RESUMO

A 40-year-old soldier in Guyana consulted at the end of December for skin lesions that had been developing for several weeks after he was lost overnight in the equatorial forest, near the village of Saul. He was bitten by numerous mosquitoes during the night and as he crossed marshy areas. When he arrived at the clinic he had 23 leishmaniasis sites visible.

Assuntos

RESUMO

We report the case of an immunocompetent French soldier stationed in French Guiana, who developed symptomatic pulmonary histoplasmosis.

Assuntos

Assuntos

RESUMO

A complex vascular abnormality in the lungs, termed alveolar capillary dysplasia (ACD) and misalignment of the lung vessels, has been recently recognized in some infants with persistent pulmonary hypertension. These infants die despite maximal medical support including extracorporeal membrane oxygenation (ECMO). Inhaled nitric oxide has been reported to improve oxygenation in neonates with persistent pulmonary hypertension of the newborn, and may allow some infants to avoid the need for ECMO. We identified five infants who had received inhaled nitric oxide to treat refractory hypoxemia caused by persistent pulmonary hypertension of the newborn, and who subsequently died and had autopsy confirmation of ACD. Each infant received care at a different medical center. In each patient, inhaled NO increased the arterial partial pressure of oxygen dramatically. Despite initial clinical improvement, the response to NO was not sustained in any patient. As responsiveness was lost, each infant with ACD required inhaled NO concentrations of 80 ppm or higher to sustain oxygenation. Each infant died, four after extensive periods of ECMO support. This experience demonstrates that a short-term improvement after inhalation of nitric oxide does not lead to long-term survival in ACD. Further, in three infants the diagnosis of ACD was established by lung biopsy before death. Increasing awareness of this clinical entity may allow for the avoidance of costly, invasive procedures such as ECMO until more specific therapies become available.

Assuntos

RESUMO

Excess nitric oxide is a mediator of the hypotension in septic shock. Nitric oxide dilates vascular smooth muscle through activation of soluble guanylate cyclase. We report the increase in blood pressure caused by methylene blue (MB), a soluble guanylate cyclase inhibitor, in five neonates with presumed septic shock unresponsive to colloids, inotropic agents, and corticosteroids. MB was given intravenously at a dose of 1 mg/kg during a 1-hour period. MB increased blood pressure in each patient (average, 33% +/- 20%). Blood pressure subsequently decreased to near baseline values in three patients, who then received a second infusion of MB. Blood pressure again increased in these patients. Three of five patients were weaned from inotropic support within 72 hours. Three of five patients survived and were discharged home. We suggest that MB increased blood pressure in these neonates with refractory hypotension.

Assuntos

RESUMO

OBJECTIVE: To determine the efficacy of partial liquid ventilation (PLV) by means of a medical-grade perfluorochemical liquid, perflubron (LiquiVent), in premature lambs with respiratory distress syndrome (RDS). Further, to determine the compatibility of perflubron with exogenous surfactant both in vitro and in vivo during PLV. DESIGN: Prospective, randomized, controlled study, with in vitro open comparison. SUBJECTS: Twenty-two premature lambs with RDS. INTERVENTIONS: In vitro assays were conducted on three exogenous surfactants before and after combination with perflubron. We studied four groups of lambs, which received one of the following treatment strategies: conventional mechanical ventilation (CMV); surfactant (Exosurf) plus CMV; PLV; or surfactant plus PLV. MEASUREMENTS AND MAIN RESULTS: In vitro surface tension, measured for three exogenous surfactants, was unchanged in each animal after exposure to perflubron. Lung mechanics and arterial blood gases were serially measured. All animals treated with PLV survived the 5 hours of experiment without complication; several animals treated with CMV died. During CMV, all animals had marked hypoxemia and hypercapnia. During PLV, arterial oxygen tension increased sixfold to sevenfold within minutes of initiation, and this increase was sustained; arterial carbon dioxide tension decreased to within the normal range. Compliance increased fourfold to fivefold during PLV compared with CMV. Tidal volumes were increased during PLV, with lower mean airway pressure. Resistance was similar for both CMV and PLV; there was no difference with surfactant treatment. CONCLUSIONS: We conclude that PLV with perflubron improves lung mechanics and gas exchange in premature lambs with RDS, that PLV is compatible with exogenous surfactant therapy, and that, as a treatment for RDS in this model, PLV is superior to the surfactant studied.

