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Acute liver failure (ALF) is defined as a severe, sudden liver dysfunction that induces encephalopathy and coagulopathy (prothrombin time [PT/INR] > 1.5) within 26 weeks of the onset of symptoms (usually jaundice) in patients without previous liver disease. Quantitative and qualitative platelet dysfunction, reduced synthesis of clotting factors, increased consumption of factors (mainly II, V, VII, X), reduced clearance of both activated factors, and/or factor inhibitor complexes are among the most important proposed pathogenetic factors. A possible role might be also played by the diminished degradation of anticoagulants. Plasminogen activator inhibitor 1 (PAI-1) is increased, shifting the balance toward hypofibrinolysis, despite the elevated levels of tissue plasminogen activator (tPA). Although changes in coagulation parameters provide crucial information for the management of the patient with ALF, the optimal management of the hemostatic defects is far from being defined. Because spontaneous bleeding occurs rarely during ALF, measures to improve the bleeding diathesis (fresh frozen plasma, cryoprecipitate, platelet transfusion) are recommended only in patients with clinically significant bleeding or before placement of invasive devices. Antifibrinolytic drugs are used in some cases, but often empirically. The role of rFVIIa, even if promising, is still under debate.

OMBINED kidney‐pancreas transplantation (KPTx) is an accepted and ever-increasing therapeutic option for patients suffering for diabetes mellitus (DM) type I who had developed end-stage renal failure (ESRF). Two of the main goals of this surgical procedure are capable of improving significantly the quality of life of these subjects: (1) recovery of renal function; (2) euglicemic state without insulin supplementation. 1 Correction of the metabolic abnormalities could prevent (or delay) the onset of severe secondary complications. Patients considered for combined KPTx manifest most of the multisystem dysfunctions associated with both diseases; generally, they are in poor medical condition and more prone to develop perioperative complications. Arterial hypertension and preoperative cardiac dysfunction secondary to autonomic neuropathy and microvascular changes are frequent findings in these patients and could be responsible for the cardiovascular complications occurring during surgery or in the immediate postoperative period: silent coronary artery disease has been reported in 20% to 40% of the candidates and hypertensive cardiomyopathy is a frequent echocardiographic finding in individuals affected by ESRF. 2 Because preoperative cardiovascular impairment has been associated with high morbidity and mortality and decreased graft survival, perioperative hemodynamic stability has been considered essential for the early functional recovery of the grafts and for the containment of postoperative complications. 3 Recent advances in invasive hemodynamic monitoring and anesthetic techniques made it possible to preserve or improve cardiovascular homeostasis. However, studies dealing with the hemodynamic profile during KPTx are scarce. In this paper we will describe the cardiovascular changes occurring during the various phases of surgery, specifically addressing the problem of hypotension following pancreatic reperfusion. 3 PATIENTS AND METHODS Our series includes 17 patients (mean age, 32 6 17 years) admitted to combined KPTx for ESRF and severe DM type 1. Eighty percent of the patients were affected by severe hypertension; one had ejection fraction lower than 40%. Heart rate and rhythm, pulse oxymetry, right atrial (RAP), and radial artery pressures were continuously monitored in all the cases. Right heart catheterization with a modified Swan‐Ganz catheter (SG cath Intellicath, Baxter) for complete invasive hemodynamic monitoring (pulmonary capillary wedge pressure [PWP] and cardiac output [CO] for continuous monitoring) was used in eight patients. Systemic vascular resistance (SVR, dynes sec 21 /cm 25 ) was calculated according to standard formulae. Hemodynamic data reported in this paper were recorded after the induction of the anesthesia (baseline, A), 5 minutes before (pre-pancreas reperfusion, B) and 2 minutes after pancreas reperfusion (post-pancreas reperfusion, C), 2 minutes after renal reperfusion (post-kidney reperfusion, D), and at the end of surgery (end of surgery, E). Severe arterial hypotension following pancreas reperfusion was considered mean arterial pressure (MAP) less than 70 mm Hg or less than 70% of the baseline values. General anesthesia and mechanical ventilation were used in all the patients: anesthesia was induced with thiopental and maintained with fentanyl and isoflurane (0.8 to 1.2% in air/O2 mixture 50%); atracurium besylate was used for muscle relaxation. Data are presented as mean 6 SD. Statistical analysis was performed using ANOVA. A P value # .05 was considered statistically significant.