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עמוד בית
Fri, 22.11.24

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December 2013
Arie Drugan, Irena Ulanovsky, Yechiel Burke, Shraga Blazer and Amir Weissman
 Background: Reduction of fetal number has been offered in high order multiple gestations but is still controversial in triplets. Since recent advances in neonatal and obstetric care have greatly improved outcome, the benefits of multifetal pregnancy reduction (MFPR) may no longer exist in triplet gestations.

Objectives: To evaluate if fetal reduction of triplets to twins improves outcome.

Methods: We analyzed the outcome of 80 triplet gestations cared for at Rambam Health Care Campus in the last decade; 34 families decided to continue the pregnancy as triplets and 46 opted for MFPR to twins.

Results: The mean gestational age at delivery was 32.3 weeks for triplets and 35.6 weeks for twins after MFPR. Severe prematurity (delivery before 32 gestational weeks) was experienced in 37.5% of triplets and in 7% of twins. Consequently, the rate of severe neonatal morbidity (respiratory distress syndrome, bronchopulmonary dysplasia, intraventricular hemorrhage) and of neonatal death was significantly higher in unreduced triplets, as was the length of hospitalization in the neonatal intensive care unit (31.4 vs. 15.7, respectively). Overall, the likelihood of a family with triplets to take home all three neonates was 80%; the likelihood to take home three healthy babies was 71.5%.

Conclusions: MFPR reduces the risk of severe prematurity and the neonatal morbidity of triplets. A secondary benefit is the reduction of cost of care per survivor. Our results indicate that MFPR should be offered in triplet gestations.

July 2012
R. Marom, R. Lubetzky, F.B. Mimouni, H. Bassan, L. Ben Sira, I. Berger, S. Dollberg and D. Mandel

Background: Infants with severe intraventricular-periventricular hemorrhage (IVH) have higher absolute nucleated red blood cell counts (aNRBC) at birth (a marker of intrauterine hypoxia) than controls. Periventricular leukomalacia (PVL) is known to be associated with prenatal and postnatal events. Whether PVL is also linked to intrauterine hypoxia is unknown.

Objectives: To test the hypothesis that infants with PVL have higher aNRBC counts at birth than controls.

Methods: We studied 14 very low birth weight infants with PVL and compared them with 14 pair-matched controls without PVL. Head ultrasound scans were performed in all infants on days 3–5 and 21–25 of life. Paired tests, Fisher exact tests and stepwise logistic regression were performed for analysis.

Results: Groups were similar for gestational age (GA), birth weight (BW), prolonged rupture of membranes (PROM), Apgar scores, IVH, and aNRBC counts. PVL correlated significantly with low partial pressure of CO2 (pCO2) and IVH (P < 0.01). In logistic regression, when GA, gender, PROM, antenatal steroid therapy, 1 (or 5) minute Apgar scores, IVH grade, nosocomial sepsis, patent ductus arteriosus, necrotizing enterocolitis (NEC), need for pressors, aNRBC counts and lowest pCO2 were used as independent variables, pCO2 (P = 0.002), IVH grade (P = 0.001), GA (P = 0.038), NEC (P = 0.061) and use of dopamine (P = 0.010) remained in the analysis (total R2 = 68.2%).

Conclusions: In contrast to severe IVH, aNRBC counts do not predict the development of PVL.

August 2010
November 2009
September 2008
July 2008
A. Malkiel, P. Mor, H. Aloni, E. Gdansky and S. Grisaru-Granovsky

Background: Intrapartum risk is based mainly on obstetric history, which is lacking in primiparous women.

Objectives: To ascertain whether the traditional known risk of primiparity is an independent variable for both maternal and neonatal outcome.

Methods: All women admitted to labor during March-April 2002 were canvassed for eligibility for participation in the study based on an obstetric risk scoring system developed and validated for our population. During the study period, 1473 women presented for delivery. Of these, 298 women (20%) were eligible according to the exclusion criteria as "low risk" parturients: 135 (45%) were primiparous and 163 (55%) were multiparous (2–5 births).

Results: After correction for significant confounding factors, primiparity was revealed as an independent significant risk factor for instrumental delivery (odds ratio 15.5, 95%confidence interval 1.88–125) and for early postpartum hemorrhage (OR[1] 5.6, 95%CI[2] 1.9–16.6).

Conclusions:
This study highlights early postpartum hemorrhage as a significant risk for primiparous women, independent of mode of delivery, and also confirms previous reports of maternal complications requiring transfer from birth centers/home deliveries to tertiary centers.






[1] OR = odds ratio

[2] CI = confidence interval


November 2006
D. Soffer
 Cerebral amyloid angiopathy is characterized by deposition of amyloid in the walls of leptomeninged and cerebral blood vessels. Its most common form, sporadic CAA[1] that results from deposition of β-amyloid peptide, which is the subject of this short review, is present in virtually all cases of Alzheimer diseases and is also common among non-demented subjects where its prevalence increases with age. Stroke due to massive cerebral lobar hemorrhage is the main clinical presentation of CAA, but transient neurologic symptoms due to microhemorrhages may also occur. CAA is also a risk factor for cerebral infarction and there is increasing evidence that CAA contributes to cognitive impairment in the elderly, usually in association with white matter abnormalities on imaging. Although the definitive diagnosis of CAA is neuropathologic, reliable diagnosis can be reached clinically, based on the occurrence of strictly lobar hemorrhages, particularly in the cortico-subcortical area when using gradient-echo or T2*-weighted magnetic resonance imaging. Experimental studies have shown that the origin of the vascular amyloid is neuronal, and age-related degenerative changes in the vessel walls prevent its clearance from the brain along perivascular spaces and promote Aβ[2] aggregation and CAA formation. The entrapped Aβ aggregetes are toxic to various vascular wall components, including smooth muscle cells, pericytes and endothelial cells, leading to their eventual destruction and predisposition of the vessel wall to rupture and hemorrhage. However, more research is necessary to decipher the mechanism of CAA formation and its relation to cognitive decline in the elderly.







[1] CAA = cerebral amyloid angiopathy

[2] Aβ = β-amyloid peptide


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