Clinical efficacy of total laparoscopic splenectomy for portal hypertension and its influence on hepatic hemodynamics and liver function

BACKGROUND The liver hemodynamic changes caused by portal hypertension(PH)are closely related to various complications such as gastroesophageal varices and portosystemic shunts,which may lead to adverse clinical outcomes in these patients,so it is of great clinical significance to find treatment strategies with favorable clinical efficacy and low risk of complications.AIM To study the clinical efficacy of total laparoscopic splenectomy(TLS)for PH and its influence on hepatic hemodynamics and liver function.METHODS Among the 199 PH patients selected from October 2016 to October 2020,100 patients[observation group(OG)]were treated with TLS,while the remaining 99[reference group(RG)]were treated with open splenectomy(OS).We observed and compared the clinical efficacy,operation indexes[operative time(OT)and intraoperative bleeding volume],safety(intraperitoneal hemorrhage,ascitic fluid infection,eating disorders,liver insufficiency,and perioperative death),hepatic hemodynamics(diameter,velocity,and flow volume of the portal vein system),and liver function[serum alanine aminotransferase(ALT),serum aspartate aminotransferase(AST),and serum total bilirubin(TBil)]of the two groups.RESULTS The OT was significantly longer and intraoperative bleeding volume was significantly lesser in the OG than in the RG.Additionally,the overall response rate,postoperative complications rate,and liver function indexes(ALT,AST,and TBil)did not differ significantly between the OG and RG.The hepatic hemodynamics statistics showed that the pre-and postoperative blood vessel diameters in the two cohorts did not differ statistically.Although the postoperative blood velocity and flow volume reduced significantly when compared with the preoperative values,there were no significant inter-group differences.CONCLUSION TLS contributes to comparable clinical efficacy,safety,hepatic hemodynamics,and liver function as those of OS in treating PH,with a longer OT but lesser intraoperative blood loss.

Hepatic pseudolesions caused by alterations in intrahepatic hemodynamics

Hepatic pseudolesion may occur in contrast-enhanced computed tomography and magnetic resonance imaging due to the unique haemodynamic characteristics of the liver.The concept of hepatic arterial buffer response(HABR)has become mainstream for the understanding of the mechanism of the reciprocal effect between hepatic arterial and portal venous flow.And HABR is thought to be significantly related to the occurrence of the abnormal imaging findings on arterial phase of contrast enhanced images,such as hepatic arterial-portal vein shunt and transient hepatic attenuation difference,which mimic hypervascular tumor and may cause clinical problems.Third inflow to the liver also cause hepatic pseudolesion,and some of the cases may show histopathologic change such as focal hyperplasia,focal fatty liver,and focal sparing of fatty liver,and called pseudotumor.To understand these phenomena might be valuable for interpreting the liver imaging findings.

QUANTITATIVE ANALYSIS ON CHANGES OF HEPATIC HEMODYNAMICS AFTER TRANSCUTANEOUS ELECTRIC PULSE STIMULATION OF LOCAL POINTS BY USING COLOR DOPPLER ULTRASOUND DIAGNOSTIC APPARATUS

Objective: To evaluate the effect of transcutaneous electric pulse stimulation (TEPS) on hepatic blood flow and parenchymal microcirculation in patients with fatty liver. Methods: A total of 31 fatty liver volunteer patients were observed in this study. Changes of color Doppler energy (CDE) images before and after TEPS of local points nearby the liver were recorded by using color Doppler ultrasound diagnostic apparatus (ACUSON 128XP/10C). Sum of color pixel area (SCPA), average of color value (ACV) and SCPA×ACV (integral) of the hepatic flow images were analyzed by an image processing system, single blind method and paired t-test. Programmed TEPS (0.5- 150 Hz / 2 000 Hz , 10- 25 V ) was applied to the right Qimen (期门 LR 14)-Jingmen (京门 GB 25), Fuai (腹哀 SP 16)-Ganshu (肝俞 BL 18) respectively for 15 min. Results: Compared with basic values of pretreatment, SCPA, ACV and SCPA×ACV increased significantly (t=2.71, P<0.02; t=3.42, P<0.01; and t=8.15, P<0.001) after TEPS, meaning improvement of hepatic blood flow supply. Conclusion: TEPS of acupoints near the liver can improve hepatic blood flow and hepatic parenchymal microcirculation in patients with fatty liver.

EFFECTS OF HEMOGLOBIN ON SERUM NITRIC OXIDECONCENTRATION AND HEMODYNAMICS PATTERN CHANGES IN CIRRHOTIC RATS

Objective To investigate the effects of hemoglobin (Hb) on serum nitric oxide (ON) concentrationand hemodynamics pattern changes in rats with cirrhosis. Methods Cirrhosis model was induced in male SDrats by injection of 60% CCl4 oily solution subcutaneously. Cirrhotic rats were treated with erythropoietin(100U/kg) injected subcutaneously for 2 weeks. Mean arterial pressure (MAP), cardiac output (CO), cardiac index(CI), splanchnic vascular resistance (SVR), splanchnic blood flow (SBF) and serum NO concentration weredetermined in erythropoietin - treated, erythropoietin - untreated cirrhotic rats and controls by using 57Co - labelledmicrosphere technique and a fluorometric assay, respectively. In addition, blood Hb levels were also measured inthe 3 groups. Results Untreated cirrhotic rats had significantly lower MAP, SVR, Hb and higher Co, CI, SBFand NO concentration than those of the controls (P<0.01). In treated cirrhotic rats, erythropoietin significantlyattenuated the increase of CO, CI, SBF, NO concentration and the decrease of MAP and SVR. In cirrhotic rats,opoetin beta in subcutaneous dose of 100U·kg-1·d-1 induced a markedly increment of blood Hb levels anddecrement of NO concentration in comparison with untreated cirrhotic rats (181±11g/L vs 120±15g/L,1.14±0.62μmol/L vs 4.20±1.25μmol/L). Conclusion The endogenous NO may play an important role in thechanges of hemodynamics pattern in cirrhosis, and hyperdynamic circulatory status in rats with cirrhosis might beameliorated by inactivation of overproduced NO by increasing hemoglobin with erythropoietin.