be a history of failed induction. In our case there was mild bleeding pervaginum which has been reported due to breakdown of decidual cast. Ultrasound examination is the first line diagnostic procedure. MRI8 provides additional information regarding surgical planning by evaluating the anatomical relationship between the placenta and invasion area. Features of intra abdominal pregnancy on MRI are the absence of uterine wall between the fetus and maternal abdominal wall, unusual fetal position, oligohydramnios, extra uterine fetus and placenta, enlarged uterus and close relationship between the placenta and maternal bowel. About 21% of babies born after an extra uterine abdominal pregnancy have birth defects like limb defects, craniofacial asymmetry, torticollis, plagiocephaly etc presumably due to compression of the fetus in lack of amniotic fluid9. The massive bleeding that occurs when the placenta is removed is due to adherence of the placenta to the broad ligament which unlike the uterus does not contract. Early

Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

REVIEW ARTICLE diagnosis of intra abdominal pregnancy is important to plan delivery and achieve good results. If undiagnosed, it carries the risk of haemorrhage secondary to placental separation, hypo fibrinogenaemia following fetal demise and abscess formation. The mainstay of management is laparotomy but there is controversy regarding the optimal time to operate. For less than 24 weeks of gestation, early laparotomy is recommended. In rare cases with a fetus near viability, it is justified to postpone the operation in view of saving a baby provided there is • Absence of fetal malformation • Absence of maternal decompensation • Continued surveillance of fetal well being • Placental implantation away from liver or spleen • Continuous hospitalization in appropriate center • Informed consent of the patient Successful treatment using laparoscopy in early cases has been reported. Preoperatively we can take the help of angiography to identify all feeding vessels to the placenta and to embolize vessels that could be difficult to ligate like hypogastric artery. In our case since the patient was already in her 36th week of gestation with a live fetus,urgent laparotomy was planned. The principal controversy concerning the management of "Advanced Abdominal Pregnancy" (AAP) is whether or not to remove the placenta. Complete removal of the placenta should be done only when the blood supply can be identified and careful ligation performed. If the placenta is not removed completely, it has been estimated that the remnant can remain functional for approximately 50 days after the operation and total regression of placental function is usually complete within 4 months. The risks associated with leaving the placenta in situ include bowel obstruction, fistula formation and sepsis as the placental tissue degenerates10. Use of methotrexate11 or actinomycin D has been advocated by some.

Conclusion Advanced abdominal pregnancy (AAP) with a healthy newborn is very rare and is challenging diagnostically and

Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

therapeutically. High index of suspicion, careful clinical and ultrasound examination is the key to diagnosis though MRI can be very useful. Since the overall incidence of advanced abdominal pregnancy is one in 8099 hospital deliveries, a medical officer responsible for a population of 100000 might expect to encounter an AAP every few years, hence this case report is aimed at creating awareness on the part of the doctors catering to peripheral population and thus reducing the maternal mortality.

Acknowledgement The author would like to thank Department of Radio Diagnosis, Alam Hospital & Research Centre for their help in diagnosis of the rare condition.

References 1. Ludwig M, Kaisi M, Bauer O, Diedrich K. The forgotten child-a case of heterotopic, intra-abdominal and intrauterine pregnancy carried to term. Hum Reprod 1999;14:1372-4 2. Nkusu Nunyalulendho D, Einterz EM. Advanced abdominal pregnancy: case report and review of 163 cases reported since 1946 Rural and Remote Health8: 1087. (Online)2008. 3. Atrash H.K., Friede A., Hogue C.J.R. (1987) Abdominal pregnancy in the United States: frequency and maternal mortality. Obstet. Gynecol. 69: 333. 4. Krishna D, Damyanti S. Advanced abdominal pregnancy: a diagnostic and management dilemma. J Gynecol Surg. 2007;23:69–72. doi: 10.1089/gyn.2007.B-02259-1. 5. Studdiford WE. Primary peritoneal pregnancy. Am J Obstet Gynecol. 1942;44:487–91. 6. Bayless RB: Non-tubal ectopic pregnancy. Clin Obstet Gynecol 1987; 30(1):191-4 7. Pasternoster DM, Santarossa C: Primary abdominal pregnancy. A case report. Ninerva Ginecol 1999;51(6):251-3. 8. Malian V, Lee JH: MR imaging and MR angiography of an abdominal pregnancy with placental infarction. AJR Am JRoentgenol 2001, 177:1305-1306 9. Stevens CA. Malformations and deformations in abdominal pregnancy. Am J Med Genet.1993;47:1189–1195. doi: 10.1002/ajmg.1320470812. 10. Ang LP, Tan AC, Yeo SH: Abdominal pregnancy: a case report and literature review. Singapore Med J 2000, 41:454-457. 11. Bajo JM, Garcia-Frutos A, Huertas MA. Sonographic follow-up of a placenta left in situ after delivery of the fetus in an abdominal pregnancy. Ultrasound Obstet Gynecol 1996; 7: 285-288.

CLINICAL STUDY

Mammoth Myoma - challenges in Management *Radha V, †Palaniappan N, ‡Diviya nanchil Kumaran

ABSTRACT Giant Leiomyomas are known to arise from uterus and very rarely from the broad ligament. The surgical management of these cases can pose a challenge. We report a case of giant broad ligament fibroid weighing 8500 grams posing problems in diagnosis and management. With the clinical examination, investigatory modalities, a diagnosis of malignant ovarian tumour was made and turned out to be a broad ligament fibroid. Intra operatively patient went into coagulopathy which was effectively managed by timely abdomino pelvic packing. Key words: Leiomyoma, Broad ligament fibroid, Abdomino pelvic packing

xtra uterine fibroid though do occur, are not as common as uterine fibroids. Among them the most common is a broad ligament fibroid although its overall incidence is rare¹. It can pose diagnostic difficulties causing an error in final diagnosis and management due to rarity of this condition. We are reporting an unusual case operated with a pre operative diagnosis of malignant ovarian tumour, which turned out to be a giant broad ligament fibroid confirmed by histopathological examination and the intra operative problem encountered which was managed successfully. A 50 years old parous , post menopausal for one year, presented with abdominal distension for 2 months, rapidly increasing over the past 1 week. It was associated with pain abdomen, epigastric discomfort, breathlessness, decreased appetite and swelling of the legs for 1 week. She had no history of weight loss, bladder or bowel disturbance. On examination, vitals were normal, had bilateral pitting peal edema, no pallor or lymphadenopathy. BMI was 26kg/m² with weight being 65kgs. Systemic examination was normal. Abdomen examination showed a mass arising

*Associate Professor † Professor & Unit Chief ‡ Assistant Professor Dept. of Obstetrics & Gynecology Sri Ramachandra University, Chennai 600116, Tamil Nadu Address for correspondence Dr Vembu Radha Associate Professor, Department of Obstetrics & Gynecology Sri Ramachandra University, Chennai 600116 E-mail: ganesh_radha@yahoo.in

from the pelvis occupying all the quadrants corresponding to 36 weeks, varied consistency, restricted mobility and no free fluid. Speculum examination revealed normal cervix and vagina. On bimanual examination, cervix was drawn up, uterus was normal size, and a firm mass was felt through all the fornices. Per rectal examination was normal. Pre operative investigations were normal. Ultra sound abdomen and pelvis showed a huge heterogenous solid mass lesion with areas of cystic changes occupying the entire abdomen with marked vascularity. Both ovaries were not visualized. Mass lesion causing posterior displacement of liver, spleen, kidneys. There is no free fluid in the peritoneal cavity. CT scan (Fig. 1) showed a well defined heterogenous mass of 32 x 27 x 21 cms with solid and cystic components with septations in the abdomen and pelvis probably ovarian mass with prominent Para aortic lymph nodes of 9mm. CA 125 and CA 19.9 were 17.8 and 4.2 U/ml respectively which were within normal limits. Considering the age, rapid progression of symptoms, ultra sound and CT scan report, a probable diagnosis of malignant ovarian tumour was made and planned for Staging Laparotomy and procedure. Intra operatively, there was no free fluid, a huge right sided broad ligament solid and cystic mass occupying all the quadrants up to the under surface of the diaphragm and extending into the retroperitoneal space was noted (Fig. 2). Appendix, omentum and bowel loop were adherent. Bilateral tubes and ovaries were normal. The specimen sent for frozen section revealed spindle cell tumour probably leiomyoma. We proceeded with total abdominal hysterectomy with bilateral salphingo oophorectomy after delineating the

Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

CLINICAL STUDY

Figure 1. CT Scan- Abdomen & Pelvis showing the mass occupying the entire abdomen.

Figure 2. Broad Ligament Fibroid of 8500gms

course of ureters. The mass measured 32x27x21 cms weighing 8500 grams. Intra operatively, there was a continuous ooze from myoma bed and hemoglobin dropped from 11 to 3.3 g%, rapid INR was 2.15. Patient was transfused 3 units packed cells, 4 units FFP and 2 units platelets. As generalized ooze continued, we proceeded with abdomino pelvic packing using 2 long abdominal packs soaked in warm saline, tied at the edges and one of the edges was brought out through a separate incision on the anterior abdominal wall (Fig. 3). Total duration of surgery was 3 hours and 15 min. Post operatively, patient was managed in ICU, was Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

Figure 3. Exit point of the Abdomino pelvic pack through a separate incision.

transfused 3 units packed cells, 4 units FFP and 4 units of platelets. Hemoglobin improved to 9.9 g%. Once the general condition of the patient was stable, pack was removed after 48 hours, rectus sheath of the pack site was sutured, and patient was extubated. Skin was sutured on post operative day (POD) 4. All the skin sutures were removed on POD 10 and was discharged on POD 12 in a stable condition. Post surgery the patient weighed 54kgs (weight loss of 11kgs). Histopathology report confirmed leiomyoma.(broad ligament fibroid based on its location)

Discussion Giant leiomyomas are known to arise from the uterus but very rarely from broad ligament. Veronica et alÂ˛ in a case

CLINICAL STUDY report have reported a broad ligament fibroid of 2800gms. Probably ours is one of the largest broad ligament fibroid of 8500gms reported in the literature. The broad ligament fibroid unlike in our case usually present with pressure symptoms. Larger fibroids distort the pelvic anatomy, compress the ureters causing hydroureteronephrosis. So delineation of the ureteric course is very important to avoid ureteric injury.

the pack is removed only after the cardiopulmonary function, coagulation factors, hypothermia and acidosis are stabilized³. In our case, as the patient was stable after 48 hours, the decision to remove the pack was considered. Many reports have suggested the need for relaparotomy 1 to 7 days after primary surgery³. In our case, as the pack had a separate exit point, it was removed without a need for relaparotomy.

Abdominal packing is most commonly used for uncontrollable hemorrhage in hepatic surgeries³ in the face of hypothermia, acidosis and coagulopathy. This may be a life saving procedure even though the morbidity and mortality is high due to continued hemorrhage, abscess, compartment syndrome, small bowel obstruction.

Conclusion

The decision to abdomino pelvic packing is based on the surgeon’s opinion that coagulopathy has developed or that the patient was too unstable to undergo further blood loss. In our case, as the hemoglobin dropped grossly with the onset of coagulopathy, the decision to proceed with abdomino pelvic packing was considered in addition to timely blood and blood products administration which saved the life of the patient. Only few studies have reported the role of packing in caesarean hysterectomies4 and during pelvic posterior exenteration in gynecological surgeries5. The role of uterine artey embolization, Internal Iliac Artery ligation prior to the surgery to reduce the vascularity could not be considered in view of the suspicion of malignant ovarian tumour and giant size of the mass. The timing of removal of pack and the route varies. Usually

The broad ligament fibroid, even though being uncommon, can grow to a large size and can be a nightmare in the diagnosis and management. So timely decision of abdominopelvic packing with other resuscitative measures can be a life saving measure.

