Hepatic Blood Flow Index Research Articles

Diagnostic value of shear wave velocity measured by virtual touch tissue imaging quantification combined with hepatic blood flow index measured by single-photon emission computed tomography first-pass method for hepatitis B fibrosis

Diagnostic value of shear wave velocity measured by virtual touch tissue imaging quantification combined with hepatic blood flow index measured by single-photon emission computed tomography first-pass method for hepatitis B fibrosis

Feasibility of semiquantitative liver perfusion assessment by ferucarbotran bolus injection in double-contrast hepatic MRI

To evaluate the feasibility of semiquantitative measurement of liver perfusion from analysis of ferucarbotran induced signal-dynamics in double-contrast liver MR-imaging (DC-MRI). In total 31 patients (21 men; 58 ± 10 years) including 18 patients with biopsy proven liver cirrhosis prospectively underwent clinically indicated DC-MRI at 1.5 Tesla (T) with dynamic T2-weighted gradient-echo imaging after ferucarbotran bolus injection. Breathing artefacts in tissue and input time curves were reduced by Savitzky-Golay-filtering and semiquantitative perfusion maps were calculated using a model free approach. Hepatic blood flow index (HBFI) and splenic blood flow index (SBFI) were determined by normalization of arbitrary perfusion values to the perfusion of the erector spinae muscle resulting in a semiquantitative perfusion measure. In 30 of 31 patients the evaluated protocol could successfully be applied. Mean HBF was 7.7 ± 2.46 (range, 4.6-12.8) and mean SBF was 13.20 ± 2.57 (range, 8.5-17.8). A significantly lower total HBF was seen in patients with cirrhotic livers as compared to patients with noncirrhotic livers (P < 0.05). In contrast, similar SBF was observed in cirrhotic and noncirrhotic patients (P = 0.11). Capturing the signal dynamics during bolus injection of ferucarbotran in DC-MRI of the liver allows for semiquantitative assessment of hepatic perfusion that may be helpful for a more precise characterisation of liver cirrhosis and focal liver lesions.

The Effects of Thoracic Epidural Anesthesia on Hepatic Blood Flow in Patients Under General Anesthesia

Hepatic hypoperfusion is regarded as an important factor in the pathophysiology of perioperative liver injury. Although epidural anesthesia (EDA) is a widely used technique, no data are available about the effects on hepatic blood flow of thoracic EDA with blockade restricted to thoracic segments in humans. In 20 patients under general anesthesia, we assessed hepatic blood flow index in the right and middle hepatic vein by use of multiplane transesophageal echocardiography before and after induction of EDA. The epidural catheter was inserted at TH7-9, and mepivacaine 1% with a median (range) dose of 10 (8-16) mL was injected. Norepinephrine (NE) was continuously administered to patients who demonstrated a decrease in mean arterial blood pressure below 60 mm Hg after induction of EDA (EDA-NE group). The other patients did not receive any catecholamine during the study period (EDA group). A further 10 patients without EDA served as controls (control group). In five patients, administration of NE was necessary to avoid a decrease in mean arterial blood pressure below 60 mm Hg. Thus, the EDA-NE group consisted of five patients and the EDA group of 15. In the EDA group, EDA was associated with a median decrease in hepatic blood flow index of 24% in both hepatic veins (P < 0.01). In the EDA-NE group, all five patients showed a decrease in the blood flow index of the right (median decrease 39 [11-45] %) and middle hepatic vein (median decrease 32 [7-49] %). Patients in the control group showed a constant blood flow index in both hepatic veins. Reduction in blood flow index in the EDA group and the EDA-NE group was significant in comparison with the control group (P < 0.05). In contrast to hepatic blood flow, cardiac output was not affected by EDA. We conclude that, in humans, thoracic EDA is associated with a decrease in hepatic blood flow. Thoracic EDA combined with continuous infusion of NE seems to result in a further decrease in hepatic blood flow.

The Effects of Intraabdominally Insufflated Carbon Dioxide on Hepatic Blood Flow During Laparoscopic Surgery Assessed by Transesophageal Echocardiography

Conflicting results have been published about the effects of carbon dioxide (CO(2)) pneumoperitoneum on splanchnic and liver perfusion. Several experimental studies described a pressure-related reduction in hepatic blood flow, whereas other investigators reported an increase as long as the intraabdominal pressure (IAP) remained less than 16 mm Hg. Our goal in the present study was to investigate the effects of insufflated CO(2) on hepatic blood flow during laparoscopic surgery in healthy adults. Blood flow in the right and middle hepatic veins was assessed in 24 patients undergoing laparoscopic surgery by use of transesophageal Doppler echocardiography. Hepatic venous blood flow was recorded before and after 5, 10, 20, 30, and 40 min of pneumoperitoneum, as well as 1 and 5 min after deflation. Twelve patients undergoing conventional hernia repair served as the control group. The induction of pneumoperitoneum produced a significant increase in blood flow of the right and middle hepatic veins. Five minutes after insufflation of CO(2) the median right hepatic blood flow index increased from 196 mL/min/m(2) (95% confidence interval (CI), 140-261 mL/min/m(2)) to 392 mL/min/m(2) (CI, 263-551 mL/min/m(2)) (P < 0.05) and persisted during maintenance of pneumoperitoneum. In the middle hepatic vein the blood flow index increased from 105 mL/min/m(2) (CI, 71-136 mL/min/m(2)) to 159 mL/min/m(2) (CI, 103-236 mL/min/m(2)) 20 min after insufflation of CO(2). After deflation blood flow returned to baseline values in both hepatic veins. Conversely, in the control group hepatic blood flow remained unchanged over the entire study period. We conclude that induction of CO(2) pneumoperitoneum with an IAP of 12 mm Hg is associated with an increase in hepatic perfusion in healthy adults.

