| JOURNAL HOME | CME HOME | THIS MONTH | PAST ISSUES | ETOC | COLLECTIONS |
| AUTHORS | REVIEWERS | EDITORIAL BOARD | FEEDBACK | RSS | HELP |
 
|
|
|
||
|
|
© 2001 International Anesthesia Research Society
|
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Despite clinical and laboratory evidence of perioperative hypercoagulability, there are no consistent data evaluating the extent, duration, and specific contribution of platelets and procoagulatory proteins by in vitro testing. We tested the hypothesis that the parallel use of standard and abciximab-cytochalasin D-modified thromboelastography (TEG®) can assess 7 days’ postoperative hypercoagulability and can estimate the independent contribution of procoagulatory proteins and platelets. Thromboelastograms were performed before surgery, at the end of surgery, 6 h after surgery, and on postoperative days 1, 2, 3, and 7; they were analyzed for the reaction time and the maximal amplitude (MA). We calculated the elastic shear modulus of standard MA (Gt) and modified MA (Gc), which reflect total clot strength and procoagulatory protein component, respectively. The difference was an estimate of the platelet component (Gp). There was a 10% perioperative increase of standard MA, corresponding to a 50% increase of Gt (P < 0.0001) and an 86%–90% contribution of the calculated Gp to Gt. We conclude that serial standard and modified thromboelastography may reveal prolonged postoperative hypercoagulability and the independent contribution of platelets and procoagulatory proteins to clot strength.
Implications: Postoperative hypercoagulability, occurring for at least 1 wk after major abdominal surgery, may be demonstrated by standard and modified thromboelastography. This hypercoagulability is not reflected by standard coagulation monitoring and seems to be predominantly caused by increased platelet reactivity.
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Arterial and venous thrombotic events are the clinical manifestation of postoperative hypercoagulability (1–3). Although thrombotic events may be attenuated by anticoagulatory substances (3), the in vitro verification of the underlying imbalance has been only incompletely evaluated. This may, in part, be because of the complex coagulation system, which involves coagulatory proteins and platelets, as well as the lack of appropriate coagulation tests, reflecting both the dynamic fibrin-platelet interaction and the individual activity of coagulatory proteins and platelets. Although several studies have shown a postoperative increase of procoagulatory proteins and parallel reductions of anticoagulatory and fibrinolytic factors relative to the extent of tissue trauma, data on platelet function are controversial (2,4–9).
Thromboelastography (TEG®) has been established as a sensitive test for the global assessment of hemostatic function in several clinical settings (10–13). Standard thromboelastography, however, cannot distinguish between the quantitative contribution of plasmatic procoagulatory proteins and platelets to postopera-tive hypercoagulability. Recently introduced modified thromboelastography with substances inhibiting platelet fibrin interaction (abciximab) (14–16) and platelet actin polymerization (cytochalasin D) (17,18) may provide a more specific, though indirect, estimate of the independent contribution of plasmatic proaggregatory proteins and platelets to perioperative hypercoagulability.
In this investigation, we tested the hypothesis that the parallel use of standard and modified thromboelastography can assess hypercoagulability and the independent contribution of plasma proteins and platelets to this hypercoagulability for 7 days after elective major abdominal surgery. Furthermore, we evaluated the association of thromboelastographic variables to standard coagulation tests and platelet count and the impact of standard thrombosis prophylaxis on thromboelastographic variables.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
After ethics committee approval and informed consent, 20 consecutive patients (16 men, 4 women, ages 58.6 ± 11.7 yr [mean ± SD]) scheduled for major abdominal surgery under general anesthesia were included in this study. Exclusion criteria were a history or clinical signs of coronary artery disease, anticipated large intraoperative transfusion requirements, preexisting coagulation disorders, preoperative anticoagulation, use of nonsteroidal antiinflammatory drugs or aspirin within 1 wk before surgery, renal dysfunction (creatinine >120 µmol/L), and surgery under regional anesthesia. Four patients were treated for hypertension (ß-blocker, n = 2; angiotensin-converting enzyme inhibitor, n = 2), 12 patients were hypercholesterolemic (lipid-lowering therapy with statins, n = 4), and five patients were active smokers. The patients underwent gastrectomy (n = 6), colonic resection (n = 6), or Whipple procedure (n = 8) under general anesthesia. The mean (± SD) duration of surgery was 303 ± 146 min. Sixteen of the 20 patients suffered from cancer.
