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La instauracion de una hipotermia peroperatoria, en la mayoria de los casos moderada (≈ 34,5-35,5 °C), es la regla si no se toman medidas de prevencion en un paciente sometido a anestesia general o locorregional perimedular. La causa principal es la redistribucion interna de calor, con un descenso inicial rapido de la temperatura central. La constitucion de una perdida calorica, favorecida por la alteracion de la termorregulacion, agrava la hipotermia hasta una temperatura central que ronda los 34,5 °C, nivel en que la reaparicion de la vasoconstriccion termorreguladora va a permitir la estabilizacion tardia de la temperatura central. Sin embargo, el cuadro sigue agravandose debido a las perdidas caloricas en el compartimento periferico. Se ha demostrado la responsabilidad de la hipotermia en el desarrollo de algunas complicaciones perioperatorias (isquemia del miocardio y arritmias, aumento de la hemorragia quirurgica, absceso de pared, retraso de la cicatrizacion) que pueden prolongar la duracion de la hospitalizacion. La hipotermia puede prevenirse de manera eficaz mediante el calentamiento cutaneo (usualmente mediante mantas con aire caliente), siempre que este metodo se aplique de forma correcta. Entre las demas medidas preventivas, solo el calentamiento de los productos sanguineos es indispensable en caso de transfusion rapida. En la actualidad, mantener la normotermia peroperatoria forma parte del procedimiento de rutina ante un paciente anestesiado.

L’installazione di un’ipotermia intraoperatoria di solito moderata (≈ 34,5-35,5 °C) e la regola, in assenza di misure preventive sotto anestesia generale o locoregionale perimidollare. La ridistribuzione interna del calore ne e la causa principale, portando a una rapida caduta iniziale della temperatura centrale. La creazione di un debito calorico favorito dall’alterazione della termoregolazione aggrava, in seguito, l’ipotermia, fino a una temperatura interna di circa 34,5 °C, dove la ricomparsa della vasocostrizione termoregolatrice permettera la stabilizzazione tardiva della temperatura centrale a questo livello. Tuttavia, il debito calorico continua a peggiorare a causa delle perdite di calore a livello del compartimento periferico. La responsabilita propria dell’ipotermia nella comparsa di complicanze perioperatorie (ischemia miocardica e disturbi del ritmo, aggravamento del sanguinamento chirurgico, ascesso della parete, cicatrizzazione ritardata), che possono prolungare la durata del ricovero, e stata dimostrata. L’ipotermia puo essere efficacemente prevenuta riscaldando la cute (di solito con coperte ad aria calda), a condizione di un utilizzo ottimale di tali mezzi. Tra le altre misure preventive, solo il riscaldamento di prodotti ematici labili e indispensabile in caso di trasfusione rapida. Il mantenimento della normotermia intraoperatoria fa ora parte della gestione di routine di tutti i pazienti anestetizzati.

To test the hypothesis that only one hour of preinduction skin-surface warming decreases the rate at which core hypothermia develops during the first hour of anesthesia.Randomized, prospective study.Operating theater of a university hospital.16 ASA status I and II adult patients scheduled for laparoscopic cholecystectomy under general anesthesia.Eight patients were assigned to receive forced-air warming for one hour before induction of anesthesia (prewarmed group); the other eight patients were covered only with a wool blanket during a similar preinduction period (control group).Tympanic membrane (core) and mean skin-surface temperatures were measured at 15-minutes intervals, starting one hour before induction of anesthesia. Mean skin temperature increased from 34.0 +/- 0.1 C to 37.0 +/- 0.2 degrees C in the pre-warmed group (p0.05), but remained unchanged at 34.7 +/- 0.3 degrees C in the control group. Core temperature during the preinduction period did not change significantly in either group. Following induction of anesthesia, core temperature decreased at a rate of 1.1 +/- 0.1 degrees C/hr in the control group, but only 0.6 +/- 0.1 degrees C/hr in the pre-warmed group (p0.05). After one hour of anesthesia, six of eight pre-warmed patients had core temperatures of at least 36.5 degrees C, whereas only one of the eight control patients did (p0.05).A single hour of preoperative skin-surface warming reduced the rate at which core hypothermia developed during the first hour of anesthesia. Preoperative skin surface warming is particularly helpful during short procedures because redistribution hypothermia is otherwise difficult to treat.

