Hypothermia Can Cause Errors in Activated Coagulation Time

Kopriva, Charles J.; Sreenivasan, Nandini; Stefansson, S.; Farrell, Debra; Shaffer, W. B.; Geha, Alexander S.

doi:10.1097/00000542-198009001-00085

Cited by 13 publications

(6 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Some studies 83,84 have shown that temperature reductions were associated with significantly prolonged activated clotting time and prolongation of partial thromboplastin time and prothrombin time. Other investigators 85 have recommended the use of warm compresses at a temperature of 49°C to accelerate hemostasis in surgically incurred wounds and that cold compresses to open surgical wounds should be avoided.…”

Section: Effects Of Temperature On Bt and Clotting Time In Normal Malmentioning

confidence: 99%

Nonsurgical bleeding diathesis in anemic thrombocytopenic patients: role of temperature, red blood cells, platelets, and plasma‐clotting proteins

2007

View full text Add to dashboard Cite

Research at the Naval Blood Research Laboratory (Boston, MA) for the past four decades has focused on the preservation of red blood cells (RBCs), platelets (PLTs), and plasma-clotting proteins to treat wounded servicemen suffering blood loss. We have studied the survival and function of fresh and preserved RBCs and PLTs and the function of fresh and frozen plasma-clotting proteins. This report summarizes our peer-reviewed publications on the effects of temperature, RBCs, PLTs, and plasma-clotting proteins on the bleeding time (BT) and nonsurgical blood loss. The term nonsurgical blood loss refers to generalized, systemic bleeding that is not corrected by surgical interventions. We observed that the BT correlated with the volume of shed blood collected at the BT site and to the nonsurgical blood loss in anemic thrombocytopenic patients after cardiopulmonary bypass surgery. Many factors influence the BT, including temperature; hematocrit (Hct); PLT count; PLT size; PLT function; and the plasma-clotting proteins factor (F)VIII, von Willebrand factor, and fibrinogen level. Our laboratory has studied temperature, Hct, PLT count, PLT size, and PLT function in studies performed in non-aspirin-treated and aspirin-treated volunteers, in aspirin-treated baboons, and in anemic thrombocytopenic patients. This monograph discusses the role of RBCs and PLTs in the restoration of hemostasis, in the hope that a better understanding of the hemostatic mechanism might improve the treatment of anemic thrombocytopenic patients. Data from our studies have demonstrated that it is important to transfuse anemic thrombocytopenic patients with RBCs that have satisfactory viability and function to achieve a Hct level of 35 vol percent before transfusing viable and functional PLTs. The Biomedical Excellence for Safer Transfusion (BEST) Collaborative recommends that preserved PLTs have an in vivo recovery of 66 percent of that of fresh PLTs and a life span that is at least 50 percent that of fresh PLTs. Their recommendation does not include any indication that preserved PLTs must be able to function to reduce the BT and reduce or prevent nonsurgical blood loss. One of the hemostatic effects of RBC is to scavenge endothelial cell nitric oxide, a vasodilating agent that inhibits PLT function. In addition, endothelin may be released from endothelial cells, a potent vasoconstrictor substance,to reduce blood flow at the BT site. RBCs, like PLTs at the BT site, may provide arachidonic acid and adenosine diphosphate to stimulate the PLTs to make thromboxane, another potent vasoconstrictor substance and a PLT-aggregating substance. At the BT site, the PLTs and RBCs are activated and phosphatidyl serine is exposed on both the PLTs and the RBCs. FVa and FXa, which generate prothrombinase activity to produce thrombin, accumulate on the PLTs and RBCs. A Hct level of 35 vol percent at the BT site minimizes shear stress and reduces nitric oxide produced by endothelial cells. The transfusion trigger for prophylactic PLT transfusion should consider both the H...

show abstract

Section: Effects Of Temperature On Bt and Clotting Time In Normal Malmentioning

confidence: 99%

Nonsurgical bleeding diathesis in anemic thrombocytopenic patients: role of temperature, red blood cells, platelets, and plasma‐clotting proteins

