Dr. Indhra Nedumaran, Consultant Obstetrics & Gynaecology

Introduction: Placenta percreta is diagnosed usually in the third trimester as massive postpartum hemorrhage, when an attempt to remove the placenta reveals lack of a cleavage plane between placenta and uterus. However, placenta percreta may also present in the second trimester with vaginal bleeding. Placenta Percreta is a complication of pregnancy that can be life threatening to both the mother and the fetus. There are three types of abnormal placentation called placenta Accreta, Increta and Percreta. Miller and colleagues by reviewing 155,670 deliveries at their hospital between 1985 and 1994, found that 62 (one in 2,510) were complicated by placenta accreta. A recent study by Wu and colleagues looking at placenta accreta over a 20-year period (1982–2002) found an incidence of 1 in 533 pregnancies at their institution.

We presenting a case of placenta percreta presented at 17 weeks with vaginal bleeding.


Case Report: 31 years old school teacher from Thiruvannamalai came with complaints of bleeding PV on and off, and watery discharge from the vagina in between bleeding for 3 months. 

3 months back patient had undergone medical termination of pregnancy at 6 weeks of pregnancy following which she developed the above symptoms. She did not have any follow-up with gynecologist in between. She had undergone LSCS and  D & C 8 years and 7 years ago respectively in the past. No other significant medical history. On clinical examination she was anemic and other systemic examinations were normal. Abdominal examination showed that uterus was 14 -16 weeks size. Supra-pubic transverse scar was present. On speculum examination watery discharge was present, swab was taken for culture and sensitivity. On vaginal examination, cervix was 1 cm long and os was closed. On evaluation Hemoglobin was 6.8 gms/dl and 2 units of packed cells were transfused.

Ultrasound examination showed Single viable intrauterine pregnancy of 17 weeks size with oligohydromnios, placenta anterior and not low lying with no obvious anomalies of the fetus. She was started on 200 mgm of mifepristone and after 36 hours single dose of oral misoprostol 200 mcg was given. She developed contractions after 12 hours, she has progressed well and expelled the fetus within 18 hours following misoprostol. Placenta expulsion was delayed and her vitals were stable and no bleeding at that time, hence syntocinon infusion started with 2.5 units in 500ml RL at a rate of 30ml/hour. After one hour she started to bleed heavily and decision was taken to examine the patient in the operation theatre. After examination under anaesthesia, was done an attempt was made to remove the placenta by curettage. she had torrential bleeding followed by hypotension. It was then decided to proceed with exploratory Laparotomy. Per-operatively there was no hemoperitoneum, lower segment was intact and showed abnormal vascular pattern. We proceeded with sub-total hysterectomy. Patient had an approximate total blood loss of about 3 liters and patient got stabilized with 10 units of PCV, 4 units of FFP and 2 units of platelet in total. Postoperative course in the hospital was uneventful and she made good recovery. She was discharged on fifth post-operative day. Histo pathological examination confirmed the diagnosis as Placenta Percreta. Now she is doing well on one year follow up.


Discussion: Placenta accreta represents a specific abnormality of placentation in which placental villi attach directly into the myometrium without intervening decidua. Risk factors for placenta percreta include multiparity, prior cesarean section or other uterine surgery, prior curettage, placenta previa, endometrial infection or prior manual removal of placenta, causing trauma to endometrium. Decidual formation in the lower segment is generally regarded as poor as compared to the upper uterine segment. This may be the mechanism for the increased incidence of placenta accreta in cases of placenta previa. Approximately one third of patients with placenta accreta have a history of cesarean section (1, 2). Failure of differential growth of the scarred lower uterine segment results in the inability to migrate from low implantation site. Our patient had significant risk factors for placenta accreta i.e LSCS and  Dilatation & Curettage.

The most common clinical presentation of placenta accreta occurs in the third trimester with massive haemorrhage after during an attempt to removal of a densely adherent placenta. Our patient presented in second trimester with an attempt removal of retained placenta. Cases of placenta accreta presenting in early pregnancy have been reported. The patient had a history of two prior low transverse cesarean sections. She appeared as cervical pregnancy with a placenta percreta and required a total hysterectomy (3). Another case presented at 17 weeks of gestation with an acute abdomen and an unexplained elevation in alpha feto protein.(4). Two other cases presented at 18 weeks and 21 weeks gestation, respectively, with a one day history of abdominal discomfort (5,6). These patients had no risk factors other than a single episode of pelvic inflammatory disease  (5) and a history of in utero exposure to diethyl stillbesterol (6). At laparotomy a ruptured uterus with placenta percreta was found and hysterectomy was necessary to control the bleeding in both cases. 

