Liver transplantation in a Jehovah's witness.
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Biomedical subjects
Publications and source records attributed to O Detry.
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During orthotopic liver transplantation (OLT) for fulminant hepatic failure (FHF), some patients develop cerebral injury secondary to intracranial hypertension. We monitored intracranial pressure (ICP) and cerebral perfusion pressure (CPP) before and during OLT in 12 FHF patients undergoing transplantation. All four patients who had normal ICP preoperatively maintained normal ICP/CPP throughout OLT. During OLT, four of the eight patients with pretransplant intracranial hypertension had six episodes of ICP increase. These episodes of intracranial hypertension occurred during failing liver dissection (n=3) and graft reperfusion (n=3). At the end of the anhepatic phase, the ICP was lower than the preoperative ICP in all patients, and was below 15 mmHg in all but one patient. These data suggest that in FHF patients who develop intracranial hypertension before OLT, dissection of the native liver and graft reperfusion are associated with a risk of brain injury resulting from intracranial hypertension and cerebral hypoperfusion.
OBJECTIVE: The mechanism of sustained alterations in pulmonary hemodynamics during endotoxin shock remains unclear. To gain more detailed knowledge we used the four-element windkessel model as a descriptor of the pulmonary circuit. METHODS: Consecutive changes in characteristic resistance (R1), vascular compliance (C), input resistance (R2) and inductance (L) were continuously assessed following injection of endotoxin in 6 anaesthetised pigs, and were compared with the corresponding values measured in a similar group of sham-operated animals. RESULTS: Endotoxin challenge resulted in a biphasic pulmonary artery pressure response. Blood flow decreased progressively from 2.8 +/- 0.2 l/min to 2 +/- 0.2 l/min. Ohmic pulmonary vascular resistance (PVR) increased gradually from 0.2 +/- 0.04 to 0.76 +/- 0.1 mm Hg s ml-1. The early increase in PAP (from 14 +/- 2 to 27 +/- 4 mm Hg) was mediated by changes in both R1 (from 0.04 +/- 0.01 to 0.06 +/- 0.01 mm Hg s ml-1) and R2 (from 0.16 +/- 0.04 to 0.61 +/- 0.2 mm Hg s ml-1). These responses, in turn, altered the proximal vascular compliance. A subsequent increase in PAP (from 27 +/- 2 to 32 +/- 3 mm Hg) paralleled the specific decline in distal pulmonary vasculature compliance from 0.84 +/- 0.1 to 0.65 +/- 0.1 ml/mmHg. Analysis of the time course of PVR did not allow us to distinguish between vasoconstriction and stiffening of the vascular tree as mechanisms accounting for PAP changes. CONCLUSIONS: Endotoxemia leads to pulmonary hypertension, which is a result of constriction of proximal pulmonary arteries during the early phase, whereas the late phase is characterised by a decline in distal pulmonary vasculature compliance.
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Transplanting a kidney graft harvested from a live donor has been proposed and used to shorten the waiting time of kidney transplant candidates and to increase the graft pool. Live donor renal transplants have demonstrated better results in term of graft survival rates, compared to renal transplants harvested from brain dead donor. Recently, laparoscopic live donor nephrectomy has been introduced to reduce the live procurement morbidity. This lower morbidity may result in increased acceptance of the donor operation. We initiated a program of laparoscopic live donor nephrectomy in January 1997 and up until June 1998, three cases were successfully performed in our department. The purpose of this paper was to report the first case of this program and its first year of follow-up.
Patients with acetaminophen-induced fulminant hepatic failure (FHF) who meet the King's College Hospital criteria have a high mortality risk (>90%) if they do not undergo liver transplantation. We have developed a treatment strategy for these patients based on the use of an extracorporeal bioartificial liver (BAL) support system. In this study, we report the results of the clinical application of BAL support in patients with acetaminophen-induced FHF. All patients were admitted to a dedicated surgical intensive care unit. They were evaluated for urgent liver transplantation and received the standard medical measures, including N-acetylcysteine administration and intracranial pressure monitoring. Moreover, they underwent daily 6-hour BAL treatments. Eight patients were treated. Three patients were bridged to liver transplantation, and five patients recovered without a transplant. All patients experienced neurological and metabolic improvement after treatments with the BAL support system. The BAL support system seems to improve the outcome of high-risk patients with acetaminophen-induced FHF, even in the absence of liver transplantation. Avoiding liver transplantation is particularly important in an era of organ shortage and high cost of transplants.
