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Signa Vitae

Journal of Anaesthesia, Intensive Care and Emergency Medicine

Impact of gestational age at PPROM on the short-term outcome of children born after extreme and prolonged preterm prelabor rupture of membranes in an experienced care center


Introduction. Survival of infants born after extreme PPROM (preterm prelabor rupture of membranes) has increased dramatically in the past 20 years, up to 90% in some tertiary neonatal centres, due to the progress in neonatal cardiorespiratory management.

Known risk factors of poor outcomes are lower gestational age at PPROM and prolonged and severe oligohydramnios.

Methods. We performed a retrospective study over a 6-year-period (2009-2015), including 14 pregnant women who experienced PPROM, before 25 weeks of gestation, with prolonged (>14 days) and severe oligohydramnios (amniotic fluid index<5). Each live neonate was matched with a control patient who was born the same year, of the same gender, with the same gestational age (+/- 6 days) and who received treatment to induce fetal lung maturation at least 48 hours before birth.

Results. Live birth rate was 14/20 (70%) and neonatal survival was 13/14 (93%). Apgar scores at 5 and 10 minutes were lower in the PPROM group (p<0.01). Intubation was necessary for all babies with PPROM and for 5/13 (38%) of the controls (p < 0.01). In a subgroup analysis of the PPROM group, we found that all babies with PPROM < 20 weeks presented refractory hypoxemia and required iNO (inhaled nitric oxide) administration compared to one in the PPROM group > 20 weeks (p < 0.01).

In all infants requiring iNO, the oxygenation index improved dramatically and rapidly with treatment.

We found no difference in the rate of bronchopulmonary dysplasia, necrotizing enterocolitis, retinopathy of prematurity or intraventricular hemorrhage.

Conclusion. PPROM before 20 weeks of gestation exposes the neonate to a high risk of refractory hypoxemia compared to PPROM after 20 weeks. The initial care management requires more aggressive treatment with administration of iNO in all of them.

After the initial period, the evolution of all babies born after PPROM is comparable to that of their controls.

Key words: preterm prelabor rupture of membranes, oligohydramnios, pulmonary hypertension, pulmonary hypoplasia.

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Pulmonary reperfusion injury


Pulmonary reperfusion injury is a clinical syndrome with no single and recognized pathophysiologic mechanism. It is a major cause of morbidity and mortality following lung transplantation, cardiogenic shock, or cardiopulmonary bypass. The underlying mechanisms remain uncertain. Lung inflammatory injury induced by lipopolysaccharide, characterized by rapid sequestration of neutrophils in response to inflammatory chemokines and cytokines released in the lungs is an acceptable theory. Structural or functional impairment of surfactant has been noted in pulmonary reperfusion injury. The pathological changes may include bilateral pulmonary infiltrates, reduced lung compliance and worsening of gas exchange in the immediate posttransplant period. Recruitment maneuver and high positive end-expiratory pressure can relieve postoperative respiratory failure, especially in the patient with reperfusion pulmonary edema after pulmonary thromboendarterectomy. Pharmaceutical agents, including inhaled nitric oxide, soluble complement receptor type 1, prostaglandin E1 and exogenous surfactant, attenuate pulmonary reperfusion injury through distinct mechanisms. Extracorporeal membrane oxygenation and Novalung are temporary assistance in bridging to lung transplantation, stabilization of hemodynamics during transplantation and treatment of severe lung dysfunction and primary graft failure. Modulation of heme oxygenase-1 expression, ischemic conditioning and gene therapy are future directions for pulmonary reperfusion injury management.

Key words: cardiopulmonary bypass, pulmonary hypertension, respiratory insufficiency

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Pulmonary hypertension leading to right heart failure in a patient with IgA gammapathy


Amyloidosis is a rare disorder characterized by the deposition of amorphous, extracellular, insoluble fibrillar protein in various tissues of the body. Pulmonary hypertension usually occurs in the last stages of the disease with co-existing left ventricular failure. Amyloidosis causing pulmonary hypertension in a patient with no evidence of left ventricular failure is rarely mentioned in literature. Here, we present a patient with IgA gammopathy presenting with pulmonary hypertension leading to progressive right heart failure and death.

Key words: amyloidosis, pulmonary hypertension, IgA gammopathy


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