Volume 2 Issue 8, August 2015

Gupta AS

Tracheal Stenosis In Pregnancy
Patil YS, Wajekar AS, Patel RD, Samant PY.

True Knot in a Nuchal Cord : A Dual fetal tragedy
Dwivedi JS, Gupta AS.

Labial Adhesions Following Herpes Genitalis And Management Options: A Case Report
Sinha S, Tiwari N, Samant PY, Chauhan AR.

Postcesarean Anterior Preperitoneal Abscess
Parulekar SV, Hira P.

Endometrial Stromal Sarcoma: A Masked Foe
Shilotri M,  Panchbudhe S,  Satia MN, Gupte P.

Villar’s Umbilical Nodule: A Rare Case Of  Umbilical Endometriosis
Joylene DAlmeida J, Backthan L, Rao SV.

Caesarean Scar Ectopic Pregnancy–An Unusual Presentation
Ramesh B, Gupta P, Chandana A.

Myomectomy During Cesarean Section - An Interesting Case Report
Changede P, Gupta S, Thakur V, Chavan N.

Adhesion of Labia Minora
Parulekar SV


Gupta AS

Labial adhesions or agglutination or fusion is an acquired condition that results from the adhesions of the inner mucosal surface of the labia minora. This can be complete or partial. When it is complete the vaginal opening cannot be seen at all.A small opening anterior or in front of the sealed labia minora permits the flow of urine and this sealed labia form a pocket which acts as a container to hold the urine.Labial adhesions may be primary or secondary. Primary are present from birth and secondary usually occur after menopause. The labial fusion occurs in two age groups. The girl child or the adult woman.
Causes of labial adhesions
Estrogen deficient states: This is the commonest cause of fused labia. It affects young girls usually aged 6 months to 6 years, women during lactation, after menopause, following use of SERMs, aromatose inhibitors, GnRH agonists or anatagonists or women having hyperprolactinemia. Usually at birth maternal circulating estrogen's are present in the neonatal circulation preventing labial adhesions. Any irritant that can cause chronic inflammation to the labia like use of diapers, stools, urine, foreign bodies, undetected chronic sexual abuse can lead to adhesion formation between the inner surface of the labia minora resulting in their fusion. The condition may be detected if the girl complaints of dribbling of the urine that leaks out of the pocket formed by the sealed labia or it may remain undiagnosed. Most of the times it spontaneously resolves at puberty with the surge of endogenous estrogen's. In menopausal women lack of estrogen results in atrophic vulvovaginitis increasing the adhesiveness of the thinned out labia and the vagina. The adult woman may present with apareunia, dyspareunia, infertility, difficulty in introducing a vaginal tampon or dribbling of urine or menstrual blood.
Other causes can be inflammation due to infections like herpes genitalis, autoimmune disorders like Behcet syndrome, pemphigoid conditions of the mucous membranes, erosive lichen planus causing vulvovaginal gingival syndrome , or serious drug reactions like Steven-Johnson syndrome or toxic epidermal necrolysis affecting the vulva as a part of the systemic disorder. Inflammation and trauma following parturition or after vulvectomy for vulval cancer or after female circumcision can also predispose to labial adhesions.
Treatment can be medical or surgical. Always a trial of medical treatment should be given especially in girls and women in hypoestrogenic states. Estrogen creams applied to the in the mid line over the fused junction which can be identified as a white red or brown line daily for 4-6 weeks usually opens up the fused labia. However, an emollient cream should be continuously applied daily to prevent reformation of the adhesions. Patients with autoimmune disorders will need treatment of the cause along with local estrogen and emollient creams. In patients where the labia are densely stuck and estrogen, emollient or steroid creams fail will need to undergo surgical adhesiolysis.

We bring you two interesting articles on labial adhesion in this issue and we hope that readers gain useful scientific insight from these and the remaining interesting case reports. We have omitted the section on multiple choice questions for management reasons. While we will continue to use it in our institute locally, making it available to everyone reading our journal was not manageable.

Tracheal Stenosis In Pregnancy : Anesthetic Dilemma

Author Information

Patil YS*, Wajekar AS**, Patel RD***, Samant PY****.
(* Associate Professor, ** Assistant Professor, *** Professor, Department of Anesthesiology; **** Additional Professor, Department of Obstetrics and Gynecology, Seth G S Medical College & KEM Hospital, Mumbai, India.)

