Hepatic Blood Flow and Splanchnic Oxygen Consumption in Patients With Liver Failure. Effect of High–Volume Plasmapheresis

Clemmesen, J; Gerbes, Alexander L.; Gülberg, Veit; Hansen, Bent Adel; Larsen, Fin Stolze; Skak, C.; Tygstrup, Niels; Ott, Peter

doi:10.1002/hep.510290206

Cited by 75 publications

(45 citation statements)

References 64 publications

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“…This corresponds well with previous findings that treatment with high-volume plasmapheresis has similar effects on systemic hemodynamics in patients with acute liver failure. 2,3,21 In a previous phase I trial in a population of mixed acute and chronic liver failure, albumin dialysis had no effect on hemodynamics. 9 However, a modified MARS system without the anion-exchange column was used, which suggests that hemodynamic effects of MARS may be associated with the specific removal of substances by the anion-exchange column.…”

Section: Discussionmentioning

confidence: 99%

Systemic hemodynamic effects of treatment with the molecular adsorbents recirculating system in patients with hyperacute liver failure: A prospective controlled trial

Schmidt

Wang

Hansen

et al. 2003

Liver Transplantation

211

106

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The aim of the study is to evaluate the effect of a single treatment with the molecular adsorbents recirculating system (MARS) on systemic hemodynamics and oxygen consumption (VO 2 ) in patients with hyperacute liver failure (HALF). In a controlled design, eight patients with HALF were assigned to a 6-hour MARS treatment, and five patients, to a control group that was mechanically cooled to match the MARS group. Systemic hemodynamic variables were determined hourly during the study period. In the MARS group, systemic vascular resistance index increased by 46% from 1,215 ؎ 437 to 1,778 ؎ 710 dynes ⅐ s ⅐ cm ؊5 ⅐ m ؊2 (P < .0001), which significantly exceeded a 6% increase in the control group. Mean arterial pressure increased from 69 ؎ 5 to 83 ؎ 11 mm Hg in the MARS group (P < .0001) and was unchanged in the control group. Cardiac index decreased by 20% from 4.6 ؎ 1.8 to 3.7 ؎ 1.1 L/min ⅐ m ؊2 (P ‫؍‬ .0007) in the MARS group and by 7% in the control group. Heart rate decreased from 105 ؎ 21 to 85 ؎ 15 beats/min in the MARS group (P < .0001) and was unchanged in the control group. In the MARS group, oxygen delivery decreased from 621 ؎ 198 to 486 ؎ 141 mL/min ⅐ m ؊2 (P < .05), and VO2, from 142 ؎ 31 to 112 ؎21 mL/min ⅐ m ؊2 (P < .05). Arterial lactate and pH levels were unchanged. In conclusion, systemic hemodynamic values tend to normalize, whereas systemic VO 2 decreases during MARS treatment in patients with HALF. These effects cannot be explained by the degree of cooling associated with MARS. (Liver Transpl 2003;9: 290-297.)

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Section: Discussionmentioning

confidence: 99%

Systemic hemodynamic effects of treatment with the molecular adsorbents recirculating system in patients with hyperacute liver failure: A prospective controlled trial

Schmidt

Wang

Hansen

et al. 2003

Liver Transplantation

211

106

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“…24 Hepatic blood flow was calculated as described earlier. 25 If the uncertainty was above 30%, the estimate was not included, as described earlier. 21 Data are expressed as mean Ϯ SD.…”