References 1. Bhatla N. Tumours of Corpus uteri, Jeffcoat principles of Gynecology 6th edn Arnold printers London; 2001: pp 470. 2. Veronica Irene Yuel, Vaneet Kaur. Broad Ligament fibroid An unusual presentation; Vol 8, No.4, Oct -Dec 2006, JK Science. 3. Kenneth W. Sharp, Richard J. Locicero. Abdominal packing for surgically uncontrollable Hemorrhage; Ann Surg vol 215, No. 5, pp 467- 474, May 1992. 4. S.Ghourab, Abdomino pelvic packing to control severe hemorrhage following caesarean hysterectomy;, Journal of Obstetrics & Gynecology 1999.Vol 19, No.2, pp 155-1585. 5. Wydra D, Emerich J, Ciach k, Dudziak M, Marciniak A. Surgical pelvic packing as a means of controlling massive intra operative bleeding during pelvic posterior exenteration - a case report & review of the literature; Int J Gynecol Cancer 2004, sept -oct 14(5): 1050-4.

Preventive effects of folic acid supplementation on adverse maternal and fetal outcomes. Although there is accumulating evidence regarding the additional protective effect of folic acid against adversepregnancy outcomes other than neural tube defects, these effects have not been elucidated in detail. We evaluated whether folic acid supplementation is associated with favorable maternal and fetal outcomes. This was a secondary analysis of 215 pregnant women who were enrolled in our prior study. With additional data from telephone interviews regarding prenatal folic acid supplementation, existing demographic, maternal and fetal data were statistically analyzed. The concentration of folic acid in maternal blood was significantly higher following folic acid supplementation (24.6 ng/ mL vs.11.8 ng/mL). In contrast, homocysteine level in maternal blood decreased with folic acid supplementation (5.5 µmol/mL vs. 6.8 µmol/mL). The rates of both preeclampsia (odds ratio [OR], 0.27; 95% confidence interval [CI], 0.09-0.76) and small for gestational age (SGA; 9.2% vs. 20.0%; OR, 0.42; 95% CI, 0.18-0.99) were lower in the folic acid supplementation group than those in the control group. Other pregnancy outcomes had no association with folic acid supplementation. The findings indicate that folic acid supplementation may help to prevent preeclampsia and SGA. Further studies are warranted to elucidate the favorable effects of folic acid supplementation on pregnancy outcomes. PLoS One. 2014 May 19;9(5):e97273. doi: 10.1371/journal.pone.0097273. eCollection 2014.

Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

CLINICAL STUDY

A Comparative Study to Analyse the Association of Metabolic Syndrome in Females with Polycystic Ovarian Syndrome *Richa S, †Saroj S, ‡Poonam Y, ≠Harpreet K

ABSTRACT Objectives: Polycystic ovarian syndrome is common female endocrinopathy affecting 5-6% of women within the age group 12-45 years. This study was contemplated with the aim to study the prevalence of metabolic syndrome in patients of PCOS and to study the spectrum of clinical features of metabolic syndrome in patients of PCOS. Methods: This case controlled study was conducted on 50 cases of diagnosed PCOS females and compared with 50 healthy age and BMI matched controls. Results: The prevalence of metabolic syndrome in PCOS patients was found 24% and in control group was 6%. Among patients with metabolic syndrome 14% of patients had high BP, 12% had impaired fasting glucose, 38% have high waist hip ratio, 14% have raised serum triglycerides and 44% had decreased HDL. Conclusion: It is observed that MBS manifests at an early age in women with PCOS. In order to prevent metabolic syndrome one should maintain BMI lower than 25 and waist circumference less than 35 inches. Key words: Metabolic syndrome, polycystic ovarian syndrome, hyperinsulinemia

Polycystic ovarian syndrome one of the most common female endocrinopathy affecting 5-6% of women within the age group 12-45 years. These patients are at high risk of developing infertility, dysfunctional uterine bleeding, endometrial carcinoma and a number of metabolic disorders including insulin resistance, hyperinsulinemia, type 2 diabetes mellitus, hypertension, dyslipidemia and cardiovascular disease. Due to these facts, early diagnosis of the syndrome should be emphasized. This background knowledge demands the necessity to work out the prevalence of MBS in women with PCOS in our society and to measure the strength of their association in the Indian scenario.

Aims And Objectives 1. To study the prevalence of metabolic syndrome in patients of polycystic ovarian syndrome. 2. To study the spectrum of clinical features of metabolic syndrome in patients of polycystic ovarian syndrome.

Material And Methods This study was conducted on 50 cases of diagnosed polycystic ovarian syndrome coming to our hospital and was compared with 50 healthy age and BMI matched women (control group) over a period of one year. Inclusion Criteria

Around 50 cases diagnosed to have PCOS by Rotterdam ESHRE/ASRM PCOS group’s revised 2003 criteria, with presence of any two of the three criteria, were recruited for the study. These criteria are

• Oligo and/or anovulation • Clinical and/or biochemical signs of hyperandrogenism • Polycystic ovaries (as confirmed on USG). The criteria for metabolic syndrome in women with PCOS.

*Professor † Professor ‡ Lecturer

According to NCEP, ATP III 2001 (Adult treatment panel III).

≠ JR-III Department of Obstetrics and Gynaecology S.N. Medical College, Agra - 282003

Three out of these five will qualify for the syndrome

Address for correspondence Dr Richa Singh Professor, Chauhan Nursing home, 1/120-G,Delhi Gate, Agra-282002 E-mail: chauhan.richavishal@gmail.com

Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

• Abdominal obesity (waist circumference ≥ 88 cm or 35 inches) and ≥ 80 cm for asian females. • Triglycerides ≥ 150 mg/dl • HDL-C ≤ 50 mg/dl

CLINICAL STUDY • Blood pressure ≥130/85 mmHg • Fasting plasma glucose ≥ 100 mg/dl or previously diagnosed type 2 diabetes. After taking careful history from the patient and conducting examination, following investigations were carried out – haemogram, fasting blood sugar, oral GTT, fasting insulin, fasting lipid profile, hormonal estimations for LH, FSH, testosterone, estrogen, progesterone and ultrasound abdomen. In these women fasting blood was drawn for glucose, insulin and lipid profile, which included triglycerides, total cholesterol, high density lipoprotein (HDL) and low density lipoprotein (LDL) cholesterol. A 2 hour 75 g glucose tolerance test was done in all PCOS patients. Two markers for obesity – such as body mass index and waist hip ratio, which depicts central obesity were used to study relationship of obesity to lipid parameters. Height (m) and weight (kg) measurements can be used to calculate the body mass index (BMI = weight in kg/ height in m2). Waist hip ratio can be calculated after measuring waist circumference between pelvic brim and costal margin, while hip circumference is taken at the level of the greater trochanter. Waist to hip ratio >0.85 is considered abnormal, while < 0.85 normal. The results were subjected to statistical analysis wherever applicable.

Results Table 1: Patient Profile Age group

Socio economic status

15-25

26-35

Total

Low

High

No.

100

No.

100

Cases

Control

(p value <0.04).

Discussion Our study was a cross sectional case control study of 100 females attending our OPD over a period of one year. If we compare BMI matched cases and control, then also lipid profile derangement is associated more with PCOS

Table 2. Distribution of cases and control according to BMI (kg/m2) Category according to BMI (kg/m2)

Cases No.

Control %

No.

Underweight (≤19.9)

Normal (20-24.9)

Overweight (25-29.9)

Obese (≥ 30)

Total

100

Table 3. Distribution of cases according to fasting insulin levels Category

Cases

Control

No.

Normal

Increased

Table 4. Distribution of cases according to components of metabolic syndrome in patients of PCOS Clinical components

Cases

Control

Positive

BP >130/85 mmHg

Impaired fasting blood glucose (>100 mg/dl)

Waist hip ratio >0.85 cm

↑STG (>150 mg/dl)

↓HDLc (<50 mg/dl)

Table 5. Comparative evaluation of clinical spectrum of MBS in Cases and Control Clinical parameters Age (years)

Control (50) Case (50)

P value

0.52

23.75

24.25

0.78

SBP (mmHg)

110

120

0.06

DBP (mmHg)

0.06

S. Cholesterol (mg/dl)

175.2

201.2

0.02

S. TG (mg/dl)

110.7

133.3

0.03

HDL (mg/dl)

35.2

25.4

0.04

LDL (mg/dl)

105.2

130.8

0.04

VLDL (mg/dl)

12.2

18.12

0.02

Insulin (µIU/ml)

5.1

6.5

0.04

Fasting glucose (mg/dl)

0.04

BMI

ANOVA test is used for calculating p value.

Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

CLINICAL STUDY TABLE-VI Study

Year

Prevalence of MBS

2012-13

24%

Gluceck et al (USA)1

2003

43-46%

Dev Ram Prasad (India)2

2011

42%

Ehrman et al3

2006

33.4%

Dokra’s et al4

2005

47.3%

Our study

obese than non PCOS obese (p value <0.04). This is in accordance with the study of Macut D et al5 who found that overweight and normal weight women with PCOS have higher incidence of lipid profile derangement than their controls. Wild RA Fertil Steril et al Oklahama USA 20116 found that dyslipidemia is more common in PCOS.

control, which shows a statistically significant difference (p<0.05) and thus PCOS per se is responsible for prevalence of MBS.

Conclusion It is observed that MBS manifests at an early age in women PCOS. Hyperinsulinemia, a central factor in the pathogenesis of PCOS, also appears to be a critical link between PCOS and MBS. Thus there is an urgent necessity to assess the rising trend of MBS among the women with PCOS and to take early measures for primary prevention of its long term sequel. In order to prevent metabolic syndrome maintain BMI lower than 25 and waist circumference less than 35 inches to prevent the development of metabolic syndrome or CVD.

In our study among patients with lipid profile derangement, 44% had decreased HDL as compared to 12% of control (p value <0.05). low HDL is having more detrimental effect on lipid profile derangement predictions among cases which is in accordance with a study in Teharian women by A. Mohini et al., 20127 where low HDL

An independent panel convened by the National Institutes of Health has recommended that well designed, multicentric studies be conducted to determine factors such as obesity, that exacerbate a genetic predisposition. The panel also determined the need for additional research to identify risks and treatments for complications and how to manage the common symptoms.

was found in 96.9% of cases of MBS in PCOS. Study by Dev Ram Prasad et.al. 20112 showed deceased HDL in 50% cases.