A retrospective study was made of 34 patients who underwent major liver resection with a single period of vascular occlusion exceeding 60 min. The liver remnant was normal in all cases. Vascular occlusion was achieved by continuous portal trial clamping (15 patients), hepatic vascular exclusion (15) or a sequential combination of both procedures (four). Liver cooling was not used. The mean(s.e.m.) duration of continuous normothermic liver ischaemia was 73·6(2·5) (range 60–127) min. The mean(s.e.m.) amount of blood transfused during operation was 5·3(0·8) units packed red cells. There were no deaths after surgery and the postoperative course was uneventful, or limited to asymptomatic pleural effusion, in 18 patients. Three patients suffered postoperative bleeding necessitating further surgery and one of these required reintervention for a prolonged bile leak. Four patients had transient liver failure that resolved spontaneously within 15 days. There was a 13-fold increase in serum transaminase activities and the proaccelerin level was 45 per cent that of normal on day 1 after operation. These changes were returning to normal levels within 15 days. Continuous vascular occlusion during major liver resection is a useful manoeuvre that may be performed safely on normal hepatic parenchyma for up to 90 min.

Experimental studies have shown that liver ischemia-reperfusion induces Kupffer cell activation and tumor necrosis factor- α (TNF α ) release. The aim of this work was to determine whether severe hepatic ischemia and subsequent reperfusion triggers TNF α release in man. Serum TNF α was measured before and 3, 10, 30, 60, 120 min after revascularization and postoperatively at day 1 and 2 in 11 patients with orthotopic liver transplantation (group 1 and 4 patients with liver resection with vascular occlusion (group 2). In group 1, TNF α levels decreased during the first few minutes of reperfusion, then increased slightly to peak at 120 min (40 ± 13 pg/ml). Primary non-function occurred in 1 patient in whom low peroperative levels of TNF α levels were measured. In group 2, no significant changes in TNF α levels were observed. These data, in a small number of patients: (a) show that hepatic ischemia reperfusion does not result in major TNF α production; (b) do not support a primary pathogenic role for TNF α in damage after ischemia-reperfusion in humans.

The increased metabolic and respiratory demand during naloxone recovery from opioid-based anesthesia could be related to the return of thermoregulation in hypothermic patients and thus be avoided by preventing intraoperative hypothermia. In this study, we measured O2 uptake (VO2) during naloxone-induced recovery in two groups of patients to determine the effect of intraoperative heat loss on postoperative VO2 changes. In seven patients, intraoperative hypothermia was prevented (normothermic group), whereas hypothermia was allowed to develop in seven other patients (hypothermic group). Core and skin temperatures were measured throughout the study to calculate changes in body heat content. Before naloxone antagonism of fentanyl-supplemented anesthesia, core temperature (mean +/- SEM) was 36.8 +/- 0.1 degrees C in the normothermic group and 34.2 +/- 0.2 degrees C in the hypothermic group (P less than 0.001). After titrated administration of naloxone during recovery, VO2 and minute ventilation (VE) increased in the hypothermic group, by 114 +/- 37% and 97 +/- 52% respectively (P less than 0.05), with a three-fold increase in four patients. In the normothermic group, VO2 increased significantly less (25 +/- 5%), without any significant change in VE. The change in VO2 and VE was significantly greater in patients who were hypothermic. VO2 was integrated throughout the recovery period to calculate recovery energy expenditure. Recovery energy expenditure and intraoperative heat loss were highly correlated (r = 0.88; P less than 0.01). This study demonstrates that the metabolic and respiratory stresses associated with naloxone-induced recovery from opioid-based anesthesia depend on the intraoperative heat loss and can therefore be reduced by preventing intraoperative hypothermia.

