Management of extensive retrohepatic vena cava defect in recipients of living donor liver transplantation.

Certain complexities, such as extensive vena caval injury, unexpected dense adhesions between liver and retrohepatic vena cava, and liver tumor abutting retrohepatic vena cava, sometimes warrant resection of vena cava during living-donor liver transplantation. Because the donor graft is devoid of vena cava, reconstruction of the retrohepatic cava is required, which can be done with the use of either a cryopreserved venous graft or an artificial conduit. With only a few published reports, the experience in vena cava reconstruction with the use of expanded polytetrafluoroethylene (ePTFE) during living-donor liver transplantation remains limited. We present our experience of 4 patients who successfully underwent vena caval resection during liver transplantation for various indications, which was subsequently reconstructed with the use of ePTFE grafts. All of these patients except 1 recovered well without any undue complications, such as thrombosis or outflow inadequacies, thus proving this extensive surgical treatment to be a successful and life-saving procedure, though meticulous skills are prerequisite.

A high model for end-stage liver disease score should not be considered a contraindication to living donor liver transplantation.

OBJECTIVE: To analyze the outcomes of patients with high Model for End-Stage Liver Disease (MELD) scores who underwent adult-to-adult live donor liver transplantation (A-A LDLT). MATERIALS AND METHODS: From September 2002 to October 2010, a total of 152 adult patients underwent A-A LDLT in our institution. Recipients were stratified into a low MELD score group (Group L; MELD score≤30) and a high MELD score group (Group H; MELD score>30) to compare short-term and long-term outcomes. RESULTS: Of the 152 adult patients who underwent A-A LDLT, 9 were excluded from the analysis because they received ABO-incompatible grafts. Group H comprised 23 and Group L 120 patients. The median follow-up was 21.5 months (range, 3 to 102 m). The mean MELD score was 15.6 in Group L and 36.7 in Group H. There were no significant differences in the mean length of stay in the intensive care unit (Group L: 3.01 days vs Group H: 3.09 days, P=.932) or mean length of hospital stay (Group L: 17.89 days vs. Group H: 19.91 days, P=0.409). There were no significant differences in 1-, 3-, or 5-year survivals between patients in Groups L versus H (91.5% vs 94.7%; 86.4% vs 94.7%; and 86.4% vs 94.7%; P=.3476, log rank). CONCLUSION: The short-term and long-term outcomes of patients with high MELD scores who underwent A-A LDLT were similar to those of patients with low MELD scores. Therefore, we suggest that high MELD scores are not a contraindication to LDLT.

Hepatic artery reconstruction in living donor liver transplantation: running suture under surgical loupes by cardiovascular surgeons in 180 recipients.

OBJECTIVES: The aim of our study was to retrospectively investigate the outcomes of hepatic artery (HA) reconstruction by cardiovascular surgeons in adult-to-adult living donor liver transplantation (A-A LDLT). METHODS: From April 2007 to April 2011, 187 recipients underwent A-A LDLT. After excluding seven ABO-incompatible transplant recipients, we reviewed the courses of 180 patients including 125 men and 55 women of mean age 52.5±9.2 years (range=23-71). One hundred seventy-seven patients received right-lobe grafts with inclusion of middle hepatic vein (MHV); two, right-lobe grafts without MHV; and one, left-lobe graft. A continuous, single-stitch, running suture with the parachute technique was used for HA reconstruction. The anastomosis was performed by cardiovascular surgeons employing surgical loupes with 4.5× magnification. RESULTS: The mean time for an arterial reconstruction was 10.7±4.0 minutes (median=10, range=4-30). Hepatic arterial thrombosis (HAT) was encountered in 3 (1.66%) patients. One HAT that developed on postoperative day 1 was successfully rescued by the intra-arterial infusion of urokinase. Another patient required reoperation due to a redundant kinked HA. A third HAT patient underwent successful retransplantation with a cadaveric graft on postoperative day 6. In our series, no delayed HAT was detected and no recipient deaths were related to HAT. CONCLUSION: HA reconstruction with a running suture under surgical loupes is a feasible technique in A-A LDLT. A speedy reconstruction can be performed by an experienced cardiovascular surgeon with a low incidence of HAT.

Living donor right hepatectomy with inclusion of the middle hepatic vein: outcome in 200 donors.