BACKGROUND: The aim of this study was to compare the effects of Euro-Collins and University of Wisconsin solutions on pulmonary mitochondrial function after cold ischemia and subsequent warm reperfusion. METHODS: Seventeen pigs underwent lung harvesting after classical lung flush with either University of Wisconsin or Euro-Collins solutions. The mitochondria were isolated from fresh swine lungs, from swine lungs subjected to 24 hr of cold ischemia, and from swine lungs subjected to 24 hr of ischemia followed by 30 min of subsequent ex vivo reperfusion at 37 degrees C with Krebs-Henseleit buffer solution and air ventilation. Mitochondrial oxidative phosphorylation parameters were determined in isolated mitochondria by in vitro measurement of oxygen consumption rates. During reperfusion, the lung function was assessed by the pulmonary aerodynamic parameters and the pulmonary vascular resistance. RESULTS: Relative to controls, mitochondria submitted to cold ischemia showed an alteration in the oxidoreductase activities of the respiratory chain. However, the yield of oxidative phosphorylation was conserved. After reperfusion, pulmonary mitochondria underwent a significant worsening in the oxidoreductase activities of the respiratory chain, and a decrease in the respiratory control and the efficiency of oxidative phosphorylation. Meanwhile, the reperfused lungs showed evidence of early dysfunction, assessed by the aerodynamic parameters and pulmonary vascular resistance. In this model, there was no advantage of University of Wisconsin solution over Euro-Collins solution. CONCLUSIONS: The mild mitochondrial alterations after cold ischemia were not sufficient to explain the limited tolerance of lung to ischemia. After reperfusion, the mitochondrial damage was more severe and could be involved in the posttransplant lung dysfunction.
OBJECTIVE: We tested the hypothesis that right heart failure during endotoxin shock may result from altered ventriculovascular coupling responsible for impeding power transfer to the pulmonary circulation. METHODS: The changes in vascular pulmonary input impedance and right ventricular contractility produced by low-dose endotoxin infusion were studied in 6 intact anesthetized dogs. RESULTS: Endotoxin insult resulted in pulmonary hypertension (from 22 +/- 2 to 33 +/- 3 mmHg) associated with significant decreases in stroke volume (from 26.9 +/- 4 to 20.2 +/- 3 ml) and right ventricular ejection fraction (from 41 +/- 3 to 32 +/- 2%). The first minimum of input impedance spectrum and zero phase were shifted towards higher frequencies. Input resistance and characteristic resistance were dramatically increased. The latter change contributed to a significant increase in the pulsatile component of total right ventricular power output from 13 to 21%, indicating a reduction in the hydraulic right ventricle power output delivered into the main pulmonary artery. Overall changes in input pulmonary impedance were indicative of increased afterload facing the right ventricle leading to depressed performance. In contrast, right ventricular systolic elastance was simultaneously increased from 0.56 to 0.93 mmHg/ml indicating an increase in right heart contractility. CONCLUSION: These data suggest that pulmonary hypertension in the setting of experimental endotoxin shock is accompanied by deleterious changes in the pulmonary impedance spectrum, which are responsible for a mismatch of increased contractile state of the right ventricle to the varying hydraulic load ultimately leading to ventricular-vascular uncoupling.
The aim of the present study was to determine effects of positive end expiratory pressure (PEEP) application on peripheral venous capacitance and relate them to concomitant central hemodynamic disturbances. The venous volume-pressure (V/P) relationships were studied in 6 intact anesthetized pigs to describe the effects of PEEP on systemic venous compliance (computed as the slope of the V/P relationship) and unstressed volume (referred to as the extrapolated volume intercept). Cardiac volumes as well as partitioning of circulating blood volume between central (ITBV) and peripheral (PBV) compartments were assessed by thermo-dye dilution techniques. During a 15 cm H2O PEEP application, venous compliance was reduced by 48%, while unstressed volume was increased by 25% and peripheral blood pooling increased from 63 to 74%. As a result, left heart and right ventricular end diastolic volumes were decreased by 8% and by 44%, respectively. It is concluded that increased venous unstressed volume and reduced compliance depicted the distension of the venous tree secondary to PEEP which acted as an impediment to venous return. As a consequence, cardiac output was reduced because of decreased preload.
Lumped models are frequently used to provide a satisfactory description of the hemodynamic properties of the pulmonary vasculature. The purpose of this study is to describe a method to identify simultaneously the parameters values of windkessel models components. The following equation was used to obtain R1 (characteristic resistance), R2 (peripheral resistance), C (total compliance) and L (inertance): [formula: see text] where ki are the following functions of L, R1, R2 and C: [formula: see text] To assess the accuracy of the method, estimates of R1, R2, and C were compared to characteristic impedance Rc, vascular resistance PVR and pulmonary arterial compliance Cd respectively computed from referenced methods. Comparison between R1 and Rc, PVR and R1 + R2, C and Cd were obtained in 5 anaesthetised pigs during basal conditions and after endotoxin-shock. The results indicate that in both conditions, comparisons evidenced highly significant correlations between values computed by the different approaches (p < 0.0001). Although our method yielded to consistently lower values than values provided by referenced methods, the results were concordant with respect to the expected response of pulmonary vasculature to endotoxin insult. We conclude that our method of identification is suitable for the assessment of lumped parameters windkessel model estimates. The main interest is that actual resistance and compliance values can be obtained easily and simultaneously by a global method approach.