Anesthesia and perioperative care were at the discretion of the attending anesthesiologist. Postoperative analgesia with piritramide IV or subcutaneously was administered on demand. Perioperative hematocrit was maintained close to 30%. A total of 20 packed red blood cells (range 0–7) was administered during the entire study period. Neither platelets nor fresh frozen plasma nor other coagulation factors were used. Patients received the recommended thrombosis prophylaxis of 40 mg enoxaparin subcutaneously once daily (19), starting before surgery (n = 13) or on the evening of surgery (n = 7), according to the surgeon’s preference. No patient suffered from perioperative cardiac morbidity, pneumonia, or renal insufficiency. Four patients sustained late surgical complications, all of which occurred after the study period.
Two 4.5-mL blood samples were drawn from a central venous line into siliconized Vacutainer tubes (Becton Dickinson, Meylan, France) containing 0.5 mL sodium citrate (0.129M), and the initial 3 mL of blood was discarded. Blood samples were collected after the induction of anesthesia, after surgery on arrival at the intensive care unit, 6 h after surgery, on the morning of postoperative day (POD) 1, on the morning of POD 2, on the morning of POD 3, and on the morning of POD 7.
Prothrombin time, thrombin clotting time, partial thromboplastin time, fibrinogen (Clauss method), and antithrombin III were measured with the Behring Coagulation System® (Dade-Behring Marburg GmBH, Marburg, Germany). Platelet count, red blood cells, and hematocrit were determined by using the Coulter STKS (Coulter Electronics Inc, Hialeah, FL).
Three different thromboelastographic assays were performed within 1 to 2 h of blood sampling (20) on a computerized thromboelastographic coagulation analyzer (roTEG Coagulation Analyzer®; Dynabite GmbH, Munich, Germany). Clot formation was triggered by recalcification of 300 µL whole blood with 20 µL 0.2M calcium chloride (StartTEG®; Fa Nobis, Endingen, Germany) and 20 µL of an intrinsic activator (InTEG-LS Aktivator®; Fa Nobis) in all three assays. The thromboelastographic trace was analyzed for the reaction time (r-time), which reflects the rate of initial fibrin formation, and for the maximal amplitude (MA), which reflects the absolute strength of the clot (21,22).
The assays were the following:
- Activated whole-blood thromboelastogram. The reference levels (mean ± SD) in our laboratory are r-time (176.2 ± 27.2 s) and MA (62.2 ± 3.3 mm).
- Abciximab-cytochalasin D-modified thromboelastogram. To assess the independent contributions of platelets and fibrinogen to clot strength, thromboelastography was performed after inhibiting platelets with 10 µL of 2 mg/mL abciximab (Reopro®; Centocor B.V., CB Leiden, Netherlands) together with 10 µL of 0.2 mg/mL cytochalasin D (Sigma Chemical Co, St Louis, MO). The reference levels (mean ± SD) in our laboratory are r-time (166.0 ± 22.8 s) and MA (14.1 ± 3.5 mm).
- Activated whole-blood thromboelastography with heparinase (heparinase-modified thromboelastography). To eliminate trace amounts of heparin, thromboelastography was performed with 20 µL heparinase (Dade Hepzyme®, 5.5IU/mL; Dade-Behring Marburg GmbH, Marburg, Germany).
Accounting for the exponential increase of the elastic shear modulus in relation to the MA (17), we calculated the elastic shear modulus (G) of the activated whole-blood MA, reflecting total clot strength (Gt) and the elastic shear modulus of the abciximab-cytochalasin D MA, reflecting the contribution of procoagulatory proteins to clot strength (Gc). The difference of Gt and Gc was calculated as an estimation of the platelet contribution to clot strength (Gp) (15,18). We further calculated the percentage contribution of Gc and Gp to Gt. The elastic shear modulus was calculated as follows: G = (5000 MA)/(100 - MA) in dynes/cm2.