References

In our study waist circumference which depicts central obesity ≥ 80 cm. was found in 38% of cases and 14% of control (p <0.05). It is different from study done by Ehrman et. al., 20063 which supports high value of waist circumference by citing 80% of subjects above 88 cm. In our study fasting insulin level showed increase in 24% of cases and 10% of control (p value <0.05) it shows a significant difference among women with MBS in comparison to those without MBS as supported by Dokras et. al.4 study in 2005. We observed that while USA women and Indian woman have similar androgen levels, similar BP, similar total cholesterol and LDL, USA women have higher body weight, higher fasting insulin, higher fasting glucose level, lower HDL and raised triglycerides. Most of these difference occurred as a result of higher prevalence of obesity in USA group but other factors including characteristics of diet may also be responsible. Thus in our study prevalence of metabolic syndrome is 24% among case and 6% among age and BMI matched

Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

1. Glueck CJ, Papua R, Wang P, Goldenberg N and Sieve Smith. Incidence and treatment of MBS in newly referred women with confirmed PCOS Journal of Clinical Endocrinology & Metabolism 2003;52:908-915. 2. DevRamprasad, Mukharjee Shiuli Roy, Roy Biswas Ranu, Mukhopadhyay, Biswas SC. Association of MBS in PCOS: an observational study; Journal of Obst. & Gynae. of India, March/April 2011;176-181. 3. Ehrmann DA, David R, Liljenquist DR, Kasza K, Azziz R, Legro RS, Ghazzi MN 2006 Prevalence and predictors of the metabolic syndrome in women with polycystic ovary syndrome. J Clin Endocrinol Metab 2006, 91:48-53. 4. Dokras A, Bochner M, Jagasia DH. Screening women with PCOS for MBS, Obstet Gynaecol 2005 July; 106(1): 131-7. 5. Macut D, Damjanovic S, Panidis D, Spanos N, Glisic B, Petakov M, Rousso D, Kourtis A, Bjekic J, Milic N (July 2006) Oxidised low-density lipoprotein concentrationearly marker of an altered lipid metabolism in young women with PCOS. Eur J Endocrinol 2006 July 155 (1):131-136. 6. Wild RA, Rizzo M. Clifton S. Carmina E. Lipid levels in polycystic ovary syndrome: systematic review and meta-analysis. Fertil Steril 2011;95(3):(1073)-9.e I-11. Epub 2011 Jan 17. 7. Ashraf Mohini, Falenun Javan Mard, Bita Eslami, Najmeh Aletaha MD “Prevalence of Metabolic Syndrome in PCOS women in a hospital of Tehran”. Human Reprod Med., 2012; Vol. 10 No. 2: 127-130.

CLINICAL STUDY

Prophylactic Preoperative use of Rectal Misoprostol vs Intravenous Oxytocin Infusion During Cesarean section to Reduce Intraoperative and Postoperative Blood Loss *Rekha R, †Shikha S, ‡Saroj S, *Urvashi V, *Ruchika G, *Rachana A, ≠Latica

ABSTRACT Objective: To compare the effectiveness of per-rectal misoprostol administered immediately after spinal anaesthesia ,before giving skin incision , with intravenous oxytocin infusion just after delivery of neonate in prevention of uterine atony and thereby reducing blood loss at cesarean section. Methods: Four hundred women with singleton term pregnancy undergoing elective lower segment cesarean section under spinal anesthesia were included in this study. They were randomly allocated to receive either misoprostol 400 μg per-rectally or intravenous infusion of 10 units of oxytocin soon after delivery of the neonate. The main outcome measures were blood loss at cesarean section, change in hemoglobin levels, need for additional oxytocics and drug related side effects. Results: The mean blood loss estimated was almost equal in misoprostol group and oxytocin group (578 ml versus 620 ml; p = 0.67). The incidence of side effects such as pyrexia, shivering and was significantly higher in misoprostol group compared to oxytocin group. Conclusion: Per-rectal misoprostol appears to be as effective as intravenous infusion of oxytocin in reducing blood loss at cesarean section. However, occurrence of transient side effects such as shivering and pyrexia and nausea were noted more frequently with the use of misoprostol. Key words: Misoprostol, Oxytocin, Blood loss, Cesarean section

ostpartum hemorrhage is defined as loss of blood greater than 500ml from the genital tract in the first 24hrs following delivery (WHO,2003) and this compares with 1000ml of blood loss for cesarean section. We can also define postpartum hemorrhage as hemoglobin difference of ˃10% between before and 24 hrs after cesarean delivery. About 57,000 women dies in child birth every year in India (2010). The Millennium Development Goal (MDG) related to maternal health as one maternal death is being reported every 10 minutes in the country now. The current Maternal Mortality Rate (MMR) of India is 200 per one lakh live births (2010), whereas the country`s MDG in this respect is 109 per one lakh live births by 2015. Uterine atony is the commonest cause of severe postpartum hemorrhage. Consequently the administration of uterotonic drugs during cesarean

section has become essential to diminish the risk of postpartum haemorrhage and improve maternal safety. The aim of our study was to evaluate and compare the effect of preoperative rectal administration of misoprostol and intravenous oxytocin on blood loss in selected cases of caesarean delivery. Materials And Methods The study was conducted in SNMC Agra from Dec’2011 – Aug’2013 on 400 patients. An informed consent was taken from all women included in the study. Thorough history taking and physical examination was done in all patients.

Inclusion Criteria • Reproductive age group (21-35 year) • Parity ( ≤4 ) • Elective cesarean cases

*lecturer †

Asso. Professor

• Hb ≥ 11gm%.

‡

Professor and Head

Exclusion Criteria

≠

IIIrd yr junior resident Department of Obstetrics and Gynaecology, S.N.Medical college, Agra,U.P. Address for correspondence Dr.Rekha Rani (Lecturer) Department of Obstetrics and Gynaecology, SN Medical College, Agra E-mail: drrekha.gynae@gmail.com

• Patients booked in antenatal period

• Age >35 years. • Grand multipara >4 children. • Previous h/o postpartum placenta

hemorrhage or retained

Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

CLINICAL STUDY • Any risk factor associated with pph (including abnormal placentation, multiple gestation, uterine fibroids, history of postpartum haemorrhage or uterine atony, and previous classical uterine incision), • Patients undergoing emergency cesarean section. • Patients with previous h/o scar rupture or dehiscence in which repair of uterus or hysterotomy done.

Following are the outcome measures• Postoperative hemoglobin deficit in 24 hrs • Intraoperative & postoperative (8hrs) estimation.

• Frequency of primary postpartum hemorrhage. • Side effects of misoprostol.

• Malpresentation, medical and coagulation disorders (diabetes, epilepsy, heart diseases), history of bronchial asthma

• Side effects of oxytocin

In the above mentioned criteria 400 patients were selected. They were divided into two groups. In study group (n=200) 600µg misoprostol was administered per-rectally just before the start of cesarean section after giving required anaesthesia. In control group (n=200) 10 units i/v oxytocin started just after delivery of baby.

Discussion

• The main outcome measures were intraoperative and postoperative blood loss within 24 hours and the difference between preoperative and postoperative haemoglobin, hematocrit values, mean arterial pressure and heart rate. The amount of blood loss was measured in the kidney tray applied after drainage of liquor which was decanted into measuring cylinder. Blood soaked mops and linen were weighed, the known ‘dry weight’ was subtracted and the calculated volume added to that cylinder/kidney tray. (Each gm ↑ in linen & mops wt was equivalent to 1 ml of blood loss). Postoperative blood loss was measured on standard sized pad applied locally. The blood loss estimation was done as shown in fig.I.

Investigations • Blood grouping, hemogram ,urine-routine and microscopy, Random Blood Sugar, Blood urea, HIV, HbsAg, Clotting factors done before cesarean section. • Hemoglobin was repeated 24 hrs after cesarean section. • Obstetric USG

blood loss

• Acceptability of drug (misoprostol) by per-rectal route.

Result

In this study there were no differences in preoperative and postoperative hemoglobin concentration as well as the amount of intraoperative blood loss between the two groups ( table II ). Vimala et al(4) in their study on comparision of 400µg sublingual misoprostol with oxytocin found that intraoperative bleeding was more significant in oxytocin group, although postoperative hemoglobin level was not different. In Chaudhuri et al(6) study with 800µg rectal misoprostol, although postoperative hemoglobin level was not different in the two groups, the intraoperative bleeding was significantly lesser in misoprostol group. Although in different studies, intraoperative blood loss was equal in both groups but intraoperative blood loss with the use of misoprostol has a wide ranged from 500ml(6)-1000ml(9). This wide range of blood loss may be due to differences in the dose,route and timing of administration of misoprostol. Chaudhuri(6) used 800 µg rectal misoprostol before making incision on the Table 1. Mean ±SD of Age, no. of Pregnancies, Weeks of Pregnancy and Duration of Operation in 2 Groups Variables

Study Group

Control Group (Misoprost. Grp) (Oxytocin Grp)

P-VALUE

Age(yrs)

26.6 ± 5.4

27.1 ± 5.3

0.64

No. of pregnancies

1.85 ± 0.92

1.91 ± 0.85

0.73

Duration of pregnancy (wks)

38.65 ± 0.58

38.66 ± 0.85

0.94

• Chi- Square test was used to compare blood loss and postoperative hemoglobin in both groups.

Duration of operation (min)

38.5 ± 5.8

40.42 ± 6.1

0.11

• P-value < 0.05 was considered significant.

There was no significant difference between the groups in age, duration and number of pregnancy and surgery.

Results • Mean and standard deviation was calculated for numerical value i.e. age and parity. • Frequency and percentage were presented for amount of blood loss and postoperative hemoglobin.

Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

CLINICAL STUDY Table 2. Mean ± SD of Amount of Intra-operative Bleeding and Mean pre, and Post-operative Hemoglobin Level in the Two Groups Variables 1. Hb% (gm/dl)

2. Amount of bleeding (ml)

Study Group (Misoprost. Grp)

Control Group (Oxytocin Grp)

P-VALUE

Preoperative

11.45 ± 1.o2

11.29 ± 0.62

0.72

postoperative

10.32 ± 0.83

10.19 ± 0.58

0.36

Mean Hb deficit

01.13 ± 0.19

1.10 ± 0.03

0.52

intraoperative

578 ± 234

620 ± 375

0.39

185 ± 95

224 ± 167

postoperative

There were no differences in preoperative and postoperative hemoglobin concentration . The amount of intraoperative blood loss was less in the misoprostol group but the difference between the two groups was not statistically significant.

STUDY GROUP (Misop. Grp ) BEFORE

AFTER

CONTROL GRP. (Oxytocin Grp) BEFORE

AFTER

P-VALUE

VARIABLES

P-VALUE

Table 3. Mean ± SD of Mean Arterial Pressure and Heart Rate in the Two Groups

mean arterial pressure (mm Hg) 82.4 ±15.5

78.3 ± 14.8

0.24

83.3 ±13.3

75.1 ±11.5

0.003

Heart rate (beats/min)

99 ± 18

0.48

104 ± 17

122 ± 21

0.005

96 ± 21

The heart rate of patients in oxytocin group significantly increased from 104 ± 17 beats/min to 122 ± 21 beats/min (p=0.005). There was no change in the heart rate in the patients who received rectal misoprostol (96 ± 21 bpm vs. 99 ± 18 bpm; p= 0.48).