Desmosomes are intercellular junctions that tether intermediate filaments to the plasma membrane. Desmogleins and desmocollins, members of the cadherin superfamily, mediate adhesion at desmosomes. Cytoplasmic components of the desmosome associate with the desmosomal cadherin tails through a series of protein interactions, which serve to recruit intermediate filaments to sites of desmosome assembly. These desmosomal plaque components include plakoglobin and the plakophilins, members of the armadillo gene family. Linkage to the cytoskeleton is mediated by the intermediate filament binding protein, desmoplakin, which associates with both plakoglobin and plakophilins. Although desmosomes are critical for maintaining stable cell-cell adhesion, emerging evidence indicates that they are also dynamic structures that contribute to cellular processes beyond that of cell adhesion. This article outlines the structure and function of the major desmosomal proteins, and explores the contributions of this protein complex to tissue architecture and morphogenesis.

We have evaluated the efficacy of new electric warming blankets, which meet the requirements of the international standard for perioperative electrical and thermal safety, in preventing intraoperative hypothermia. We studied 18 patients undergoing abdominal surgery, allocated to one of two groups: in the control group, there was no prevention of intraoperative hypothermia (n = 8) and in the electric blanket group, two electric blankets covered the legs and upper body (n = 10). Anaesthesia duration was similar in the two groups (mean 201 (SEM 11) min), as was ambient temperature (20.5 (0.1) degrees C). Core temperature decreased during operation by 1.5 (0.1) degrees C in the control group, but only by 0.3 (0.2) degree C in the electric blanket group (P < 0.01). Five patients shivered in the control group compared with one in the electric blanket group (P < 0.05). We conclude that cutaneous warming with electric blankets was an effective means of preventing intraoperative hypothermia during prolonged abdominal surgery.

Since the first attempts at resection of Klatskin tumours, an increasingly aggressive surgical treatment has been proposed. Results obtained after examination of the specimen have shown that a significant proportion of resections were palliative. Curative resection appears to be difficult to perform selectively.This retrospective study evaluates the results of a surgically-oriented management of hilar bile duct cancers. Thirty-nine patients were operated on in the period 1982-1994. Eighteen resections were carried out, requiring liver resection in 13 cases. Pathology of the specimen showed that the resection had been curative in 14 cases. The remaining 21 patients had surgical palliation, i.e. bypass and/or stenting.In the resection group, there was no death but four patients suffered severe complications. The 1- and 5-year survival rates were 67 and 47 per cent respectively, with a median survival of 26 months. In the palliation group, the mortality rate was 14 per cent and median survival was 7 months.In the absence of evident contraindications, surgical exploration is worthwhile as it allows detection of the cases where curative resection is possible. Curative resection often requires a major hepatectomy, but mortality and morbidity may be kept low, and it offers a real hope of cure.

Hepatic vascular exclusion allows the performance of major hepatic resections with minimal intraoperative blood loss. We have previously shown that normothermic ischemia can be tolerated by a healthy liver for up to 90 minutes, and this period is increased to 4 hours if the liver is cooled to 4 degrees C using University of Wisconsin solution.This study assessed whether these techniques could be successfully applied for patients requiring resection of a diseased liver, which is more sensitive to ischemic damage. Between July 1990 and May 1994, 12 patients (6 men, 6 women; mean age, 57.8 years) in whom the planned hepatic resection was believed to require hepatic vascular exclusion for more than 1 hour were treated with perfusion with the University of Wisconsin solution. The surgical procedures were right hepatectomy (one patient), extended right hepatectomy (seven patients), and extended left hepatectomy (four patients). The underlying hepatic disease was cirrhosis or severe fibrosis with hepatocellular carcinoma (four patients), cholestasis (due to cholangiocarcinoma and biliary stricture, one patient each), and more than 30 percent steatosis after treatment of hepatic metastases with chemotherapy (six patients). The University of Wisconsin solution that had been cooled to 4 degrees C was perfused through a cannula placed in the portal vein or the hepatic arterial branch of the segment to be resected, but with flow directed toward the liver that should be retained and effluent fluid drained through a cavotomy. Before reperfusion, the liver was rinsed with Ringer's lactate solution, which was also 4 degrees C.The mean duration of hepatic ischemia was 121 minutes (range, 65 to 250 minutes), and venovenous bypass was used in three cases. The mean amount of blood transfused intraoperatively was 4.3 +/- 4 U; four cases required no transfusion. One patient died on postoperative day seven of portal vein thrombosis. The median hospital stay was 21 days (range, 12 to 56 days). Postoperative complications consisted of pneumonia (one patient), liver insufficiency (one patient, who recovered spontaneously), and subphrenic abscess (one patient). The postoperative tests of hepatic function were altered to the same degree as that seen after hepatic vascular exclusion of less than 1-hour duration in healthy livers. All patients who left the hospital were alive at 1 year.Cooling of the hepatic parenchyma allowed us to perform major hepatic resection in patients with diseased livers using hepatic vascular exclusion for longer than 1 hour without increased morbidity or mortality. However, because of particular difficulties due to the size or location of the lesions, the application of these new techniques should only be considered for the largest and most complex hepatic resections for which hepatic vascular exclusions longer than 1 hour are foreseen.

