Individualized early goal-directed therapy in systemic Inflammation: is full utilization of preload reserve the optimal strategy?

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Individualized early goal-directed therapy in systemic Inflammation: is full utilization of preload reserve the optimal strategy? / Wodack, Karin H; Poppe, Annika M; Tomkötter, Lena; Bachmann, Kai A; Strobel, Cilly M; Bonk, Sarah; Havel, Jan; Heckel, Kai; Gocht, Andreas; Saugel, Bernd; Mann, Oliver; Izbicki, Jakob R; Goetz, Alwin E; Trepte, Constantin J C; Reuter, Daniel A.

In: CRIT CARE MED, Vol. 42, No. 12, 01.12.2014, p. e741-51.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

Harvard

Wodack, KH, Poppe, AM, Tomkötter, L, Bachmann, KA, Strobel, CM, Bonk, S, Havel, J, Heckel, K, Gocht, A, Saugel, B, Mann, O, Izbicki, JR, Goetz, AE, Trepte, CJC & Reuter, DA 2014, 'Individualized early goal-directed therapy in systemic Inflammation: is full utilization of preload reserve the optimal strategy?', CRIT CARE MED, vol. 42, no. 12, pp. e741-51. https://doi.org/10.1097/CCM.0000000000000657

APA

Wodack, K. H., Poppe, A. M., Tomkötter, L., Bachmann, K. A., Strobel, C. M., Bonk, S., Havel, J., Heckel, K., Gocht, A., Saugel, B., Mann, O., Izbicki, J. R., Goetz, A. E., Trepte, C. J. C., & Reuter, D. A. (2014). Individualized early goal-directed therapy in systemic Inflammation: is full utilization of preload reserve the optimal strategy? CRIT CARE MED, 42(12), e741-51. https://doi.org/10.1097/CCM.0000000000000657

Vancouver

Bibtex

@article{df16a457f1244d0aa13c701c8ca7053e,
title = "Individualized early goal-directed therapy in systemic Inflammation: is full utilization of preload reserve the optimal strategy?",
abstract = "OBJECTIVES: In severe acute pancreatitis, the administration of fluids in the presence of positive fluid responsiveness is associated with better outcome when compared to guiding therapy on central venous pressure. We compared the effects of such consequent maximization of stroke volume index with a regime using individual values of stroke volume index assessed prior to severe acute pancreatitis induction as therapeutic hemodynamic goals.DESIGN: Prospective, randomized animal study.SETTING: University animal research laboratory.SUBJECTS: Thirty domestic pigs.INTERVENTIONS: After randomization, fluid resuscitation was started 2 hours after severe acute pancreatitis induction and continued for 6 hours according to the respective treatment algorithms. In the control group, fluid therapy was directed by maximizing stroke volume index, and in the study group, stroke volume index assessed prior to severe acute pancreatitis served as primary hemodynamic goal.MEASUREMENTS AND MAIN RESULTS: Within the first 6 hours of severe acute pancreatitis, the study group received a total of 1,935.8 ± 540.7 mL of fluids compared with 3,462.8 ± 828.2 mL in the control group (p < 0.001). Pancreatic tissue oxygenation did not differ significantly between both groups. Vascular endothelial function, measured by flow-mediated vasodilation before and 6 hours after severe acute pancreatitis induction, revealed less impairment in the study group after treatment interval (-90.76% [study group] vs -130.89% [control group]; p = 0.046). Further, lower levels of heparan sulfate (3.41 ± 5.6 pg/mL [study group] vs 43.67 ± 46.61 pg/mL [control group]; p = 0.032) and interleukin 6 (32.18 ± 8.81 pg/mL [study group] vs 77.76 ± 56.86 pg/mL [control group]; p = 0.021) were found in the study group compared with control group. Histopathological examination of the pancreatic head and corpus at day 7 revealed less edema for the study group compared with the control group (1.82 ± 0.87 [study group] vs 2.89 ± 0.33 [control group, pancreatic head]; p = 0.03; 2.2 ± 0.92 [study group] vs 2.91 ± 0.3 [control group, pancreatic corpus]; p = 0.025).CONCLUSIONS: Individualized optimization of intravascular fluid status during the early course of severe acute pancreatitis, compared with a treatment strategy of maximizing stroke volume by fluid loading, leads to less vascular endothelial damage, pancreatic edema, and inflammatory response.",
keywords = "Acute Disease, Animals, Disease Models, Animal, Endothelium, Vascular, Enzyme-Linked Immunosorbent Assay, Fluid Therapy, Glycocalyx, Hemodynamics, Heparitin Sulfate, Inflammation, Pancreatitis, Prospective Studies, Random Allocation, Severity of Illness Index, Stroke Volume, Swine, Syndecan-1",
author = "Wodack, {Karin H} and Poppe, {Annika M} and Lena Tomk{\"o}tter and Bachmann, {Kai A} and Strobel, {Cilly M} and Sarah Bonk and Jan Havel and Kai Heckel and Andreas Gocht and Bernd Saugel and Oliver Mann and Izbicki, {Jakob R} and Goetz, {Alwin E} and Trepte, {Constantin J C} and Reuter, {Daniel A}",
year = "2014",
month = dec,
day = "1",
doi = "10.1097/CCM.0000000000000657",
language = "English",
volume = "42",
pages = "e741--51",
journal = "CRIT CARE MED",
issn = "0090-3493",
publisher = "Lippincott Williams and Wilkins",
number = "12",

