scholarly journals Premature Closure of the Ductus Arteriosus in an Otherwise Healthy Fetus

2019 ◽  
Vol 35 (3) ◽  
pp. 235-239
Author(s):  
Michaela Operle ◽  
Sharlette Anderson

Premature closure of the ductus arteriosus is a rare phenomenon. It is thought to be caused by one of three things: abnormal levels of produced and circulating prostaglandin, maternal ingestion of prostaglandin synthase inhibitors, or it can be idiopathic. Idiopathic premature closure of the ductus arteriosus, not caused by maternal exposure to nonsteroidal anti-inflammatory drugs, is an uncommon event that can cause increased pressure on the right ventricle, resulting in pulmonary hypertension. If left untreated, it can result in fetal death.

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Edin Medjedovic ◽  
Zijo Begic ◽  
Edin Begic ◽  
Amer Iglica ◽  
Nedim Begic ◽  
...  

Abstract Objectives The aim of this article was to present a case of premature fetal closure of the ductus arteriosus (DA) of unknown cause. Case presentation A 32-year-old pregnant woman came for the regular prenatal visit at 36 + 1 weeks of gestation (WG) at which oligohydramnios and premature closure of DA were revealed. Use of non-steroidal anti-inflammatory drugs was excluded by the history, although the patient had the symptoms of common cold 2 weeks before the check-up taking more than 1,000 mL of strong chamomile tea daily till the day before the prenatal visit. The patient was hospitalized at 36 + 1 weeks of gestation due to premature closure of DA and oligohydramnios (amniotic fluid index = 4.5/3), which was the indication to deliver the baby by cesarean section at 36 + 6 WG (birth weight was 2,830 g, birth length 49 cm and head circumference 34 cm, Apgar score at 1 and 5 min were 9/9). Postnatal course was uneventful, and postnatal echocardiography at 12 h of life revealed functionally closed DA and mild dysfunction of the right ventricle, which completely resolved after 7 days. The mother and the baby were discharged home healthy, and were doing well 3 months after delivery. Conclusions Although the cause of premature closure of DA in most of the cases will remain undetected, thorough history sometimes with unexpected events should be taken under the consideration as possible causative factor for premature DA closure, as was drinking of high quantities of chamomile tea in our case.


2021 ◽  
Vol 12 ◽  
Author(s):  
Kévin Le Duc ◽  
Sixtine Gilliot ◽  
Jean Benoit Baudelet ◽  
Sébastien Mur ◽  
Mohamed Riadh Boukhris ◽  
...  

Background: The use of non-steroidal anti-inflammatory drugs (NSAIDs) during the third trimester of pregnancy can cause premature constriction of the ductus arteriosus. This report describes a case of in utero narrowing of the ductus arteriosus (DA) diagnosed postnatally in a baby with Persistent Pulmonary Hypertension of the Newborn (PPHN), after maternal use of Diclofenac-Epolamine 140 mg patch during the second and third trimester.Case Presentation: A fetal ultrasounds revealed an enlarged hypertrophic right ventricle at 32 weeks of gestation. Detailed questioning of the mother highlighted that topical Diclofenac (FLECTOR®) had been used at 26 and at 31 weeks of gestation. An echocardiography performed 8 h postnatally showed supra-systemic pulmonary hypertension, a restrictive ductus arteriosus and a dilated right ventricle. The newborn was treated by inhaled nitric oxide and oral Sildenafil and was discharged from hospital on day 24. He had a complete normalization of his pulmonary vascular resistance on day 48.Conclusion: This case illustrates the potential fetal and neonatal complications associated with maternal topical Diclofenac medication during pregnancy resulting in antenatal closure of the DA.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J Vos ◽  
T Leiner ◽  
A.P.J Van Dijk ◽  
F.J Meijboom ◽  
G.T Sieswerda ◽  
...  

