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Therapeutic plasma exchange does not reduce vasopressor requirement in severe acute liver failure: a retrospective case series.

Wiersema UF, Kim SW, Roxby D, Holt A - BMC Anesthesiol (2015)

Bottom Line: MAP was significantly higher immediately after TPE compared to baseline (p = 0.039), however when corrected for change in vasopressor requirement there was no significant change in VDI with TPE (p = 0.953).Twelve hours after TPE the MAP, vasopressor score and VDI were not significantly different from baseline (p = 0.563, p = 0.317 and p = 0.214 respectively).In this cohort of patients with severe ALF centrifugal TPE did not significantly affect vasopressor requirements.

View Article: PubMed Central - PubMed

Affiliation: Department of Critical Care Medicine, Flinders Medical Centre, Bedford Park, South Australia Australia.

ABSTRACT

Background: In acute liver failure (ALF) therapeutic plasma exchange (TPE) improves laboratory measures of liver function. In patients with ALF requiring minimal vasoactive support TPE has also been shown to provide haemodynamic benefits including an increase in systemic blood pressure. However the haemodynamic effects of TPE in patients with severe ALF requiring moderate or high dose vasopressor therapy has not been reported. We retrospectively examined the haemodynamic effects of TPE in a cohort of patients with severe ALF requiring vasopressor therapy.

Methods: Physiological, laboratory and treatment data were collected on all patients with ALF who received TPE between January 2000 and December 2012. All patients were managed in the intensive care unit of a tertiary referral centre for ALF and liver transplantation. The primary outcome measures were changes in mean arterial pressure (MAP), vasopressor score and the ratio of vasopressor score to MAP (vasopressor dependency index (VDI)) from baseline prior to TPE through to 12 hours after completion of TPE. Secondary outcome measures were changes in other routinely collected physiological variables and laboratory results. Results are presented as median (interquartile range (IQR)). Outcome measures were evaluated using a mixed effect model.

Results: Thirty nine TPE were performed in 17 patients with ALF (13 paracetamol poisoning). All TPE were performed with a centrifugal apheresis system (duration 130 minutes (IQR 115 - 147.5), plasma volume removed 5.1% body weight (IQR 4.6 - 5.5). Baseline values for primary outcome measures were: MAP 82 mmHg (IQR 72 - 92.5), vasopressor score 8.35 (IQR 3.62 - 24.6) and VDI 0.10 (IQR 0.05 - 0.31). MAP was significantly higher immediately after TPE compared to baseline (p = 0.039), however when corrected for change in vasopressor requirement there was no significant change in VDI with TPE (p = 0.953). Twelve hours after TPE the MAP, vasopressor score and VDI were not significantly different from baseline (p = 0.563, p = 0.317 and p = 0.214 respectively).

Conclusion: In this cohort of patients with severe ALF centrifugal TPE did not significantly affect vasopressor requirements.

No MeSH data available.


Related in: MedlinePlus

Box plots for temporal trends in (a) MAP, (b) vasopressor score and (c) VDI for every TPE treatment. The time points extend from less than 1 hour before TPE (pre treatment), through every hour of TPE (treatment 1 hr, 2 hr etc.) to 12 hours after TPE (post treatment 1 hr, 2 hr etc.). Note that only a few TPE were as long as 4 or 5 hours so the data values for treatment 4 hr and 5 hr are calculated from only a few TPE treatments.
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Fig2: Box plots for temporal trends in (a) MAP, (b) vasopressor score and (c) VDI for every TPE treatment. The time points extend from less than 1 hour before TPE (pre treatment), through every hour of TPE (treatment 1 hr, 2 hr etc.) to 12 hours after TPE (post treatment 1 hr, 2 hr etc.). Note that only a few TPE were as long as 4 or 5 hours so the data values for treatment 4 hr and 5 hr are calculated from only a few TPE treatments.

Mentions: The temporal trends in MAP, vasopressor score and VDI for every TPE performed are shown in Figure 2. The temporal trends in VDI for the first TPE treatment for each patient are shown in Figure 3. The temporal trends in MAP and vasopressor score for the first TPE treatment for each patient are shown in Additional files 1 and 2. For 7 TPE treatments in 4 patients the patient did not require any vasoactive agent at some (1 TPE) or all time points (6 TPE in 3 patients). The VDI was thus zero for these data points. Physiological variables pre-treatment and 1 hour post-treatment are shown in Table 3. The effect size of TPE on MAP, vasopressor score and VDI, comparing 1 hour post-treatment and 12 hours post-treatment with pre-treatment values and 12 hours post-treatment with 1 hour post-treatment values is shown in Table 4. This demonstrates a significant increase in MAP with treatment (P1 – Pre) (p = 0.038), but when corrected for vasopressor dose there was no significant treatment effect on VDI (P1 – Pre) (p = 0.953). Twelve hours after TPE the VDI was not significantly different from baseline (p = 0.214). No association was found between haemodynamic response and repetition of treatment for the same individual. Analysis of data including only the 13 patients with paracetamol toxicity produced results very similar to analysis of all 17 patients (VDI (P1 – Pre) p = 0.865).Figure 2


Therapeutic plasma exchange does not reduce vasopressor requirement in severe acute liver failure: a retrospective case series.