BACKGROUND The infusion of several liters of crystalloid solution at room temperature may significantly contribute to intraoperative hypothermia because warming fluid to core temperature requires body heat. The aim of this study was to evaluate the effect of delivering warmed intravenous (IV) fluid to the patient on preventing intraoperative hypothermia. METHODS Intraoperative core and mean skin temperatures were measured during prolonged abdominal surgery in 18 patients randomly divided into two groups according to intraoperative IV fluid management. In 9 patients (control group) all IV fluids infused were at room temperature. In the other 9 patients (group receiving warmed fluids) all IV fluids were warmed using an active IV fluid tube-warming system. In all 18 patients a warming blanket covered the skin surface available for cutaneous warming. Intraoperative changes in total body heat content (kJ) were calculated from core and mean skin temperatures. RESULTS At the end of surgery, core temperature was 36.7 +/- 0.2 degrees C in the group receiving warmed fluids and 35.8 +/- 0.2 degrees C in the control group (P < 0.05). The estimated reduction in heat loss provided by warming IV fluid was 217 kJ, a value very close to the theoretical value expected from thermodynamic calculation. During recovery, one patient shivered in the group receiving warmed fluids and seven in the control group (P < 0.05). CONCLUSION In conclusion, infusion of warmed fluids, combined with skin-surface warming, helps to prevent hypothermia and reduces the incidence of postoperative shivering.

Intraoperative hypothermia initially results from internal redistribution of heat facilitated by anesthesia-induced vasodilation. Preinduction skin-surface warming minimizes postinduction hypothermia in anesthetized volunteers. However, its efficacy might be reduced in surgical situations, because of multiple sources of heat loss.Intraoperative core and mean skin temperatures were measured during total hip arthroplasty in 16 patients, randomly assigned to be covered preoperatively with a warming blanket foror = 90 min (prewarmed group) or not covered (unwarmed group).During the first hour of anesthesia, core temperature decreased more than twice as much in the unwarmed group (-0.7 +/- 0.1 degree C; mean +/- SE) than in the prewarmed patients (-0.3 +/- 0.1 degree C). At the end of surgery, core temperature was 36.3 +/- 0.1 degree C in the prewarmed group and 35.2 +/- 0.2 degree C in the unwarmed group. During recovery, seven patients obviously shivered in the unwarmed group and none in the prewarmed group.Preanesthetic skin-surface warming reduces the initial postinduction hypothermia in surgical patients, preventing intraoperative hypothermia and postoperative shivering even for procedures lasting 3 h or longer.

Experimental studies have shown that liver ischemia-reperfusion induces Kupffer cell activation and tumor necrosis factor-alpha (TNF alpha) release. The aim of this work was to determine whether severe hepatic ischemia and subsequent reperfusion triggers TNF alpha release in man. Serum TNF alpha was measured before and 3, 10, 30, 60, 120 min after revascularization and postoperatively at day 1 and 2 in 11 patients with orthotopic liver transplantation (group 1) and 4 patients with liver resection with vascular occlusion (group 2). In group 1, TNF alpha levels decreased during the first few minutes of reperfusion, then increased slightly to peak at 120 min (40 +/- 13 pg/ml). Primary non-function occurred in 1 patient in whom low peroperative levels of TNF alpha levels were measured. In group 2, no significant changes in TNF alpha levels were observed. These data, in a small number of patients: (a) show that hepatic ischemia-reperfusion does not result in major TNF alpha production; (b) do not support a primary pathogenic role for TNF alpha in damage after ischemia-reperfusion in humans.

