Terlipressin-induced modifications of Doppler ultrasound signals of systemic arteries in preterm infants with vasoactive-resistant patent ductus arteriosus: A pilot study.

PURPOSE: To study the effects of terlipressin (TP) infusion on systemic perfusion, estimated with pulsed-wave Doppler ultrasonography of systemic arteries, in a population of extremely low birth-weight (ELBW) preterm infants with vasoactive-resistant ductus arteriosus. METHODS: This prospective, observational cohort included, during five years, 12 ELBW infants with hemodynamically significant patent ductus arteriosus and absent or reversed diastolic flow at Doppler ultrasonography of systemic arteries, despite treatment and high-dose vasoactive support. We measured flow velocity of the anterior cerebral, right renal, and superior mesenteric arteries before and after TP infusion. Changes were evaluated by Spearman's rho coefficient analysis, Wilcoxon signed-rank, and Friedman test. RESULTS: Time-averaged mean velocity of the renal artery (P = .028) increased, while renal pulsatility (P = .010) and resistance (P = .004) indexes, and cerebral artery resistance index (P = .021) decreased after TP infusion. Time-averaged mean velocity of the anterior cerebral artery proportionately increased with dopamine dose (rho = 0.678; P = .015), but showed opposite shifts after TP (rho = -0.662; P = .024). CONCLUSIONS: These changes suggest that TP may improve systemic perfusion in the ELBW infants with vasoactive-resistant ductus arteriosus.

Effects of terlipressin on pulmonary artery pressure in a septic cooled infant: an echocardiographic assessment.

Experience with terlipressin (TP) in the neonatal field is scarce. We describe the effects of TP on pulmonary circulation, studied with echocardiography, in an asphyxiated septic cooled infant with pulmonary hypertension (PH) who developed catecholamine-resistant hypotension and exacerbation of PH shortly after the beginning of the rewarming. TP was added to norephinephine and adrenaline infusions at the dose of 0.02 mg kg(-1) every 6 h, because of refractory hypotension and oliguria. After 10 min, blood pressure dramatically and definitely increased, and urinary output was re-established after 60 min. Echocardiographic evaluation 30 min after the second bolus of TP showed unchanged velocity of the tricuspidal valve regurgitation and improved biventricular functional indexes respect to the pre-treatment assessment. TP was continued for 12 h (three doses) without significant adverse effect except for a transient increase in troponin levels. Addition of TP boluses to catecholamine infusion in our newborn was effective in increasing systemic vascular resistance without increasing pulmonary vascular resistance, successfully reversing the hemodynamics of severe PH, and suggesting a potential primary vasodilator effect on pulmonary circulation. Transient increase of troponin levels during TP treatment confirms the risk of excessive coronary vasoconstriction when TP boluses are added to high dose catecholamines.

Evidence for heavy hyperhydrogen (Λ)(6)h.

Evidence for the neutron-rich hypernucleus (Λ)(6)H is presented from the FINUDA experiment at DAΦNE, Frascati, studying (π+,π-) pairs in coincidence from the K(stop)(-) + (6)Li →(Λ)(6)H + π+ production reaction followed by (Λ)(6)H → (6)He + π- weak decay. The production rate of (Λ)(6) undergoing this two-body π- decay is determined to be (2.9 ± 2.0) × 10(-6)/K(stop)(-). Its binding energy, evaluated jointly from production and decay, is BΛ((Λ)(6)H) = (4.0 ± 1.1) MeV with respect to (5)H+Λ. A systematic difference of (0.98 ± 0.74) MeV between BΛ values derived separately from decay and from production is tentatively assigned to the (Λ)(6)H 0(g.s.)(+) → 1+ excitation.

Congenital fetal and neonatal visceral chylous effusions: neonatal chylothorax and chylous ascites revisited. A multicenter retrospective study.

This retrospective study was carried out at eight Neonatal Intensive Care Units (NICU) Centers worldwide on 33 newborns presenting at birth with pleural, pericardial, or abdominal chylous effusions. Diagnosis of chylous effusion is based on findings of fluid with a milk-like appearance, a concentration of triglycerides in pleural effusion >1.1 mmol/l, and a total cell count >1,000 cells/ml with a predominance of >80% lymphocytes. Thirty-three newborns met the inclusion criteria and were studied. Six subjects who presented at birth with fetal effusion were treated by in-utero pleuro-amniotic shunt. Five of these patients are alive at follow-up. At birth, pleural drainage was performed in 29/33 patients and abdominal drainage was carried out in 3/33. Total parenteral nutrition (TPN) was given to 32/33 patients; 19/23 patients were fed a medium-chain triglycerides (MCT). No adverse effects were observed. Eight patients were treated with Octreotide at dosages ranging from 1 to 7 mcg/kg/hour for 8 to 35 days. All patients showed decreased chylous production. Two patients were treated by pleurodesis. Twenty-two babies are alive after at least 6 months follow-up, 9/33 are deceased, and 2 were lost to follow-up. Clinical conditions of survivors are basically good except for lung involvement [chronic lung disease (CLD) or lung lymphangiectasia] and lymphedema. All patients were using a MCT diet at follow-up with good control of chylous effusion. Visceral chylous effusions of the fetus and neonate are rare disorders, and there currently is only partial agreement on decision-making strategies. We suggest the need for an international prospective trial in an effort to establish the efficacy and effectiveness of diagnostic and therapeutic options described in this article.

Evidence for a kaon-bound state K(-)pp produced in K(-) absorption reactions at rest.

We have searched for a deeply bound kaonic state by using the FINUDA spectrometer installed at the e(+)e(-) collider DAPhiNE. Almost monochromatic K(-)'s produced through the decay of phi(1020) mesons are used to observe K(-) absorption reactions stopped on very thin nuclear targets. Taking this unique advantage, we have succeeded to detect a kaon-bound state K(-)pp through its two-body decay into a Lambda hyperon and a proton. The binding energy and the decay width are determined from the invariant-mass distribution as 115(+6)(-5)(stat)(+3)(-4)(syst) MeV and 67(+14)(-11)(stat)(+2)(-3)(syst) MeV, respectively.