[Interlobar pleural effusion in cardiac insufficiency].
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We describe a case of extreme primary pulmonary hypoplasia. No other congenital anomalies and none of the conditions known to be associated with pulmonary hypoplasia were present. Pregnancy had been complicated by substantial polyhydramnios. The hypoplasia was due to a marked deficiency of the respiratory parenchyma in the presence of normal upper airways and bronchi. Virtually no parenchymal development had occurred and there were very few bronchioles, alveolar ducts, and alveoli. The changes differ from those seen in pulmonary hypoplasia secondary to congenital diaphragmatic hernia, bilateral renal agenesis, anomalies of the urinary outflow tracts, and malformations of the thoracic cavity, in which the pulmonary hypoplasia appears to be compressive in nature. While neither the etiology or pathogenesis of the pulmonary hypoplasia are apparent in this case, the presence of substantial polyhydramnios during pregnancy suggests the possibility that the developing lungs may offer an important surface area for reabsorption and recycling of constituents of amniotic fluid.
Mechanical complications of central vein catheterization for hyperalimentation typically become manifest shortly after insertion. We present a case report describing a delayed innominate vein perforation by a central venous catheter. Use of the adult internal jugular vein for central venous catheterization should be limited to situations in which a subclavian vein is unavailable. Ongoing watchfulness and a vigorous diagnostic and therapeutic approach to such complications are mandatory in the treatment of patients receiving total parenteral nutrition.
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By chance, we had the opportunity to make serial sonographic observations of the extrusion of meconium in a case of meconium peritonitis. Inflammation leads to exudative processes and production of fluid (ascites) in the fetal abdomen. Sonography at that stage of the disease may lead to a misdiagnosis such as 'fetal ascites' or 'non-immune hydrops'. After bowel perforation and extrusion of meconium, the latter appears as a solitary mass inside fetal ascites or as disseminated echogenic masses distributed subdiaphragmatically or perihepatically. Within a couple of days, in most cases the echogenicity of the masses increases. Calcifications lead to distinct shadowing. These calcifications are often the only visible signs of a previous meconium peritonitis. Serial sonograms are essential for the management of pregnancies with meconium peritonitis. If the amount of fetal ascites does not increase and no signs of cardiovascular stagnation appear, no invasive intrauterine diagnostic and therapeutic steps are required. In none out of the nine cases was a cause found.
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Twenty cases of hemothorax in newborns, including 4 of our own patients, are reviewed in detail. This unusual cause of acute respiratory distress within the neonatal period was observed in 14 males and 6 females. Most of the patients were fullterm newborns. As causal factors hemorrhagic disease of the newborn (vitamin K deficiency), disseminated intravascular coagulation, arteriovenous malformations and pleural/vascular rupture are considered. The time of occurrence of bleeding symptoms ranged from 1 to 28 days of life. Sixteen out of 20 patients survived without sequelae, but in 4 cases the outcome was lethal.
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Demonstration of peritoneopleural communication in patients with cirrhotic ascites has an important impact on treatment planning. We studied 12 such patients and found presence of peritoneopleural communication in five. Two had bilateral, one right-side and two left-side, pleural effusion. Pleural fluid protein content was less than 2 g/dL in all patients.
Clinical parameters alone have repeatedly been proven unreliable in assessing cardiopulmonary status, especially in hemodynamically unstable patients. To learn if we had a diagnostic problem in our hospital, we compared physician assessment of cardiac index (CI) and thoracic fluid content (TFC) to values obtained using impedance cardiography (ICG). We selected the newest available ICG monitor, the BioZ, which employs this noninvasive technology. For CI measurements we have shown it to be equivalent to thermodilution and to be more reproducible (variability: 6.3% vs. 24.7%). Physician assessment of CI and TFC (high, normal, or low) was compared to the BioZ monitor's results in 186 patients, considered to be hemodynamically unstable, from the emergency room, the intensive care units, and the floors. Normal values were defined for CI (2.5-4.2 L/min m(2)) and for TFC (males: 30-50 kohm(-1) and females: 21-37 kohm(-1)). The concordance between physician assessment and the BioZ was 51% for CI with Kappa of 0.14 and 58% for TFC with Kappa of 0.19. Attendings did slightly better than the surgical residents with CI (52% vs. 48%) but slightly worse with TFC (57% vs. 61%). The potentially serious conditions of low CI and high TFC were misdiagnosed 42% and 46% of the time, respectively, by all physicians. Analysis of the data revealed that physician use of clinically available objective hemodynamic data, such as heart rate, blood pressure, and pulse pressure index, would not have been helpful. Furthermore, assistance from the pulmonary artery catheter (PAC) is often not available in our hospital, which has experienced a 90% decrease in its utilization over the past six years. Considering the increasing acuity of our aging patient population, accurate assessment of cardiopulmonary status is needed. The use of ICG could be a valuable addition to the physician's armamentarium.