Postoperative Fibrinogen Levels Research Articles

Fibrinogen Supplementation in Cardiac Surgery: Where Are We Now and Where Are We Going?

Fibrinogen Supplementation in Cardiac Surgery: Where Are We Now and Where Are We Going?

Fibrinogen Levels Following Amicar in Surgery for Idiopathic Scoliosis

Prospective evaluation of fibrinogen levels before surgery and after surgery in patients with idiopathic scoliosis undergoing posterior spinal fusion (PSF) and segmental spinal instrumentation (SSI) who received Amicar to decrease perioperative blood loss. To assess a possible association between postoperative fibrinogen levels and Amicar administration. Our previous randomized, double-blind (Amicar and control) study demonstrated a rise in fibrinogen levels on the first postoperative day in the Amicar group, but not in the control group. Fibrinogen levels were not measured on the remaining postoperative days. We subsequently measured fibrinogen levels on all postoperative days in 21 consecutive patients with idiopathic scoliosis and found a dramatic increase throughout the postoperative hospitalization. This study is a continuation of our analysis of postoperative fibrinogen levels. We analyzed fibrinogen levels before surgery and on all postoperative days (4 or 5 days) until discharge in 51 consecutive patients, including our 21 previously reported patients, who received Amicar and underwent a PSF and SSI. We also analyzed the same factors with respect to perioperative blood loss as in our previous Amicar studies. There were 41 females and 10 males with a mean age at surgery of 14.2 +/- 1.8 years. Their mean hospitalization was 4.6 +/- 0.8 days. Their mean estimated intraoperative blood loss was 766 +/- 308 mL and postoperative suction drainage 532 +/- 186 mL for a total perioperative blood loss of 1297 +/- 311 mL. The perioperative transfusion requirements were 0.5 +/- 0.6 U per patient. The preoperative fibrinogen was 255.5 +/- 58.3 mg/dL, and it rose steadily throughout the postoperative period to 680.9 +/- 111.9 mg/dL on the fifth postoperative day. There were no complications related to the use of Amicar. Fibrinogen levels rise steadily throughout the postoperative period. The significance of this increase is unknown. Was it due to the use of Amicar or just the effects of surgery itself? Further investigations will be necessary.

Inflammatory response and platelet activation after off-pump coronary artery bypass surgery

Background. Cardiac surgery induces a systemic inflammatory activation and alterations in the hemostatic cascade. The responses contribute to postoperative complications but may also have protective effects. We investigated the relationship between inflammation, hemostasis and bleeding after off-pump coronary artery bypass surgery (OPCAB). Methods. Ten OPCAB patients were included in a prospective descriptive study. Selected markers of inflammation (IL-6, IL-8, PMN-elastase, C3a, and SC5b-9), and hemostasis (platelet count, β-thromboglobulin, anti-thrombin, D-dimer and fibrinogen) were measured before and immediately after surgery. Postoperative bleeding was registered. Results. Inflammatory variables did not alter significantly during surgery while β-thromboglobulin concentrations increased and anti-thrombin and fibrinogen decreased. There were significant postoperative correlations between PMN-elastase and β-thromboglobulin (r = 0.82, p = 0.004), between PMN-elastase and fibrinogen (r = 0.69, p = 0.03) and between C3a and β-thromboglobulin (r = 0.71, p = 0.02). In addition, there were significant inverse correlations between postoperative bleeding and pre- and postoperative fibrinogen levels (r = − 0.76, p = 0.011 and r = − 0.84, p = 0.002 respectively), between bleeding and postoperative β-thromboglobulin levels (r = − 0.66, p = 0.04) and between bleeding and postoperative PMN-elastase (r = − 0.75, p = 0.01). Conclusions. The results give further evidence for an association between the inflammatory response and hemostasis after cardiac surgery.

Influence of Hypotensive and Normotensive Anesthesia on Platelet Aggregability and Hemostatic Markers in Orthognathic Surgery

This prospective randomized study investigated the influence of normotensive and hypotensive general anesthesia on platelet aggregability, intraoperative blood loss and parameters of plasmatic coagulation during extensive orthognathic surgery. A total of 30 patients were randomly allocated for either normotensive anesthesia maintained by continuous infusion of propofol and remifentanil (NORMO, n=10) or hypotensive anesthesia, whereby hypotension was induced by increasing the infusion rate of remifentanil (HYPO-R, n=10) or by administration of nitroglycerin (HYPO-N, n=10). Whole blood platelet aggregability was significantly reduced during hypotension compared to normotensive anesthesia ( P<.01, HYPO-N and HYPO-R vs. NORMO). Mean arterial blood pressure during hypotension correlated well with adenosinediphosphate- ( R=.712, P<.001) and collagen-induced platelet aggregability ( R=.685, P<.001). Within hypotensive study groups, postoperative fibrinogen levels were significantly different, whereas intraoperative platelet aggregability, postoperative platelet count, prothrombin time, activated partial thromboplastin time and antithrombin levels were not different. Normotensive anesthesia, however, caused significant decreases in platelet count (−29%), prothrombin time (−24%), fibrinogen (−41%) and antithrombin (−28%) and a significant prolongation in activated partial thromboplastin time (+21%) and thrombin time (+18%). There was a trend to reduced intraoperative blood loss in hypotensive study groups; however, differences were not significant. In conclusion, induced hypotension — independent of substances used for induction of hypotension — reduces intraoperative platelet aggregability, subsequently protecting the coagulation system against subclinical consumption coagulopathy. Induced hypotension-caused platelet dysfunction does not lead to an increased intraoperative blood loss, but quite on the contrary shows a trend to reduced intraoperative blood loss, possibly by preventing platelet-induced subclinical consumption coagulopathy.