Venous congestion of segments V and VIII of the graft is observed frequently in right-lobe living donor liver transplants (LDLT) without middle hepatic vein (MHV) drainage. It can cause graft dysfunction and failure. Inclusion of the MHV in the right lobe graft allows optimal venous drainage but can pose adverse effects for the donor. From May 2005 to April 2011, we performed 202 right-lobe LDLTs using grafts that all (except two) contained the MHV. The mean duration of donor surgery was 558±132 minutes (median 540, range 332-1100), and estimated blood loss 441±309 mL (median 350, range 35-3200). No donor was admitted to the intensive care unit postoperatively. The mean hospital stay was 8.7±2.1 days (median 8, range 6-22). Postoperatively, 39 donors (19.5%) experienced Clavien grade I and II complications, mostly minor wound infections or massive ascites necessitating diuretic therapy. Seven (3.5%) donors displayed Clavien grade III complications, including five bile leakages requiring endoscopic retrograde biliary drainage and two abdominal wound dehiscences requiring repair under general anesthesia. There was no donor death. In conclusion, inclusion of the MHV in a right-lobe LDLT was safe for most donors.

Simultaneous liver and kidney transplantation from different living donors.

OBJECTIVES: To present our experience with simultaneous living donor liver and kidney (SLK) transplantation from two different living donors. PATIENTS AND METHODS: We performed five SLK transplantations from two different living donors from November 2006 to December 2010. Four patients were males and one, female. Their age range was 47 to 66 years (mean, 55 years). The primary liver diseases included hepatitis B virus (n=2), alcoholic liver cirrhosis (n=2), cryptogenic liver disease (n=1), and hepatitis C virus with hepatocellular carcinoma (n=1). All five patients had chronic renal failure: four were on hemodialysis (H/D) and one on chronic ambulatory peritoneal dialysis for 1 to 20 years. Liver implantation was performed first, followed by kidney transplantation. The liver and kidney teams worked closely to shorten the ischemia time. RESULTS: All surgical procedures were performed uneventfully and all recipients and donors survived the operations. Good liver graft function was noted in all five patients. The patient with both anti-T- and anti-B-cell positive crossmatch tests developed hyperacute rejection of the kidney graft requiring its immediate removal. This patient was maintained on regular H/D afterward. The other four patients displayed good renal function. No evidence of severe acute rejection was noted during the follow-up period (range, 9-55 months) among patients treated with tacrolimus-based immunosuppression. CONCLUSION: We suggest that SLK transplantation be performed with organs from two different instead of a single live donor.

Persistent dizziness and nausea in patients receiving postoperative epidural pain control after living donor liver transplantation: case reports.

Dizziness and nausea are frequent problems among patients receiving patient-controlled epidural analgesia (PCEA) after major surgery. It is important to consider the various etiologies that might cause these adverse events, especially among patients who have undergone massive hepatic resection for living donor liver transplantation (LDLT). We have described 2 LDLT cases with persistent dizziness and nausea postoperatively despite several adjustments in PCEA management. Their symptoms were quickly relieved after suspension of PCEA medication. Our 2 cases of LDLT represented a unique setting for this type of complication.

Innovative technique to reconstruct two branches of the right hepatic artery in living donor liver transplantation.

Hepatic arterial thrombosis is a critical complication in living donor liver transplantation (LDLT). Two separate branches of the right hepatic artery (RHA) are sometimes observed and addressed by anastomosis of the larger branch first, then checking backflow from the smaller branch. If not good, the smaller branch must be reconstructed. We used the cystic artery as a conduit for the reconstruction. Meticulous dissection was performed to identify all branches of the hepatic artery in the donor operation. The length of cystic artery preserved was as long as possible. The cystic arterial stump was anastomosed to the stump of the posterior branch the of RHA under microscopic guidance on the back table. Patency was checked through the stump of the anterior branch of the RHA. With this technique, only one orifice, the stump of right anterior hepatic artery, was used for hepatic artery reconstruction. We have performed this technique in two patients. Both had good arterial flow after living donor liver transplantation. This innovative technique is easy and safe, and requires only one anastomosis, which, in theory, decreases the adds of developing hepatic arterial thrombosis.

Polytetrafluoroethylene patch venoplasty for outflow reconstruction in living donor liver transplantation: two case reports.

Outflow obstruction may lead to liver congestion and eventual graft failure after living donor liver transplantation. Various methods of venoplasty provide wider outflow tracts. Most series have suggested use of autologous or allogenic grafts for patch venoplasty. We used a polytetrafluorethylene patch in two patients. Both showed good patency of the outflow tract at Doppler ultrasonography at 7 months and 4 months posttransplantation. A polytetrafluoroethylene patch may be a good alternative when no other autologous or allogeneic vascular patch is available or when the situation is critical.