Considering the perioperative change of the platelet count, we created a platelet index, defined as Gp per 1000 platelets, as a calculated measure of the platelet contribution to clot strength.
All data were tested for normal distribution and are expressed as mean ± SD. Effects over time were analyzed by a one-way repeated measures analysis of variance model. The correlation between fibrinogen and the MA of the activated whole blood and the abciximab-cytochalasin D-modified thromboelastography, as well as the correlation between the platelet count and the MA of activated whole blood and the Gp, was performed by simple linear regression analysis (Stat View 4.5; Abacus Concepts, Berkeley, CA). The intercept was not removed. P < 0.05 was used to indicate statistical significance.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The perioperative trend of the r-time in the activated whole-blood thromboelastography as compared with the heparinase thromboelastography is depicted in Figure 1. There was a significant and parallel perioperative change of the r-time in both thromboelastographic traces, with an initial r-time decrease at the end of surgery and a return to the preoperative baseline on POD 7 (P < 0.0001).
|
The perioperative trend of the MA in the activated whole-blood thromboelastography as compared with the heparinase thromboelastography is depicted in Figure 2. There was an equal and continuous perioperative increase of the MA in both thromboelastographic traces until POD 7 (P < 0.0001). This 10% perioperative increase of the MA corresponded to a 50% increase of the calculated elastic shear modulus.
|
Prothrombin time, partial thromboplastin time, thrombin clotting time, and antithrombin III, respectively, changed slightly over time but remained within the reference limits ( Table 1). Fibrinogen increased substantially on POD 2 and had a peak on POD 3, exceeding the preoperative baseline by 90%. Platelet count remained stable until an increase on POD 7.
|
After an initial decrease of the abciximab-cytochalasin D-modified MA on the day of surgery, the MA increased until POD 3 and exceeded the preoperative baseline by 40% (Fig. 3). This increase persisted until POD 7 (P < 0.0001). The biphasic change of the MA coincided with a parallel change of fibrinogen levels (Table 1).
|
There was a weak correlation between fibrinogen and the activated whole-blood MA (adjusted r2 = 0.442; P < 0.0001) and a strong correlation between fibrinogen and the abciximab-cytochalasin D MA (adjusted r2 = 0.767) ( Fig. 4). Small levels of fibrinogen were associated with a small MA, and increased levels of fibrinogen corresponded to a large MA.
|
The platelet count did not correlate with the activated whole-blood MA (adjusted r2 = 0.165), and there was a weak correlation with Gp (adjusted r2 = 0.371). The relative contribution of Gp to Gt varied over time but remained between 86% and 90%.
Figure 5 depicts the perioperative trend of the platelet index. There was an immediate increase after surgery that reached its peak on POD 3 and exceeded the preoperative baseline on POD 7 by 25% (P < 0.0001).
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Clinical evidence of postoperative hypercoagulability has been incompletely evaluated by in vitro coagulation monitoring. The results of the present investigation clearly demonstrate a substantial postoperative hypercoagulability lasting for at least seven days after major uneventful abdominal surgery under general anesthesia. This hypercoagulability comprised an accelerated clot formation, as evidenced by an early decrease of the r-time, and an increase of the clot strength, as evidenced by a continuous postoperative increase of the MA. It is unclear when coagulation returned to preoperative baseline values, but the present data suggest that hypercoagulability after major abdominal surgery persists beyond the known duration of surgical stress response after similar procedures (23,24).
The principles and the methods of the thromboelastogram, reflecting the dynamic interaction between platelets and the protein coagulation cascade, are well described in the literature (20–22). Thromboelastography is being increasingly used to guide therapeutic decisions during liver transplantation and cardiac surgery and in preeclamptic and eclamptic parturients (10–13). Data on perioperative changes of thromboelastographic variables in noncardiac surgery are rare and limited to a short postoperative period (1,25–27).
