H.K Cheung

Minimal blood loss living donor hepatectomy.

BACKGROUND Donor hepatectomy with maximal safety while preserving graft viability is of principal concern in living donor liver transplantation. There are compelling reasons for avoiding blood transfusion, even with autologous blood, to avoid the potential risks it imposes on healthy donors. This study aims to describe the surgical technique and clinical outcomes of living donor hepatectomy with minimal blood loss requiring no blood transfusion. METHODS Donor hepatectomy was performed in 30 living donors according to a detailed preoperative imaging study of the vascular and biliary anatomy. Liver parenchymal transection was carried out with strict adherence to a meticulous surgical technique without vascular inflow occlusion to either side of the liver. Pre-, intra-, and postoperative data were gathered, and factors related to blood loss were analyzed retrospectively. RESULTS The intraoperative blood loss ranged from 20 to 300 ml with a mean of 72.0+/-58.9 ml (median, 55 ml), and neither homologous nor autologous blood transfusion was required in any of the donors intra- and postoperatively. All 30 donors were discharged with minimal complications, and remain well at a mean follow-up of 24 months after donation. Excellent graft viability was verified by the fact that all 30 recipients are alive and well with a few manageable complications. The actual graft and patient survival are both 100% at the time of writing. CONCLUSIONS Regardless of the extent of donor hepatectomy, blood loss can and should be kept to a minimum, and living donor hepatectomy without blood transfusion is a realistic objective.

Outflow tract reconstruction in living donor liver transplantation.

Background. Hepatic venous reconstruction is critical in living donor liver transplantation because outflow obstruction may lead to graft dysfunction or loss. We describe our e-perience and analyze outcomes with a technique of creating a single outflow tract using venoplasties of the graft and recipient hepatic veins. Patients and Methods. A retrospective study was done on 38 consecutive living donor liver transplants performed from June 1994 to March 2000. The grafts included 36 left-side grafts and 2 right-side grafts. Nine grafts had multiple hepatic veins and required a venoplasty of two or three hepatic veins to create a single outflow orifice. Triple recipient hepatic venoplasty was performed in 32 patients, double venoplasty in 5 and none in 1. Results. There were four cases of outflow obstruction, three occurring in patients with a double recipient venoplasty. Two of the problems were remedied intraoperatively by adjusting the position of the graft although two were structural in nature and required the insertion of expandable metallic vascular stents. All donors and recipients with their original grafts are alive at a mean follow-up period of 27 months. Conclusion. A triple recipient venoplasty with a matching venoplasty of multiple graft hepatic veins to create a single wide outflow orifice is recommended in living donor liver transplantation using left side grafts.

Soluble thrombomodulin antigen as a marker for endothelial damage during liver transplantation.

RTHOTOPIC liver transplantation (OLT) is now being performed with improved survival rates in a high number of patients suffering from different liver diseases. Despite better control of blood loss, hemorrhages still occur, particularly after reperfusion. Problems arising from defective hemostasis during major abdominal surgery are a major risk for patients with terminal chronic liver disease. 1 Liver transplantation, most often performed in such patients, differs from operations because the recipients start with a diseased liver and end up with a healthy liver, the function of which, however, is compromised by preservation damage. Thrombomodulin (TM), an integral glycoprotein on the surface of endothelial cells, serves as a receptor for thrombin. Thrombin bound to TM greatly reduces procoagulatory and platelet-stimulating effects but activates the zymogen, protein C. 2 Activated protein C together with protein S inactivates two blood coagulation cofactors, factor Va and factor VIIIa, and indirectly stimulates fibrinolysis. Thus, TM plays an important role as an anticoagulant protein on the blood vessel wall. Immunohistochemically, TM has been found to be mainly present on endothelial cell surfaces of blood and lymphatic vessels in all organs except the brain. 3,4 A smaller from of TM, the soluble thrombomodulin (sTM), has been isolated from human blood and urine. 5 The structure of sTM is not known but is thought to be similar to the soluble protein obtained after proteolytic modification of TM with elastase 6 —a cleaved form of tissue TM with loss of part of the transmembrane domain, and the cytoplasmatic tail. 7 Therefore, sTM in plasma appears to be derived from injured endothelial cells or to be proteolytically cleaved from TM by proteases. In vitro, sTM has been shown to be a marker of endothelial damage 8 and several previous clinical studies have shown that plasma levels of sTM are increased in various diseases associated with endothelial cell damage or proteolytic activity on the endothelial cell surface, including DIC, 9,10 adult respiratory distress syndrome (ARDS), 10 thromboembolic disease, 9,10 thrombotic thrombocytopenic purpura, 11,12 diabetes mellitus with microangiopathy, 9,13 systemic lupus erythematosus (SLE), 14 and chronic myelogenous leukemia. 15 Because they are usually associated with vascular endothelium alterations, 10,16 TM plays an important role as an anticoagulant protein on the blood vessel wall. However, in the context of liver transplantation, the understanding of pathophysiology of TM in the coagulation-fibrinolysis equilibrium is still in its infancy. There are only few reports 17,18 on sTM in liver transplantation. In orthotopic liver transplantation, both platelet and leukocyte activation as well as prothrombin activation are suspected of being caused by damaged endothelial cells in the grafted liver. In this study, plasma sTM levels as an endothelial marker were measured in the course of 11 consecutive liver transplantation. Samples were taken at nine different time points perioperatively as well as the perfusate released from the graft outflow vein during the flushing procedure.