}

RIS

TY - JOUR

T1 - Individualized early goal-directed therapy in systemic Inflammation: is full utilization of preload reserve the optimal strategy?

AU - Wodack, Karin H

AU - Poppe, Annika M

AU - Tomkötter, Lena

AU - Bachmann, Kai A

AU - Strobel, Cilly M

AU - Bonk, Sarah

AU - Havel, Jan

AU - Heckel, Kai

AU - Gocht, Andreas

AU - Saugel, Bernd

AU - Mann, Oliver

AU - Izbicki, Jakob R

AU - Goetz, Alwin E

AU - Trepte, Constantin J C

AU - Reuter, Daniel A

PY - 2014/12/1

Y1 - 2014/12/1

N2 - OBJECTIVES: In severe acute pancreatitis, the administration of fluids in the presence of positive fluid responsiveness is associated with better outcome when compared to guiding therapy on central venous pressure. We compared the effects of such consequent maximization of stroke volume index with a regime using individual values of stroke volume index assessed prior to severe acute pancreatitis induction as therapeutic hemodynamic goals.DESIGN: Prospective, randomized animal study.SETTING: University animal research laboratory.SUBJECTS: Thirty domestic pigs.INTERVENTIONS: After randomization, fluid resuscitation was started 2 hours after severe acute pancreatitis induction and continued for 6 hours according to the respective treatment algorithms. In the control group, fluid therapy was directed by maximizing stroke volume index, and in the study group, stroke volume index assessed prior to severe acute pancreatitis served as primary hemodynamic goal.MEASUREMENTS AND MAIN RESULTS: Within the first 6 hours of severe acute pancreatitis, the study group received a total of 1,935.8 ± 540.7 mL of fluids compared with 3,462.8 ± 828.2 mL in the control group (p < 0.001). Pancreatic tissue oxygenation did not differ significantly between both groups. Vascular endothelial function, measured by flow-mediated vasodilation before and 6 hours after severe acute pancreatitis induction, revealed less impairment in the study group after treatment interval (-90.76% [study group] vs -130.89% [control group]; p = 0.046). Further, lower levels of heparan sulfate (3.41 ± 5.6 pg/mL [study group] vs 43.67 ± 46.61 pg/mL [control group]; p = 0.032) and interleukin 6 (32.18 ± 8.81 pg/mL [study group] vs 77.76 ± 56.86 pg/mL [control group]; p = 0.021) were found in the study group compared with control group. Histopathological examination of the pancreatic head and corpus at day 7 revealed less edema for the study group compared with the control group (1.82 ± 0.87 [study group] vs 2.89 ± 0.33 [control group, pancreatic head]; p = 0.03; 2.2 ± 0.92 [study group] vs 2.91 ± 0.3 [control group, pancreatic corpus]; p = 0.025).CONCLUSIONS: Individualized optimization of intravascular fluid status during the early course of severe acute pancreatitis, compared with a treatment strategy of maximizing stroke volume by fluid loading, leads to less vascular endothelial damage, pancreatic edema, and inflammatory response.

