Infusion of Escherichia coli endotoxin (0.12-1.5 micrograms/kg) into unanesthetized sheep causes transient pulmonary hypertension and several hours of increased lung vascular permeability, after which sheep recover. To produce enough lung injury to result in pulmonary edema with respiratory failure, we infused larger doses of E. coli endotoxin (2.0-5.0 micrograms/kg) into 11 chronically instrumented unanesthetized sheep and continuously measured pulmonary arterial, left atrial and aortic pressures, dynamic lung compliance, lung resistance, and lung lymph flow. We intermittently measured arterial blood gas tensions and pH, made interval chest radiographs, and calculated postmortem extravascular bloodless lung water-to-dry lung weight ratio (EVLW/DLW). Of 11 sheep 8 developed respiratory failure; 7 died spontaneously 6.3 +/- 1.1 h, and one was killed 10 h after endotoxin infusion. All sheep that had a premortem room air alveolar-arterial gradient in partial pressure of O2 (PAo2-Pao2) greater than 42 Torr (58 +/- 5 (SE) Torr) died. Of eight sheep that had radiographs made, six developed radiographically evident interstitial or interstitial and alveolar edema. Pulmonary artery pressure rose from base line 22 +/- 2 to 73 +/- 3 cmH2O and remained elevated above baseline levels until death. There was an initial fourfold decrease in dynamic compliance and sixfold increase in pulmonary resistance; both variables remained abnormal until death. EVLW/DLW increased with increasing survival time after endotoxin infusion, suggesting that pulmonary edema accumulated at the same rate in all fatally injured sheep, regardless of other variables. The best predictor of death was a high PAo2-Pao2. The marked increase in pulmonary resistance and decrease in dynamic compliance occurred too early after endotoxin infusion (15-30 min) to be due to pulmonary edema. The response to high-dose endotoxin in sheep closely resembles acute respiratory failure in humans following gram-negative septicemia. Respiratory failure and death in this model were not due to pulmonary edema alone.

Primary CT findings are not specific for mediastinitis through postoperative day 14; after day 14, they are highly indicative of mediastinitis.

We investigated the clinical significance of time of onset, duration, and type of pulmonary edema after orthotopic liver transplantation by retrospectively reviewing 93 consecutive recipients. Pulmonary edema was diagnosed by means of radiographic criteria and PaO 2 /FIO 2 ratio <300. Type was identified by pulmonary artery wedge pressure (hydrostatic, >18 mm Hg; permeability, <18 mm Hg O rthotopic liver transplantation is an accepted treatment for patients with end-stage liver disease. Survival after transplantation has been improving steadily, with a current one-year survival rate of 86.9% for patients and 81.3% for grafts. 1 Nonetheless, early pulmonary complications are common and known to contribute significantly to morbidity and mortality. 2 The most frequent pulmonary complications are pleural effusion, atelectasis, pulmonary edema, and pneumonia. [3][4][5] Pulmonary edema occurs in 14% to 47% of liver transplant recipients. [6][7][8][9][10] It is diagnosed clinically by the combination of bilateral radiographic infiltrates and impaired oxygenation. 11 The purpose of this study was to investigate the clinical significance of the time of onset and the duration of pulmonary edema after orthotopic liver transplantation in consecutive liver transplant recipients. In addition, we investigated whether the traditional classification of pulmonary edema 12 into hydrostatic or permeability types is associated with different outcomes. Methods Patients and Transplantation ProceduresThe medical records of all consecutive patients who underwent orthotopic liver transplantation at Mayo Clinic, Jacksonville, Florida, from February 25, 1998, to October 1, 1999, were retrospectively reviewed. This series represents the first 93 consecutive liver transplant recipients in our transplantation program.All liver transplantation procedures were performed using the piggyback technique without venovenous bypass. Pulmonary arterial catheters were inserted intraoperatively to facilitate hemodynamic management. Patients routinely received small amounts of epinephrine boluses at the time of graft reperfusion but had no sustained need for vasoconstrictor or inotropic support. Decisions regarding administration of fluids and blood products were made according to standards for care to provide hemodynamic stability and correction of unexpected coagulation abnormalities and bleeding. All patients were admitted to the intensive care unit (ICU) immediately after surgery and then extubated as soon as they met standard criteria for termination of mechanical ventilation, such as presence of adequate gas exchange function, hemodynamic stability, and ability to protect the airway. Pulmonary EdemaRadiographic, arterial oxygenation, and hemodynamic data were collected to evaluate patients for pulmonary edema preoperatively on the day of surgery and postoperatively on admission to the ICU and 16 to 24 hours after the operation. A chest radiologist and two pulmonary intensivists evaluated

Analysis

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