Our study differs from previous work in several regards. We included only patients without a history or clinical signs of coronary artery disease. All of our patients underwent major abdominal surgery, which is known to trigger a substantial stress response and activation of the coagulation cascade (4,7,23,24). Most importantly, we evaluated our patients until the seventh POD.
Because of the exponential increase of the elastic shear modulus, the perioperatively observed 10% increase of the MA corresponds to a 50% perioperative increase of the clot strength. This is in accordance with the findings of Khurana et al. (17), who showed a similar increase of the elastic shear modulus after maximally triggering coagulation with tissue factor. Comparing conventional with laparoscopic cholecystectomy, Caprini et al. (25) demonstrated thromboelastographic signs of hypercoagulability on the first POD in the laparoscopic group.
In morbidly obese patients, Pivalizza et al. (27) demonstrated an already preoperatively accelerated coagulability and clot strength without additional changes of the thromboelastographic variable after minor surgical procedures. In contrast to patients undergoing major vascular surgery under epidural anesthesia, Tuman et al. (1) demonstrated thromboelastographic evidence of hypercoagulability on the first POD after comparable procedures under general anesthesia. This early postoperative hypercoagulability was associated with the occurrence of arterial thrombotic events (1).
Likewise, Gibbs and Bell (28) demonstrated evidence of hypercoagulability on the second POD after abdominal aortic surgery, which was attenuated by small-dose unfractionated heparin. Their findings are in line with the available literature, which demonstrates dose-dependent alterations of the r-time and the MA and their reversibility with heparinase, both in vitro and in vivo (12,28,29). In contrast to a similar dose-dependent effect of low molecular weight heparin in vitro, there are no conclusive data in vivo (29). The results of this investigation, however, suggest that thromboelastographic variables are unable to monitor an in vivo effect of standard thrombosis prophylaxis with low molecular weight heparin. This is most likely because of the prophylactic dose and the time window between subcutaneous administration and thromboelastographic assessment.
Modified thromboelastography, which uses platelet-inactivating substances such as abciximab and cytochalasin D, has been introduced to estimate the independent contribution of procoagulatory proteins and platelets to clot strength (14–17) to specifically correct coagulation defects (14,15,30). The difference between the calculated elastic shear modulus of the whole-blood MA and that of the modified MA has been suggested to represent the platelet contribution to clot strength (15,17,18). Whether these considerations apply to hypercoagulable states is unknown. The perioperative change of the abciximab-cytochalasin D-modified MA in our study coincided with a parallel change of fibrinogen that peaked on the third POD, similarly to previously published data (2,4,8). Despite this substantial 60%–90% increase of fibrinogen concentration, there were only minimal changes of the relatively small contribution of the plasmatic component to the clot strength (10%–14%). This small contribution of the plasma protein component to the clot strength is in agreement with recent findings (17,18). Similar to the findings of Khurana et al. (17) and Nielson et al. (18), the relative perioperative contribution of the platelet component to clot strength ranged from 86% to 90% in this study. Correction for the perioperative change of the platelet count revealed an estimated peak platelet reactivity on the second and third PODs. This is in agreement with the findings of Rosenfeld et al. (8), who used whole-blood aggregometry to demonstrate maximal platelet reactivity 48 hours after major abdominal surgery. However, because we did not measure platelet activation variables, the calculated platelet component of clot strength is only indirect evidence of the possible role of platelet reactivity in postoperative hypercoagulability.
Our study was designed to evaluate whether major abdominal surgery induces hypercoagulability, which may be detected by changes in the thromboelastographic trace and calculated variables. Because of the seven-day study period and the fluid requirements associated with major abdominal surgery, we cannot exclude a potential impact of the administration of hydroxyethyl starch, saline, or both on thromboelastographic variables, as has been precisely described to occur after in vitro hemodilution and in healthy volunteers (31–33).
