Timing and antecedents of periventricular haemorrhage and of cerebral atrophy in very preterm infants

Thorburn, RosalindJ.; Lipscomb, A.P.; Stewart, Ann; Reynolds, E. O. R.; Hope, P L

doi:10.1016/0378-3782(82)90085-8

Cited by 65 publications

(32 citation statements)

References 35 publications

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“…We found the incidence of PIVH to be on average twice as high in infants with than in those without IRDS. Our odds ratio of 2.2, with a confidence interval of 1.4 to 3.5, further specifies and substantiates the known association between IRDS and PIVH [5,10,23,24]. The mechanism of the association is believed to be related to hypoxia and hypercapnia, consequences of IRDS, which cause an increase in cerebral blood flow that may lead to rupture of the immature capillary bed in the germinal matrix, thus resulting in PIVH [18,24].…”

Section: Discussionsupporting

confidence: 76%

Incidence and prediction of periventricular-intraventricular hemorrhage in very preterm infants

Bor¹,

Verloove-Vanhorick²,

Brand³

et al. 1987

Journal of Perinatal Medicine

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Section: Discussionsupporting

confidence: 76%

Incidence and prediction of periventricular-intraventricular hemorrhage in very preterm infants

Bor¹,

Verloove-Vanhorick²,

Brand³

et al. 1987

Journal of Perinatal Medicine

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“…Although several other investigators observed significant univariate associations between IVH in premature infants and specific maximum PaCO 2 cutoff values: >45 mm Hg, 11 X50 mm Hg, 8 >60 mm Hg, 11,15,16 and >65 mm Hg, 10 in multivariate analyses a significant association was not found. 10,11,15 Only one small observational trial using multivariate analysis found that hypercapnia was a statistically significant antecedent to IVH. 12 In contrast, three trials found no association between hypercapnia and IVH.…”

Section: Discussionmentioning

confidence: 70%

“…4 Further, hypercapnia in animals has been shown to abolish intact cerebral autoregulation. 5,6 In addition to low gestational age, low birth weight, male gender, worse acute lung disease, etc., hypercapnia has also been identified as an important risk factor for intraventricular hemorrhage (IVH), [7][8][9][10][11][12][13][14][15][16] the most common acute brain injury of premature infants. Although it is unclear whether hypercapnia causes IVH or results from circulatory disturbances that follow severe IVH, hypercapnia may influence the development of IVH by causing vasodilation of cerebral resistance arterioles, increasing CBF, and by impairing intact cerebral autoregulation.…”

Section: Introductionmentioning

confidence: 99%

Hypercapnia during the first 3 days of life is associated with severe intraventricular hemorrhage in very low birth weight infants

et al. 2006

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Objective: To examine whether hypercapnia in very low birth weight (VLBW) infants during the first 3 days of life is associated with severe intraventricular hemorrhage (IVH).Study design: Retrospective cohort study of inborn VLBW infants between January 1999 and May 2004 with arterial access during the first 3 days of life. A multiple logistic regression analysis was used where IVH was dichotomized ((grades 0/1/2) ¼ non-severe; (grades 3/4) ¼ severe). Measures of hypercapnia were entered into the model to ascertain their association with severe IVH.Results: In total, 574 VLBW infants met entry criteria. Worst IVH grade was 0 in 400; 1: 54; 2: 42; 3: 47; and 4: 31 infants. The logistic regression model consisted of the following predictors of severe IVH: gestational age, gender, 1 min Apgar score (dichotomized into two groups: >3 vs p3), multifetal gestation, vasopressor use, and maximum PaCO 2 .Conclusion: In addition to traditional risk factors, it appears maximum PaCO 2 is a dose-dependent predictor of severe IVH during the permissive hypercapnia era.

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“…Temporary obstruction of the airways might have caused an acute episode of impaired gas exchange. Alternatively, if the lung rapidly became more compliant as a result of treatment, it is possible that the intrathoracic circulation became obstructed, creating a situation analogous to the development of tension pneumothorax, which can be an important antecedent of PVH (23). Although these are many ways in which the cerebral circulation might be affected by the administration of surfactant, our results show that the procedure need not cause persistent major perturbations.…”

Section: >S Et Almentioning

confidence: 70%

Cerebral Hemodynamic Effects of Treatment with Modified Natural Surfactant Investigated by Near Infrared Spectroscopy

et al. 1992

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ABSTRACT. The purpose of this study was to investigate PAP, peak airway pressure the effects on cerebral hemodynamics of administering EEP, end expiratory pressure modified natural surfactant (Curosurf, to FiOz, inspired oxygen fraction infants requiring mechanical ventilation for hyaline mem-PVH, periventricular cerebral hemorrhage brane disease. Observations were made using near infrared Paoz, arterial oxygen tension spectroscopy on 20 infants for between 26 and 109 (median Pacoz, arterial carbon dioxide tension 57) min before and 22 to 112 (median 46) min after surfactant instillation. Changes in cerebral oxyhemoglobin concentration and cerebral blood volume (CBV) were monitored continuously; cerebral blood flow, oxygen delivery, and the response of CBV to changes in arterial carbonThere is abundant evidence that surfactant replacement therdioxide tension were measured while the infants were apy improves pulmonary gas exchange and reduces mortality in stable shortly before and after surfactant was given. Cere-infants with hyaline membrane disease (surfactant-deficient resbra1 oxyhemoglobin concentration fell transiently in all piratory distress syndrome) (1). The effects of this therapy on infants immediately after surfactant by a median of -0.21 intracerebral complications, such as PVH, that lead to later (range -0.46 to 0.05) m L 100 g-I, but quickly recovered morbidity are less certain. Most randomized trials show no so that the median change during the 10 min after surfac-evidence of a change in the incidence of PVH in infants treated tant was 0.01 (-0.46 to 0.46) mL.lOO g-I. Alterations in with either natural or artificial surfactant (1). However, in one CBV also occurred ranging from -0.44 to 0.40 (median 0) recent multicenter trial in which an enriched extract of bovine mL. 100 g-I, which represented -12 to 16% of total CBV; lung was used, a substantial increase in the incidence of PVH these changes rapidly resolved. When the infants were was found (2). Hemorrhages graded as severe occurred in 39% stable before and after surfactant, the values for mean (SD) of treated infants compared with 15% of controls. Concern about cerebral blood flow were 20.5 (7.5) and 23.1 (5.2) mL. 100 the high incidence of PVH in the treated infants prompted the g-' . min-I, respectively (n = 9); for mean cerebral oxygen U.S. Food and Drug Administration to terminate this trial before delivery, values were 2.71 (0.89) and 3.15 (0.73) mL. 100 planned enrollment was completed. g-' . min-' (n = 9); and for response of CBV to changes in Little information is available about intracerebral consearterial carbon dioxide tension, they were 0.14 (0.09) and quences of surfactant administration that might provoke PVH, 0.11 (0.11) m L 100 g-' . kPa-' (n = 16); these changes although abnormalities of EEG recordings (3) and falls in cerebral were not statistically significant. We conclude that ( I ) arterial blood velocity (4)

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Timing and antecedents of periventricular haemorrhage and of cerebral atrophy in very preterm infants

Cited by 65 publications

References 35 publications

Incidence and prediction of periventricular-intraventricular hemorrhage in very preterm infants

Incidence and prediction of periventricular-intraventricular hemorrhage in very preterm infants

Hypercapnia during the first 3 days of life is associated with severe intraventricular hemorrhage in very low birth weight infants

Cerebral Hemodynamic Effects of Treatment with Modified Natural Surfactant Investigated by Near Infrared Spectroscopy

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