Wiersema UF, Kim SW, Roxby D, Holt A - BMC Anesthesiol (2015)

Box plots for temporal trends in (a) MAP, (b) vasopressor score and (c) VDI for every TPE treatment. The time points extend from less than 1 hour before TPE (pre treatment), through every hour of TPE (treatment 1 hr, 2 hr etc.) to 12 hours after TPE (post treatment 1 hr, 2 hr etc.). Note that only a few TPE were as long as 4 or 5 hours so the data values for treatment 4 hr and 5 hr are calculated from only a few TPE treatments.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4359494&req=5

Fig2: Box plots for temporal trends in (a) MAP, (b) vasopressor score and (c) VDI for every TPE treatment. The time points extend from less than 1 hour before TPE (pre treatment), through every hour of TPE (treatment 1 hr, 2 hr etc.) to 12 hours after TPE (post treatment 1 hr, 2 hr etc.). Note that only a few TPE were as long as 4 or 5 hours so the data values for treatment 4 hr and 5 hr are calculated from only a few TPE treatments.
Mentions: The temporal trends in MAP, vasopressor score and VDI for every TPE performed are shown in Figure 2. The temporal trends in VDI for the first TPE treatment for each patient are shown in Figure 3. The temporal trends in MAP and vasopressor score for the first TPE treatment for each patient are shown in Additional files 1 and 2. For 7 TPE treatments in 4 patients the patient did not require any vasoactive agent at some (1 TPE) or all time points (6 TPE in 3 patients). The VDI was thus zero for these data points. Physiological variables pre-treatment and 1 hour post-treatment are shown in Table 3. The effect size of TPE on MAP, vasopressor score and VDI, comparing 1 hour post-treatment and 12 hours post-treatment with pre-treatment values and 12 hours post-treatment with 1 hour post-treatment values is shown in Table 4. This demonstrates a significant increase in MAP with treatment (P1 – Pre) (p = 0.038), but when corrected for vasopressor dose there was no significant treatment effect on VDI (P1 – Pre) (p = 0.953). Twelve hours after TPE the VDI was not significantly different from baseline (p = 0.214). No association was found between haemodynamic response and repetition of treatment for the same individual. Analysis of data including only the 13 patients with paracetamol toxicity produced results very similar to analysis of all 17 patients (VDI (P1 – Pre) p = 0.865).Figure 2

Bottom Line: MAP was significantly higher immediately after TPE compared to baseline (p = 0.039), however when corrected for change in vasopressor requirement there was no significant change in VDI with TPE (p = 0.953).Twelve hours after TPE the MAP, vasopressor score and VDI were not significantly different from baseline (p = 0.563, p = 0.317 and p = 0.214 respectively).In this cohort of patients with severe ALF centrifugal TPE did not significantly affect vasopressor requirements.

View Article: PubMed Central - PubMed

Affiliation: Department of Critical Care Medicine, Flinders Medical Centre, Bedford Park, South Australia Australia.

ABSTRACT

Background: In acute liver failure (ALF) therapeutic plasma exchange (TPE) improves laboratory measures of liver function. In patients with ALF requiring minimal vasoactive support TPE has also been shown to provide haemodynamic benefits including an increase in systemic blood pressure. However the haemodynamic effects of TPE in patients with severe ALF requiring moderate or high dose vasopressor therapy has not been reported. We retrospectively examined the haemodynamic effects of TPE in a cohort of patients with severe ALF requiring vasopressor therapy.

Methods: Physiological, laboratory and treatment data were collected on all patients with ALF who received TPE between January 2000 and December 2012. All patients were managed in the intensive care unit of a tertiary referral centre for ALF and liver transplantation. The primary outcome measures were changes in mean arterial pressure (MAP), vasopressor score and the ratio of vasopressor score to MAP (vasopressor dependency index (VDI)) from baseline prior to TPE through to 12 hours after completion of TPE. Secondary outcome measures were changes in other routinely collected physiological variables and laboratory results. Results are presented as median (interquartile range (IQR)). Outcome measures were evaluated using a mixed effect model.

Results: Thirty nine TPE were performed in 17 patients with ALF (13 paracetamol poisoning). All TPE were performed with a centrifugal apheresis system (duration 130 minutes (IQR 115 - 147.5), plasma volume removed 5.1% body weight (IQR 4.6 - 5.5). Baseline values for primary outcome measures were: MAP 82 mmHg (IQR 72 - 92.5), vasopressor score 8.35 (IQR 3.62 - 24.6) and VDI 0.10 (IQR 0.05 - 0.31). MAP was significantly higher immediately after TPE compared to baseline (p = 0.039), however when corrected for change in vasopressor requirement there was no significant change in VDI with TPE (p = 0.953). Twelve hours after TPE the MAP, vasopressor score and VDI were not significantly different from baseline (p = 0.563, p = 0.317 and p = 0.214 respectively).

Conclusion: In this cohort of patients with severe ALF centrifugal TPE did not significantly affect vasopressor requirements.

No MeSH data available.


Related in: MedlinePlus