Table 4. The comparison of side-effects during and after operation in the two groups Variables

Study Group (Misoprost.Grp)

Control Group (Oxytocin Grp)

P -value

N=200

Chest pain

1.0%

7.0%

0.03

Nausea

5.0%

7.0%

Vomiting

2.0%

4.0%

Shivering

10.0%

1.0%

0.03

Hyperpyrexia >40°C

4.0%

1.0%

The incidence of shivering was statistically higher in the misoprostol group while the incidence of chest pain was statistically higher in the oxytocin group. Other side effects were not statistically different between the two groups. Oxytocin reduces mean arterial blood pressure and peripheral vascular resistance, increases heart rate and creates ST-segment changes and consequently will lead to chest pain

uterus followed by infusion of 6 units of oxytocin in half an hour but Vimala(4) used 400µg of oxytocin in half an hour. In measuring hemoglobin level the changes are almost similar in different studies e.g. in spite of 500cc difference in amount for intraoperative blood loss in Chaudhuri &

Vimala studies the difference in hemoglobin changes is only 0.3mg/dl (0.411 vs 0.1mg/dl respectively). The rate of bleeding and the hemoglobin changes found in our study was similar to most other studies(8,9). The differences between our study and that of Chaudhury may be due to the lower dose of rectal misoprostol (400µg vs 800µg) and higher dose of oxytocin in our study. Changes in blood pressure and heart rate are side-effects of oxytocin. In our study, decrease in mean arterial blood pressure and increase in heart rate were significantly more common in patients receiving oxytocin. Vimala has reported shivering in 26% of patients with 400µg of sublingual misoprostol and 4% in oxytocin group. In Lapaire study with 800µg of misoprostol; the incidence of shivering was 36% in comparision with 8% in oxytocin group. Chaudhuri reported 8.3% and 1.1% in misoprostol and oxytocin group respectively. Shivering was seen in 16% of our patients in misoprostol group and 2% in oxytocin group. These findings are compatable to previous studies. The difference of nausea and vomiting in the two groups was not significant. Similar findings were reported in previous studies(6,7). Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

CLINICAL STUDY

25 mL

50 mL

100 mL

Figure 1. Estimated Blood Loss

Hyperpyrexia was seen in 8% of patients who received misoprostol and 2% with oxytocin. The difference was not significant. Previous studies have reported similar findings(6,7).

Conclusions Leading cause 0f postpartum hemorrhage is uterine atony, can be successfully treated with misoprostol. Misoprostol is potent uterotonic drug . Its per-rectal use is much better in controlling postpartum hemorrhage , lesser side effects , better tolerability , cheaper ,and does not require refrigeration. Its route of administration is non-invasive than other uterotonic drugs. It has long half life. The features discussed above makes the misoprostol much better option in developing countries. Misoprostol is a synthetic analogue of prostaglandin E1 which its using is very simple; there is no need to intramuscular or intravenous administration and can be kept at room temperature and is easily carried. Misoprostol is administered as rectal, vaginal, oral, and sublingual and there is no need to ringer serum or injection. It is saved very easily results and is resistant at room temperature. Misoprostol may therefore be considered as an alternative agent when oxytocin is relatively contraindicated in patients with pre-eclampsia, prolonged labour, or cardiac disease.

References 1. Khan FA, Khan M, Ali A et al. - Estimation of blood loss during Caesarean section: an audit. J Pak Med Assoc,

Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

2006;56:572-577. 2. Magann EF, Evans S, Hutchinson M et al. - Postpartum hemorrhage after cesarean delivery: an analysis of risk factors. South Med J, 2005;98:681-686. 3. Acharya G, Al-Sammarai MT, Patel N et al. - A randomized, controlled trial comparing effect of oral misoprostol and intravenous syntocinon on intra-operative blood loss during cesarean section. Acta Obstet Gynecol Scand, 2001; 80:245-250. 4. Vimala N, Mittal S, Kumar S - Sublingual misoprostol versus oxytocin infusion to reduce blood loss at caesarean section. Int J Gynaecol Obstet, 2006;92:106-110. 5. Eftekhari N, Doroodian M, Lashkarizadeh R - The effect of sublingual misoprostol versus intravenous oxytocin in reducing bleeding after caesarean section. J Obstet Gynaecol, 2009;29:633-639. 6. Chaudhuri P, Banerjee GB, Mandal A - Rectally administered misoprostol versus intravenous oxytocin infusion during cesarean delivery to reduce intraoperative and postoperative blood loss. Int J Gynaecol Obstet, 2010;109:25-34. 7. Combs CA Murphy EL Laros Jr RK: Factors associated with hemorrhage in caesarean deliveries. Obstet Gynecol,1991,77;77-82 8. Prendivelli W Elbourne D ;Care during the third stage of labour. In Chalmers I Enkin M Keirse MJMC. Editors Effective care in pregnancy and childbirth. Oxford 7 University Press; 1989,p. 1145-69. 9. Pregnancy and Childbirth Module In Keirse MJMC , Renfrew MJ Neilson JP Crowther C editors Cochrane Database of Systemic Reviews. The Cochrane Collaboration. Issue 2. Oxford Update Software: 1995; Review NoTs 2974, p 2999-5352.

Bilateral PSOAS Abscess in Surgery PUNEET MALIK

ABSTRACT Iliopsoas abscess is a relatively uncommon condition that can present with vague clinical features. Its insidious onset and occult characteristics can cause diagnostic delays, resulting in high mortality and morbidity.We present the case of 25 year old male patient who initially presented in urology department with polycystic kidney disease. Further imaging investigations later revealed bilateral psoas abscess with pott’s spine. Pott’s spine must always be considered as an important cause of psoas abscess, particulary in developing nations. In our case abscess was surgically drained and anti-tubercular treatment was started early which resulted in a favorable outcome. Key words: Psoas abscess, tuberculosis, polycystic kidney disease

soas abscess is usually unilateral but can be bilateral in upto 3% of cases. Psoas abscess may be clinically difficult to diagnose because of its rarity, insidious onset of the disease and non specific clinical presentation which can cause diagnostic delays. In patients with psoas abscess associated with pott’s spine a delay in diagnosis can result in severe and irreversible neurologic sequelae. We describe 25 year male with bilateral psoas abscess associated with pott’s spine which was treated successfully with antitubercular drugs and bilateral open drainage of the psoas abscess. Case Report A 25 year old male patient initially presented to urology department with chief complaint of backache for past one year and left flank lump for past 2 months. Backache was dull aching, continuous, mild to moderate in severity, which was partially relieved by medication. History of mildly painful lump in left flank was present which progressively increased in size over past 2 months. History of low grade fever and malaise was present.

Patient was tobacco chewer and occasional smoker. On physical examination, patient was vitally stable, afebrile, preferred lying with hip flexed. His gait was antalgic. On abdominal inspection, fullness was noted in both iliac fossas, extending below inguinal region. On palpation, mild tenderness was elicited and it was soft in consistency. Examination of rest of the abdomen was normal. There was no spinal tenderness and all four limbs power was 5/5. On investigating, patients haemoglobin was found to be 13.3 gm/dl, WBC count was 9600/cu mm. of which 68% was neutrophils and 30% was lymphocytes, ESR was 30 mm/hr, renal and liver function tests were within normal range. Ultrasonography revealed large 15 x 10 cm cystic mass with fluid and internal echoes and debris in left paracolic gutter, most likely suggestive of an abscess along with multiple small cystic areas in both kidneys with poor cortico-medullary differentiation. Following USG, CECT whole abdomen with urography was done which showed large bilateral psoas abscess, bilateral polycystic

Professor Address for correspondence All India Instiute of Medical Sciences Figure 1. Ct Image showing bilateral psoas abscess.

Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

CLINICAL STUDY

Figure 2. Image showing associated bilateral polycystic kidney disease. Figure 4. Image showing associated pott‘s spine

Discussion Iliopsoas abscess was first described by Mynter in 1881 who referred to this as psoitis.1 Psoas muscle originates from 12th thoracic to 5th lumbar vertebrae and inserts at the lesser trochanter of femur. Its fibres blends with those of iliacus, together known as iliopsoas. Iliopsoas muscle is located in an extraperitoneal space called the iliopsoas compartment. Iliopsoas abscess is collection of pus in this compartment. It is surrounded by rich vertebral plexus which explains its predisposition to infections by haematogenous route.11 Figure 3. Bilateral psoas abscess in sagittal section.

kidney disease, right renal calculus and destruction of adjoining part of second and third lumbar vertebrae with pre-para vertebral and epidural collections with secondary spinal canal stenosis, findings were in favour of pott’s spine. MRI of lumbosacral spine with screening rest of the spine revealed findings suggestive of pott’s spine showing osteitis of L2 to L4 vertebral bodies, L2-3 discitis, minimal pre-paravertebral and ventral epidural abscess component L2-3, bilateral ilio-psoas abscesses and degenerative changes were seen in cervical spine. There was ventral ridging of thecal sac at C5-6 due to posterior osteophytic ridges and protruding disc. Patient was advised strict bed rest and anti-tubercular treatment was started. Patient was planned for surgery and open drainage of psoas abscess was done bilaterally with drain placement. Around 300ml of pus was found in left sided and 100ml in right sided psoas abscess. Both drains were removed on third post-op day. On post op day five, he was discharged home in stable condition. Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

Iliopsoas abscess is common in the young (less than 20 years) compared with the elderly. It is reported to be commoner in males than females with 3:1 ratio.5,6,7,10 It is more frequently found in people with low socio economic status. Iliopsoas abscess is classified as primary or secondary, depending on the presence or absence of underlying disease. Primary iliopsoas abscess occurs as a result of haematogenous or lymphatic spread of an infectious process from an occult source in the body. It is commonly seen in immunosupressed states, diabetics, renal failure, etc. Secondary iliopsoas abscess is because of contagious spread from nearby structures. The psoas muscle is situated near a number of important anatomical structures including the vertebral bodies, the abdominal aorta, the sigmoid colon, the appendix, the hip joint, and iliac lymph nodes.13 Infection may spread directly between these structures and the psoas muscle. Of all these structures, lumbar vertebral osteomyelitis because of tubercular pathology is an important cause of secondary psoas abscess, particularly in developing nations. Crohn’s

CLINICAL STUDY disease is most common cause of secondary psoas abscess in developed nations.2 Other causes include appendicitis, diverticulitis, aortic mycotic aneurysm, endocarditis, instrumentation in and around the spine.2,3 Mostly primary abscess is because of Staphylococcus Aureus and secondary because of mixed flora of the gut like E.coli and Bacteroides.12 Classic triad of symptoms in psoas abscess includes chronic backache, fever and limitation of hip joint movement. It is present in only 30% of cases.8 Chronic back pain is most common symptom associated with psoas abscess, in particular when it is associated with pott’s spine.8 It is usually progressive, duration may vary from weeks to months, may or may not be associated with muscle spasm. Hip movements are restricted. Patients usually prefer lying with hip joint flexed and resists the hyperextension or active flexion of hip joint done by the examiner.3 Patient may present with limp or lump in inguinal region. Other constitutional symptoms includes loss of appetite, weight loss, evening rise of temperature. Symptoms are mostly non specific which is main reason behind delay in diagnosis, particularly in tubercular patients where classic symptoms can even be absent. Patients presenting late can present with septic shock or neurologic sequelae like paraplegia. Complete blood count, ESR, CRP, urine analysis, blood culture is helpful in knowing the source of infection in psoas abscess. USG is diagnostic in 60% of cases.2 IV contrast enhanced spiral CT has become the gold standard modality.10 MRI is better imaging technique to evaluate spinal canal and to rule out other potential causes of backache.10 In cases of secondary abscess, one must give consideration to CT abdomen with IV and oral contrast. In cases of primary abscess clinician may empirically start iv anti-staphylococcal antibiotics like vancomycin, clindamycin and linezolid. In secondary cases, antibiotic spectrum must cover gram negative and anaerobic flora of the gut. Antibiotics preferred are third and fourth generation cephalosporins, fluoroquinolones, antipseudomonal penicillins with or without metronidazole.7,8 Antibiotics can be changed after culture and sensitivity report and to be continued after two weeks of abscess drainage. Definitive treatment requires pus drainage, CT-guided percutaneous drainage is gold standard particularly in primary etiologies where as open surgical drainage is preferred where secondary abdominal pathology is

present and in cases where percutaneous drainage fails. Surgical drainage is associated with shorter hospital stay due to higher incidence of concurrent intra abdominal pathology.9 Mortality rates are 2.4% and 18.9% for primary and secondary types.7 Mortality reaches close to 100% in cases without drainage because of sepsis.4,7

Conclusion Psoas abscess should be diagnosed as early as possible. In cases diagnosed with unilateral psoas abscess, a search for contra lateral abscess must be made, both clinically as well as with contrast enhanced CT. CECT may also help in identifying the cause of secondary psoas abscess as illustrated by our case who had bilateral psoas abscess secondary to pott’s spine. Pott’s spine must always be considered as an important cause of psoas abscess, particulary in developing nations.

