Download the Free Unbound MEDLINE PubMed App to your smartphone or tablet.
Available for iPhone, iPad, iPod touch, and Android.
Erythroblastosis Fetalis [keywords]
- Bilirubin-induced neurologic damage. [Comment, Letter]
- N Engl J Med 2014 Mar 6; 370(10):978-9.
- Bilirubin-induced neurologic damage. [Comment, Letter]
- N Engl J Med 2014 Mar 6; 370(10):979.
- Mirror syndrome after fetoscopic laser therapy for twin-twin transfusion syndrome due to transient donor hydrops that resolved before delivery. A case report. [Case Reports, Journal Article]
- J Reprod Med 2014 Jan-Feb; 59(1-2):90-2.
Mirror syndrome is a rare complication of twin-twin transfusion syndrome (TTTS). Its clinical picture includes massive edema, oliguria, and hemodilution in the context of fetal hydrops. The occurrence of mirror syndrome after fetoscopic laser therapy for TTTS has been well documented, but resolution of mirror syndrome before delivery has not been reported in the literature.A 33-year-old woman was referred to our institution at 23(6)/7 weeks' gestation for TTTS, which had been treated with amnioreduction twice: at 21 and 22 gestational weeks, respectively. Mirror syndrome was diagnosed after fetoscopic laser therapy for TTTS at 24 weeks' gestation due to maternal manifestations of pulmonary edema, skin edema, anemia, low blood protein concentration and proteinuria accompanied by donor hydrops. The maternal respiratory symptoms then gradually abated in <2 weeks along with improved fetal condition, resulting in a delivery with favorable outcomes at 36 weeks' gestation.Manifestation of mirror syndrome after fetoscopic laser therapy in twin-twin transfusion due to donor hydrops doesn't necessarily predict a poor perinatal outcome.
- Non-immune hydrops fetalis. [Journal Article, Review]
- Niger J Med 2013 Oct-Dec; 22(4):266-73.
Non-immune hydrops fetalis (NIHF) is a rare fetal condition with a very high mortality in spite of advances in prenatal diagnostic techniques, early detection, and individualized management. Despite advancement in fetal therapy and rapidly developing new knowledge about the aetiology and prenatal diagnosis, its management has remained controversial.This is a descriptive review ofNIHF.NIHF is a rare fetal condition that presents in an extremely acute manner with almost 90% mortality. Fetal cardiac anomalies are the most common cause and chromosome anomalies are the second-most-common cause. The worst prognosis was related to prematurity, severe hydrops, anaemia, cardiac malformations, chromosomal disorders and congenital infections. Fetal interventions includeboth medical and surgical modalities.NIHF is a rare condition with high prenatal mortality. The exact pathophysiology is still poorly understood. It is important to detect NIHF early, diagnose the underlying cause and institute appropriate treatment. There is need for autopsy of all fetuses or neonates who die from NIHF.
- Relation of placental diagnosis in stillbirth to fetal maceration and gestational age at delivery1). [JOURNAL ARTICLE]
- J Perinat Med 2013 Nov 21.:1-15.
Abstract Aim: To study the relation of retention of dead fetus resulting in its maceration and gestational age at delivery to placental diagnosis. Methods: Some 75 clinicoplacental phenotypes have been retrospectively analyzed in 520 consecutive stillbirths, 329 macerated and 191 nonmacerated, and at three gestational age interval cohorts (330 second trimester, 102 preterm third trimester, and 88 term). Chi-square and clustering methods (Ward dendrograms and multidimensional scaling) were used for statistical analysis. Results: Maternal diabetes mellitus, induction of labor, fetal growth restriction, various umbilical cord abnormalities, and placental clusters of sclerotic/hemosiderotic chorionic villi were more common in macerated stillbirths, while clinicoplacental signs and symptoms of ascending infection and placental abruption, i.e., retroplacental hematoma, premature rupture of membranes, and acute chorioamnionitis in nonmacerated stillbirths. Placental abnormalities were less common in the second trimester, other than the acute chorioamnionitis. Patterns of chronic hypoxic placental injury were common in preterm third trimester, while signs of in-utero hypoxia (abnormal cardiotocography, meconium, and histological erythroblastosis of fetal blood) in term pregnancy. In addition to classical statistics, the clustering analyses added new information to placental investigation of cause of stillbirth. Conclusions: Macerated third trimester stillbirths have multifactorial etiology more likely than the second trimester stillbirths and the likely stasis-induced fetal thrombotic vasculopathy secondary to occult umbilical cord compromise should be sought in placental investigation in such cases. Nonmacerated stillbirths are associated with ascending infection and placental abruption.
- Bilirubin-induced neurologic damage--mechanisms and management approaches. [Journal Article, Review]
- N Engl J Med 2013 Nov 21; 369(21):2021-30.
- [Diagnostic value of amplitude-integrated electroencephalography in predicting outcome of newborn patients in neonatal intensive care unit]. [English Abstract, Journal Article, Research Support, Non-U.S. Gov't]
- Zhonghua Er Ke Za Zhi 2013 Aug; 51(8):614-20.
