INTRAVENOUS KETOROLAC TROMETHAMINE DOES NOT WORSEN PLATELET-FUNCTION DURING KNEE ARTHROSCOPY UNDER GENERAL-ANESTHESIA

Citation
Bk. Thwaites et al., INTRAVENOUS KETOROLAC TROMETHAMINE DOES NOT WORSEN PLATELET-FUNCTION DURING KNEE ARTHROSCOPY UNDER GENERAL-ANESTHESIA, Anesthesia and analgesia, 81(1), 1995, pp. 119-124
Citations number
27
Categorie Soggetti
Anesthesiology
Journal title
ISSN journal
00032999
Volume
81
Issue
1
Year of publication
1995
Pages
119 - 124
Database
ISI
SICI code
0003-2999(1995)81:1<119:IKTDNW>2.0.ZU;2-J
Abstract
Ketorolac (KT) prolongs bleeding time and inhibits platelet aggregatio n and platelet thromboxane production in healthy, awake volunteers. Ho wever, platelet function may be accentuated during the stress of gener al anesthesia (GA) and surgery. The purpose of this study was to inves tigate platelet function changes during a standard GA technique and su rgery, as well as after a single intraoperative dose of intravenous (I V) KT. The study comprised 30 ASA physical status I patients undergoin g GA for knee arthroscopy. Subjects were randomized to receive either KT 60 mg IV 15 min after skin incision or placebo IV. Platelet functio n testing consisted of an Ivy bleeding time (BT), platelet aggregometr y (PA) with adenosine diphosphate (ADP) and collagen, thromboelastogra phy (TEG), and serum thromboxane B-2 assays (TxB(2)). Platelet functio n testing was performed: 1) 15 min prior to the induction of GA, 2) 10 min after skin incision, and 3) 45 min after administration of study drug. BT decreased significantly in the placebo group from 263 +/- 133 s (mean +/- so) preoperatively to 207 +/- 89 s postincision. BT did n ot change in the KT group. PA was unchanged after IV KT. TEG data was unchanged in both groups during anesthesia and surgery. TxB(2) levels decreased markedly in the KT group from 106.9 +/- 96.2 ng/mL preoperat ively to 0.4 +/- 1.2 ng/mL poststudy drug, P = 0.002. Platelet functio n appears to be accentuated during GA and surgery as evaluated by BT i n the placebo group. Further, platelet function by BT, PA, and TEG was not inhibited after IV KT despite near complete abolition of TxB(2) p roduction.