Fatal duodenal hemorrhage complicated after living donor liver transplantation: case report.

Fatal hemorrhage caused by duodenal ulcer is rarely seen after liver transplantation. We report a case with penetrating duodenal ulcer resulting in massive gastrointestinal tract hemorrhage from a ruptured pseudoaneurysm of the hepatic artery. The patient, a 54-year-old man, had undergone living donor liver transplantation with a graft from his son. Massive hematelnesis occurred 7 days after transplantation. Endoscopy revealed a penetrating duodenal ulcer. Repeated episodes of hemorrhage resulted in shock. Angiography showed a ruptured pseudoaneurysm of the proper hepatic artery. Embolization controlled the bleeding; however, the grafted liver became ischemic. The patient subsequently developed ischemic cholangitis, which was treated with percutaneous transhepatic cholangial drainage. Repeat transplantation was performed 30 months later. The patient was doing well at 10-month follow-up.

Procoagulant surface exposure and apoptosis in rabbit platelets: association with shortened survival and steady-state senescence.

BACKGROUND: The signal(s) for removal of senescent platelets from the circulation are not fully understood; phosphatidylserine (PS) expression on platelets and another marker of apoptosis, loss of mitochondrial inner membrane potential (DeltaPsim), have been implicated in platelet clearance. OBJECTIVE: To investigate whether shortened platelet survival and steady-state platelet senescence are associated with increased surface exposure of PS and DeltaPsim collapse. METHODS: Survival of in-vitro biotinylated rabbit platelets treated with thrombin or Ca(2+)-ionophore A23187 was tracked by flow cytometry after injection. Steady-state platelet senescence was investigated by infusing biotin to label a platelet cohort. PS expression and DeltaPsim of in-vitro biotinylated platelets and of the aging platelet cohort biotinylated in-vivo were measured by flow cytometry using annexin V-FLUOS and the DeltaPsim-sensitive dye CMXRos, respectively. RESULTS: Although PS expression, DeltaPsim and survival of thrombin-degranulated platelets were similar to those of control platelets, increasing concentrations of A23187 caused increased surface exposure of PS and progressive shortening of platelet survival; only one-sixth of PS-expressing platelets also exhibited DeltaPsim loss. The cohort of senescent, biotinylated platelets remaining in the circulation at 96 h had increased exposure of PS and collapsed DeltaPsim; of the 17% of PS-expressing platelets, one-third did not exhibit DeltaPsim loss. There was also an increase in platelets with collapsed DeltaPsim but not expressing PS. CONCLUSIONS: Platelets with shortened survival and senescent platelets have increased surface exposure of PS, that may be involved in their clearance. PS expression can occur independently of DeltaPsim collapse and conversely, in aged platelets, DeltaPsim loss can occur independently of PS expression.

Inflammatory pseudotumor of the urinary bladder: a report of five cases and review of the literature.

We describe five patients who recently presented with gross hematuria secondary to inflammatory pseudotumors of the bladder along with a review of the literature. At presentation, four of the five patients were clinically misdiagnosed as malignancies of which two were further believed to be leiomyosarcomas on initial histological examination because of their spindle-cell appearance. Conservative excision either by transurethral resection or partial cystectomy was curative in all cases. The main importance of these rare, benign lesions is to differentiate them from malignant tumors for which they may be mistaken, thus avoiding radical surgery and its attendant complications.

Truncal rigidity as a result of epidural sufentanil--a case report.

It is well known that intravenous opioids may cause truncal rigidity. To the best of our knowledge truncal rigidity induced by epidural opioid has never been reported. Recently, we came across an accident of truncal rigidity following epidural sufentanil. The victim was a 65-year-old female who received cholecystectomy, choledochotomy, and cholangiography. For post-operative pain control, an epidural catheter was inserted cephalad [corrected] at L1-2 interspace with a length of 4 cm of the catheter retained in the epidural space. The epidural catheter was secured and tested for correct placement with 3 ml of 2% lidocaine with 1:200,000 epinephrine prior to induction of general anesthesia. No opioid was ever given in the operative course. When the patient was fully awake and complained of wound pain in the recovery room 50 mg of sufentanil in 10 ml normal saline was given via the epidural catheter after a negative evacuation test. About one minute after the epidural shot, she was found to lose consciousness without any slightest warning sign. Truncal rigidity and locked jaw that followed entailed respiratory arrest and rapid deterioration of oxygenation which evidenced a life-threatening airway emergency. It spite of our efforts we could not manage to ventilate her with ordinary means. It was not until the administration of 80 mg of succinylcholine and oral endotracheal intubation could an adequate ventilation be reestablished. She regained spontaneous breathing 15 min after the episode but for safety's sake she remained intubated for 6 h until the dissipation of analgesia. Another test dose was attempted, which reconfirmed that the epidural catheter was in proper position. She stayed in the recovery room for 24 h and returned to ward in satisfactory condition. The incidence disclosed that epidural sufentanil even with a dose as small as 50 micrograms could cause truncal rigidity. Thus when epidural sufentanil is applied for post-operative pain control constant vigilance is necessary in order to avoid accident.