We present the anesthesia management of a pregnant patient with acquired subglottic stenosis for elective lower segment caesarean section (LSCS) under spinal anesthesia with severe postoperative desaturation requiring emergency intubation and tracheal dilatation. Presence of tracheal stenosis during pregnancy significantly affects maternal and foetal oxygenation and ventilation making anesthesia management very challenging. Congestion and edema of the airway in pregnant patients combined with increased respiratory load can worsen the obstruction in such patients. The goals of anesthesia are avoiding maternal loss of airway, maintaining both maternal and fetal oxygenation and ventilation. Although the surgery was successfully managed with neuraxial anesthesia, the patient still remained at high risk of postoperative complications. Emergency airway management may be required at any stage in such patients and preparation for difficult airway should include keeping bronchoscopy, bougie and tracheal dilators, jet ventilation and tracheostomy ready. In some scenarios, femoro-femoral cardiopulmonary bypass may also be required.

Pregnancy is considered as difficult airway  and failed intubation can give rise to catastrophic consequences. Presence of tracheal stenosis during pregnancy significantly affects maternal and foetal oxygenation and ventilation making anesthesia management very challenging.[1–3] Post intubation tracheal stenosis affects 4-13% of adults in United States and 90% of them progress to chronic subglottic stenosis.[4]
We present the perioperative anesthesia management of a pregnant patient with acquired subglottic stenosis for elective lower segment cesarean section (LSCS). Although the surgery was conducted under combined spinal epidural anesthesia, she had postoperative severe hypoxia necessitating emergency intubation and tracheal dilatation.

Case Report

A 24 year old primigravida with history of tracheal stenosis was posted for elective LSCS in view of cephalopelvic disproportion. During first trimester, she contracted pneumonia and acute respiratory distress necessitating endotracheal intubation for 8 days. 15days later she developed acute stridor. Flexible bronchoscopy done by ear-nose-throat (ENT) surgeons, at the time and again 3 months later showed grade III soft tracheal stenosis near 5th tracheal ring with tracheal lumen of 0.5 cm which required tracheal dilatation with bougie. Elective tracheostomy was avoided since it was a soft stenosis responsive to tracheal dilatation. Currently, she had inspiratory stridor which increased in supine position and with effort tolerance of one flight. Her haemoglobin was 9.1 g%. All other routine investigations were normal. Standard monitors including electrocardiography, automated blood pressure, pulse oximetry (SPO2) and end-tidal carbon dioxide were applied. Her pulse was 42/min with blood pressure 130/70 mm hg and SPO2 98%. Left uterine displacement was maintained. Combined spinal epidural (CSE) anesthesia was planned. ENT surgeon was present in the operating room throughout procedure. Difficult airway preparation included laryngeal mask airways (LMA) and different sizes of endotracheal tubes, Frova’s ventilating and intubating bougie, transtracheal jet ventilation, rigid bronchoscope with tracheal dilators of various sizes and tracheostomy tubes. Epidural catheter was inserted at L2-3 space and bupivacaine 0.5% 2cc was injected intrathecally in L3-4 space with a 25G spinal needle. T6 level was achieved. A healthy neonate with a good APGAR score was delivered. The intraoperative period was uneventful. No other sedatives were given. Post procedure 30mg tramadol diluted in 10cc was injected epidurally. Paracetamol 1g IV was given 8hrly. She was shifted to recovery room with oxygen by mask.
Four hours after surgery, she had hypotension up to 80/60 mm hg and desaturation up to 88%. Ventimask with reservoir bag at 8L/min brought her saturation up to 92%.  Two packed cell transfused since she appeared pale and blood loss was around 900ml. She was shifted to intensive care unit (ICU) in propped up position. She maintained 100% saturation with overnight continuous positive pressure ventilation. After chest physiotherapy in ICU, she probably had loosened secretion which obstructed the stenotic airway and she suddenly desaturated up to 67% with peripheral cyanosis. She was intubated with 5.5mm endotracheal tube. Her arterial blood gases 1 hour later were pH 7.098, pCO2 83.7, pO2 161.9, HCO3 18.3 and Sao2 98.4%. Emergency bronchoscopy and tracheal dilation under intermittent apneic technique with jet ventilaton under total intravenous anesthesia (TIVA) was done. After successfully dilating with 26 size tracheal bougie, she was intubated with 7mm endotracheal tube. She was electively ventilated and weaned off and extubated after 12 hours. She was shifted to ward on day 3 and discharged on day 8.


