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Deep venous thrombosis (DVT) has been reported extensively following ovarian hyperstimulation syndrome during in-vitrofertilization (IVF).
16.Douketis JD, Julian JA, Kearon C, Anderson DR, Crowther MA, Bates SM, et al.Does the type of hormone replacement therapy influence the risk of deep vein thrombosis? NB: We prefer the term "vascular dysplasias" for "vascular malformations" because of the risk of confusion with the malformations of vessels (vascular malformations). Division of Pediatric Cardiology, Mattel Children's Hospital, University of California, Los Angeles, California.
In 2004, the interventional treatment of patent ductus arteriosus (PDA) is definitive and curative. BACKGROUND: Large patent ductus arteriosus can present in infancy with congestive cardiac failure and superadded pulmonary infection can necessitate mechanical ventilation. Pulmonary and aortic valve endocarditis in an adult patient with silent patent ductus arteriosus.
Department of Cardiovascular Surgery, Abant Izzet Baysal University, Izzet Baysal Medical Faculty. Pulmonary and aortic valve endocarditis are uncommon especially in an adult patient with patent ductus arteriosus. Praus R, Parizek P, Cervinka P, Haman L, Tauchman M, St'asek J, Pudil R, Gregor J, Hudik M, Hodac M. The case-report describes a 48-year-old-female patient with patent ductus arteriosus with the following structural changes leading to the malignant arrhythmias manifested as a syncope.
Hernandez-Ronquillo L, Tellez-Zenteno JF, Weder-Cisneros N, Salinas-Ramirez V, Zapata-Pallagi JA, da Silva O. BACKGROUND: Advances in neonatal care over the past decades have meant that an increasing number of very premature infants survive today than in years past.
Department of Medicine, Section of Cardiology, Baylor College of Medicine, Houston, Texas 77030, USA. Patent ductus arteriosus as a natural cause of pulmonary hemorrhage in infants: a medicolegal dilemma. Division of Forensic Pathology, University of Leicester, Leicester Royal Infirmary, Leicester, UK. Patent ductus arteriosus (PDA) is a recognized risk factor for massive pulmonary hemorrhage (MPH) in the newborn and is generally seen in association with other MPH risk factors such as prematurity.
Ductus arteriosus aneurysm, a rare and potentially fatal condition, has been reported as a complication after surgical ductus arteriosus closure. Persistent ductus arteriosus (PDA) murmurs become silent probably due to the direction of the jet across the ductus arteriosus when entering the pulmonary artery. Division of Pediatric Cardiology, Saint Louis University School of Medicine, Cardinal Glennon Children's Hospital, 1465 South Grand Boulevard, St.
A number of patent ductus arteriosus (PDA) occluding devices have been studied in an attempt to develop a transcatheter method of closure of PDA. Transcatheter occlusion of patent ductus arteriosus: which method to use and which ductus to close.
Zanardo V, Trevisanuto D, Dani C, Milanesi O, Secchieri S, Guglielmi A, Brentegani L, Cantarutti F.
We report on 14 observations undertaken by ourselves of silent persistent ductus arteriosus (SPDA). A clinically undetectable, small ductus arteriosus was identified by Doppler ultrasonography in 21 individuals. Doppler evaluations were done when congestive heart failure and pulmonary edema were clinically evident. Three cases are presented of patent uncomplicated ductus arteriosus in children, with short systolic murmur, in which the noninvasive diagnosis could not be possible without the echo-Doppler help. Prophylactic closure of the patent ductus arteriosus has been recommended as a means of decreasing the morbidity of the very low birth weight neonate. Purpose: To attempt to describe the natural history and disease process of untreated PDA - from birth to late adulthood - especially pertaining to spontaneous closure and mortality rate. Methods: Review of data on clinical course of patients with PDA over a 20 yr period from the early nineteen hundreds.
Provides a good idea of natural history (with respect to mortality vs spontaneous closure or development of CHF) of PDA during the advent of antibiotic therapy and surgical closure. Case 1 is a 21 yr female presented with pulmonary embolus found to have silent PDA on catheterization; refused surgery and was placed on antibiotic prophylaxis for endocarditis. Case 2 is a 10 yr girl who presented with syncopal attacks (diagnosed as vasovagal episodes) was found to have AS and AR as well as a "silent" PDA (masked PDA); she underwent surgical ligation.