References 1. Mynter H. Acute psoitis. Buffalo Med Surg J1881;21:202-10. 2. Riyad MN, Sallam MA, Nur A. Pyogenic psoas abscess: discussion 1. of its epidemiology, etiology, bacteriology, diagnosis, treatment and prognosis-case report. Kuwait Med J 2003;35:44-7. 3. Mallick IH, Thoufeeq MH, Rajendran TP. Iliopsoas abscess. Postgrad Med J 2004;80:459-62. 4. Thongngarm T, McMurray RW. Primary psoas abscess [letter] Ann Rheum Dis 2001;60:173-6. 5. Walsh TR, Reilly JR, Hanley E, et al. Changing etiology of iliopsoas abscess. Am J Surg 1992;163:413-16. 6. Dinc H, Onder C, Turhan AL et al. Percutaneous drainage of tuberculosis and nontuberculosis psoas abscess. Eur J Radiol 1996;23:130-4. 7. Gruenwald I, Abrahamson J, Cohen O. Psoas abscess: case report and review of the literature. J Urol 1992;147:1624-6. 8. Chern CH, Hu SC, Kao WF, et al. Psoas abscess: making an early diagnosis in the ED. Am J Emerg Med1997;15:83-8. 9. Procaccino JA, Laury IC, Fazio VW, et al. Psoas abscess: difficulties encountered. Dis Colon Rectum 1991;34:784-9. 10. Isdale AH, Nolan DF, Butt WP, et al. Psoas abscess in rheumatoid arthritis-an inperspicuous diagnosis. Br J Rhuemato 1994;33:853-8. 11. Taiwo B. Psoas abscess: a primer for the internist. South Med J 2001;94:2-5. 12. Vandenberge M, Marie S, Kuipers T, et al. Psoas abscess: report of a series and review of the literature. Neth J Med. 2005;63:413-6. 13. Postgrad Med J 2004;80:459-462 doi:10.1136/pgmj 2003.017665

Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

CASE REPORT

Progesterone and Prevention of Preterm Labour *Ruchika Garg, *Urvashi Verma, *Rajni Rawat, †Somya Shrivastava, ‡Renu Rajvanshi

ABSTRACT Objectives: To evaluate the effect of vaginal progesterone in the prolongation of duration of pregnancy in women at high risk of developing preterm labour. Material and Method: This is a prospective case control study carried out in the department of Obstetrics & Gynaecology S.N. Medical College Agra on 100 patients chosen from in patients and outpatient department (50 cases and 50 control).Women with singleton pregnancy having history of preterm labour, uterine malformation, prophylactic cerclage, currently suffering from premature pains were given daily vaginal progesterone 200mg from 24 weeks and discontinued at 34 weeks of gestation. In both groups rate of preterm labour and neonatal outcome was determined. Results: The incidence of preterm labour in progesterone group was 17.8% and in control group 36%, p value is <0.05. Conclusion: Administration of progesterone in women at high risk developing preterm labour reduces the incidence of preterm labour, neonatal mortality and morbidity and increases baby weight <2.5kg. Key words: Preterm labour, Progesterone.

reterm labour is defined by WHO as contraction of sufficient strength and frequency to effect progressive effacement of cervix between 2037 weeks. Worldwide incidence of preterm labour is 6-10%.1 Csapo et al promoted the progesterone see-saw theory, according to it high progesterone level prevent uterine contractions and low level facilitate such contraction.2

Aims of Study To compare the effect of vaginal progesterone Vs placebo on the prevention of preterm labour, among women at increased risk of preterm labour. Material and methods: Study was conducted at the department of obstetrics and gynaecology S. N. Medical College Agra (U.P.). High risk patients seen in outpatient department and admitted in emergency were recruited. Women with singleton pregnancy with age group 20-35 years having history of preterm labour, *Assistant Professor †

Senior Resident

‡

Resident

Dept. of obstetrics and gynaecology S. N. Medical college Agra- 282003 (U.P.) Address for correspondence Dr Ruchika Garg Assistant Professor, Department of obstetrics and gynaecology S. N. Medical College Agra D 1, Sulahkul Nagar, Bodla road, Agra UP E-mail: ruchikagargagra@gmail.com Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

prophylactic cerclage, uterine malformation or currently suffering from premature pains on the basis of clinical information and evaluation of USG were included in study. 50 antenatal women were given 200mcg micronized sustained released progesterone while another 50 antenatal women were provided placebo. Daily micronized sustained released vaginal progesterone 200mcg 12 hourly was started beyond 12-14 weeks and discontinued after 36 weeks gestation or early if passes in labour. Patients with multiple pregnancy, major fetal anomaly, allergy to progesterone, premature rupture of membrane, cervical dilation >4cm, coexisting maternal medical disease, fetal distress and chorioamnionitis were excluded from the study.

Result and Discussion The incidence of preterm labour was 36% in placebo and 17.8% in progesterone group in our study (p<0.05) (table 1). The incidence of preterm labour was 54.9% in placebo group 36.3% in progesterone group in study of Meis et al3. In study of fonseca EB4 et al it was 28.5% and 13.8% respectively. 35.9% and 26.2% in study of Luis sanchez et al. In Meis et al5 babies with birth weigth <2.5kg were 27% in progesterone treated group and 41% in control with relative risk (0.66) CI. 51-0.87. In our study babies with birth weight <2.5kg

CLINICAL STUDY Table 1. Distribution of Women According to Profile Patient profile

Group A (progesterone)

GroupB (placcebo)

Mean age(years)

28.6yrs

27.6yrs

Gravida 2

24(48%)

22(44%)

Gravida >3

26(52%)

28(56%)

Socioeconomic status

Class III20(40%)

Class III28(44%)

Class IV30(60%)

Class IV22(56%)

16(32%)

24(48%)

18(36%)

10(20%)

8(16%)

Preterm delivariesl

Study

In cases

In controls

Meis et al (RR = 0.66)

27%

41%

Present study (RR = 0.65)

38.02%

55%

Table 4. Mean gestational age in progesterone group vs placebo Study Jhonson et al

Cases

Controls

38.6weeks

35.2weeks

Da fonseca et al

37weeks

36weeks

Our study

38weeks

34.5weeks

Conclusion

In cases (In progesterone treated group)

In controls(In placebo group)

Meis et al

36.3%

54.9%

Fonseca et al

13.8%

28.5%

Luis Sanchez Ramos et al

26.2%

35.9%

Preterm birth complicates one in eight deliveries and remains a major cause of perinatal morbidity and mortality. Appropriate candidates should be counseled about the potential benefits of progesterone supplementation from 16 - 20 weeks up to 36 weeks of gestation to prevent preterm birth in any subsequent pregnancy. The result of current study has shown promising result in reducing the incidence of preterm birth and low birth weight babies.

Johnson JW et al

12.8%

40.9%

References

Present study(p=<0.05)

17.8%

36%

Table 2. Incidence of Preterm Labour in Progesterone Treated Group v/s Placebo Study done by

were 28% in progesterone treated group and 54% in control (table) it was found that labour was postponed by 2-4 weeks in 88% of cases. In study done by Jhonson et6 al and Da fonseca et7 al delivery occur at 38.6 weeks and 35.2 weeks respectively of cases, 37 weeks and 36 weeks respectively of controls. In our study delivery of cases postponed up to 38 weeks and of controls up to 34.5 weeks. In the study of Meis et8 al infant treated with progesterone had significantly lower rate of necrotizing enterocolitis, intraventricular haemorrhage and need for supplemental oxygen. Joddie M Dodd et,9 al found that infant with itraventricular haemorhage were very less in progesterone treated group. In our study it was found that number of days of NICU stay was significantly reduced in infant delivered to progesterone treated group.

Table 3. Birth weight (<2.5kg) in progesterone group vs placebo

1. Goldenberg RL .The management of preterm labour obstet Gynecol 2002;100(5):1020-37 2. Vidaeff AC Ramin SM From concept to practice the recent history of preterm delivery prevention. part 1: cervical incompetence. Am J perinatol 2006:23(1): 3. Meis et al AMJ obstet gynecol 2005;193(3pt):1181-6. 4. Fonseca EB et al.journal obstet Gynacol 1990;97;149-54. 5. Meis PJ. 17- OHPC for prevention of preterm delivery. Obstet Gynecol 2005;105:1128-35. 6. Johnson JW et al. Obstet Gynecol1979;54(4):412-8. 7. ACOG Committee Opinion No. 291.Use of progesterone to reduce preterm birth. Obstet Gynecol 2003;102:11158. Catherine Y, Spong MD, Meis PJ.Progesterone for prevention of recurrent preterm birth-impact of gestational age at previous delivery. 9. Dodd JM, Flenady V, Cincotta R, Crowther CA. Prenatal administration of progesterone for preventing preterm birth. Cochrane Database Syst Rev 2006;1:CD004947.

Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

CASE REPORT

A rare case of spinal muscular dystrophy/atrophy Sunanda kulkarni., Savitha C

Introduction Spinal muscular atrophy is a rare genetic disease which causes muscular weakness leading to increased morbidity and mortality. Early recognition and MTP saves the agony of the parents. Case is reported because of its rarity and to enhance the awareness of the condition. A 28 year old by name M G2P1L1 came to OPD with history of amenorrhoea of 3 months. Her past cycles were regular. Her married life of 5 years, was non consanguineous. She had undergone LSCS for PROM for the first baby which was a female baby weighing 3.75 kg. As baby had delayed milestones and was not able to walk even after one year, they had consulted the paediatrician. Muscle biopsy and genetic DNA was done which confirmed the diagnosis of spinal muscular atrophy. There was deletion of exon 7 of SNM 1 gene. Menstrual history – cycles were regular. Family history Professor Address for correspondence

Professor of OBG AIMS Bellur OBG BMC Bangalore

revealed that husband’s 2nd cousin had a female baby with similar complaints but the diagnosis was not confirmed. Past and personal history did not reveal anything significant. On examination the patient’s vitals were normal, and pelvic examination showed pregnancy about 12 weeks.

Investigations All routine investigations were within normal limits. Ultrasound confirmed pregnancy and foetus was corresponding to gestational age. In view of the SMA of the first baby – CVS was done and it was confirmed that this foetus also had homozygous deletion of exon7 of SNM1 gene. Couple were counselled for MTP for which they readily agreed. MTP was carried out with mifeprostone 200 mg and 3 doses of misoprostol 200microgram 4th hourly and patient expelled after 16 hours. Foetal post mortem was done. Autopsy showed that anthropometry was corresponding to the age of the foetus and there was no dysmorphic features and no associated anomaly. Brain and spinal cord was normally developed.