Influence of Enteral and Parenteral Nutrition on Splanchnic Hemodynamics in Septic Patients

Enteral nutrition is believed to augment splanchnic perfusion, thereby preserving splanchnic integrity, whereas parenteral nutrition does not offer this benefit. In an effort to study this, we compared splanchnic oxygen exchange and blood flow in critically ill, septic patients to normal controls during enteral or total parenteral nutrition. Splanchnic oxygen exchange and hepatic blood flow characteristics in 14 critically ill, septic patients were compared to 19 normal controls while fasting and during nutrient administration. Nutrients were delivered as intraduodenal feedings or parenteral nutrition. Splanchnic hemodynamics were measured at baseline, 90 min, and 210 min during nutrient administration. Hepatic blood flow index (HBFI) by indocyanine green dye (ICG) clearance, splanchnic oxygen consumption index (SplVO(2)I), and hepatic venous oxygen saturation (ShvO(2)) were measured using hepatic venous catheterization. Plasma volume (PV) was measured from the volume of ICG distribution. Results were analyzed using population means (+/-SD) and one-way analysis of variance. There was no statistical change in HBFI, SplVO(2)I, PV or ShvO(2) over the study time interval within any group (p < 0.05), irrespective of whether enteral or parenteral nutrition was the nutrient source. Septic patients, whether fasting or receiving nutrition, demonstrated higher HBFI and SplVO(2)I levels, whereas ShvO(2) levels were uniformly lower throughout the study compared to normal controls. Critically ill patients exhibited a hyperdynamic splanchnic state as indicated by the marked increase in HBFI and SplVO(2)I. However, neither nutrient regimen at clinically relevant rates altered splanchnic hemodynamics over the course of study. Thus, enteral nutrients do not appear to offer hemodynamic protection to the splanchnic system in critically ill patients.

Hypocapnia does not alter hepatic blood flow or oxygen consumption in patients with head injury.

To evaluate the effects of hypocapnia on the systemic and hepatic circulations and oxygenation values in patients with head injury. Open-label, prospective study. University hospital, department of anesthesiology and intensive care unit. Eleven mechanically ventilated patients with isolated head trauma and stable hemodynamic status. At the beginning of the study, each patient presented with normocapnic ventilation. Mechanical hyperventilation was then adjusted to obtain stable hypocapnia over an interval of 24 hrs. Cardiac output and other systemic hemodynamic parameters were measured, using a pulmonary artery catheter. Hepatic parameters were measured via a catheter inserted into the hepatic vein. Total hepatic blood flow was determined by the Fick principle using a continuous infusion of indocyanine green. Arterial and hepatic venous blood gases were sampled to determine systemic and hepatic-splanchnic oxygenation. Measurements were done at the end of the four phases: a) 30 mins of normocapnia (N); b) 30 mins of hypocapnia (H0); c) 3 hrs of hypocapnia (H3); and d) 24 hrs of hypocapnia (H24). Intracranial pressure and cerebral perfusion pressure were hourly monitored throughout the study. There were no significant changes in systemic hemodynamic parameters. The hepatic blood flow index did not differ from normocapnia (N 1.8 +/- 0.4 L/min/m2) to hypocapnia (H0 1.6 +/- 0.3 L/min/m2; H3 1.7 +/- 0.4 L/min/m2; H24 1.7 +/- 0.4 L/min/m2). The ratio of hepatic blood flow index to cardiac index remained stable throughout the study. Hypocapnia did not affect hepatic-splanchnic oxygen delivery and consumption. Hypocapnic hyperventilation does not alter hepatic hemodynamic parameters in patients with head injury. This result may be related to the lack of changes in cardiac output or in the hepatic vasoreactivity. Moreover, hypocapnia does not modify hepatic-splanchnic oxygenation. Thus, in case of intracranial hypertension, hypocapnia might be used without undesirable effect on the hepatic-splanchnic perfusion.

Measurement of hepatic blood flow using 111In colloid.

The reduced hepatic blood flow calculated from hepatic scintigram with 198Au colloid was elucidated as the primary responsible factor for postoperative hepatic insufficiency. However 198Au colloid is no longer in use because of the high levels of radiation. Although 99mTc-phytate behaves similarly to 198Au on imaging, there were discrepancies between the hepatic blood flow index (KL) value and the severity of cirrhosis determined by laboratory data or by histology. In the measurement of hepatic blood flow using a radioactive colloid, factors like organ distribution, stability and uniformity of the colloid particles influence the values. In the present study, a 111In colloid was prepared and administered to rats to investigate the usefulness: as much as 95.4 (0.8) [Mean (+/- SD)]% of the colloid accumulated in the liver at pH 6.8. The distribution of particle diameter was within a relatively narrow range with the peak at 0.2 to 0.4 microns. Moreover, the KL values were not affected by condition of the reticuloendothelial system. The values showed a significant correlation with the measurements of the hepatic tissue blood flow obtained by the hydrogen gas clearance method (gamma = 0.83, P < 0.001). Thus, the 111In colloid can be clinically used as a substitute for 198Au colloid in the preoperative examination for estimation of the limit of resection.