Difficult intubation can lead to significant airway related injuries leading to adverse maternal and fetal outcomes.[5] Congestion and edema of the airway in pregnant patients combined with increased respiratory load can worsen the obstruction in such patients.[1] Mother and foetus are at high risk of impaired oxygenation and ventilation. Definitive treatment with stents for tracheal stenosis are licensed only for malignant conditions.[1,6] Surgical morbidity and mortality associated with tracheal reconstruction prevents its use in benign stenosis. Generally such tracheal stenosis are managed with serial tracheal dilatations. Radiological evaluation with computed tomography or lateral neck x-ray was avoided in our patient due to her pregnancy and as prior bronchoscopy reports were available.
The goals of anesthesia are avoiding maternal loss of airway, maintaining both maternal and foetal oxygenation and ventilation. Preoperative bradycardia in the supine position can be attributed to inferior vena cava compression, relieved by left uterine displacement. Although the surgery was successfully managed with neuraxial anesthesia, patient still remained at high risk of postoperative complications. As occurred in our patient, any kind of airway irritation such as coughing or instrumentation can precipitate catastrophic complete airway obstruction.[6] Ventilation through 5.5 mm endotracheal tube led to severe hypercarbia and emergency tracheal dilatation with bronchoscopic passage of a large size tube was required under TIVA.
Common causes of tracheal stenosis are inflammatory diseases, benign and malignant tumours, collagen vascular diseases etc. Prolonged intubation is one of the leading causes of acquired tracheal stenosis with incidence of almost 4-13% intubated adults.[4] The tracheal wall in contact with the endotracheal cuff is generally the site of this stenosis.[6] Local inflammation and mucosal ischaemia  near cuff leads to ulceration, granulation tissue, tracheal chondritis and fibrotic stenosis.[5]  The site of tracheal stenosis is very important since upper stenosis may be treated with an endotracheal tube passed beyond the cords. But mid-level tracheal stenosis may require unilateral or differential bronchial intubation or even cardiopulmonary bypass.[6]
If surgery demands, then elective intubation can be attempted in topical airway anesthesia or bilateral cervical plexus block.[6,7] Salama et al reported a case of pregnant woman with tracheal stenosis whose stenotic area was preoperatively dilated by a balloon with fibre optic bronchoscopy under local anesthesia.[2] Kuczkowski et al performed preoperative elective tracheostomy under local anesthesia in the 36th week of pregnancy which was kept till the end of her pregnancy.[8] We did not perform elective tracheostomy in our patient, because ENT surgeons felt she can undergo tracheal dilatation if need arises. Parsa et al and Sutcliffe et al described the general anesthesia management for bronchoscopic dilatation of stenotic airway in pregnancy.[1,3] Laryngeal mask airway is a valuable tool for ventilation and passing a guidewire, allowing flexible bronchoscopy.[6]
Conclusion : Airway management of pregnant patients with critical tracheal stenosis can be tricky and the key step is prevention of loss of airway, maintenance of adequate oxygenation and ventilation. Although regional anesthesia is a boon in such patients for conduct of anesthesia, need for emergency airway management must be kept in mind. Multidisciplinary approach along with availability of experienced personnel and difficult airway equipments at hand ensures successful outcome.

  1. Parsa T, Dabir S, Reza H, Darjani J, Radpay B. Anesthesia Management in a Pregnant Woman with Severe Subglottic Stenosis. Tanaffos 2008;7(3):76–80.
  2. Salama DJ, Body SC. Management of a term parturient with tracheal stenosis. 1994.
  3. Sutcliffe N, Remington SAM, Ramsby TM, Mason C. Severe tracheal stenosis and operative delivery. Anaesthesia 1995;50(1):26–9.
  4. McCaffrey T V. Classification of laryngotracheal stenosis. In: Laryngoscope. 1992. page 1335–40.
  5. Zarogoulidis P, Kontakiotis T, Tsakiridis K, Karanikas M, Simoglou C, Porpodis K, et al. Difficult airway and difficult intubation in postintubation tracheal stenosis: A case report and literature review. Ther Clin Risk Manag 2012;8:279–86.
  6. Juvekar NE Al. Anesthetic management for tracheal dilatation and stenting. Indian J Anaest 2003;47(4):307.
  7. Cho A-R, Kim H-K, Lee E-A, Lee D-H. Airway management in a patient with severe tracheal stenosis: bilateral superficial cervical plexus block with dexmedetomidine sedation. J Anesth [Internet] 2014;29(2):292–4. Available from: http://link.springer.com/10.1007/s00540-014-1912-9
  8. Kuczkowski KM, Benumof JL. Subglottic tracheal stenosis in pregnancy: Anaesthetic implications. Anaesth Intensive Care 2003;31(5):576–7.