These history illustrate that the the diagnosis of placenta percreta early in gestation is difficult because signs and symptoms may be modified by the presence of enlarged uterus. When hemo peritoneum is suspected a laparotomy is indicated immediately. In almost all cases hysterectomy needed. One case was described in which the surgeon was able to suture the myometrial defect created by the protruding placenta and to prolong the pregnancy until 32 weeks (7). 

one case was reported at 17 weeks of pregnancy with vaginal bleeding and 3 previous LSCS and with USG findings  of  placenta located anterior and right lateral wall. She developed symptoms of hemo peritoneum which needed laparotomy and found to have placenta percreta, ruptured uterus with broad ligament hematoma and underwent hysterectomy with evacuation of hematoma (8). The total blood was 5000 ml and treated with 12 units of PCV, 1800 ml of FFP and 10 units of platelets to prevent the dilution coagulopathy. 


The postoperative period in our patient was uneventful. She was discharged on fourth post-operative day.



Conclusion : When patient presents with

1.     Failed termination of pregnancy 

2.     Risk factors for abnormal placentation 

3.     Painless vaginal bleeding ,then we should  suspect abnormal placentation .This          should be ruled out by USG or MRI. This could minimize the morbidity by doing the     procedure electively and possibly even result in conservative therapy.


References :

1.    Breen JL,Neubecker R,Gregori CA,Franklin JE.Placenta accreta, increta, a survey of     40 cases. Obstet Gynecol 1977;49:43-47

2.    Clark SL,Koonings PP, Phelan JP.placenta previa/accreta and prior cesarean section. Obstet Gynecol 1985;66:89-92

3.    Woolcottrj,Nichol M,Gibson JS. A case of placenta percreta presenting in the first 

trimester of pregnancy.Aust N Z J Obstet Gynecol 1987;27:258-260

4.    Mcduffie RS, Harkness L, mcvay R M, Haverkamp AD. Mid trimester hemoperitoneum caused by placenta percreta in association with elevated maternal serum alpha etoprotein.Am J Obstet Gynecol 1994;171:565-566

5.    Innes G, Rosen P. An unusual cause of abdominal pain and shock in pregnancy:Case     report and review of literature. J Emerg Med 1985;2:361-366

6.    Archer GE, Furlong LA. Acute abdomen caused by placenta percreta in the second 

trimester. Am J Obstet Gynecol 1987;157:146-147

7.    Aboulafia Y, Lavie O, Granovsky-Grisaru S, Shen O, Diamant YZ.Conservative surgical

management of acute abdomen caused by placenta percreta in the second trimester. Am J Obstet Gynecol 1994;170:1388-1389

8.    Zeemangg,Allaire A,Whitecar P, Moise KJ Jr. Second –trimester presentation of 

placenta percreta. Am J Perinatol, 1999;16(9):475-478

Dr. V. Ravi Sekar  DNB., FNB., 

(Interventional Cardiologist)


Introduction : With the wide expansions of horizons in the field of percutaneous coronary interventions (PCI) , we see a lot of patients with previous bypass surgery presenting for native vessel or graft interventions. With the recent advances in devices and pharmacology various complex lesions could be addressed through PCI.

Case History : 66 year old male who is a known diabetic, hypertensive who has undergone coronary artery bypass grafting (CABG ) in 2006 with 3 bypass grafts (LIMA to LAD and SVG to OM) presented with recent onset exertional angina for 4 months duration. 

Echocardiogram showed preserved LV systolic function and TMT was positive for inducible ischemia. Coronary angiogram done showed significant progression of native Triple Vessel Disease with patent bypass grafts. PDA showed significant stenosis near the origin of the vessel, which was at pathway of Retrograde flow from graft to PLV Branch. Hence to make blood flow possible to PLV it was decided to stent the PDA origin.



Patient was taken up for PCI of PDA. The PCI of the lesion was attempted wiring through femoral approach with 7F multipurpose catheter but failed. After repeated attempts with hydrophilic coated wire, still the lesion could not be crossed. 

Then the lesion was crossed with balloon support with a buddy wire placed in posterolateral branch (PLB) and balloon inflated at low atmospheres.

Subsequently repeated attempts to cross the lesion with complaint balloon failed due to poor support guide.


Then a 5F mother and child catheter (Guideliner) was used as an extension of original guide till the proximal bend so that the balloon could be negotiated. 


Then the lesion was stented with a short everolimus eluting stent (2.75 x 12  mm) in an similar fashion using the guideliner catheter .Final result showed well deployed stent with TIMI III flow.


Conclusion: Adequate guide support is an essential pre-requisite for delivery of interventional materials during coronary angioplasty. Poor guide support can be managed with choosing a proper  supportive guide, using buddy wire  or with balloon entrapment. If all the measures fail guide extension with a guideliner could be a very handy and useful tool for delivery of devices in complex PCI.