Abstract 1228

Primary pulmonary hypertension of the newborn (PPHN) requires cardiopulmonary stabilization to reverse the right to left shunt & admixture of oxygenated with deoxygenated blood. This entails supplemental oxygen via conventional or high frequency ventilation, sedation/paralysis, inotropic support, alkalinization, selective pulmonary vasodilation (inhalation nitric oxide = iNO), & frequent blood volume expansion prior to consideration for ECMO. While several studies have focused on many aspects of these interventional strategies, not much information exists regarding the role of volume expansion in the initial phase of PPHN. To define the importance of fluid resuscitation & determine the necessary fluid volume to achieve cardiopulmonary stabilization, we undertook a retrospective pilot study in which all full term neonates with the diagnosis of PPHN that were admitted between June-Nov. 1998 to our NICU were included. PPHN was confirmed by echocardiography. We analyzed total fluid requirement (crystalloid+colloids) & the duration of fluid administration necessary to achieve cardiopulmonary stabilization after admission to the NICU. Colloids were infused to alleviate hypotension, tachycardia or hypoxemia. Fluid resuscitation was considered complete when the patient did not require colloid infusion for > 6 h. A total of 10 patients were enrolled (B.W.=3.3±0.31 kg, G.A.=38.6±0.45) with the primary diagnosis of meconium aspiration syndrome (3), presumed sepsis (2), primary PPHN in Trisomy 21 (4) & air-leak syndrome (1). All patients were treated with 100% FiO2, mechanical ventilation, sedation/paralysis, exogenous surfactant, high doses of inotropes (dopamine/dobutamine/epinephrine) & iNO. Of the 10 infants, 2 required ECMO of which 1 died. It took 30±4.3 hrs (range 10-56) & 380±60 ml/kg of total fluids (colloids 260±50 ml/kg) to achieve cardiopulmonary stabilization. Urine output during this period was 2.95±0.55 ml/kg/hr. One patient with presumed sepsis developed the abdominal compartment syndrome, necessitating removal of ∼60 ml of transudate by paracentesis, with marked improvement in her cardiopulmonary status. We conclude: 1] Neonates with PPHN require large amounts of fluid (∼ 3 times the estimated blood volume) to expand the intravascular volume during the early stage of the disease process, despite the concomitant use of other therapeutic strategies, 2] Abdominal compartment syndrome can be a complication of PPHN, & 3) Patients with Trisomy-21 may have a higher incidence of PPHN than previously recognized. We speculate that the hypoxemia associated with PPHN results in capillary damage resulting in enhanced permeability causing excessive interstitial fluid leakage. This excessive capillary leak complicates the management of these infants.