Patil YS, Wajekar AS, Patel RD, Samant PY. Tracheal Stenosis In Pregnancy : Anesthetic Dilemma. JPGO 2015. Volume 2 No. 8. Available from: http://www.jpgo.org/2015/08/tracheal-stenosis-in-pregnancy.html

True Knot in a Nuchal Cord : A Dual fetal tragedy

Author Information

Dwivedi JS*, Gupta AS**. 
(* Third Year Resident **Professor, Department of Obstetrics & Gynecology, Seth G.S.Medical College & KEM Hospital, Mumbai, India.)


The incidence of true knot of the umbilical cord which compromises the blood flow is 0.04%-3% [1]. Umbilical cord with one loop around the neck is found in about 20%-34% of cases but the incidence of two or three loops is 2.5% to 5% and 0.2% to 0.5% respectively[2]. The following image shows a rare incidence of two loops of umbilical cord around the neck with a true knot being the probable cause of intra-uterine fetal demise. This is the first case reported in world literature with a true knot in a twice wound nuchal cord.


There are many maternal and fetal causes for intra uterine fetal demise. Presence of tight loop of cord around the neck or presence of knot in the cord is one amongst those multiple causes. When these two conditions are simultaneously present the chances of fetal compromise increase tremendously. We hereby present a rare case of intrauterine fetal demise due to two tight loops of cord around the fetal neck with a co existing true knot.

Case Report

A 34 years old woman married since 8years G3P2L1IUFD1 with previous lower segment caesarean section with 35 weeks of gestation came with a ultrasound (USG) scan suggestive of intrauterine fetal demise. The cause of her previous intrauterine fetal demise was undetermined.  Her serological and biochemical tests were within normal range. Pre-induction ripening of the cervix with Foley’s catheter was done followed by oxytocin augmentation. Patient delivered vaginally after 18 hours of induction. She delivered a female fetus of 2.5kg with two tight loops of cord around the neck and also the presence of a true knot in the nuchal umbilical cord as shown in figure 1.

Figure1: Fresh still birth with the true knot (blue arrow) of umbilical cord and the two loops of cord around the neck (green arrow).


Umbilical cord (Funis) is the connecting link between the fetus and placenta through which fetal blood flows to and fro from the placenta. In general the cord diameter is about 1.5cm and its length varies from 30-100 cm[3]. An average umbilical cord is 55cm long and approximately 1-2 cm in diameter.  When this umbilical cord passes around the neck 360 degrees it is called nuchal cord[4]. Umbilical cord has nodes or swelling like structure at places. These swellings may be due to accumulation of Wharton’s jelly (false knots) or may be due to actual twisting of the cord upon itself (true knots). True knot is the type B pattern of nuchal cord which is described as a hitch, which can’t be removed. True knots are most likely to develop in early pregnancy when there is more liquor and are common in cases of mono-amniotic twins, advanced maternal age, long umbilical cord and fetal movements[5]. Due to the true knot, the blood flow to the fetus is compromised as the knot tightens due to either fetal movements or during labor at the time of descent. Decreased venous return from the placenta leads to asphyxia and sometimes intra uterine fetal demise. Perinatal morbidity and mortality in the form of stillbirth is increased four to ten times in case of true knot of umbilical cord[2]. Prenatal detection of cord knot is very challenging and not always possible. However detection of true knot antenatally by ultrasonography and four dimensional color doppler and its vigilant management in the form of elective caesarean section if required, can reduce the perinatal loss[6]. A medline, google, MD consult, Pubmed search did not yield any case reports documenting a nuchal cord having a true knot. Case reports with true knots or nuchal cords are well documented but this unfortunate dual tragedy is not yet reported.