AB - OBJECTIVES: In severe acute pancreatitis, the administration of fluids in the presence of positive fluid responsiveness is associated with better outcome when compared to guiding therapy on central venous pressure. We compared the effects of such consequent maximization of stroke volume index with a regime using individual values of stroke volume index assessed prior to severe acute pancreatitis induction as therapeutic hemodynamic goals.DESIGN: Prospective, randomized animal study.SETTING: University animal research laboratory.SUBJECTS: Thirty domestic pigs.INTERVENTIONS: After randomization, fluid resuscitation was started 2 hours after severe acute pancreatitis induction and continued for 6 hours according to the respective treatment algorithms. In the control group, fluid therapy was directed by maximizing stroke volume index, and in the study group, stroke volume index assessed prior to severe acute pancreatitis served as primary hemodynamic goal.MEASUREMENTS AND MAIN RESULTS: Within the first 6 hours of severe acute pancreatitis, the study group received a total of 1,935.8 ± 540.7 mL of fluids compared with 3,462.8 ± 828.2 mL in the control group (p < 0.001). Pancreatic tissue oxygenation did not differ significantly between both groups. Vascular endothelial function, measured by flow-mediated vasodilation before and 6 hours after severe acute pancreatitis induction, revealed less impairment in the study group after treatment interval (-90.76% [study group] vs -130.89% [control group]; p = 0.046). Further, lower levels of heparan sulfate (3.41 ± 5.6 pg/mL [study group] vs 43.67 ± 46.61 pg/mL [control group]; p = 0.032) and interleukin 6 (32.18 ± 8.81 pg/mL [study group] vs 77.76 ± 56.86 pg/mL [control group]; p = 0.021) were found in the study group compared with control group. Histopathological examination of the pancreatic head and corpus at day 7 revealed less edema for the study group compared with the control group (1.82 ± 0.87 [study group] vs 2.89 ± 0.33 [control group, pancreatic head]; p = 0.03; 2.2 ± 0.92 [study group] vs 2.91 ± 0.3 [control group, pancreatic corpus]; p = 0.025).CONCLUSIONS: Individualized optimization of intravascular fluid status during the early course of severe acute pancreatitis, compared with a treatment strategy of maximizing stroke volume by fluid loading, leads to less vascular endothelial damage, pancreatic edema, and inflammatory response.

KW - Acute Disease

KW - Animals

KW - Disease Models, Animal

KW - Endothelium, Vascular

KW - Enzyme-Linked Immunosorbent Assay

KW - Fluid Therapy

KW - Glycocalyx

KW - Hemodynamics

KW - Heparitin Sulfate

KW - Inflammation

KW - Pancreatitis

KW - Prospective Studies

KW - Random Allocation

KW - Severity of Illness Index

KW - Stroke Volume

KW - Swine

KW - Syndecan-1

U2 - 10.1097/CCM.0000000000000657

DO - 10.1097/CCM.0000000000000657

M3 - SCORING: Journal article

C2 - 25402295

VL - 42

SP - e741-51

JO - CRIT CARE MED

JF - CRIT CARE MED

SN - 0090-3493

IS - 12

ER -