This investigation demonstrates thromboelastographic evidence of substantial hypercoagulability lasting for at least seven days after major and uneventful abdominal surgery. Despite a significant increase of fibrinogen, this hypercoagulability seems to be predominantly caused by a substantial platelet activity. Postoperative hypercoagulability is not reflected by standard coagulation monitoring but can be easily and quickly determined by serial analyses of standard and modified thromboelastography. Standard thromboelastography is unable to monitor prophylactic doses of low molecular weight heparin.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
-
Tuman KJ, McCarthy RJ, March RJ, et al. Effects of epidural anesthesia and analgesia on coagulation and outcome after major vascular surgery. Anesth Analg 1991; 73: 696–704.
[Abstract/Free Full Text] - Rosenfeld BA, Beattie C, Christopherson R, et al. The effects of different anesthetic regimens on fibrinolysis and the development of postoperative arterial thrombosis. Perioperative Ischemia Randomized Anesthesia Trial Study Group. Anesthesiology 1993; 79: 435–43.[Web of Science][Medline]
-
Clagett GP, Anderson FA, Heit J, et al. Prevention of thromboembolism. Chest 1995; 108: 312S–334S.
[Free Full Text] - Gibbs NM, Crawford GP, Michalopoulos N. Postoperative changes in coagulant and anticoagulant factors following abdominal aortic surgery. J Cardiothorac Vasc Anesth 1992; 6: 680–5.[Medline]
- Gibbs NM, Crawford GP, Michalopoulos N. A comparison of postoperative thrombotic potential following abdominal aortic surgery, carotid endarterectomy, and femoro-popliteal bypass. Anaesth Intensive Care 1996; 24: 11–4.[Web of Science][Medline]
- Dahl OE. The role of the pulmonary circulation in the regulation of coagulation and fibrinolysis in relation to major surgery. J Cardiothorac Vasc Anesth 1997; 11: 322–8.[Web of Science][Medline]
- Kambayashi J, Sakon M, Yokota M, et al. Activation of coagulation and fibrinolysis during surgery, analyzed by molecular markers. Thromb Res 1990; 60: 157–67.[Web of Science][Medline]
- Rosenfeld BA, Faraday N, Campbell D, et al. Perioperative platelet reactivity and the effects of clonidine. Anesthesiology 1993; 79: 255–61.[Web of Science][Medline]
- Naesh O, Hindberg I, Friis J, et al. Platelet activation in major surgical stress: influence of combined epidural and general anaesthesia. Acta Anaesthesiol Scand 1994; 38: 820–5.[Web of Science][Medline]
-
Kang YG, Martin DJ, Marquez J, et al. Intraoperative changes in blood coagulation and thrombelastographic monitoring in liver transplantation. Anesth Analg 1985; 64: 888–96.
[Abstract/Free Full Text] -
Shore Lesserson L, Manspeizer HE, DePerio M, et al. Thromboelasto-graphy-guided transfusion algorithm reduces transfusions in complex cardiac surgery. Anesth Analg 1999; 88: 312–9.
[Abstract/Free Full Text] - Tuman KJ, McCarthy RJ, Djuric M, et al. Evaluation of coagulation during cardiopulmonary bypass with a heparinase-modified thromboelastographic assay. J Cardiothorac Vasc Anesth 1994; 8: 144–9.[Medline]
- Sharma SK, Philip J, Whitten CW, et al. Assessment of changes in coagulation in parturients with preeclampsia using thromboelastography. Anesthesiology 1999; 90: 385–90.[Web of Science][Medline]
- Greilich PE, Alving BM, O’Neill KL, et al. A modified thrombo-elastographic method for monitoring c7E3 Fab in heparinized patients. Anesth Analg 1997; 84: 31–8.[Abstract]
-
Kettner SC, Panzer OP, Kozek SA, et al. Use of abciximab-modified thrombelastography in patients undergoing cardiac surgery. Anesth Analg 1999; 89: 580–4.