  1. Srinivasan A, Graves L, Mortimer B. Four true umbilical cord knots-JOGC http://www.jogc.com/abstracts/200601_Obstetrics_3.pdf
  2. Cunningham FG, Leveno KJ, Bloom SL, Spong CY , Dashe JS, HoffmanBL, et al, Placental abnormalities. Williams Obstetrics.24th ed, New York, Mc Graw Hill education books; 2014, pg123-124.
  3. Dutta DC, The placenta and fetal membranes. In Konnar HL, editor, Textbook of obstetrics including perinatology and contraception.7th ed, Delhi, New Central Agency(P) limited; 2011, pg40.
  4. Schaffer L, Zimmermann R. Nuchal cords. Available from http://www.uptodate.com/contents/nuchal-cords
  5. Beall MH, Ross MG. Umbilical cord complications. Available from http://emedicine.medscape.com/article/262470-overview#aw2aab6b6
  6. Ramon Y, Cajal CL, Martinez RO. Four dimensional ultrasonography of a true knot of the umbilical cord.Am J Obstet Gynecol.10/2006; 195:896-8.

Dwivedi JS, Gupta AS. True Knot in a Nuchal Cord : A Dual fetal tragedy. JPGO 2015. Volume 2 No. 8. Available from: http://www.jpgo.org/2015/08/true-knot-in-nuchal-cord-dual-fetal.html

Labial Adhesions Following Herpes Genitalis And Management Options: A Case Report

Author Information

Sinha S*, Tiwari N**, Samant PY***, Chauhan AR***.
(* Second year resident, ** Assistant Professor, *** Additional Professor, Department of Obstetrics and Gynaecology, Seth G S Medical College and KEM Hospital, Mumbai, India.)


Genital herpes is a common sexually transmitted disease but labial adhesions following this infection are a rare but recognized local complication. Chronic labial adhesion in the reproductive age group is extremely rare. It occurs most often in infants, prepubertal girls, postpartum and postmenopausal women. It is usually associated with low estrogen levels. We present a case of almost complete labial adhesion with dysuria, altered stream of urine, and perineal discomfort in a 35-year-old female secondary to herpes genitalis.

The incidence of genital herpes nearly doubled over 20 years (11.4% to 20.5%) from 1977 to 2000 as observed in a review from North India1. The infection is transmitted through contact with lesions on mucosal surfaces, and from genital and oral secretions. The incubation period ranges from 2 to 21 days2. Vesicles on or around the genital area, rectum or mouth which may later ulcerate are typical lesions. Ulcers take two to four weeks to heal. Complications like secondary bacterial infection of lesions, blindness due to corneal infection, meningitis, and labial adhesions have been known to occur.

Case Report:

A 35- year old married parous woman presented in emergency with complaints of vulvar and lower abdominal pain, dysuria and fever for two days. She had regular menstrual cycles. She was afebrile. Minimal tenderness was present in hypogastrium. No lesion or lymphadenopathy was present on local vulvar examination. On speculum examination, copious vaginal discharge and hypertrophied congested cervix were seen. The discharge was collected for bacterial culture and antibiotic sensitivity. Patient did not allow bimanual examination as she was in severe pain. She was advised personal hygiene, testing for HIV and VDRL, urine routine microscopy with culture sensitivity, and pelvic ultrasonography. She was prescribed oral clindamycin and metronidazole and was asked to follow up in a week.
After 5 days she presented again to the emergency room in view of vaginal discharge, pain, and fever not responding to antibiotics. On examination she was afebrile and vitally stable. Multiple vesicles and papules in various stages of eruption were now noted on vulva. Her routine pathological, biochemical investigations, pelvic ultrasonography and urine analysis were unremarkable. Culture and sensitivity tests of vaginal discharge and urine did not yield any bacterial growth. Diagnosis of herpes genitalis was made. Oral acyclovir (1000 mg per day in divided doses) and antibacterial ointment for local application were prescribed. Patient’s partner did not report symptoms suggestive of herpes.
She followed in the outpatient department 10 days after the second visit with complaint of altered stream of urine. At this time, healed herpetic lesions on both labia majora and agglutination of labia minora were noted on local examination.
For her voiding difficulty, manual separation of the labial adhesions with local lignocaine jelly application was done gradually in 4 daily sittings after counseling the couple. Patient was advised to continue antibacterial ointment with additional use of liberal application of lignocaine jelly after urination, washing, bathing. Adhesions were completely separated over the course of these 4 days. Patient was asked to maintain genital hygiene and continue ointment application for 2 weeks before resuming sexual activity. Partner was referred to dermatology department for further advice. Follow up examination of the patient after two weeks showed normal appearance of genitalia. She could void urine normally and was otherwise asymptomatic.