Abstract Introduction Precapillary pulmonary hypertension (pPH) causes right ventricular (RV) pressure overload inducing RV remodeling, often resulting in dysfunction and dilatation, heart failure, and ultimately death. The ability of the right ventricle to adequately adapt to increased pressure loading is key for patients' prognosis. RV ejection fraction (RVEF) by cardiac magnetic resonance (CMR) is related to outcome in pPH patients, but this global measurement is not ideal for detecting early changes in RV function. Strain analysis on CMR using feature tracking (FT) software provides a more detailed assessment, and might therefore detect early changes in RV function. Aim 1) To compare RV strain parameters in pPH patients and healthy controls, and 2) to compare strain parameters in a subgroup of pPH patients with preserved RVEF (pRVEF) and healthy controls. Methods In this prospective study, a CMR was performed in pPH patients and healthy controls. Using FT-software on standard cine images, the following RV strain parameters were analyzed: global, septal, and free wall longitudinal strain (GLS, sept-LS, free wall-LS), time to peak strain (TTP, as a % of the whole cardiac cycle), the fractional area change (FAC), global circumferential strain (GCS), global longitudinal and global circumferential strain rate (GLSR and GCSR, respectively). A pRVEF is defined as a RVEF >50%. To compare RV strain parameters in pPH patients to healthy controls, the Mann-Whitney U test was used. Results 33 pPH-patients (55 [45–63] yrs; 10 (30%) male) and 22 healthy controls (40 [36–48] yrs; 15 (68%) male) were included. All RV strain parameters were significantly reduced in pPH patients compared to healthy controls (see table), except for GCS and GCSR. Most importantly, in pPH patients with pRVEF (n=8) GLS (−26.6% [−22.6 to −27.3] vs. −28.1% [−26.2 to −30.6], p=0.04), sept-LS (−21.2% [−19.8 to −23.2] vs. −26.0% [−24.0 to −27.9], p=0.005), and FAC (39% [35–44] vs. 44% [42–47], p=0.02) were still significantly impaired compared to healthy controls. The RV TTP was significantly increased in pPH patients compared to healthy controls (47% [44–57] vs. 40% [33–43], p≤0.001). Conclusions Several CMR-FT strain parameters of the right ventricle are impaired in pPH patients when compared to healthy controls. Moreover, even in pPH patients with a preserved RVEF multiple RV strain parameters (GLS, sept-LS, and FAC) remained significantly impaired, and TTP significantly prolonged, in comparison to healthy controls. This suggests that RV strain parameters may be used as an early marker of RV dysfunction in pPH patients. Funding Acknowledgement Type of funding source: None


Author(s):  
Gayathri Viswanathan ◽  
Argen Mamazhakypov ◽  
Ralph T. Schermuly ◽  
Sudarshan Rajagopal

2022 ◽  
Vol 12 ◽  
Author(s):  
Matthieu Petit ◽  
Edouard Jullien ◽  
Antoine Vieillard-Baron

Acute respiratory distress syndrome (ARDS) is characterized by protein-rich alveolar edema, reduced lung compliance and severe hypoxemia. Despite some evidence of improvements in mortality over recent decades, ARDS remains a major public health problem with 30% 28-day mortality in recent cohorts. Pulmonary vascular dysfunction is one of the pivot points of the pathophysiology of ARDS, resulting in a certain degree of pulmonary hypertension, higher levels of which are associated with morbidity and mortality. Pulmonary hypertension develops as a result of endothelial dysfunction, pulmonary vascular occlusion, increased vascular tone, extrinsic vessel occlusion, and vascular remodeling. This increase in right ventricular (RV) afterload causes uncoupling between the pulmonary circulation and RV function. Without any contractile reserve, the right ventricle has no adaptive reserve mechanism other than dilatation, which is responsible for left ventricular compression, leading to circulatory failure and worsening of oxygen delivery. This state, also called severe acute cor pulmonale (ACP), is responsible for excess mortality. Strategies designed to protect the pulmonary circulation and the right ventricle in ARDS should be the cornerstones of the care and support of patients with the severest disease, in order to improve prognosis, pending stronger evidence. Acute cor pulmonale is associated with higher driving pressure (≥18 cmH2O), hypercapnia (PaCO2 ≥ 48 mmHg), and hypoxemia (PaO2/FiO2 < 150 mmHg). RV protection should focus on these three preventable factors identified in the last decade. Prone positioning, the setting of positive end-expiratory pressure, and inhaled nitric oxide (INO) can also unload the right ventricle, restore better coupling between the right ventricle and the pulmonary circulation, and correct circulatory failure. When all these strategies are insufficient, extracorporeal membrane oxygenation (ECMO), which improves decarboxylation and oxygenation and enables ultra-protective ventilation by decreasing driving pressure, should be discussed in seeking better control of RV afterload. This review reports the pathophysiology of pulmonary hypertension in ARDS, describes right heart function, and proposes an RV protective approach, ranging from ventilatory settings and prone positioning to INO and selection of patients potentially eligible for veno-venous extracorporeal membrane oxygenation (VV ECMO).