Discussion SMA is an autosomal recessive genetic defect where SNM a protein expressed in the yolk sac cells, which is necessary

Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

CLINICAL STUDY for survival of motor neurones. Deficiency of this protein leads to death of neuronal cells of anterior horn of spinal cord and subsequent muscle wasting leading to atrophy. It manifests from newborn to adulthood. Depending on the age of onset and appearance of symptoms it is classified into 3 types. Infantile type is from 0 to 6 months( Werdnig Hoffmans disease), Intermediate type from 6 to 18 months, (Dubowitz disease)where baby cannot stand and walk and life expectancy is also short. Juvenile kugelberg welanders disease is seen > 18 months where child can walk with support and life expectancy is near normal. Lastly adult onset manifests in 3rd decade of life. It affects extremities rendering the patient to wheelchair but life expectancy is not affected. Treatment needs respiratory, nutritional, mental health, cardiac and orthopaedic care. SMA is a rare hereditary disease and it could also be due to mutation of gene. Incidence is 1:10000 live birth. Approximately 90% of patients suffering is from lack of 2 copies of SNM gene on exon SNM1 on 7 and 8. It is slow progressive disease and there is no specific treatment. Disease can be diagnosed by clinical tests of motor disabilities, serum creatinine kinase, EMG testing for muscle atrophy. Muscle biopsy is absolutely necessary when genetic investigation is not confirmatory. In the present case genetically though it was confirmed by CVS, autopsy did not show the same results as the disease may manifest in later weeks of pregnancy. Prenatal diagnosis of SMA may be diagnosed by genetic analysis of circulating foetal cells from maternal blood1. Ultrasound evaluation of foetal movements in pregnancy at risk of SMA in 1st trimester were not confirmatory2.

if both parents were carrier or any family member had SMA ,prenatal diagnosis by DHPLC( denaturing high performance liquid chromatography) using DNA extracted from blood, chorionic villi and amniotic fliud can be done3.DNA from amniocytes and CVS can be analysed and MTP can be done if disease is confirmed4. SMA can also be diagnosed by PCR and MTP can be advised5.

Conclusion If there is family history of SMA, CVS should be done to confirm the disease by genomic studies. If the disease is confirmed the couple should be counselled for MTP to save them from agony and reduce burden to the society.

Reference 1. Prenatal diagnosis of SMA by genetic analysis of circulating foetal cells. Lancet volume 361, issue 9362, 22nd march 2003, pg 1013 â&#x20AC;&#x201C; 1014. C. Berond, M. Karlinova, J.P. Bonfont, A. Benachi, A.Munich, Y. Dumez, B. Lacour, Dr P. Paterine, Brechot 2. Ultrasound evaluation of fetal movements in pregnancies at risk of SMA . Neuromuscular disorders. volume 21, issue 2, February 2011, pg 97-101. Juan parra, Rebecca Martinez, Hernadez, Eva Also-Ralo, Laura Ahias, Maria Jesus, Barcello Maria Amanedo, Carmen Medina, Raqual Senosiain, Joaquim Calal, Montserrat Baiget, Sara.Elsevier. 3. Rapid prenatal diagnosis of SMA by denaturing high performance liquid chromatography system. Acta obstet gynecol scand 2008;87(a): 960-8. Shaw SN,Cheng P, Chong SD, Lin YT, Huig CC, Chen CP, Su YN 4. Prenatal diagnosis of SMA in Macedonian families. Genet test 2008 sep â&#x20AC;&#x201C; 12(3); 391-3. Kocheua SA, Plaseka Karnafilska D, Trivodaleiva S, Katarec M, Vlaski Jekic S, Efremoy GD Prenatal diagnosis of SMA in Chinese by genetic analysis of fetal cells. Chin Med J(Engl) 2005 aug 5:118(115): 1274-7. Vilu T, Diq XS, Li WL, Yao J, Derg XX.

Impact of metformin on reproductive tissues: an overview from gametogenesis to gestation. Metformin is an oral anti-hyperglycemic drug that acts as an insulin sensitizer in the treatment of diabetes mellitus type 2. It has also been widely used in the treatment of polycystic ovary syndrome (PCOS) and gestational diabetes. This drug has been shown to activate a protein kinase called 5' AMP-activated protein kinase or AMPK. AMPK is present in many tissues making metformin's effect multi factorial. However as metformin crosses the placenta, its use during pregnancy raises concerns regarding potential adverse effects on the mother and fetus. The majority of reports suggest no significant adverse effects or teratogenicity. However, disconcerting reports of male mouse offspring that were exposed to metformin in utero that present with a reduction in testis size, seminiferous tubule size and in Sertoli cell number suggest that we do not understand the full suite of effects of metformin. In addition, recent molecular evidence is suggesting an epigenetic effect of metformin which could explain some of the long-term effects reported. Nevertheless, the data are still insufficient to completely confirm or disprove negative effects of metformin.

Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

ORIGINAL ARTICLE

Iron Deficiency Anemia Evaluation and Management MATTHEW W. SHORT, LTC, MC, USA, and JASON E. DOMAGALSKI, MAJ, MC, USA

ABSTRACT Iron deficiency is the most common nutritional disorder worldwide and accounts for approximately one-half of anemia cases. The diagnosis of iron deficiency anemia is confirmed by the findings of low iron stores and a hemoglobin level two standard deviations below normal. Women should be screened during pregnancy, and children screened at one year of age. Supplemental iron may be given initially, followed by further workup if the patient is not responsive to therapy. Men and postmenopausal women should not be screened, but should be evaluated with gastrointestinal endoscopy if diagnosed with iron deficiency anemia. The underlying cause should be treated, and oral iron therapy can be initiated to replenish iron stores. Parenteral therapy may be used in patients who cannot tolerate or absorb oral preparations. (Am Fam Physician. 2013;87(2):98-104.

ron deficiency anemia is diminished red blood cell production due to low iron stores in the body. It is the most common nutritional disorder worldwide and accounts for approximately onehalf of anemia cases.1,2 Iron deficiency anemia can result from inadequate iron intake, decreased iron absorption, increased iron demand, and increased iron loss.3 Identifying the underlying etiology and administering the appropriate therapy are keys to the evaluation andmanagement of this condition. Diagnosis Diagnosis of iron deficiency anemia requires laboratoryconfirmed evidence of anemia, as well as evidence of low iron stores.4 Anemia is defined as a hemoglobin level two standard deviations below normal for age and sex (Table 1).5 A complete blood count can be helpful to determine the mean corpuscular volume or red blood cell size. Although iron deficiency is the most common cause of microcytic anemia, up to 40 percent of patients with iron deficiency anemia will have normo- cytic erythrocytes.2 As such, iron deficiency should still be considered in all cases of anemia unless the mean corpuscular volume is greater than 95 Îźm3 (95 fL), because this cutoff has a sensitivity of 97.6 percent.6 Other causes of microcytosis include chronic inflammatory states, lead poisoning, thalas- semia, and sideroblastic anemia.1 The following diagnostic approach is recommended in patients with anemia and is outlined in Figure 1.2,6-11 A serum ferritin level should be obtained in patients with Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

anemia and a mean corpuscular volume less than 95 Îźm3. Ferritin reflects iron stores and is the most accurate test to diagnose iron deficiency anemia.7 Although levels below 15 ng per mL (33.70 pmol per L) are consistent with a diagnosis of iron deficiency anemia, using a cutoff of 30 ng per mL (67.41 pmol per L) improves sensitivity from 25 to 92 percent, and specificity remains high at 98 percent.8,12 Ferritin is also an acute phase reactant and can be elevated in patients with chronic inflammation or infection. In patients with chronic inflammation, iron deficiency anemia is likely when the ferritin level is less than 50 ng per mL (112.35 pmol per L).7 Fer- ritin values greater than or equal to 100 ng per mL (224.70 pmol per L) generally exclude iron deficiency anemia.9,10 In patients with no inflammatory states and in whom the ferritin level is indeterminate (31 to 99 ng per mL [69.66 to 222.45 pmol per L]), further tests can be performed to ascertain iron status. Values consistent with iron deficiency include a low serum iron level, low transferrin saturation, and a hightotal iron-binding capacity.2 Soluble transferrin receptor anderythrocyte protoporphyrin testing,or bone marrow biopsy can be considered if the diagnosis remains unclear.2The soluble transferrin receptor level is an indirect measure of erythropoiesisand is increased in patients with irondeficiency anemia.8 Another benefit of this test is that the soluble transferrin receptor level is unaffected by inflammatory states and can help identify concomitant iron deficiency anemia in patients with anemia of chronic disease.12 Erythrocyte protoporphyrin is a heme precursor and accumulates in the absence of adequate iron stores.11 If other tests are indeterminate and suspicion for iron deficiency anemia persists, the absence of stainable

ORIGINAL ARTICLE Table 2. Etiologies of Iron Deficiency Anemia Etiology

Prevalence %

Abnormaluterine bleeding

20 to 30

Long-term use of aspirin or other monsteroidal anti-inflammatory drugs

10 to 15

Colonic carcinoma

5 to 10

Angiodysplasia

Blood donation

Gastric carcinoma

Peptic ulcer disease

CHILDREN

diagnostic standard.2

The American Academy of Pediatrics recommends universal hemoglobin screening and evaluation of risk factors for iron deficiency anemia in all children at one year of age.16 Risk factors include low birth weight, history of prematurity, exposure to lead, exclusive breastfeeding beyond four months of life, and weaning to whole milk and complementary foods without iron-fortified foods.16 The Centers for Disease Control and Prevention recommends screening children from low-income or newly immigrated families at nine to 12 months of age, and consideration of screening for preterm and low-birth-weight infants before six months of age if they are not given iron-fortified formula.14 The U.S. Preventive Services Task Force found insufficient evidence for screening in asymptomatic children six to 12 months of age and does not make recommendations for other ages.4 A meta-analysis showed that infants in whom cord clamping was delayed for up to two minutes after birth had a reduced risk of low iron stores for up to six months.17 Larger randomized studies that include maternal outcomes are needed before delayed cord clamping can be recommended for general practice.