Extracorporeal liver surgery has been proposed with the aim to increase the resectability rate in patients with advanced tumors. In order to avoid the inherent section of the hepatic pedicle we propose ex situ-in vivo liver surgery. The surgical procedure comprises complete mobilization and exteriorization of the liver which is rocked on the axis of the porta hepatis following section of the hepatic veins. Protection of the liver parenchyma against prolonged ischemia is obtained through cold portal perfusion (UW solution) and the use of an heat exchanger on which liver resections and vascular procedures are performed. The procedure also encompasses the use of veno-venous bypass during liver vascular exclusion. This procedure was performed in 2 patients with tumoral invasion of the 3 main hepatic veins and in 1 patient whose hemangioma was surrounding the hepatocaval confluence. Duration of hypothermic ischemia was 205, 225 and 230 minutes respectively. Postoperative course was uneventful in the 3 cases with an hospital stay of 25, 28 and 18 days. Ex situ-in vivo liver surgery allows completion of a surgical treatment in patients whose tumor appears unresectable with the use of conventional technics. This procedure may constitute an alternative to liver transplantation in highly selected cases.

Major liver resections with complex vascular reconstruction require ischemia lasting from 2 h 30 to 5 h thus exceeding hepatic tolerance to warm ischemia. We describe a new technique of "ex situ-in vivo" liver surgery with prolonged ischemia with an intact hepatic pedicle. The surgical procedure encompasses complete mobilization of the liver and inferior vena cava, inferior mesenteric and femoral to axillary vein bypass, complete vascular exclusion of the liver, cold perfusion (U. W. solution), section of the hepatic veins allowing exteriorization of the liver ("ex situ") which remains connected by the hepatic pedicle ("in vivo"). The liver is placed on a heat exchanger at 4 degrees C. This procedure was performed in three patients: one each with hepatocellular carcinoma, huge metastasis of colorectal carcinoma and a "diffuse" hemangioma. Duration of ischemia was 225, 205, and 230 min respectively. The postoperative course was uneventful in all 3 cases and patients are alive at 15, 12, and 6 months. As it improves resecability rate of liver tumors and provides radical margins of resection, this procedure may be a beneficial alternative to liver transplantation for which poor results in cancer therapy with a high rate of recurrence are mainly due to immunosuppression.

Intra-operative hemorrhage is the main surgical risk during liver resections. Nowadays hepatectomies for large or posterior liver tumors close to the hepatocaval junction can benefit from total hepatic vascular exclusion (HVE) involving portal triad exclusion and clamping of the inferior vena cava (IVC) below and above the liver. Anatomical aspects of HVE have been studied in 64 subjects by segmental occlusive phlebographies of the IVC, injection of corrosive substances into the hepatocaval network, biometry of the retrohepatic IVC and serial sections of injected livers. A total HVE should exclude the right suprarenal and phrenic veins. Clamping of the suprahepatic IVC depends on the termination of the left inferior phrenic vein. Clamping of the subhepatic IVC must be retrohepatic: the right lobe of the liver has to be mobilized to free the right border of the retrohepatic IVC into which flows the right suprarenal vein 40 +/- 20 mm above the right renal vein and under the superior right hepatic vein. Both suprahepatic and retrohepatic clamps excluding the retrohepatic portion of the IVC (46.6 +/- 13 mm) and the hepatocaval junction should come in contact behind the IVC without overlapping.

The acid-base disorders after hepatic vascular exclusion (HVE) were studied in 30 major liver resections. HVE included portal triad clamping and occlusion of the inferior vena cava below and above the liver, without venous shunt nor cooling. Clamping of the supra-coeliac abdominal aorta (AoC) was associated with HVE in 12 patients. HVE lasted 18 to 65 min (mean 37 min). Liver ischemia and splanchnic blood pooling resulted in metabolic acidosis and hyperlactatemia. In order to prevent his acidosis, prophylactic administration of NaHCO23 was used during the first 19 cases. This induced significant metabolic alkalosis during HVE and the early postoperative period; increasing experience made us reduce the amount of NaHCO3. After the release of the clamps, Paco2 increased 25% following HVE without AoC (p less than 0.001) and 53% following HVE with AoC (p less than 0.001). In an attempt to distinguish between the effects of the metabolic acidosis and the rise of Paco2 in the fall of pH which occurred after removal of the clamps, NAaHCO3 was deliberately not given in the last 11 patients. Acidosis appeared to be greater with AoC than without and mainly related to the rise of Paco2. A fall of Paco2 to its initial value was always followed by the return of pH to the normal range. This study demonstrated the human ability to correct spontaneously the acidosis which followed HVE. The need for NaHCO3 after HVE reflected a poor hemodynamic state after major liver resection rather than a metabolic consequence of hepatic ischaemia.