Section: Calculations and Statisticsmentioning

confidence: 99%

Cerebral Herniation in Patients With Acute E Liver Failure Is Correlated With Arterial Ammonia Concentration

et al. 1999

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Cerebral edema leading to cerebral herniation (CH) is a common cause of death in acute liver failure (ALF). Animal studies have related ammonia with this complication. During liver failure, hepatic ammonia removal can be expected to determine the arterial ammonia level. In patients with ALF, we examined the hypotheses that high arterial ammonia is related to later death by CH, and that impaired removal in the hepatic circulation is related to high arterial ammonia. Twenty-two patients with ALF were studied retrospectively. In addition, prospective studies with liver vein catheterization were performed after development of hepatic encephalopathy (HE) in 22 patients with ALF and 9 with acute on chronic liver disease (AOCLD). Cerebral arterial-venous ammonia difference was studied in 13 patients with ALF. In all patients with ALF (n ‫؍‬ 44), those who developed CH (n ‫؍‬ 14) had higher arterial plasma ammonia than the non-CH (n ‫؍‬ 30) patients (230 ؎ 58 vs. 118 ؎ 48 mol/L; P F .001). In contrast, galactose elimination capacity, bilirubin, creatinine, and prothrombin time were not different (NS). Cerebral arterial-venous differences increased with increasing arterial ammonia (P F .001). Arterial plasma ammonia was lower than hepatic venous in ALF (148 ؎ 73 vs. 203 ؎ 108 mol/L; P F .001). In contrast, arterial plasma ammonia was higher than hepatic venous in patients with AOCLD (91 ؎ 26 vs. 66 ؎ 18 mol/L; P F .05). Net ammonia release from the hepatic-splanchnic region was 6.5 ؎ 6.4 mmol/h in ALF, and arterial ammonia increased with increasing release. In contrast, there was a net hepatic-splanchnic removal of ammonia (2.8 ؎ 3.3 mmol/h) in patients with AOCLD. We interpret these data that in ALF in humans, vast amounts of ammonia escape hepatic metabolism, leading to high arterial ammonia concentrations, which in turn is associated with increased cerebral ammonia uptake and CH. (HEPATOL-OGY 1999;29:648-653.)

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“…Arteriolar dilation, both in the splanchnic and the systemic circulation, is responsible. 3 Such an imbalanced vasodilatation results in a restricted cardiac output and low arterial blood pressure. The other major complication in patients with ALF is brain edema, which in some cases results in increased intracranial pressure (ICP).…”

mentioning

confidence: 99%

Brain edema in liver failure: Basic physiologic principles and management

Larsen

Wendon

2002

Liver Transpl

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In patients with severe liver failure, brain edema is a frequent and serious complication that may result in high intracranial pressure and brain damage. This short article focuses on basic physiologic principles that determine water flux across the blood-brain barrier. Using the Starling equation, it is evident that both the osmotic and hydrostatic pressure gradients are imbalanced across the blood-brain barrier in patients with acute liver failure. This combination will tend to favor cerebral capillary water influx to the brain. In contrast, the disequilibration of the Starling forces seems to be less pronounced in patients with cirrhosis because the regulation of cerebral blood flow is preserved and the arterial ammonia concentration is lower compared with that of patients with acute liver failure. Treatments that are known to reverse high intracranial pressure tend to decrease the osmotic pressure gradients across the blood-brain barrier. Recent studies indicate that interventions that restrict cerebral blood flow, such as hyperventilation, hypothermia, and indomethacin, are also efficient in preventing edema and high intracranial pressure, probably by decreasing the transcapillary hydrostatic pressure gradient. In our opinion, it is important to recall that rational fluid therapy, adequate ventilation, and temperature control are of direct importance to controlling cerebral capillary water flux in patients with acute liver failure. These simple interventions should be secured before more advanced experimental technologies are instituted to treat these patients.

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Hepatic Blood Flow and Splanchnic Oxygen Consumption in Patients With Liver Failure. Effect of High–Volume Plasmapheresis

Cited by 75 publications

References 64 publications

Systemic hemodynamic effects of treatment with the molecular adsorbents recirculating system in patients with hyperacute liver failure: A prospective controlled trial

Systemic hemodynamic effects of treatment with the molecular adsorbents recirculating system in patients with hyperacute liver failure: A prospective controlled trial

Cerebral Herniation in Patients With Acute E Liver Failure Is Correlated With Arterial Ammonia Concentration

Brain edema in liver failure: Basic physiologic principles and management

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