Klebsiella pneumoniae carbapenemase (KPC)-producing K. pneumoniae is spreading globally and represents a challenge in infection control and treatment. Solid organ transplant (SOT) recipients are especially at risk for infection by multidrug-resistant bacteria, and little is known about infection with KPC-producing organisms in this setting. The aim of this study was to describe the clinical and microbiologic aspects of KPC-producing K. pneumoniae infections in SOT recipients. A KPC-2-producing K. pneumoniae outbreak was identified in a public teaching tertiary care hospital in São Paulo, Brazil, in June 2009. During the outbreak, cases of KPC-2-producing K. pneumoniae infection in SOT recipients occurred between July 2009 and February 2010; these cases were retrospectively reviewed. Overall, 12 episodes of infection with KPC-producing K. pneumoniae occurred in 2 heart, 4 liver, and 6 kidney transplant recipients with incidence rates of 16.7%, 12.9%, and 26.3% in heart, liver, and kidney transplantation, respectively. Infection occurred at a median time of 20 days after transplantation. Primary infection sites were as follows: 4 urinary tract infections, 4 bloodstream infections, 2 pneumonias, and 2 surgical site infections. All patients except one had received antibiotics in the last 30 days, mostly piperacillin-tazobactam or glycopeptides. All strains exhibited susceptibility to amikacin and gentamicin. Patients were treated with tigecycline plus polymyxin B (3 cases), polymyxin B plus carbapenem (3 cases), polymyxin B alone (3 cases), or tigecycline plus imipenem (1 case). In 2 cases, patients received only carbapenem, and death occurred before the final culture result. The overall 30-day mortality rate was 42%. In this series of KPC-producing K. pneumoniae infection in SOT recipients, the infection occurrence was high during an institutional outbreak and was potentially life threatening.

During the anhepatic phase of conventional liver transplantation (LT), the inferior vena cava (IVC) is crossclamped and venovenous bypass (VVB) is usually indicated for diversion of IVC and portal blood flow. VVB can theoretically lead to pulmonary complications due to the contact of the blood with the surfaces of the circuit. In the piggyback method, preservation of the IVC avoids VVB. The aim of this study is to compare pulmonary alterations after conventional with VVB versus piggyback LT. Sixtyseven patients were randomized for conventional VVB (n ‫؍‬ 34) or piggyback (n ‫؍‬ 33) LT. Pulmonary static compliance (C st ) and Pa O2 /F IO2 ratio were measured preand post-LT. Chest X-rays were obtained daily from the 1st to the 5th postoperative day. Pre-and post-LT C st were 73.4 ؎ 36.0 mL/cm H 2 O and 59.7 ؎ 22.0 mL/cm H 2 O in the conventional group and 69.1 ؎ 20.0 mL/cm H 2 O and 58.7 ؎ 27.1 mL/cmH 2 O in the piggyback group. The difference between the two groups was not significant (P ‫؍‬ .702). C st significantly decreased after LT (P ‫؍‬ .008). The pre-and post-LT Pa O2 /F IO2 were 455.6 ؎ 126.6 mm Hg and 463.1 ؎ 105.9 mm Hg in the conventional group and 468.9 ؎ 114.1 mm Hg and 483.3 ؎ 119.8 mm Hg in the piggyback group. The difference among the two groups was not significant (P ‫؍‬ 0.331). There was no significant difference after LT (P ‫؍‬ .382). Upon the radiological evaluation, piggyback group presented a higher frequency of pulmonary infiltrates (80.6% vs. 50.0%; P ‫؍‬ .025). In conclusion, piggyback LT recipients have a higher rate of pulmonary infiltrates when compared to those operated upon using the conventional VVB method. (Liver Transpl 2004;10:425-433.) C urrently, 2 main methods of liver transplantation (LT) are employed. 1 In the conventional method, the retrohepatic portion of the inferior vena cava (IVC) is cross-clamped and resected in block with the native liver. This maneuver can lead to pulmonary complications secondary to the temporary reduction of the venous blood return of the lower extremities and splanchnic bed. 2 Patients with poor hemodynamic tolerance to IVC and portal vein clamping will require fluid infusion during the anhepatic phase. 2 After graft reperfusion, the restoration of the venous return results in a sudden central volume overload that can cause pulmonary edema. 2 A concurrent mechanism is the release into the systemic circulation of proinflammatory substances produced in the graft itself during the ischemia-reperfusion injury, and in the obstructed venous beds during blood stagnation. 3 These substances may produce left ventricle dysfunction, increase pulmonary capillary pressure, and alter capillary permeability. 3 All these actions can contribute to pulmonary dysfunction.To overcome these disorders, venovenous bypass (VVB) is usually indicated, allowing the diversion of the IVC and portal blood flow to the superior vena cava. 2 Despite these advantages, VVB can also cause pulmonary complications. Although rare, some can be fatal, like air or thrombotic pulmonary em...

The aim of this study was to evaluate the bacterial translocation in liver transplantation (LT), comparing the conventional and the piggyback methods. A total of 32 patients were randomized into the 2 groups. Samples of blood were collected from the radial artery, portal vein (PV) and hepatic vein (HV), in up to 120 minutes postreperfusion. The samples were sent for endotoxin level, as well as samples up to 2 minutes post-perfusion were sent to culture. Hepatic artery and PV blood flows were measured at postreperfusion collection times. The results analyzed were: endotoxin concentration, its quantity, and hepatic clearance. The statistical treatment consisted of analyzing each group's mean profile. The analysis for endotoxin concentration in the radial artery was the deviation related to presurgery measure, and in the PV the deviation related to preclamping (PC) measure. The overall mean level of endotoxin concentration was 0.99 EU/mL in the artery, 1.30 EU/mL in the PV, and 1.22 EU/mL in the HV. The deviation was significant in the portal (P ϭ 0.0031), but not in the artery samples (P ϭ 0.2092). We detected a significant quantity of endotoxin in the artery and in the portal and the HVs (P Ͻ 0.001). There was no difference between the 2 groups and no hepatic clearance of endotoxin was detected either (P ϭ 0.1515). All the cultures were negative. In conclusion, the study detected a significant translocation of endotoxin, but not of bacteria. The study also detected the absence of endotoxin hepatic clearance in both the piggyback and the conventional methods without any difference between them. Liver Transpl 13: 488-496, 2007.

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Systemic and hepatic hemodynamics were prospectively studied in 11 patients with Manson's schistosomiasis and portal hypertension, as well as alterations resulting from the use of propranolol. It was decided that patients whose portal pressure was reduced by 30% with the use of the drug would not undergo surgery and that treatment would consist of the chronic use of propranolol, associated with sclerosis of esophageal varices. This objective was not met by any of the patients whose portal pressure was measured and the study was interrupted. Results show that patients with Manson's schistosomiasis and portal hypertension have hyperdynamic circulation, mild pulmonary hypertension, greatly increased splenic blood flow, and preservation of total hepatic blood flow. Administration of propranolol corrects hyperdynamic circulation, aggravates pulmonary hypertension, does not alter portal pressure and reduces the sectorial portal blood flows, especially of the azygos vein, with maintenance of total hepatic blood flow. These data favor the hypothesis of portal overflow in the physiopathology of portal hypertension of schistosomiasis.