To assess the diagnostic value of amplitude-integrated electroencephalography (aEEG) in predicting outcome of newborns who were at high risk for central nervous system without severe hypoxic-ischemic encephalopathy.Forty-two consecutive patients at risks for neurological disorders referred to our level-III NICU were prospectively enrolled in the study over a period of 3 years. They were classified on the basis of their primary diagnoses including hypoglycemic brain damage, meningoencephalitis, bilirubin encephalopathy, and metabolic disease. Clinical data were collected. Amplitude-integrated and raw EEG tracings were assessed for background pattern, sleep-wake cycling, and epileptiform activity. The neuromotor development of survivors was assessed by using the Infant Neurological International Battery (INFANIB).The characteristic of aEEG tracings in 42 infants showed continuous normal voltage (CNV)(n = 15), discontinuous voltage (DC)(n = 9), burst-suppression (BS) BS(+) (n = 6), BS(-)(n = 7), flat (FT, n = 5); mature sleep-wake cycling (SWC, n = 4), immature SWC (n = 14), no SWC (n = 24); 30 infants (71.4%) had electrical seizures: single seizure (n = 6); repetitive seizures (n = 7), and status epilepticus (SE) (n = 17).aEEG of 20 infants who had poor outcome showed FT (n = 5), BS(-)/SE (n = 6), BS(-)/ repetitive seizures (n = 1) , BS(+)/SE (n = 1), BS(+)/repetitive seizures (n = 1), DC/SE(n = 6). Chi-square analysis and Spearman rank correlation analysis showed the classification of aEEG background pattern, SWC and comprehensive score (score system was developed by evaluation of the above 3 variables) were correlated with the outcome of these infants at high neurological risks.Amplitude-integrated electroencephalography can provide important information of the status of cerebral function in neonates at high neurological risk and help to predict their outcome.
- Neonatal death suspected to be from sepsis was found to be kernicterus with G6PD deficiency. [Case Reports, Journal Article]
- Pediatrics 2013 Dec; 132(6):e1694-8.
We cared for a term male infant born to Burmese immigrants. At about 24 hours a total serum bilirubin (TSB) was 9.3 mg/dL, and phototherapy was begun. It was stopped 48 hours later, with a TSB of 10.9 mg/dL, and he was discharged from the hospital with an appointment for a repeat TSB check 48 hours later. A few hours before the appointment he became listless and apneic, and his parents took him to the emergency department of the regional children's hospital, where sepsis was suspected. The TSB was 41 mg/dL. He died 4 hours later, despite intensive care efforts, with opisthotonus and refractory hypotension. Blood drawn before the exchange transfusion had low glucose-6-phosphate dehydrogenase (G6PD) enzymatic activity, and sequencing of the G6PD gene revealed the G6PD Mahidol mutation (c.487G>A). Cultures and postmortem examination did not demonstrate an infectious process, but kernicterus was present. Acute kernicterus can mimic septic shock.
- [Mirror syndrome: a case report in fetal medicine]. [Case Reports, English Abstract, Journal Article]
- Rev Med Liege 2013 Sep; 68(9):440-3.
Mirror syndrome is a rare entity describing the association of foetal hydrops and maternal symptoms as general oedema and excessive weight gain mimicking preeclampsia. We report the case of a patient who developed symptoms of oedema, weight gain, headache and biological hemodilution associated with foetal hydrops due to a complex congenital heart defect. This symptomatology spontaneously resolved after foetal expulsion. Mirror or Ballantyne's syndrome needs to be identified on time and well differentiated from preeclampsia. Its consequences may involve the maternal and foetal prognosis.
- Investigation and management of non-immune fetal hydrops. [Journal Article, Practice Guideline, Review]
- J Obstet Gynaecol Can 2013 Oct; 35(10):923-38.
To describe the current investigation and management of non-immune fetal hydrops, with a focus on treatable or recurring etiologies.To provide better counselling and management in cases of prenatally diagnosed non-immune hydrops.Published literature was retrieved through searches of PubMed or MEDLINE, CINAHL, and The Cochrane Library in 2011 using key words (non-immune hydrops fetalis, fetal hydrops, fetal therapy, fetal metabolism). Results were restricted to systematic reviews, randomized controlled trials/controlled clinical trials, observational studies, and significant case reports. Additional publications were identified from the bibliographies of these articles. There were no date or language restrictions. Searches were updated on a regular basis and incorporated in the guideline to May 2012. Grey (unpublished) literature was identified through searching the websites of health technology assessment and health technology-related agencies, clinical practice guideline collections, clinical trial registries, and national and international medical specialty societies.These guidelines educate readers about the causes of non-immune fetal hydrops and its prenatal counselling and management. It also provides a standardized approach to non-immune fetal hydrops, emphasizing the search for prenatally treatable conditions and recurrent genetic etiologies.The quality of evidence in this document was rated using the criteria described in the Report of the Canadian Task Force on Preventive Health Care (Table 1).1. All patients with fetal hydrops should be referred promptly to a tertiary care centre for evaluation. Some conditions amenable to prenatal treatment represent a therapeutic emergency after 18 weeks. (II-2A) 2. Fetal chromosome analysis and genetic microarray molecular testing should be offered where available in all cases of non-immune fetal hydrops. (II-2A) 3. Imaging studies should include comprehensive obstetrical ultrasound (including arterial and venous fetal Doppler) and fetal echocardiography. (II-2A) 4. Investigation for maternal-fetal infections, and alpha-thalassemia in women at risk because of their ethnicity, should be performed in all cases of unexplained fetal hydrops. (II-2A) 5. To evaluate the risk of fetal anemia, Doppler measurement of the middle cerebral artery peak systolic velocity should be performed in all hydropic fetuses after 16 weeks of gestation. In case of suspected fetal anemia, fetal blood sampling and intrauterine transfusion should be offered rapidly. (II-2A) 6. All cases of unexplained fetal hydrops should be referred to a medical genetics service where available. Detailed postnatal evaluation by a medical geneticist should be performed on all cases of newborns with unexplained non-immune hydrops. (II-2A) 7. Autopsy should be recommended in all cases of fetal or neonatal death or pregnancy termination. (II-2A) Amniotic fluid and/or fetal cells should be stored for future genetic testing. (II-2B).