Aside from infective endocarditis, pulmonary embolus may be another complication of PDA that should warrant consideration for closure.
Purpose: To provide data on incidence and evolution of (silent) PDA with RDS, and response of treatment.

Signs and symptoms of PDA developed 24-48 hrs after radiologic diagnosis despite treatment, possibly because indomethacin was not used at that time. Purpose: The writer takes issue with Ellison for underestimating the incidence of silent PDA in premature infants. Where infants > 1kg already studied under similar circumstances in a previous study: 79% of PDA's that were treated, closed. Purpose: To present the case that incidence of PDA is higher than previously shown by less sensitive diagnostic methods (as compared with Doppler ultrasound). Methods: 21 patients older than 12 months diagnosed with silent PDA by Doppler ultrasound in a population of 7,345 children. Discussion: silent PDA due to large duct, coincident pulmonary hypertension, or trivial duct. The authors conclude that 0.5% of those presenting with innocent murmurs have a silent PDA. Kashani's estimate (in 1983) may be still lower than the actual incidence, as this was a clinical rather than Doppler diagnosis. 2) Glickstein: States that small PDA is distinguished from silent PDA by presence of reversal of diastolic flow in the thoracic aorta. 4) Lloyd: Refutes Balzer's implication that all children should be screened and treated for silent PDA. Purpose: To review different devices, techniques, complications, and indications for ductal closure.
Many PDA's don't have a continuous murmur, but only a "partial" systolic murmur - authors didn't comment on this group.
It occurs more frequently in the lower limbs than upper limbs and is associated with an increased maternal morbidity and mortality.[1] Hypercoagulability, damage of the vessel wall, stasis, or low blood flow are the common causes of DVT in pregnancy. Ante- and postnatal risk factors of venous thrombosis: A hospital-based case-control study.
Oral contraception and factor V Leiden mutation in relation to localization of deep vein thrombosis. Venous thromboembolism in relation to in vitro fertilization: An approach to determining the incidence and increase in risk in successful cycles. Incidence of pulmonary and venous thromboembolism in pregnancies after in vitro fertilisation: Cross sectional study. No evidence that assisted reproduction increases the risk of thrombosis: A Danish national cohort study. Can we identify risk factors during pregnancy for thrombo-embolic events during the puerperium and later in life? Obesity as a causal risk factor for deep venous thrombosis: A Mendelian randomization study.
The epidemiology of venous thromboembolism in Caucasians and African-Americans: The GATE Study. In current practice, coils are used for smaller PDA, and devices are employed for larger PDA. This review summarizes the current and emerging interventional technologies directed at PDA closures. A 27-year-old woman diagnosed with pulmonary and aortic valve endocarditis underwent surgical treatment. The authors discuss patent ductus arteriosus, arrhythmias and sudden cardiac death in adult patients with congenital heart disease. These cases illustrate the medicolegal dilemma faced by the pathologist, as well as the need for further research into the potential association of PDA with MPH. This report associates the persistence of ductus arteriosus with a complication considered rare, which has a rapidly fatal evolution.
Bulkiness of the device, complexity of the procedure, and significant residual complications make the majority of the devices unsuitable for routine clinical use.
During a three year period with the routine use of color doppler flow evaluation we found cases of SPDA in 14 children.
It is difficult to estimate the incidence in the general population, but it is likely to be higher than the previously published 0.065% incidence. The long-term use of hormone replacement therapy (HRT) is another critical factor associated with DVT in women. However, an association between the short-term use of HRT in oocyte donation (OD) cycles and DVT has not yet been reported. Other predisposing factors for DVT are obesity, smoking, immobilization and a past or family history of thrombosis.[7]We present a case of a 43-year-old woman who developed lower extremity DVT at around 7 weeks of pregnancy after IVF by oocyte donation (IVF-OD).
DVT was diagnosed at 7 weeks of pregnancy and was managed with low-molecular-weight heparin. We suggest that even a short-term use of HRT should be considered a risk factor for DVT especially in the presence of additional risk factors such as obesity.