2013 ◽  
Vol 4 (3) ◽  
Author(s):  
Alice I. Supit ◽  
Erling D. Kaunang

Abstract: Congenital heart disease is a structural defect due to the malformation of the heart, aorta, and or great blood vessels. It is the most frequent congenital malformation in newborn babies. Tetralogy of Fallot is one of the congenital heart diseases (CHD) with central cyanosis, and covers 5-10% of all CHD. We reported a boy of one year old with Tetralogy of Fallot and pulmonal atresia (ToF-PA), associated with bronchopneumonia. The diagnosis was based on anamnesis, physical examination, and other supporting examinations. The chest X-ray showed a normal sized heart (CTR 57%) with coer-en-sabot shape, and right and left parahilar infiltration, which resulted in bronchopneumonia and ToF. The electrocardiography showed a right deviation of axis and a hypertrophy of the right ventricle; the echocardiography showed a right ventricle hypertrophy, an over-riding aorta, a large malalignment of the ventricular septal defect, no visualization of pulmonar artery, and no visualization of patent ductus arteriosus (PDA). Conclusion: Based on all the tests performed, the diagnosis of this patient was Tetralogy of Fallot and pulmonal atresia (ToF-PA), associated with bronchopneumonia. The prognosis related to bronchopneumonia in this case was good due to the use of antibiotics. Keywords: tetralogy of Fallot, pulmona atresia, bronchopneumonia.  Abstrak: Penyakit jantung bawaan (PJB) ialah kelainan struktural akibat malformasi jantung, aorta dan atau pembuluh darah besar, dan merupakan kelainan kongenital tersering pada bayi baru lahir. Tetralogi Fallot merupakan salah satu PJB dengan sianosis sentral, dan mencakup 5-10% dari seluruh PJB. Kami melaporkan kasus seorang anak laki-laki berusia satu tahun dengan Tetralogi Fallot dan atresia pulmonal (ToF-PA) disertai bronkopneumonia. Diagnosis ditegakkan melalui anamnesis, pemeriksaan fisik, dan pemeriksaan penunjang. Hasil ekspertisi foto toraks AP memperlihatkan ukuran jantung normal (CTR 57%) berbentuk coer-en-sabot, dan pada paru-paru terlihat infiltrat parahilar kanan dan kiri serta corakan vaskular paru berkurang yang menunjukkan suspek bronkopneumonia dan ToF. Elektrokardiografi memperlihatkan deviasi aksis ke kanan dan hipertrofi ventrikel kanan, dan pada ekokardiografi tampak right ventricle hypertrophy, overriding aorta, VSD malalignment besar, tidak tampak visualisasi arteri pulmonal, dan tidak tampak patent ductus arteriosus (PDA) dengan hasil Tetralogi Fallot dan atresia pulmonal. Simpulan: Berdasarkan hasil pemeriksaan yang dilakukan, diagnosis pasien ini ialah Tetralogi Fallot dan atresia pulmonal (ToF-PA) disertai bronkopneumonia. Prognosis bronkopenumonia pada kasus ini baik yang dapat diatasi dengan antibiotika.Kata kunci: tetralogi Fallot, atresia pulmonal, bronkopneumonia.  


PVRI Review ◽  
2009 ◽  
Vol 1 (3) ◽  
pp. 180 ◽  
Author(s):  
AndrewJ Peacock ◽  
KevinG Blyth

2009 ◽  
Vol 2 (4) ◽  
pp. 294-299 ◽  
Author(s):  
Marc A. Simon ◽  
Christopher Deible ◽  
Michael A. Mathier ◽  
Joan Lacomis ◽  
Orly Goitein ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document