A case of venous air embolism occurring during liver resection is reported. Diagnosis was made early from the continuous recording of pulmonary artery pressure. The aetiology was neither surgical nor an obvious discon-nection of a venous line. It was caused by a blockage of the blood filter, resulting in subambient pressure between the filter and a peristaltic pump, leading to aspiration of numerous small air bubbles. The clinical course after replacement of the defective material was uneventful, except for transient postoperative pulmonary oedema.

Serial determinations of creatine phosphokinase isoenzymes (CPK) were made during the operative period and the first postoperative week in 60 patients undergoing coronary artery bypass surgery. Electrocardiograms (ECG) and serum levels of glutamic oxaloacetic transaminase (SGOT) and lactic dehydrogenase (LDH) were also evaluated. All patients had increased CPK MB activity which first became detectable during the operative period. The CPK MB curves usually showed a peak during the first postoperative hours and then a rapid decay. Some curves, however, showed a different profile with a prolonged liberation of CPK MB. This type of curve was more frequent in patients with electrical signs of necrosis or ischemic injury. In this group, the total amount of CPK MB released was greater than that in patients with unchanged ECG tracings (p less than 0.05). A mean curve of CPK MB activity was calculated for the patients without electric and/or enzymatic signs of myocardial injury. Serum CPK MB determination is a useful technique for identifying perioperative myocardial infarction (MI) and the time sequence of its occurrence. The appearance of this isoenzyme in every patient undergoing coronary surgery is an interesting finding, and it significance needs to be clarified.

The acid-base disorders after hepatic vascular exclusion (HVE) were studied in 30 major liver resections. HVE included portal triad clamping and occlusion of the inferior vena cava below and above the liver, without venous shunt nor cooling. Clamping of the supra-coeliac abdominal aorta (AoC) was associated with HVE in 12 patients. HVE lasted 18 to 65 min (mean 37 min). Liver ischemia and splanchnic blood pooling resulted in metabolic acidosis and hyperlactatemia. In order to prevent his acidosis, prophylactic administration of NaHCO23 was used during the first 19 cases. This induced significant metabolic alkalosis during HVE and the early postoperative period; increasing experience made us reduce the amount of NaHCO3. After the release of the clamps, Paco2 increased 25% following HVE without AoC (p less than 0.001) and 53% following HVE with AoC (p less than 0.001). In an attempt to distinguish between the effects of the metabolic acidosis and the rise of Paco2 in the fall of pH which occurred after removal of the clamps, NAaHCO3 was deliberately not given in the last 11 patients. Acidosis appeared to be greater with AoC than without and mainly related to the rise of Paco2. A fall of Paco2 to its initial value was always followed by the return of pH to the normal range. This study demonstrated the human ability to correct spontaneously the acidosis which followed HVE. The need for NaHCO3 after HVE reflected a poor hemodynamic state after major liver resection rather than a metabolic consequence of hepatic ischaemia.