Screening

Causes

Celiac disease

4 to 6

Gastrectomy

Helicobacter pylori infection

Esophagitis

2 to 4

Esophageal carcinoma

1 to 2

Gastric antral vascular ectasia

1 to 2

Small bowel tumors

1 to 2

Hematuria

Ampullary carcinoma

Bacterial overgrowth

Cameron ulcer (i.e., ulcer in large hiatal hernia)

Epistaxis

Intestinal resection

Information from references 5,7,18 and 19

iron in a bone marrow biopsy is considered the

MEN AND POSTMENOPAUSAL WOMEN

Asymptomatic men and postmenopausal women shouldnot be screened for iron deficiency anemia. Testing should be performed in patients with signs and symptoms of anemia, and a complete evaluation should beperformed if iron deficiency is confirmed.13 PREGNANT WOMEN

The American Academy of Family Physicians, U.S. Preventive Services Task Force, and Centers for Disease Control and Prevention recommend routine screening of asymptomatic pregnant women for iron deficiency anemia.4,11,14 The American College of Obstetricians and Gynecologists recommends screening for anemia and implementing iron therapy if iron deficiency anemia is confirmed.15 The defined values consistent with anemia

in pregnancy are hemoglobin levels less than 11 g per dL (110 g per L) in the first or third trimester, or less than 10.5 g per dL (105 g per L) in the second trimester.16 A maternal hemoglobin level of less than 6 g per dL (60 g per L) has been associated with poor fetal outcomes,including death.15

Once iron deficiency anemia is identified, the goal is to determine the underlying etiology. Causes include inadequate iron intake, decreased iron absorption, increased iron demand, and increased iron loss (Table 2).5,7,18,19

Iron Therapy Premenopausal women with a negative evaluation for abnormal uterine bleeding can be given a trial of iron therapy. In children and pregnant women, iron therapy should be tried initially. Current guidelines recommend empiric treatment in children up to two years of age and in pregnant women with iron deficiency anemia; however,if the hemoglobin level does not increase by 1 g per dL (10 g per L) after one month of therapy in children or does not improve in pregnant women, further evaluation may be indicated.4,15,16 In pregnant patients, poor compliance Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

ORIGINAL ARTICLE or intolerance should be considered, and parenteral iron may produce a better response.15

Evaluation The evaluation should begin with a thorough history and physical examination to help identify the cause of iron deficiency. The history should focus on potential etiologies and may include questions about diet, gastrointestinal (GI) symptoms, history of pica or pagophagia (i.e., compulsive consumption of ice), signs of blood loss (e.g., epistaxis, menorrhagia, melena, hematuria, hematemesis), surgical history (e.g., gastric bypass), and family history of GI malignancy. Patients with iron deficiency anemia are often asymptomatic and have limited findings on examination. Further evaluation should be based on risk factors (Figure 2).10,15,17-21

PREMENOPAUSAL WOMEN Excessive menstruation is a common cause of iron deficiency anemia in premenopausal women in developed countries; however, a GI source (particularly erosive lesions in the stomach or esophagus) is present in 6 to

30 percent of cases.20,22,23 If the gynecologic workup is negative and the patient does not respond to iron therapy, endoscopy should be performed to exclude an occult GI source.20,22,23 Excessive or irregular menstrual bleeding affects 9 to 14 percent of all women and can lead to varying degrees of iron deficiency anemia.24 Etiologies include thyroid disease,uncontrolled diabetes mellitus, polycysticovary syndrome, coagulopathies, uterinefibroids, endometrial hyperplasia, hyperprolactinemia,and use of antipsychotics orantiepileptics. Initial evaluation includes a history, physical examination, and pregnancy and thyroid-stimulating hormone tests. An endometrial biopsy should be considered in women 35 years and younger who have conditions that could lead to unopposed estrogen exposure, in women older than 35 years who have suspected anovulatory bleeding, and in women with abnormal uterine bleeding that does not respond to medical therapy.25

MEN AND POSTMENOPAUSAL WOMEN In men and postmenopausal women, GI sources of bleeding should be excluded. Current recommendations

Diagnosis of Iron Deficiency Anemia Patient with anemia, mean corpuscular volume < 95 µm3 (95 fL)

Ferritin ≤ 30 ng per mL

Ferritin 31 to 99 ng per mL

Ferritin ≥ 100 ng per mL

(67.41 pmol per L)

(69.66 to 222.45 pmol per L)

(224.70 pmol per L)

Increased total iron-binding capacity, low serum iron level, low transferrin saturation

In patients with any other result, order soluble transferrin receptor test

Increased

Decreased total iron-binding capacity, high serum iron level, high transferrin saturation

Decreased

Normal Erythrocyte protoporphyrin level increased? Yes

No iron deficiency anemia No

Suspicion persists; consider bone marrow biopsy

Iron deficiency anemia

Yes

Low bone marrow iron level?

Workup for other causes of anemia

Figure 1. Algorithm for diagnosis of iron deficiency anemia. Information from references 2, and 6 through 11.

Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

ORIGINAL ARTICLE

Evaluation of Iron Deficiency Anemia Iron deficiency anemia diagnosed

Premenopausal women

Men and postmenopausal women

Abnormal uterine bleeding?

No Treat with iron

If no response, initiate evaluation for occult GI blood loss

Upper endoscopy and colonoscopy; consider celiac serology

Yes Initiate workup for No evidence of GI bleeding source

Evidence of GI source

Treat underlying cause

Observe

Treat with iron (Table 3) Response

No response

Observe

Evidence of GI source

Repeat upper endoscopy and colonoscopy

No evidence of GI source

than 65 years will be diagnosed with a GI malignancy within two years of a diagnosis of iron deficiency anemia.28 Celiac serology should also be considered for all adults presenting with iron deficiency anemia.18 Upper endoscopy with duodenal biopsies should be performed to confirm the diagnosis after positive serologic testing and to evaluate for additional etiologies.29 In patients in whom endoscopy may be contraindicated because of procedural risk, radiographic imaging may offer sufficient screening. The sensitivity of computed tomographic colonography for lesions larger than 1 cm is greater than 90 percent.7 The use of barium enema is less reliable, but may be of use if colonoscopy or computed tomographic colonography is not available. If initial endoscopy findings are negative and patients with iron deficiency anemia do not respond to iron therapy, repeat upper nd lower endoscopy may be justified. In some instances, lesions may not be detected on initial examination (e.g., missed mucosal erosions in a large hiatal hernia, suboptimal preparation for colonoscopy, inadequate biopsy of a suspected lesion).13 Colonoscopy can fail to diagnose up to 5 percent of colorectal tumors.13

Additional evaluation of the small intestine is not necessary unless there is inadequate response to iron therapy, the Treat underlying cause Capsule endoscopy patient is transfusion dependent, or fecal occult blood testing suggests that the patient has had obscure GI Normal Abnormal bleeding with the source ndiscovered on initial or repeat Consider repeat Treat underlying cause; endoscopy.30 In these cases, further evaluation with capsule endoscopy push enteroscopy capsule endoscopy should be considered.30 Enteroscopy Figure 2. Algorithm for evaluation of iron deficiency anemia. is an upper endoscopy procedure using a longer scope to (GI = gastrointestinal.) visualize the proximal jejunum; it should be reserved to treat or biopsy lesions identified by capsule endoscopy. Information from references 10, 15, and 17 through 21. This test is a second-line technique for evaluating the small bowel because it is complicated by the level support upper and lower endoscopy; however, there are of sedation and duration of procedure. 13 Magnetic no clear guidelines about which procedure should be resonance imaging enteroclysis, computed tomographic performed first or if the second procedure is necessary enterography, or barium studies may also be considered, if a source is found on the first study.18 Lesions that but have a limited ability to identify most small bowel occur simultaneously in the upper and lower tracts are 18 lesions, which are mucosal and flat.7 rare, occurring in only 1 to 9 percent of patients. However, one study showed that 12.2 percent of patients Treatment diagnosed with celiac disease and iron deficiency anemia had a secondary source of anemia, including three cases UNDERLYING CAUSE of colon cancer.26 A study of patients with iron deficiency Patients with an underlying condition that causes iron anemia of unknown etiology in the primary care setting deficiency anemia should be treated or referred to a found that 11 percent had newly diagnosed GI cancer.27 subspecialist (e.g., gynecologist, gastroenterologist) for Additionally, a cohort study found that 6 percent of efinitive treatment. patients older than 50 years and 9 percent of those older

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ORIGINAL ARTICLE ORAL IRON THERAPY The dosage of elemental iron required to treat iron deficiency anemia in adults is 120 mg per day for three months; the dosage for children is 3 mg per kg per day, up to 60 mg per day.1 An increase in hemoglobin of 1 g per dL after one month of treatment shows an adequate response to treatment and confirms the diagnosis.16 In adults, therapy should be continued for three months after the anemia is corrected to allow iron stores to become replenished7 (Figure 36,28,31). Adherence to oral iron therapy can be a barrier to treatment because of GI adverse effects such as epigastric discomfort, nausea, diarrhea, and constipation. These effects may be reduced when iron is taken with meals, but absorption may decrease by 40 percent.1 Medications such as proton pump inhibitors and factors that induce gastric acid hyposecretion (e.g., chronic atrophic gastritis, recent gastrectomy or vagotomy) are associated with reduced absorption of dietary iron and iron tablets.31 PARENTERAL IRON THERAPY

Parenteral therapy may be used in patients who cannot tolerate or absorb oral preparations, such as those who have undergone gastrectomy, gastrojejunostomy, bariatric surgery, or other small bowel surgeries. The most ommon indications for intravenous therapy include GI effects, worsening symptoms of inflammatory bowel disease, unresolved bleeding, renal failureâ&#x20AC;&#x201C;induced anemia treated with erythropoietin, and insufficient absorption in patients with celiac disease.32 Parenteral treatment options are outlined in Table 3.2,16 Serious adverse effects have occurred in up to 0.7 percent of patients receiving iron dextran, with 31 recorded fatalities reported between 1976 and 1996.32,33 Iron sucrose and sodium ferric gluconate (Ferrlecit) have greater bioavailability and a lower incidence of life-threatening anaphylaxis compared with iron dextran.2 Approximately 35 percent of patients receiving iron sucrose have mild dverse effects (e.g., headache, nausea, diarrhea).7 One mall study cited similar adverse effect profiles between ntravenous iron dextran and sodium ferric gluconate, with only one serious adverse effect reported in the iron dextran group.34 If this finding is duplicated in larger studies, it could support the use of iron dextran over sodium ferric gluconate, because the total dose can be given in one sitting. A newer formulation, ferumoxytol, can be given over five minutes and supplies 510 mg of elemental iron per infusion, allowing for greater amounts

Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

Treatment of Iron Deficiency Anemia Iron deficiency anemia diagnosed

Treat underlying cause and start oral iron therapy

Not tolerated

Intravenous iron therapy

Monthly CBC showing improvedhematocrit and red blood cell indices?

Yes Continue therapy three months after hematocrit and ferritin levels normalize, then discontinue oral iron

CBC performed periodically; values normal? Yes No further monitoring needed unless symptoms arise

No Reevaluate for underlying cause Consider intravenous iron therapy Transfuse if symptomatic

Figure 3. Algorithm for treatment of iron deficiency anemia. (CBC = complete blood count.) Information from references 6, 28, and 31.

of iron in fewer infusions compared with iron sucrose.2

MONITORING There are no standard recommendations for followup after initiating therapy for iron deficiency anemia; however, one suggested course is to recheck complete blood counts every three months for one year. If hemoglobin and red blood cell indices remain normal, one additional complete blood count should be obtained 12 months later. A more practical approach is to recheck the patient periodically; no further follow-up is necessary f the patient is asymptomatic and the hematocrit level remains normal.7

BLOOD TRANSFUSION There is no universally accepted threshold for transfusing packed red blood cells in patients with iron deficiency anemia. Guidelines often specify certain hemoglobin values as indications to transfuse, but an essential part of deciding whether to transfuse.35 Transfusion is recommended in pregnant women with hemoglobin

ORIGINAL ARTICLE Table 3. Iron Therapy: Formulations and Dosing Form

Formulation

Elemental iron

Adult dosage

Intravenous Sodium ferric gluconate (Ferrlecit)

Solution for injection

12.5 mg per mL

Based on weight and amount of desired change in hemoglobin*

Iron dextran

Solution for injection

50 mg per mL

Iron sucrose

Solution for injection

20 mg per mL

Ferumoxytol

Solution for injection

30 mg per mL

Ferrous fumarate

324-mg tablet

106 mg

One tablet twice per day

Ferrous gluconate

300-mg tablet

38 mg

One to three tablets two or three times per day

Ferrous sulfate

325-mg tablet

65 mg

One tablet three times per day

Oral

*—Elemental iron (mg) = 50 × (0.442 [desired hemoglobin level in g per L – observed hemoglobin level in g per L] × lean body weight + 0.26 × lean body weight).2 Information from references 2 and 16.

levels of less than 6 g per dL because of potentially abnormal fetal oxygenation resulting in nonreassuring fetal heart tracings, low amniotic fluid volumes, fetal cerebral vasodilation, and fetal death.15 If transfusion is performed, two units of packed red blood cells should be given, then the clinical situation should be reassessed to guide further treatment.35