Obstetric history revealed one full term birth and two early abortions with no living child.
There was no history of pregnancy-induced hypertension, gestational diabetes or any other complication during that pregnancy.In 2003 and 2013, she had missed abortions at 45 days after spontaneous conception. There was no family history of VT.She had undergone laparotomy for an appendectomy in 1990 in Nigeria. In 1996, she had a diagnostic laparoscopy followed by diagnostic hysteroscopy done twice in 2009 and 2010 (all in Nigeria).
No postoperative complications were reported in the patient.In-vitro fertilization attemptsTwo IVF procedures with self-eggs in Nigeria, the last one in 2010 using long agonist protocol had failed. In November 2013, the patient had an IVF with embryo transfer (ET) using donor oocytes (IVF-OD) in India.
The patient then underwent operative hysteroscopy with adhesiolysis in December 2013 followed by HRT for 2 months. In February 2014, she again underwent another cycle of IVF-OD with the transfer of four embryos but this too did not result in pregnancy.The patient presented at our facility in March 2014.
Pap's smear, breast ultrasound sonography (USG) and routine electrocardiography were normal.
She received a total of 2 cycles of HRT before the next IVF-OD attempt.In April 2014, IVF-OD was done and 2 grade A blastocysts were transferred.
It was extremely difficult to identify the external cervical os due to the presence of a cystocoele, made worse because of the full bladder, depth of the vagina and the flush torn cervix. The bladder was half emptied by catheterization and ET catheter was negotiated after holding the cervix with an allis forceps.
During this FET cycle, the patient again received estradiol valerate (OD, 12 mg) and progesterone (BD, 400 mg).
A subcutaneous injection of lonopin (20 mg, Bharat Serums and Vaccines Ltd., Hyderabad, India) was administered on alternate days to improve implantation.
Estradiol valerate dose was dropped from 12 mg to 6 mg after identification of gestation sacs on transvaginal sonography. Ultrasound at 6 weeks revealed cardiac activity present in all the three embryos.The patient reported with pain and swelling in left leg at around 7 weeks of the pregnancy. On examination, the entire left leg showed edema, there was no discoloration or change in skin temperature. On Doppler, left common iliac, left external iliac and left common femoral in its upper one-third showed distension with soft tissue echogenicity of a thrombus, occupying the entire lumen of the vein. The patient was hospitalized and managed with enoxaparin (BD, 0.8 ml) subcutaneously in association with a hematologist. The thrombus started resolving within 3 weeks with the Doppler showing improved blood flow and was completely resolved on the scan done after 7 weeks of treatment. The patient was maintained on a daily dose of LMWH until 34 weeks of pregnancy and then in the postmartum phase. Thromboembolic deterrent stocking was given after thefirst 2 weeks of LMWH.At 34 weeks, she had a premature rupture of membranes, and an emergency lower (uterine) segment cesarean section was done. The female baby died of necrotizing enterocolitis 1-week after the birth; the other two were discharged from the hospital after 2 weeks of delivery. The additive effects of endogenous, genetic and environmental risk factors present simultaneously can cause VT [9] [Figure 1].
Hypercoagulability and hypofibrinolysis is a result of increased plasma levels of fibrinogen, von-Willebrand factor and factors VII, VIII, IX, and X, and a decreased plasma level of protein S and platelets.
A review by Richter and Rath demonstrated that pregnant women are at a six times higher risk of developing thromboembolic complications. The chance of developing venous insufficiency is reported to be increased with multiple pregnancies and obesity.[12]Previous studies have provided important evidence for considering IVF as a risk factor for VTE. At our center, she again underwent three cycles of HRT with a high dose of estradiol valerate before she had a successful pregnancy.
Ethnicity could also be a factor, an increased risk in patients of African ethnicity has been reported.[20]Patients who have undergone IVF tend to take bed rest as they feel it increases their chances of implantation and reduces chances of abortion. Immobility increases the risk of thrombosis, presumably due to stasis of blood flow in the venous system. She had an uneventful recovery and delivered three healthy babies.AcknowledgmentsThe authors acknowledge Knowledge Isotopes Pvt.

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