Assuntos

RESUMO

The aim of this study was to assess the impact of surfactant deficiency on the pathophysiology of congenital diaphragmatic hernia (CDH). Pregnant ewes were operated on at 80 days of gestation for creation of a diaphragmatic hernia in the lambs. Twenty-one lambs survived to be delivered by cesarean section and were studied. Compliance was improved when surface tension effects were removed by saline solution in lungs of both control animals and lambs with CDH; however, the lungs of the lambs with CDH still had significantly impaired compliance. In a second series of experiments, two groups were studied: a surfactant-treated and a control, nontreated group. Surfactant was given prophylactically into the liquid-filled lungs before the first breath. All lambs were paralyzed and sedated and their lungs mechanically ventilated with 100% oxygen for 30 minutes; gas exchange was then assessed, pressure-volume data were obtained, and compliance was calculated. Surfactant significantly improved gas exchange; arterial oxygen pressure increased from 39 +/- 11.4 to 316 +/- 53.6 mm Hg, arterial carbon dioxide pressure decreased from 148 to 63 mm Hg, and pH increased from 6.87 to 7.16 (p < 0.001). Lung volume at 25 cm H2O, functional residual capacity, and compliance were all increased (p < 0.02). Thus, in the CDH lamb model, pulmonary mechanics are impaired by both parenchymal and surfactant abnormalities. Both lung mechanics and gas exchange are markedly improved by exogenous surfactant therapy.

Assuntos

RESUMO

We previously showed that inhaling nitric oxide (NO) for up to 30 minutes selectively dilates the pulmonary circulation and improves oxygenation in newborn lambs with persistent pulmonary hypertension. In the current study we determined whether inhaling NO for 23 hours increased the survival rate of newborn lambs with persistent pulmonary hypertension, oxidized hemoglobin to methemoglobin, or damaged the lungs. Persistent pulmonary hypertension was created in newborn lambs by ligating the ductus arteriosus 13 days before delivery. Six lambs were randomly selected to breathe NO at 80 parts per million for 23 hours, and 7 control lambs were untreated. Each lamb was delivered at 135 days of gestation (term is 146 days), and the lungs were ventilated at a fraction of inspired oxygen of 0.92. Each of the control lambs died before the end of the study, whereas only one of the NO-treated lambs died (p < or = 0.05). Arterial oxygen tension was greater in the NO-treated lambs by 15 minutes after delivery (63 +/- 17 vs 14 +/- 4 mm Hg). Oxygen tension increased with time in the NO-treated lambs. Inhaled NO increased the concentration of methemoglobin, but this concentration reached a plateau at 3.0% +/- 0.4%. There was evidence of early airway damage in both groups of lambs but no difference between the groups. We conclude that inhaled NO increased survival rates without increasing the incidence of acute lung injury in newborn lambs with persistent pulmonary hypertension.

Assuntos

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We previously showed that fetal lambs whose ductus arteriosus is ligated prenatally will have persistent pulmonary hypertension at birth. We investigated the effect of inhaled nitric oxide on the pulmonary circulation in this animal model. The ductus arteriosus of six fetal lambs was ligated at 126 days of gestation. The lambs were delivered and studied at 136 days of gestation. Mechanical ventilation was maintained at a fraction of inspired oxygen of 0.80. Nitric oxide gas was administered at five different concentrations (6, 12, 25, 50, and 100 ppm) for 5-minute periods separated by 10-minute periods of ventilation without nitric oxide. Inhaled nitric oxide caused dose-dependent decreases in pulmonary arterial pressure and vascular resistance and dose-dependent increases in pulmonary blood flow without affecting systemic arterial pressure. Thus pulmonary arterial pressure decreased from equal to aortic pressure to less than aortic pressure. At the highest dose, mean pulmonary arterial pressure decreased by 27% +/- 2%, pulmonary blood flow increased by 86% +/- 6%, and pulmonary vascular resistance decreased by 59% +/- 4%. Nitric oxide also caused dose-dependent increases in systemic arterial oxygen tension and in the saturation of hemoglobin with oxygen. Partial pressure of arterial oxygen increased from 43 +/- 16 mm Hg at baseline to 185 +/- 72 mm Hg at the highest dose; saturation increased from 74% +/- 8% to 96% +/- 2%. In our model of persistent pulmonary hypertension of the newborn, inhaled nitric oxide selectively dilates the pulmonary circulation, thereby improving systemic arterial oxygenation. Nitric oxide is a promising new treatment of persistent pulmonary hypertension of the newborn.

Assuntos

RESUMO

We investigated the effects of PGD2 in six near-term newborn lambs with induced pulmonary hypertension (mean pulmonary arterial pressure equal to mean systemic arterial pressure). In each lamb PGD2 decreased mean pulmonary arterial pressure, increased pulmonary blood flow, and therefore decreased pulmonary vascular resistance without changing mean systemic arterial pressure. A bolus dose of 20 micrograms PGD2 decreased pulmonary arterial pressure by 30%, increased pulmonary blood flow by 45%, and decreased pulmonary vascular resistance by 54%; systemic arterial pressure increased by 4%. At all doses, pulmonary vascular resistance fell further than systemic vascular resistance, the ratio of percent change in pulmonary vascular resistance to percent change in systemic vascular resistance was approximately 2:1. Similar changes occurred with continuous infusions of PGD2. These effects suggest a role for PGD2 in the normal regulation of pulmonary vascular resistance and blood flow at birth. In addition, because PGD2 in these circumstances increases pulmonary blood flow and reduces pulmonary arterial pressure, it may merit further trials in nonhuman primates; it may be an appropriate agent for treating newborn infants with persistent pulmonary hypertension.

Assuntos