[Abstract/Free Full Text] -
Gottumukkala VN, Sharma SK, Philip J. Assessing platelet and fibrinogen contribution to clot strength using modified thromboelastography in pregnant women. Anesth Analg 1999; 89: 1453–5.
[Abstract/Free Full Text] - Khurana S, Mattson JC, Westley S, et al. Monitoring platelet glycoprotein IIb/IIIa-fibrin interaction with tissue factor-activated thromboelastography. J Lab Clin Med 1997; 130: 401–11.[Web of Science][Medline]
-
Nielson VG, Geary BT, Baird MS. Evaluation of the contribution of platelets to clot strength by thrombelastography in rabbits: the role of tissue factor and cytochalasin D. Anaesth Analg 2000; 91: 35–9.
[Abstract/Free Full Text] - Horlocker TT, Heit JA. Low molecular weight heparin: biochemistry, pharmacology, perioperative prophylaxis regimens, and guidelines for regional anesthetic management. Anesth Analg 1997; 85: 874–85.[Web of Science][Medline]
- Camenzind V, Bombeli T, Seifert B, et al. Citrate storage after thrombelastograph analysis. Anesthesiology 2000; 92: 1242–9.[Web of Science][Medline]
-
Mallett SV, Cox DJ. Thrombelastography. Br J Anaesth 1992; 69: 307–13.
[Free Full Text] - Chandler WL. The thromboelastograph and the thromboelastograph technique. Semin Thromb Hemost 1995; 21 (Suppl 4): 1–6.[Web of Science][Medline]
- Dorman T, Clarkson K, Rosenfeld BA, et al. Effects of clonidine on prolonged postoperative sympathetic response. Crit Care Med 1997; 25: 1147–52.[Web of Science][Medline]
- Naito Y, Tamai S, Shingu K, et al. Responses of plasma adrenocorticotropic hormone, cortisol, and cytokines during and after upper abdominal surgery. Anesthesiology 1992; 77: 426–31.[Web of Science][Medline]
- Caprini JA, Arcelus JI, Laubach M, et al. Postoperative hypercoagulability and deep-vein thrombosis after laparoscopic cholecystectomy. Surg Endosc 1995; 9: 304–9.[Web of Science][Medline]
- Gibbs NM, Crawford GP, Michalopoulos N. Thrombelastographic patterns following abdominal aortic surgery. Anaesth Intensive Care 1994; 22: 534–8.[Web of Science][Medline]
- Pivalizza EG, Pivalizza PJ, Weavind LM. Perioperative thrombo-elastography and sonoclot analysis in morbidly obese patients. Can J Anaesth 1997; 44: 942–5.[Web of Science][Medline]
- Gibbs NM, Bell R. The effect of low-dose heparin on hypercoagulability following abdominal aortic surgery. Anaesth Intensive Care 1998; 26: 503–8.[Web of Science][Medline]
-
Zmuda K, Neofotistos D, Ts’ao CH. Effects of unfractionated heparin, low-molecular-weight heparin, and heparinoid on thromboelastographic assay of blood coagulation. Am J Clin Pathol 2000; 113: 725–31.
[Abstract/Free Full Text] - Greilich PE, Alving BM, Longnecker D, et al. Near-site monitoring of the antiplatelet drug abciximab using the Hemodyne analyzer and modified thrombelastograph. J Cardiothorac Vasc Anesth 1999; 13: 58–64.[Web of Science][Medline]
-
Jamnicki M, Zollinger A, Seifert B, et al. Compromised blood coagulation: an in vitro comparison of hydroxyethyl starch 130/0.4 and hydroxyethyl starch 200/0.5 using thrombelastography. Anesth Analg 1998; 87: 989–93.
[Abstract/Free Full Text] -
Egli GA, Zollinger A, Seifert B, et al. Effect of progressive haemodilution with hydroxyethyl starch, gelatin and albumin on blood coagulation Br J Anaesth 1997; 78: 684–9.
[Abstract/Free Full Text] -
Ruttmann TG, James MF, Aronson I. In vivo investigation into the effects of haemodilution with hydroxyethyl starch (200/0.5) and normal saline on coagulation. Br J Anaesth 1998; 80: 612–6.
