Antenatal risk factors for germinal matrix hemorrhage and intraventricular hemorrhage in preterm infants

Jung

2014

J Korean Neurosurg Soc

ObjectiveThe purpose of this study is to identify the risk factors associated with the development of germinal matrix-intraventricular hemorrhage (GM-IVH) and the relationship of the severity of disease and prematurity.MethodsA total of 168 premature neonates whose birth weight ≤1500 g or gestational age ≤34 weeks were examined by cranial ultrasound (CUS) for detection of GM-IVH among the babies admitted between January 2011 and December 2012 in our medical center neonatal intensive care unit. The babies were divided into two groups : GM-IVH and non-IVH. Clinical presentations, precipitating factors of the patients and maternal factors were analyzed.ResultsIn univariate analysis, gestational age, birth weight, delivery method, presence of premature rupture of membrane (PROM) and level of sodium and glucose were statistically meaningful factors (p<0.05). But only two factors, gestational age and presence of patent ductus arteriosus (PDA) were statistically meaningful in multivariate logistic regression (p<0.05). Delivery method [normal vaginal delivery (NVD) to Caeserean section] was borderline significant (p<0.10).ConclusionPresence of PDA and gestational age were the important risk factors associated with development of GM-IVH.

Section: Discussionsupporting

confidence: 68%

Risk Factors Associated with Germinal Matrix-Intraventricular Hemorrhage in Preterm Neonates

Jung

2014

J Korean Neurosurg Soc

“…However, there are some recent indications that prenatal nicotine predisposes the immature brain for future hypoxic injury [10]. Epidemiologic studies link heavy maternal smoking to the risk of the offspring having germinal matrix/intraventricular hemorrhage [11][12][13] and an increased risk for neurologic morbidity [14]. Perinatal exposure to tobacco constituents is linked to a wide range of morbidities, and increases the risk for sudden intrauterine unexplained death [15].…”

Section: Introductionmentioning

confidence: 99%

Detrimental Effects of Nicotine and Endotoxin in the Newborn Piglet Brain during Severe Hypoxemia

Frøen¹,

Amerio

Stray‐Pedersen³

et al. 2002

Neonatology

Hypoxia-ischemia is a major cause of perinatal brain damage, but evidence shows that brain injury also is associated with intrauterine infections and maternal smoking. The mechanisms are not known, and we therefore explored the effects of experimental inflammation or nicotine on perinatal brain metabolism and injury during severe hypoxemia. Twenty-eight 1-week-old piglets were anesthetized and instrumented with microdialysis probes in the striatum and brainstem. We studied three pretreatment groups: (1) 20 µg/kg i.v. nicotine (n = 9); (2) 1 µg/kg i.v. endotoxin from Escherichia coli (n = 11), or (3) control (n = 8). The piglets were subsequently exposed to 30 min of hypoxemia (6% O₂). In order to minimize any ischemic component and increase survival, this was abrupted for 1 min if blood pressure fell to 30 mm Hg. During hypoxemia, both the pretreatment with endotoxin and nicotine induced higher levels of extracellular lactate and peak lactate/pyruvate ratio compared with controls (54.7 ± 9.6 (p < 0.01) and 65.2 ± 13.1 (p < 0.02) vs. 15.9 ± 7.4, respectively), reflecting a deterioration of the metabolic status in these groups. The two pretreated groups reached significantly higher peak levels of extracellular glycerol (30.9 ± 4.1 vs. 77.9 ± 12.7 and 89.4 ± 14.2 µmol/l, respectively, p = 0.01), indicating a higher level of cellular membrane disintegration or leakage. In addition, 3 endotoxin piglets and 4 nicotine piglets died during reoxygenation, while all controls survived (p = 0.13 and p < 0.04, respectively). Mortality was associated with a rise in extracellular glutamate at the end of hypoxemia/start reoxygenation (p = 0.02). These findings contribute in explaining how nicotine and inflammatory response to bacterial toxins could act as cofactors for hypoxic-ischemic neurologic injury in the immature brain.

“…In addition to the direct hemodynamic effects, toxic effects of the gaseous components released during the combustion of nicotine have been shown to damage the arterial wall [15,27]. Therefore, cigarette smoking is an important causal factor of prenatal pathology, also in unexpected and unexplained fetal death [14][15][16][17][28][29][30][31][32][33]. Hence, the strong atherogenic effect of cigarette smoking on human arteries already begins in fetal life, probably in genetically predisposed individuals.…”

Section: Discussionmentioning

confidence: 99%

Severe intra- and periventricular hemorrhage: role of arteriolosclerosis related to maternal smoke

2011

Objective The authors aimed to describe the atherosclerotic lesions of the cerebral arterioles as a substrate of their rupture and bleeding. Methods The study was performed on the brain of nine Caucasian fetal victims of intra-and periventricular hemorrhage, all grade IV, and nine control cases. Results In the nine victims of hemorrhage, the arteriolar wall structure was altered, focally transformed into a deposit of amorphous eosinophilic material. Such changes often affected the full thickness of the wall causing rupture and hemorrhage. In eight of these cases and in two victims of the control group, the mothers were heavy cigarette smokers (15-20 cigarettes/day) before and during pregnancy. Conclusion The authors conclude that intra-and periventricular hemorrhage can be ascribed to the toxic effects of prenatal absorption of nicotine.