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The impact of pre-induction fluid optimisation on post-induction hypotension

Intra-operative hypotension is a known predictor of adverse events and poor outcomes following major surgery. Hypotension often occurs on induction of anaesthesia, typically attributed to hypovolaemia and the haemodynamic effects of anaesthetic agents. We assessed the efficacy of fluid optimisation...

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Published in:Anaesthesia 2020-02, Vol.75 (5), p.634-641
Main Authors: Khan, A. I., Fischer, M., Pedoto, A. C., Seier, K., Tan, K. S., Dalbagni, G., Donat, S. M., Arslan-Carlon, V.
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container_end_page 641
container_issue 5
container_start_page 634
container_title Anaesthesia
container_volume 75
creator Khan, A. I.
Fischer, M.
Pedoto, A. C.
Seier, K.
Tan, K. S.
Dalbagni, G.
Donat, S. M.
Arslan-Carlon, V.
description Intra-operative hypotension is a known predictor of adverse events and poor outcomes following major surgery. Hypotension often occurs on induction of anaesthesia, typically attributed to hypovolaemia and the haemodynamic effects of anaesthetic agents. We assessed the efficacy of fluid optimisation for reducing the incidence of hypotension upon anaesthesia induction. This prospective protocol enrolled 283 patients undergoing radical cystectomy and randomised them to goal-directed fluid therapy (n = 142) or standard fluid therapy (n = 141). Goal-directed fluid therapy patients received fluid optimisation based on stroke volume response to passive leg raise before induction; those with positive passive leg raise received intravenous crystalloid fluid boluses until stroke volume was optimised. Baseline mean arterial pressure was measured on the morning of surgery and upon operating room arrival. This post-hoc analysis defined haemodynamic instability as either a > 30% relative drop in mean arterial pressure compared to baseline or absolute mean arterial pressure < 55 mmHg, within 15 minutes of induction. Forty-two (30%) goal-directed fluid therapy patients underwent fluid optimisation after finding an intravascular fluid deficit via passive leg raise testing; 106 (75%) goal-directed fluid therapy and 112 (79%) standard fluid therapy patients met criteria for haemodynamic instability. There was no significant difference in haemodynamic instability incidence between the goal-directed fluid therapy and standard fluid therapy groups using absolute mean arterial pressure drop below 55 mmHg (p=0.58) or using pre-surgical testing or pre-surgical mean arterial pressure values as baseline (p = 0.21, p = 0.89); however, the difference in haemodynamic instability incidence was significant using the operating room baseline mean arterial pressure (p = 0.004). We conclude that fluid optimisation before induction of general anaesthesia did not significantly impact haemodynamic instability.
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Goal-directed fluid therapy patients received fluid optimisation based on stroke volume response to passive leg raise before induction; those with positive passive leg raise received intravenous crystalloid fluid boluses until stroke volume was optimised. Baseline mean arterial pressure was measured on the morning of surgery and upon operating room arrival. This post-hoc analysis defined haemodynamic instability as either a &gt; 30% relative drop in mean arterial pressure compared to baseline or absolute mean arterial pressure &lt; 55 mmHg, within 15 minutes of induction. Forty-two (30%) goal-directed fluid therapy patients underwent fluid optimisation after finding an intravascular fluid deficit via passive leg raise testing; 106 (75%) goal-directed fluid therapy and 112 (79%) standard fluid therapy patients met criteria for haemodynamic instability. 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title The impact of pre-induction fluid optimisation on post-induction hypotension
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