References 1. World Health Organization. Iron Deficiency Anaemia: Assessment, Prevention,and Control: A Guide for Programme Managers. Geneva, Switzerland:World Health Organization; 2001. 2. Johnson-Wimbley TD, Graham DY. Diagnosis and management of iron deficiency anemia in the 21st century. Therap Adv Gastroenterol.2011;4(3):177-184. 3. WHO Global Database on Anaemia. Worldwide Prevalence of Anaemia 1993-2005. Geneva, Switzerland: World Health Organization; 2008. 4. U.S. Preventive Services Task Force. Screening for iron deficiency anemia, including iron supplementations for children and pregnant women: recommendation statement. Am Fam Physician. 2006;74(3):461-464. 5. Van Vranken M. Evaluation of microcytosis. Am Fam Physician. 2010;82(9):1117-1122. 6. Ioannou GN, Spector J, Scott K, Rockey DC. Prospective evaluation of a clinical guideline for the diagnosis and management of iron deficiency nemia. Am J Med. 2002;113(4):281-287. 7. Goddard AF, James MW, McIntyre AS, Scott BB;

British Society of Gastroenterology. Guidelines for the management of iron deficiency anaemia. Gut. 2011;60(10):1309-1316. 8. Mast AE, Blinder MA, Gronowski AM, Chumley C, Scott MG. Clinical utility of the soluble transferrin receptor and comparison with serum ferritin in several populations. Clin Chem. 1998;44(1):45-51. 9. Knovich MA, Storey JA, Coffman LG, Torti SV, Torti FM. Ferritin for the clinician. Blood Rev. 2009;23(3):95-104. 10. Galloway MJ, Smellie WS. Investigating iron status in microcytic anaemia. BMJ. 2006;333(7572):791-793. 11. Assessing the iron status of populations: report of a joint World Health Organization/Centers for Disease Control and Prevention technical consultation on the assessment of iron status at the population level, Geneva, Switzerland, 6-8 April 2004. Geneva: World Health Organization, Centers for Disease Control and Prevention; 2005. 12. Skikne BS, Punnonen K, Caldron PH, et al. Improved differential diagnosis of anemia of chronic disease and iron deficiency anemia: a prospective multicenter evaluation of soluble transferrin receptor and the sTfR/ log ferritin index. Am J Hematol. 2011;86(11):923-927. 13. Bermejo F, García-López S. A guide to diagnosis of iron deficiency and iron deficiency anemia in digestive diseases. World J Gastroenterol. 2009;15(37):4638-4643. 14. Centers for Disease Control and Prevention. Recommendations to prevent and control iron deficiency in the United States. MMWR Recomm Rep. 1998;47(RR-3):1-29. 15. American College of Obstetricians and Gynecologists.

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ORIGINAL ARTICLE ACOG practice bulletin no. 95: anemia in pregnancy. Obstet Gynecol. 2008;112(1): 201-207. 16. Baker RD, Greer FR; Committee on Nutrition, American Academy of Pediatrics. Diagnosis and prevention of iron deficiency and iron-deficiency anemia in infants and young children (0-3 years of age). Pediatrics. 2010;126(5):1040-1050. 17. Hutton EK, Hassan ES. Late vs early clamping of the umbilical cord in full-term neonates: systematic review and meta-analysis of controlled trials. JAMA. 2007;297(11):1241-1252. 18. Liu K, Kaffes AJ. Iron deficiency anaemia: a review of diagnosis, investigation and management. Eur J Gastroenterol Hepatol. 2012;24(2): 109-116. 19. British Columbia Ministry of Health. Iron deficiencyâ&#x20AC;&#x201D; investigation and management. http://www. bcguidelines.ca/guideline_iron_deficiency. html. Accessed November 13, 2012. 20. Carter D, Maor Y, Bar-Meir S, Avidan B. Prevalence and predictive signs for gastrointestinal lesions in premenopausal women with iron deficiency anemia. Dig Dis Sci. 2008;53(12):3138-3144. 21. American College of Obstetricians and Gynecologists Committee on Adolescent Health Care; American College of Obstetricians and Gynecologists Committee on Gynecologic Practice. ACOG committee opinion no. 451: Von Willebrand disease in women. Obstet Gynecol. 2009;114(6):1439-1443. 22. Green BT, Rockey DC. Gastrointestinal endoscopic evaluation of premenopausal women with iron deficiency anemia. J Clin Gastroenterol. 2004;38(2):104109. 23. Park DI, Ryu SH, Oh SJ, et al. Significance of endoscopy in asymptomatic premenopausal women with iron deficiency anemia. Dig Dis Sci. 2006;51(12):2372-2376. 24. Fraser IS, Langham S, Uhl-Hochgraeber K. Health-related quality of life and economic burden of abnormal uterine bleeding. Expert Rev Obstet Gynecol. 2009;4(2):179-189.

25. ACOG Committee on Practice Bulletinsâ&#x20AC;&#x201D;Gynecology, American College of Obstetricians and Gynecologists. ACOG practice bulletin: management of anovulatory bleeding. Int J Gynaecol Obstet. 2001;72(3):263-271. 26. Hopper AD, Leeds JS, Hurlstone DP, Hadjivassiliou M, Drew K, Sanders DS. Are lower gastrointestinal investigations necessary in patients with coeliac disease? Eur J Gastroenterol Hepatol. 2005;17(6):617-621. 27. Yates JM, Logan EC, Stewart RM. Iron deficiency anaemia in general practice: clinical outcomes over three years and factors influencing diagnostic investigations. Postgrad Med J. 2004;80(945):405-410. 28. Ioannou GN, Rockey DC, Bryson CL, Weiss NS. Iron deficiency and gastrointestinal malignancy: a population-based cohort study. Am J Med. 2002;113(4):276-280. 29. Lewis NR, Scott BB. Systematic review: the use of serology to exclude or diagnose coeliac disease (a comparison of the endomysial and tissue transglutaminase antibody tests). Aliment Pharmacol Ther. 2006;24(1):47-54. 30. Sidhu R, Sanders DS, Morris AJ, McAlindon ME. Guidelines on small bowel enteroscopy and capsule endoscopy in adults. Gut. 2008; 57(1):125-136. 31. Ajmera AV, Shastri GS, Gajera MJ, Judge TA. Suboptimal response to ferrous sulfate in iron-deficient patients taking omeprazole. Am J Ther. 2012;19(3):185-189. 32. Maslovsky I. Intravenous iron in a primary-care clinic. Am J Hematol. 2005;78(4):261-264. 33. 33. Silverstein SB, Rodgers GM. Parenteral iron therapy options. Am J Hematol. 2004;76(1):74-78. 34. Eichbaum Q, Foran S, Dzik S. Is iron gluconate really safer than iron dextran? Blood. 2003;101(9):3756-3757. 35. Murphy MF, Wallington TB, Kelsey P, et al.; British Committee for Standards in Haematology, Blood Transfusion Task Force. Guidelines for the clinical use of red cell transfusions. Br J Haematol. 2001;113(1):24-31.

Folic acid and prevention of the neural tube defects. Overview of neural tube defect in relation to use of folic acid among fertile-age women.Design: Review article. Setting: Obstetrics and gynecology department OU and FN Ostrava.Methods and results: Neural tube defects (NTDs) are one of the most common birth defects in the Czech Republic. The relation between using of folic acid and decrease of the incidence NTDs was first described in 1965. Fertile-age women are not able to get enough folate from their diet, therefore right timing and proper dosing of folic acid is the object of numerous studies. Many countries started theirs food fortification programs because of the high percentage of unplanned pregnancies and often low compliance.Conclusion: The role of folic acid in prevention of NTDs is undeniable. Due to the large number of unplanned pregnancies long-term supplementation is recommended for all fertile-age women. If pregnancy is planned, the suplementation should begin at least one month before pregnancy. In both cases it is necessary to continue until the end of the week of 12. dosage should be individualized according to risk. Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1

JOURNAL SCAN

Resveratrol suppresses inflammatory responses in endometrial stromal cells derived from endometriosis: A possible role of the sirtuin 1 pathway. Aim: Endometriosis is a chronic inflammatory disease. Sirtuin 1 (SIRT1) plays a role in regulation of inflammation. The role of SIRT1 in endometriosis remains unknown. We here addressed the anti-inflammatory effects of SIRT1 on endometriosis. Methods:The expression of SIRT1 in human ovarian endometriomas and eutopic endometria were examined using immunohistochemistry and reverse transcription polymerase chain reaction (RT–PCR). Endometriotic stromal cells (ESC) obtained from endometriomas were exposed to either resveratrol or sirtinol, an activator or inhibitor of sirtuins, respectively, and tumor necrosis factor (TNF)-α-induced interleukin (IL)-8 release from the ESC was assessed at mRNA and protein levels. Results :Both immunochemistry and RT–PCR demonstrated that SIRT1 was expressed in ESC and normal endometrial stromal cells. Resveratrol suppressed TNF-α-induced IL-8 release from the ESC in a dose-dependent manner while sirtinol increased IL-8 release. Conclusion: These opposing effects of SIRT1-related agents suggest that IL-8 release from the ESC is modulated through the SIRT1 pathway. Resveratrol may have the potential to ameliorate local inflammation in endometriomas. Source: Journal of Obstetrics and Gynaecology Research, Volume 40, Issue 3, pages 770–778, March 2014

Benefits of resveratrol in women's health. Resveratrol and trans-resveratrol are powerful phytoestrogens, present in the skins of grapes and other plant foods and wine, which demonstrate a broad spectrum of pharmacological and therapeutic health benefits. Phytoestrogens are naturally occurring plant-derived nonsteroidal compounds that are functionally and structurally similar to steroidal estrogens, such as estradiol, produced by the body. Various studies, reviewed herein, have demonstrated the health benefits of phytoestrogens in addressing climacteric syndrome including vasomotor symptoms and postmenopausal health risks, as well as their anticarcinogenic, neuroprotective and cardioprotective activities and prostate health and bone formation promoting properties. Conventional HRT drugs have been demonstrated to cause serious adverse effects including stroke and gallbladder disease, as well as endometrial, uterine and breast cancers. Recent research demonstrates that trans-resveratrol binds to human estrogen receptors and increases estrogenic activity in the body. We investigated the effects of protykin, a standardized extract of trans-resveratrol from Polygonum cuspidatum, on cardioprotective function, the incidence of reperfusion-induced arrhythmias and free radical production in isolated ischemic/ reperfused rat hearts. The rats were orally treated with two different daily doses of protykin for 3 weeks. Coronary effluents were measured for oxygen free radical production by electron spin resonance (ESR) spectroscopy in treated and drug-free control groups. In rats treated with 50 and 100 mg/kg of protykin, the incidence of reperfusion-induced ventricular fibrillation was reduced from its control value of 83% to 75% (p < 0.05) and 33% (p < 0.05), respectively. Protykin was seen to possess cardioprotective effects against reperfusion-induced arrhythmias through its ability to reduce or remove the reactive oxygen species in ischemic/reperfused myocardium. Taken together, these data suggest that trans-resveratrol supplementation may be a potential alternative to conventional HRT for cardioprotection and osteoporosis prevention and may confer other potential health benefits in women. Source: Drugs Exp Clin Res. 2001; 27(5-6):233-48 (ISSN: 0378-6501)

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CASE REPORT

Asian Journal of Obstetrics and Gynecology Practice, Vol. 1, No. 1