Figure 1: Labial agglutination.

Figure 2: Partially separated labia on day 2 of manual separation.

Figure 3: Completely separated labia.


Labial adhesions are membranous structures resulting due to fusion of the adjacent mucosal surfaces of the labia minora or majora. Infants and adolescent girls are more prone to labial adhesions due to hypoestrogenemia3. Adhesions form when apposing surfaces of labia become raw due to worm infestation, nappy rash, poor hygiene or sexual abuse. Atrophic vaginitis can cause labial adhesions in post menopausal women4. Topical application of oestrogen cream is the treatment of choice. Surgical intervention is required only in long standing cases. The entity is rare in reproductive age but can occur as a result of inflammatory skin conditions like lichen sclerosus, herpes genitalis, Stevens Johnson syndrome, surgery or childbirth trauma. Seehusen and Earwood found that estrogen therapy was ineffective and surgery was required to resolve postpartum adhesions5. In case of herpes genitalis, formation of fibrinious exudates can lead to adhesions between the labia minora6. If left untreated, this can lead to midline fusion with coital and voiding difficulty. In our patient, in a short period of 14 days after prodromal symptoms almost complete agglutination of  labia minora occurred; probably due to apposition between raw surfaces and unwashed exudates at the time of healing with resultant distortion of urinary stream.
Spontaneous resolution of prepubertal labial adhesions is reported in nearly 80% cases within 1 year7. Topical steroid application has been successfully tried of post herpetic labial adhesions in an adult woman8. Mayoglou et al in retrospective review of prepubertal cases with labial adhesions observed that topical steroid therapy resolved adhesions faster and had less recurrence and side effects as compared to topical estrogen therapy9. Obstruction to urinary flow or refactory adhesions after local therapy requires surgical intevention9. Our patient required intervention due to her urinary symptoms. Surgery and CO2 laser vaporisation are recommended for restoring voiding and sexual function impaired by adhesion10. Amniotic membrane graft on raw surfaces has been used to prevent reformation of adhesions after surgery.11


Incorrect diagnosis, poor hygiene and lack of topical treatment may predispose to development of labial adhesions in women with herpetic vulvitis. Topical therapy and saline baths in addition to antiviral medication are integral part of treatment for primary genital herpes, with manual or sugical separation reserved for obstructive symptoms.

  1. Kumar B, Sahoo B, Gupta S., Jain R.Rising incidence of genital herpes over two decades in a Sexually  transmitted disease clinic in North India.  J Dermatology. 200;29(2):74-78.
  2. BCCDC Clinical Prevention Services
Reproductive Health STI Decision Support Tool – Non-certified Practice Genital HSV - March 2012
  3. Schober J, Dulabon L, Martin-Alguacil N, Kow L, Pfaff D. Significance of topical estrogens to labial fusion and vaginal introital integrity,” Journal of Pediatric and Adolescent Gynecology 2006;19(5):337–339.
  4. Bachmann G, Nevadunsky N. Diagnosis and treatment of atrophic vaginitis. Am Fam Physician. 2000; 61(10):3090-3096.
  5. Seehusen D, Earwood J. Postpartum labial adhesions. J Am Board Fam Med 2007; 20: 408–410.
  6. Herieka E. Labial adhesions following severe primary genital herpes.  Letter to the Editor. SexTransm Inf 2001; 77:75.
  7. Pokorny SF.Prepubertal vulvovaginopathies. Obstet Gynecol Clin North Am. Mar 1992; 19(1):39-58.
  8. Markos A R. Successful management of vulvar adhesions with potent topical corticosteroids: a case report. J Reprod Med. 2004 May; 49(5):398-400.
  9. Mayoglou L.,Dulabon L., Matrtin-Alguacil N.,Pfaff D., Schober J.Success of treatment modalities for labial fusion: A Retrospective evaluation of topical and surgical treatments. Journal of Pediatric and adolescent gynecology. August 2009; 22 (4): 247–250
  10. Walzman M, Wade A. Labial Adhesions after genital herpes infection, Genitourin Med 1989; 65:187-188
  11. Lin Y, Hwang J, Huang L. Chou C. Amniotic membrane grafting to treat refractory labial adhesions postpartum. A case report. The Journal of Reproductive Medicine 2002, 47(3):235-237.