Evaluation of stress response to surgery under general anesthesia combined with spinal analgesia.

BACKGROUND: Each type of anesthesia has varying influence on the amount of catecholamine secretion during surgery. Epidural or spinal anesthesia can markedly suppress the increase of many of the stress hormones. Our purpose of this study is to evaluate metabolism change during surgery under anesthesia and to see whether general anesthesia combined with intraspinal anesthetic and narcotic is a better way to suppress such stress response. METHODS: Seventeen patients in fit physical condition (ASA class I) with normal biochemical screening scheduled for radical gastrectomy were studied. All patients were premedicated with diazepam and glycopyrrolate and an indwelling catheter was inserted into a radial artery under local anesthesia for monitoring blood pressure and obtaining blood samples for glucose and hormonal assays. A CVP line was set up via the right internal jugular vein for the administration of fluid (free of sugar). In the study group, a 32-G intraspinal catheter was placed via lumbar interspaces. Spinal blockade up to T4 by titrating 0.25% marcaine. Then anesthesia in both groups was induced with thiopental 5 mg/kg, followed by succinylcholine 1.5 mg/kg for intubation. Anesthesia was maintained with isoflurane, N2O, O2 and pancuronium. Blood samples for measurement cortisol, catecholamine and sugar were taken after induction and 30 min after surgical incision. Thirty min after skin incision all patients were subjected to glucose tolerance test, accomplished by giving 50% dextrose at 0.33 g/kg in 3 min. Arterial blood samples were then obtained at 1, 3, 5, 7, 10, 20, 30, 45 and 60 min intervals for plasma glucose determination. RESULTS: No difference was evident in cortisol values, baseline, before and after surgical incision (p > 0.05) either intragroup or inter-group. Catecholamine and glucose were significantly higher in control group after surgical incision (p < 0.05, intra-gr and inter-gr). Following a glucose load the decay of plasma glucose was similar in both groups but glycemic level was higher in the control group. CONCLUSIONS: Better control of stress response by general anesthesia combined with subarachnoid block was disclosed in this study.

Complete heart block induced by general anesthesia in a patient with suspected conduction system defect: a case report.

We report a rare incident of complete heart block occurring after induction of general anesthesia in an apparently fit patient. An external temporary pacemarker was first applied, which was then replaced by isoproterenol infusion, but permanent pacing was required postoperatively. The role of anesthesia as a precipitating factor was discussed. It is suggested that surgical patients suspicious of conduction system defect should be under continuous hemodynamic monitoring with temporary pacing at hand during perioperative period.

Endothelium-derived nitric oxide partially mediates salbutamol-induced vasodilatations.

This study examined the ability of salbutamol (selective beta 2-adrenoceptor agonist) to cause endothelium-dependent relaxation in rat aortic rings and depressor response in conscious rats. Salbutamol (0.01-100 microM) concentration dependently relaxed preconstricted aortic rings. The relaxant response was partially attenuated by either mechanical removal of the endothelium or treatment with NG-nitro-L-arginine methyl ester (L-NAME, 100 microM). In conscious rats, either i.v. infused phenylephrine (5 micrograms/kg per min) or i.v. bolus injected L-NAME (12.8 mg/kg), but not the vehicle, caused similar sustained increases in mean arterial pressure (MAP). I.v. infused salbutamol (2-128 micrograms/kg per min, each dose for 5 min) dose dependently decreased MAP in vehicle-treated rats; the depressor responses were potentiated by hypertension induced by phenylephrine. In contrast, the magnitudes of the depressor response to salbutamol in L-NAME-treated rats were less than those in rats pretreated with phenylephrine or the vehicle. I.v. bolus injections of salbutamol (0.25-16 micrograms/kg) also caused dose-dependent and transient decreases in MAP in vehicle-treated rats. The magnitude but not the duration of the depressor response to salbutamol was less in rats treated with L-NAME, compared to those in rats given phenylephrine or the vehicle. These results suggest that endothelium-derived nitric oxide is partially involved in beta 2-adrenoceptor-mediated vasodilatation.

