Pulmonary haemorrhage in preterm infants

Finlay, Eric; Subhedar, Nimish V

doi:10.1007/s004310000578

Cited by 32 publications

(20 citation statements)

References 4 publications

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“…Severity of pulmonary hemorrhage varies from limited bleedings to massive pulmonary hemorrhage that might cause death [1,2], and severe pulmonary hemorrhage is characterized by an acute onset of severe endotracheal bleeding with an acute decline in hematocrit and development of multilobar infiltrates on chest radiograph. According to a report by Finlay and Subhedar [3], in the 38 preterm infants with massive pulmonary hemorrhage, mortality was as high as 47% and chronic lung disease was observed in 75% of the survivors despite being administered with adequate supportive treatment. Symptomatic patent ductus arteriosus, culture-positive sepsis and the being small for gestational age were the major predisposing factors to mortality in these 38 preterm infants with severe pulmonary hemorrhage.…”

Section: Introductionmentioning

confidence: 97%

The use of recombinant activated factor VII in the treatment of massive pulmonary hemorrhage in a preterm infant

Çetin

Yalaz²,

Akısü³

et al. 2006

Blood Coagulation &Amp; Fibrinolysis

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Pulmonary hemorrhage is a rare but well-known complication in preterm infants. We present a case of massive pulmonary hemorrhage in a 9-day-old male infant, successfully treated with intravenous recombinant activated factor VII (rFVIIa) (NovoSeven; Novo Nordisk). The infant was diagnosed with sepsis-related disseminated intravascular coagulation and required ventilator support for respiratory distress syndrome and blood transfusions due to active bleeding from endotracheal tube. After administration of the second dose of rFVIIa (120 microg/kg per dose, every 2 h), the active bleeding subsided dramatically and a significant improvement in the oxygenation index was seen 8 h after the third dose of rFVIIa treatment. There were also significant improvements in the prothrombin time, International Normalized Ratio, activated partial thromboplastin time and plasma fibrinogen levels after the third dose of rFVIIa treatment. The infant was discharged on day 82 of life and there was no finding of thrombosis during the hospitalization period. At month 18 of follow-up, there was no morbidity related to the pulmonary and central nervous systems. This case suggests that rFVIIa is effective as an alternative therapy in controlling massive pulmonary hemorrhage of preterm infants.

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Section: Introductionmentioning

confidence: 97%

The use of recombinant activated factor VII in the treatment of massive pulmonary hemorrhage in a preterm infant

Çetin

Yalaz²,

Akısü³

et al. 2006

Blood Coagulation &Amp; Fibrinolysis

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“…1 Over the following two decades, the hemodynamic and pulmonary consequences of delayed ductal closure provided a compelling rationale for treatment to close the ductus. In landmark papers, patent ductus arteriosus (PDA) in infants with RDS was linked to bronchopulmonary dysplasia (BPD) by Northway et al, 2 prolonged ventilation by Siassi et al, 3 mortality by Gregory et al, 4 and worsening pulmonary disease by Kitterman et al 5 Subsequent studies confirmed the association of PDA with pulmonary hemorrhage, 6,7 severe RDS, 8,9 BPD, [10][11][12] necrotizing enterocolitis (NEC), 13,14 renal impairment, 15 intraventricular hemorrhage (IVH), 16,17 periventricular leukomalacia (PVL), 18 cerebral palsy, 19 and death. 20,21 Even now, the adjusted risk of death is increased four- 22 to eightfold 23 for very low birth weight (<1500 g) infants in whom the ductus remains patent after medical therapy.…”

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confidence: 99%

Treatment of persistent patent ductus arteriosus in preterm infants: time to accept the null hypothesis?

2010

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“…19 A functional PDA is recognized by the presence of a murmur, bounding peripheral pulses, cardiomegaly, increased pulmo- nary fluid, and a hyperactive pericardium, 20 and MPH has strongly been associated with a symptomatic PDA. 21 However, none of the infants we reviewed had any clinical suggestion of a functional PDA. This could be due to 1 of 2 reasons.…”

Section: Discussionmentioning

confidence: 98%

Patent Ductus Arteriosus as a Natural Cause of Pulmonary Hemorrhage in Infants

Lewis¹,

McKeever²,

Rutty³

2004

American Journal of Forensic Medicine &Amp; Pathology

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Patent ductus arteriosus (PDA) is a recognized risk factor for massive pulmonary hemorrhage (MPH) in the newborn and is generally seen in association with other MPH risk factors such as prematurity. We report 6 cases of sudden and unexpected death of infants older than 4 days with MPH and PDA at autopsy. The cases were reviewed for other factors that could contribute to MPH to ascertain whether PDA is directly linked to MPH. Histology samples were examined for distribution of hemorrhage in the lungs and iron stained for hemosiderin evaluation. All of the cases had clinical histories and scene examinations which raised the differential diagnosis of mechanical asphyxia in the form of so-called overlayings. The diagnostic dilemma of attributing the MPH to the PDA as the sole cause, dual cause, or incidental finding is discussed. These cases illustrate the medicolegal dilemma faced by the pathologist, as well as the need for further research into the potential association of PDA with MPH.

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Pulmonary haemorrhage in preterm infants

Cited by 32 publications

References 4 publications

The use of recombinant activated factor VII in the treatment of massive pulmonary hemorrhage in a preterm infant

The use of recombinant activated factor VII in the treatment of massive pulmonary hemorrhage in a preterm infant

Treatment of persistent patent ductus arteriosus in preterm infants: time to accept the null hypothesis?

Patent Ductus Arteriosus as a Natural Cause of Pulmonary Hemorrhage in Infants

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