Sinha S, Tiwari N, Samant PY, Chauhan AR. Labial Adhesions Following Herpes Genitalis And Management Options: A Case Report. JPGO 2015. Volume 2 No. 8. Available from: http://www.jpgo.org/2015/08/labial-adhesions-following-herpes.html

Postcesarean Anterior Preperitoneal Abscess

Author Information

Parulekar SV*, Hira P**
(* Professor and Head of Department, Department of Obstetrics and Gynecology, ** Associate Professor, Department of Radiology, Seth G. S. Medical college and KEM Hospital, Mumbai, India)


Puerperal sepsis after cesarean section usually presents as systemic features of sepsis plus foul smelling lochia. Sometimes the pus may collect in the uterovesical space if the lower segment sutures give way. A case of a large collection of pus in the anterior preperitoneal space is presented.


The risk of puerperal sepsis should not be high if standard aseptic and antispetic precautions are followed. If the pus drains out of the cervix, the risk to the mother would be less as compared to when it does not drain out fully and spreads to extraperitoneal space posteriorly or anteriorly. Drainage of such collections is very difficult, and risk of complications including septicemia is quite high. A case of a cesarean section with anterior extraperitoneal collection of pus behind the anterior abdominal wall is presented.

Case Report

A 30 year old woman, para 1 living 1, presented with high fever, vaginal discharge of pus, and abdominal distension for 10 days. She had undergone a lower segment cesarean section in a private hospital 10 days ago, for breech presentation and pregnancy induced hypertension.. She started getting fever from the third postoperative day. She was found to have a positive Widal test and was treated with ceftriaxone. She was sent to us on the 10th postoperative day. On examination, her general condition was poor. Her temperature was 300 C, pulse rate 86/min, respiratory rate 22/min, blood pressure 140/90 mm Hg. Respiratory system showed decreased air entry in the lung bases, accompanied by crepitations in that area. The abdomen was distended, tense, and tender. Peristaltic sounds were normal. The uterus was of 18 weeks' size. The cervix was open and purulent discharge was found to be draining from it. Her hemoglobin was 9.2 g/dl, white cell count 18000/cmm, polymorphs 73%, lymphocytes 16%, platelets 1.8 lakh/cmm, blood urea nitrogen 7 mg/dl, serum creatinine 0.8 mg/dl, fasting plasma sugar 96 mg/dl, serum bilirubin 0.8 mg/dl, SGOT 16 mIU/ml, SGPT 12 mIU/ml, PT-INR 1.19. Abdominopelvic ultrasonography showed the uterus of 16x8x6 cm, and a large collection fluid with internal echoes measuring 22x13x8 cm of above the uterus. A computed tomography of the abdomen and pelvis showed that there was a 23x7.7x21 cm collection of fluid above and in front of the uterus extraperitoneally, deep to the rectus sheath, spread in front of the anterior parietal peritoneum. It was communicating with the collection of fluid in the uterine cavity through a rent in the uterine scar.
A diagnosis of puerperal sepsis after cesarean section, with formation of a large collection of pus in the uterovesical space and the space between the posterior ectus sheat and the anterior parietal peritoneum was made. The collection was drained by insertion of a tube under ultrasonographic control. 1800 ml of pus was drained. She was administered piperacillin-tazobactum, metronidazole and amikacin parenterally. Her blood culture showed no growth of any bacteria. The pus removed through the tube grew E. coli which was sensitive to piperacillin-tazobactum. The The tube continued to drain purulent fluid measuring 200 ml, 150 ml, 110 ml, 70 ml, 50 ml and 20 ml over successive days, while the vaginal discharge of pus ceased. She became afebrile 7 days after the initial drainage. The tube was drained on 12th postoperative day, after it had stopped draining over 48 hours. Abdominopelvic USG done after two days showed no collection of any fluid in the abdominal wall or pelvis. She made an uneventful recovery. She was advised to avoid another pregnancy and counseled to use effective contraception like combination contraceptive pills or condoms.