Inhibitory actions of diphenyleneiodonium on endothelium-dependent vasodilatations in vitro and in vivo.

1. This study examined the in vitro and in vivo inhibitory effects of diphenyleneiodonium (DPI), a novel inhibitor of nitric oxide (NO) synthase, on endothelium-dependent vasodilatations. 2. DPI (3 x 10(-8)-3 x 10(-6) M) concentration-dependently inhibited acetylcholine (ACh)-induced relaxation in preconstricted rat thoracic aortic rings, with an IC50 of 1.8 x 10(-7) M and a maximal inhibition of nearly 100%. DPI (3 x 10(-6) M) also completely inhibited the relaxation induced by the calcium ionophore, A23187 but not by sodium nitroprusside (SNP). The inhibitory effect of DPI (3 x 10(-7) M) on ACh-induced relaxation was prevented by pretreatment with NADPH (5 x 10(-3) M) and FAD (5 x 10(-4) M) but not L-arginine (L-Arg, 2 x 10(-3) M). Pretreatment with NADPH did not alter the inhibitory effect of NG-nitro-L-arginine on ACh-induced relaxation. 3. The inhibitory effect of DPI on ACh-induced relaxation in the aortae lasted > 4 h after washout. In contrast to pretreatment, post-treatment (1 h later) with NADPH (5 x 10(-3) M) reversed only slightly the inhibitory effect of DPI. 4. In conscious rats, DPI (10(-5) mol kg-1) inhibited the depressor response to i.v. infused ACh, but not SNP. However, it caused only a transient pressor response which was previously shown to be due completely to sympathetic activation. 5. Thus, DPI is an efficacious and 'irreversible' inhibitor of endothelium-dependent vasodilatation in vivo and in vitro. The mechanism of the inhibition may involve antagonism of the effects of FAD and NADPH, co-factors of NO synthase. However, unlike the N0-substituted arginine analogues (another class of NO synthase inhibitors), DPI-induced suppression of endothelium-dependent vasodilatation in vivo does not lead to a sustained rise in blood pressure.

Fatal gas embolism as a complication of Nd-YAG laser surgery during treatment of bilateral choanal stenosis.

A 40-day-old infant boy underwent Nd-YAG laser surgery because of congenital bilateral choanal stenosis. Cyanosis and cardiovascular collapse occurred during the operation. Resuscitation was initiated, but in vain; the patient died. The evolution of clinical events was consistent with a diagnosis of gas embolism. In the investigation of causes, the use of a sapphire tip with the Nd-YAG laser and the cooling of the tip with N2 gas were thought to have contributed to the fatal outcome. The authors warn of the potential risk of gas embolism with the Nd-YAG laser and a coaxial gas cooling system, and they emphasize the importance of monitoring for gas embolism in high-risk patients.

[Continuous thoracic epidural fentanyl in postoperative pain control--a comparison of two different dosages].

We evaluate the postoperative pain relief using continuous epidural fentanyl infusion in two different dosages for thoracic and upper abdominal surgeries. A total of 21 ASA class III patients were studied. A thoracic epidural catheter was placed before surgery but pain control was begun when the patients became fully awake and complained of pain in the recovery room. Patients were divided into group A (n = 9) and group B (n = 12). Those in group A were given fentanyl 1.5 micrograms/kg in saline solution as initial dose followed by continuous infusion at a rate of 1 microgram/kg/h for 23 hours. In group B the initial dose and the maintenance dose were respectively 1.0 microgram/kg and 0.5 micrograms/kg/h. Following the initial dose, the intensity of pain was assessed hourly for a total of 24 hours using a visual analogue pain scale with scores from 0 to 10. In group A, the pain scale fell from the baseline level of 7.7 +/- 2.6 to 2.3 +/- 2.0 at the first hour while in group B it fell from 8.9 +/- 1.4 to 4.3 +/- 2.1. The pain scores following continuous infusion in groups A and B were respectively 1.3 +/- 1.5 and 2.9 +/- 1.7. Although the analgesic effect appeared to be better in group A, pain relief was satisfactory in both groups (p less than 0.01). Regarding respiratory depression, there was a greater degree of rise in PaCO2 in group A and some of the patients even had a PaCO2 value above 50 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)