BACKGROUND: Pressure measuring systems using fluid-filled catheters can result in the recording of distorted pressure waveforms. It results in phase delay, overestimation of systolic and, to a lesser extent, of diastolic pressure. We designed and evaluated a method to correct this pressure waveform distortion using an appropriate transfer equation obtained from the dynamic response of the fluid-filled catheter. This transfer equation is based on the principle that a fluid-filled catheter recording system is considered as an underdamped dynamic system fully characterized by its natural frequency (omega n) and damping ratio (zeta). METHODS: Pressure waveforms, simultaneously recorded in vitro or in vivo by a fluid-filled catheter (Pc) and a micromanometer-tipped catheter (Pref), were used to validate the method. Dynamic response of the catheter used was obtained from a fastflush test. The corrected signal (Ppred) was obtained using omega n, zeta and the following transfer equation: d2Pc/dt2 + 2 omega n zeta dPc/dt + omega n 2Pc = C Ppred (t) After correction of Pc, Ppred was compared, using a linear regression, with Pref taken as reference. RESULTS: Our results showed that Ppred was fitted to Pref with excellent coefficient correlation (0.99). The mean error and the standard error of estimate were respectively -1.16 mmHg and 1.4 mmHg. CONCLUSION: This new method can convert the distorted pressure waveforms transmitted by any fluid-filled catheters into high-fidelity signals. It suppresses the phase delay and the over-estimation of systolic pressure induced by fluid-filled catheters.
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Transmission of undiagnosed malignancy with the graft is a dramatic complication of liver transplantation. Alternatives in the management of the recipients of livers, harvested from donors with malignancy diagnosed shortly after transplantation, are either early re-transplantation or close follow-up without re-operation. We reported 4 cases of liver recipients whose allografts were harvested from donors who were diagnosed with malignancy shortly after the liver transplantation. One recipient underwent re-transplantation, and the three other allografts were not removed. No recipient developed recurrence in the follow-up. While graft removal may be the only way to avoid tumor recurrence in recipients of liver graft harvested from donor with malignancy, close follow-up without re-operation may also be considered. The risk of tumor transferral may depend on the histopathological aggressiveness and metastatic potential of the donor tumor, and may be low for low-grade, local tumors. This risk should be evaluated by analyzing large series, using databases of Eurotransplant or United Network for Organ Sharing.
Transplantation of kidney grafts harvested in living donors has demonstrated better results than grafts harvested from brain dead donors. Recently, laparoscopic live donor nephrectomy has been introduced to reduce the live procurement morbidity. In 1997, we performed two laparoscopic live donor nephrectomy and we report the first case of this program in this paper.
Fulminant hepatic failure is an infrequent but dreadful disease, occurring usually in young patients. Despite fulminant hepatic failure is reversible in most of the cases, some patients develop brain edema and intracranial hypertension, which are the most common cause of death in these patients. Liver transplantation significantly improves the prognosis of selected patients in who precise criteria predict a low chance of survival. This review summarizes the modern standard of care of patients with fulminant hepatic failure, with particular underlining of the management of brain oedema and intracranial hypertension.
The orthotopic liver transplantation (OLT) program of the University of Liège was initiated in 1986. Between 1986 and December 1998, 150 adult OLT have been performed in our institution, including 18 liver retransplantations, 1 combined heart and liver transplantation and 3 combined liver and kidney transplantations. The aim of this study was to report the last 3 years of our experience. From January 1996 to November 1998, we performed 50 OLT on 49 patients. Three were retransplantations and two were combined liver and kidney transplantations. Fourty-three patients were transplanted for chronic liver disease and 6 for acute or subacute hepatopathy. Mean waiting time on the list was 4 weeks. Immunosuppression was based on triple therapy (cyclosporin A/tacrolimus, steroids, azathioprine), with steroid and azathioprine withdrawal in most of the patients after 3 months. In the chronic liver disease group, operative (< 30 days) survival was 95% (peroperative myocardial infarction in 2 patients). In the acute liver disease group, postoperative survival was 66%. No perioperative death occurred in 1997 and 1998. Actuarial one year survival was 87%. In our experience, OLT has become a safe procedure.
Attempts to develop liver support systems for the treatment of patients with liver failure have ranged from use of plasma exchange to utilization of charcoal columns and extracorporeal devices loaded with liver tissue. However, no system has achieved wide clinical use and - in the absence of liver transplantation - severe hepatic failure continues to be associated with significant morbidity and mortality. In this paper, the authors review the current status of liver assist systems and summarize their clinical experience with a xenogeneic cell based-bioartificial liver.
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