Figure 1. CT Scan of the abdomen at the level of the lower segment incision. The communication between the intrauterine and preperitoneal collections of pus is pointed out by an arrow.

Figure 2. CT Scan of the abdomen at the level of the kidneys. The large collection of pus is pointed out by arrows.

Figure 3. CT Scan of the abdomen at the level of the liver and transverse colon. The large collection of pus is pointed out by arrows.


The peritoneal cavity is a closed sac within another closed sac made of the fascial layer continuous with transversalis fascia. An extraperitoneal abscess may occur between the peritoneum and the deep fascia anteriorly.[1] It may be due to an extension of an abscess in the bladder flap after a cesarean section. Since the peritoneum and the posterior rectus sheath extend upwards until the peritoneum turns backwards under the diaphragm, the pus can track upwards similarly between the fascia and the peritoneum. Though it is a potential space, it can accommodate up to 2000 ml of pus.[2,3]  In the case presented, the patient had fulminant puerperal sepsis after a cesarean section. Part of the pus generated within the uterine cavity kept draining out through the cervix. There was a breakdown of the uterine sutures in the lower segment, so that the pus escaped into the uterovesical space under the uterovesical fold. Since the uterovesical fold had healed, the pus did not enter the peritoneal cavity. It spread upwards, separating the peritoneum from the posterior rectus sheath, reaching cranially up to the level of the liver. After drainage of the collection through a tube drain inserted under ultrasonographic control, and treatment with antibiotics, the production of the pus stopped. As a result, the abscess cavity collapsed, the fascia and the peritoneum came in contact with each other, and cervical drainage of the pus also ceased. The healing of the uterine scar is most likely to be compromised, and the risk of rupture of the scar in a future pregnancy is quite high. A surgical repair of the uterine scar was not considered during the recovery phase of the patient, because the tissues would have been friable and would not heal well in the presence of infection. The patient was counseled about the risk and advised to use adequate contraception so as to avoid another pregnancy.
Use of prophylactic antibiotics indiscriminately results in development of resistant strains of bacteria, which cause nosocomial infections. The case presented had postcesarean puerperal sepsis with E. coli which was resistant to all antibiotics except piperacillin-tazobactum. This was a nosocomial infection, which was most likely due to indiscriminate use of antibiotics for prevention and treatment of surgical site infections. This trend is on the rise, as illustrated by another case report of retroperitoneal abscess formation after a criminal abortion in a private hospital.[4] The only treatment available to such extraperitoneal abscesses in the past was open drainage, if the diagnosis was made at all. With modern imaging techniques and a high degree of suspicion, the diagnosis is easier, and treatment by insertion of drainage tube under imaging control without having to resort to open surgery is possible.[5]


Preperitoneal abscess is a serious condition that may have few localizing signs. It may occur as a complication of a cesarean section. A high degree of suspicion aided by modern imaging techniques like CT and MRI helps make an accurate diagnosis. Early diagnosis and treatment by catheter help reduce morbidity and mortality associated with the condition.

  1. Maull KI. Extraperitoneal abscess. The American surgeon 1980;46(8):453-6.)
  2. Altemeier WA, Alexander JW. Retroperitoneal abscess. Arch Surg 1961;83:512-524.
  3. Stevenson EOS, Ozeran RS. Retroperitoneal space abscesses. Surg Gynecol Obstet 1969; 128:1202-1208.
  4. Kulkarni S, Parulekar SV, Hira P. Post Criminal Abortion Retroperitoneal Abscess. JPGO 2014 Volume 1 Number 11. Available from: http://www.jpgo.org/2014/11/post-criminal-abortion-retroperitoneal.html
  5. Rodgers SK, Kirby CL, Smith RJ, Horrow MM. Imaging after cesarean delivery: acute and chronic complications. Radiographics. 2012 Oct;32(6):1693-712. doi: 10.1148/rg.326125516.

Parulekar SV, Hira P. Postcesarean Anterior Preperitoneal Abscess. JPGO 2015 Volume 2 Number 8. Available from: http://www.jpgo.org/2015/08/postcesarean-anterior-preperitoneal.html