Twenty-four resections under hepatic vascular exclusion (HVE) have been performed in patients with massive liver tumors. The procedure of HVE was used to minimize blood loss and the chance of gas embolism; it included clamping of the portal triad and occlusion of the inferior vena cava above and below the liver. In 12 of these patients the HVE was associated with clamping of the abdominal aorta above the celiac axis (AoC). During the "anhepatic" phase, which lasted 24 to 65 minutes (mean 39 minutes), neither venous shunt nor refrigeration was used. When HVE was associated with AoC, the circulation to the lower part of the body was completely excluded so that the systemic circulation was reduced to a small upper compartment in which the mean arterial pressure increased by 33% while the cardiac index decreased by 40%. The diastolic pulmonary arterial pressure remained unchanged. When HVE was not associated with AoC, the body was divided into an upper vascular compartment with normal venous resistance and a lower vascular compartment with increased resistance to the venous return and increased blood volume. The cardiac index, which was distributed to these two compartments, decreased by 40% to 50% but the mean arterial pressure decreased by only 14%. The good hemodynamic tolerance to HVE without AoC that was observed in these patients confirms the efficiency of collateral venous channels in the circumstances reported. AoC appears to be unnecessary in most patients if accurate fluid volume loading has been achieved before HVE. The study of acid-base balance demonstrates the ability of the human body to correct spontaneously the acidosis that follows the release of the clamps, provided a stable hemodynamic state is maintained. Only minor disorders of coagulation, without abnormal bleeding, were observed, and no prophylactic treatment was necessary. There were no deaths during operation, but a 25% postoperative mortality rate was observed mainly related to the underlying disease and the status of the remnant liver parenchyma. Despite its apparent sophistication, HVE is a simple and safe procedure for performing otherwise hazardous liver resections for tumors of large size or that are located close to the inferior vena cava and the suprahepatic veins. Its hemodynamic and metabolic consequences appear to be moderate.

The intra- and early postoperative courses of 142 consecutive patients who underwent liver resections using vascular occlusions to reduce bleeding were reviewed. In 127 patients, the remnant liver parenchyma was normal, and 15 patients had liver cirrhosis. Eighty-five patients underwent major liver resections: right, extended right, or left lobectomies. Portal triad clamping (PTC) was used alone in 107 cases. Complete hepatic vascular exclusion (HVE) combining PTC and occlusion of the inferior vena cava below and above the liver was used for 35 major liver resections. These 35 patients had large or posterior liver tumors, and HVE was used to reduce the risks of massive bleeding or air embolism caused by an accidental tear of the vena cava or a hepatic vein. Duration of normothermic liver ischemia was 32.3 +/- 1.2 minutes (mean +/- SEM) and ranged from 8 to 90 minutes. Amount of blood transfusion was 5.5 +/- 0.5 (mean +/- SEM) units of packed red blood cells. There were eight operative deaths (5.6%). Overall, postoperative complications occurred in 46 patients (32%). The patients who experienced complications after surgery had received more blood transfusion than those with an uneventful postoperative course (p less than 0.001). The length of postoperative hospital stay was also correlated with the amount of blood transfused during surgery (p less than 0.001). On the other hand, there was no correlation between the durations of liver ischemia of up to 90 minutes and the lengths of postoperative hospital stay. The longest periods of ischemia were not associated with increased rates of postoperative complications, liver failures, or deaths. There was no difference in mortality or morbidity after major liver resections performed with the use of HVE as compared with major liver resections carried out with PTC alone, although the lesions were larger in the former group. It is concluded that the main priority during liver resections is to reduce operative bleeding. Vascular occlusions aim at achieving this goal and can be extended safely for up to 60 minutes.

Surgical resection is currently the only potentially curative treatment in some selected patients with colo-rectal liver metastases (LM). Unfortunately only a minority of patients are candidates for resection. Only solitary or unilobar LM that can be removed by partial liver resection, are considered to be resectable. The second condition for the resection of LM is that the primary cancer must be resected. The third condition for resection is that the patient must be able to undergo a major liver resection if it is necessary. Small metastases which do not exceed 5 cm, and appear on the surface of the liver can be removed by a simple wedge resection. If the tumor is larger than 5 cm, or if multiple unilobar nodules are discovered, a major liver resection becomes necessary. Hospital mortality does not exceed 5% in most published series. Five year survivals are very rare when histologically proven colo-rectal LM are left in place. After surgical resection of LM, five year survival rates are close to 25% and range from 18% to 52%. Surgical resection is of benefit to approximately one fourth of the patients, who survive five years or more, but three fourths of the patients have early recurrences. None of the studied criteria can predict which patients will benefit from surgical resection of LM. In order to try to reduce the rate of early recurrences adjuvant chemotherapy has been proposed. No positive data have yet been obtained.