Repeated hypotensive episodes due to hepatic outflow obstruction during liver transplantation in adult patients

We report two cases of unusual repeated hypotension, decreased cardiac output, decreased mixed venous oxygen saturation, decreased central venous pressure, pulmonary artery pressure, and pulmonary wedge pressure after the completion of all vascular anastamoses of liver transplantation. These unstable hemodynamics appear to reflect a clinically relevant picture of hypovolemia. However, the real cause was partial hepatic outflow obstruction. The obstruction was suspected because hypotension was alleviated by elevating the full-sized liver graft ventrally and to the left. Doppler ultrasound examination confirmed that the flow velocity of the hepatic vein outflow was insufficient when the liver fell to its resting position in the right hepatic fossa. An additional side-to-side cavo-caval anastomosis resolved the problem in one patient, whereas the other required not only the additional anastomosis, but also application of a tissue expander filled with 770 mL normal saline beneath the liver to eliminate the obstruction. We emphasize that obstruction of the hepatic outflow causes only temporal hypovolemia because of a decrease of venous return and that treatment of this complication should be surgical intervention to relieve the obstruction. Blind resuscitation with fluids will not solve the problem and, in fact, may result in fluid overload with subsequent complications.

Aspiration in transtracheal oxygen insufflation with different insufflation flow rates during cardiopulmonary resuscitation in dogs.

We investigated whether transtracheal insufflation of oxygen with different insufflation flow rates protects against aspiration of gastric contents during cardiopulmonary resuscitation (CPR). Its ventilation and oxygenation effects were also evaluated. Cardiac arrest was induced in anesthetized and paralyzed 18 mongrel dogs. Chest compression using an automatic thumper was performed while the dogs randomly received no mechanical ventilation (Group I, n = 6) or were transtracheally insufflated with 4 L/min oxygen (Group II, n = 6) or 10 L/min oxygen (Group III, n = 6). Blood samples were drawn every 5 min for 20 min for blood gas analysis. the mouths of the dogs were then filled with 70 mL mixed barium, and 10 min after chest compression, chest radiographs were taken to evaluate the incidence of pulmonary aspiration. Results showed that pulmonary aspiration occurred in all dogs of Group I and three of the six dogs in Group II, whereas dogs in Group III were free from pulmonary aspiration. Both transtracheal oxygen insufflation groups maintained oxygen saturation significantly better than Group I, but mild hypercapnia was observed in all groups after 20 min of CPR. We conclude that transtracheal oxygen insufflation, but not chest compression alone, was able to maintain oxygenation for 20 min during CPR in dogs with cardiac arrest. Mild hypercapnia was noted in all groups. Chest compression alone caused pulmonary aspiration, whereas insufflation of 10 L O2/min provided better protection against pulmonary aspiration than that of 4 L O2/min. Implications In case of difficult airway during cardiopulmonary resuscitation, insertion of an IV catheter through the trachea is easy, and insufflation of 10 L/min of oxygen through the needle can not only maintain the oxygenation but also prevent aspiration.

Aspiration in chest compression alone without mechanical ventilation in the head down position in dogs

BACKGROUND Previous work by the authors has shown that chest compressions alone without mechanical ventilation during cardiopulmonary resuscitation in the natural supine position was associated with pulmonary aspiration in dogs. The purpose of this investigation was to test the hypothesis that a head down position may prevent aspiration during chest compressions alone and whether oxygenation can be improved by simply insufflation of oral oxygen 10 min after cardiac arrest. METHODS Cardiac arrest was induced in ten mongrel dogs which were anesthetized and paralysed. Eight underwent chest compressions alone in different head down positions using an automatic compressor at 9 kg compression force and 3 cm compression depth. The study was composed of two parts. Part 1 evaluated the effect of insufflation of 10 l/min O2, into the mouth of the dogs, 10 min after initiation of resuscitation, using chest compressions alone. Part 2 was designed to test our hypothesis that the head down position may protect the lungs from aspiration during chest compression alone. The mouths of the dogs were filled with mixed barium and the dogs underwent serial episodes of chest compressions, for 10 min each, in the 20 degree head down, 10 degree head down and the natural supine positions. Chest X-rays with antero-posterior and lateral views were taken to evaluate pulmonary aspiration. Two additional dogs underwent direct chest compression alone in the natural supine position and the time of chest compression was shortened to 5 min. RESULTS All dogs in the natural position showed evidence of pulmonary aspiration of barium, five or six of the dogs showed tracheal aspiration in the 10 degree head down position, while no any barium was visualized in the tracheo-broncheal trees of the dogs in the 20 degree head down position. Supplemental oxygen in the mouth improved the mean PaO2 from 67 +/- 26 to 160 +/- 97 mmHg during chest compressions alone. CONCLUSION Chest compression alone without mechanical ventilation in the supine position caused pulmonary aspiration in the unprotected airway in dogs. This complication could be prevented by adopting a 20 degree head down position. The 10 degree head down position seemed to reduce the severity of the pulmonary aspiration, but not enough to eliminate the danger altogether. Supplemental oxygen in the mouth can improve oxygenation in chest compressions alone.