[Abstract/Free Full Text]
This article has been cited by other articles:
|
|
 |
|
  Y. Dai, A. Lee, L. A. H. Critchley, and P. F. White Does Thromboelastography Predict Postoperative Thromboembolic Events? A Systematic Review of the Literature Anesth. Analg., March 1, 2009; 108(3): 734 - 742. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. T. Ganter and C. K. Hofer Coagulation Monitoring: Current Techniques and Clinical Use of Viscoelastic Point-of-Care Coagulation Devices Anesth. Analg., May 1, 2008; 106(5): 1366 - 1375. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Holte, B. B. Kristensen, L. Valentiner, N. B. Foss, H. Husted, and H. Kehlet Liberal Versus Restrictive Fluid Management in Knee Arthroplasty: A Randomized, Double-Blind Study Anesth. Analg., August 1, 2007; 105(2): 465 - 474. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. M. Howard-Alpe, J. de Bono, L. Hudsmith, W. P. Orr, P. Foex, and J. W. Sear Coronary artery stents and non-cardiac surgery Br. J. Anaesth., May 1, 2007; 98(5): 560 - 574. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. N. Vicenzi, T. Meislitzer, B. Heitzinger, M. Halaj, L. A. Fleisher, and H. Metzler Coronary artery stenting and non-cardiac surgery--a prospective outcome study Br. J. Anaesth., June 1, 2006; 96(6): 686 - 693. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. J. McCrath, E. Cerboni, R. J. Frumento, A. L. Hirsh, and E. Bennett-Guerrero Thromboelastography Maximum Amplitude Predicts Postoperative Thrombotic Complications Including Myocardial Infarction Anesth. Analg., June 1, 2005; 100(6): 1576 - 1583. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. G. Nielsen, R. T. Lyerly III, and W. Q. Gurley The Effect of Dilution on Plasma Coagulation Kinetics Determined by Thrombelastography Is Dependent on Antithrombin Activity and Mode of Activation Anesth. Analg., December 1, 2004; 99(6): 1587 - 1592. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. E. Miller, S. R. Tosone, N. A. Guzzetta, J. L. Miller, and K. K. Brosius Fibrinogen in Children Undergoing Cardiac Surgery: Is It Effective? Anesth. Analg., November 1, 2004; 99(5): 1341 - 1346. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. G. Nielsen, W. Q. Gurley Jr, and T. M. Burch The Impact of Factor XIII on Coagulation Kinetics and Clot Strength Determined by Thrombelastography Anesth. Analg., July 1, 2004; 99(1): 120 - 123. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Boldt, G. Haisch, S. Suttner, B. Kumle, and A. Schellhaass Effects of a new modified, balanced hydroxyethyl starch preparation (Hextend(R)) on measures of coagulation Br. J. Anaesth., November 1, 2002; 89(5): 722 - 728. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. T. McCammon, J. P. Wright, M. Figueroa, and V. G. Nielsen Hemodilution with Albumin, but Not Hextend(R), Results in Hypercoagulability as Assessed by Thrombelastography(R) in Rabbits: Role of Heparin-Dependent Serpins and Factor VIII Complex Anesth. Analg., October 1, 2002; 95(4): 844 - 850. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. J. P. Harnett, K. Bhavani-Shankar, S. Datta, and L. C. Tsen In Vitro Fertilization-Induced Alterations in Coagulation and Fibrinolysis as Measured by Thromboelastography Anesth. Analg., October 1, 2002; 95(4): 1063 - 1066. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Boldt, G. Haisch, S. Suttner, B. Kumle, and F. Schellhase Are Lactated Ringer's Solution and Normal Saline Solution Equal with Regard to Coagulation? Anesth. Analg., February 1, 2002; 94(2): 378 - 384. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. M. Samama Thromboelastography: The Next Step Anesth. Analg., March 1, 2001; 92(3): 563 - 564. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