2007

View full text Add to dashboard Cite

show abstract

“…Few studies have investigated the effect of hypothermia on heparin anticoagulation (5,6,11,12). Despotis et al reported a weak inverse correlation (r = -0.2) between temperature and kaolin or celite automated ACT determination (11).…”

Section: Discussionmentioning

confidence: 99%

“…Historically, when the ACT is above 400 to 480 seconds, it is considered safe to initiate CPB (2,3), but several studies have reported ACT values below 400 seconds at CPB initiation without complications (4). A number of factors other than the heparin, including hypothermia, hemodilution, and platelet function can affect ACT during CPB (5)(6)(7)(8)(9)(10)(11). Paul et al reported that surface cooling to 20'C for 60 minutes in anesthetized dogs without cardiopulmonary bypass provoked a significant decrease in the platelet count and the constant release of a heparin-like factor which reacted identically to heparin as a specific inhibitor of factor Xa (12).…”

Section: Introductionmentioning

confidence: 99%

The Effect of Hypothermia on Heparin Anticoagulation as Measured by Activated Clotting Time and Factor Xa Inhibition

Tian,

Coffin,

Sutton

et al. 1995

J Extra Corpor Technol

View full text Add to dashboard Cite

The effect of hypothermia on heparin anticoagulation was studied using (siliceous earth) activated clotting time (ACT) measured by the modified Hattersley technique and anti-factor Xa assay measured by the modified Teien technique during cardiopulmonary bypass (CPB). Seventeen adult patients with normal blood coagulation function undergoing their first time coronary artery bypass grafting surgery or valve replacement surgery were randomly selected. Blood samples were collected 3-5 minutes after CPB initiation, before cooling at a mean temperature of 32.9°C, and then again after cooling to a mean temperature of 28.4°C. No additional heparin, citrate or packed red blood cells were added to the CPB circuit between sampling points. The mean heparin concentration measured by the anti-factor Xa assay was 4.1 ± 0.5 units/ml before cooling and 4.1 ± 0.4 units/ml after cooling. The mean ACT was 465 ± 75 seconds prior to cooling and 499 ± 69 seconds at the cold temperature (p<0.05). This suggests that the cooling process itself must induce changes in whole blood coagulation resulting in a prolongation in the ACT. The change in ACT with cooling is not due to a change in heparin concentration. The presented data supports previous research on the inadequacy of ACT to trend heparin concentration when steady state conditions are altered.

show abstract

“…Hypothermia itself exerts several anticoagulant effects, the most basic of which is kinetic: decreased temperatures slow the enzyme reactions of the coagulation cascade resulting in prolonged clotting times, regardless of clotting factor levels. Prothrombin time (PT), activated partial thromboplastin time (APTT), and thrombin time (TT) display a negative exponential correlation with temperature (22,23). These kinetic effects are presumably the major factors responsible for the prolonged ACT seen in hypothermic blood independent of heparin concentration.…”

Section: Hypothermia and Effect On Bloodmentioning

confidence: 99%

Use of Aprotinin in Patients Undergoing Deep Hypothermic Circulatory Arrest: A Review

Huffman-Egger

2003

J Extra Corpor Technol

View full text Add to dashboard Cite

Hemostatic derangements continue to be a major clinical challenge during thoracic aortic surgery using deep hypothermic circulatory arrest despite advances in surgical and pharmacologic therapy. Aprotinin, a broad-based, nonspecific serine protease inhibitor has been advocated for prophylactic use in cardiac surgery to decrease perioperative blood loss and blood transfusions. Its efficacy has been documented in several studies throughout the United States and Europe. Currently, aprotinin is advocated for use in patients undergoing cardiopulmonary bypass in the course of coronary artery bypass graft surgery. A review of current studies is provided that examines aprotinin usage under deep hypothermic circulatory arrest.

show abstract

Hypothermia Can Cause Errors in Activated Coagulation Time

Cited by 13 publications

References 0 publications

Nonsurgical bleeding diathesis in anemic thrombocytopenic patients: role of temperature, red blood cells, platelets, and plasma‐clotting proteins

Nonsurgical bleeding diathesis in anemic thrombocytopenic patients: role of temperature, red blood cells, platelets, and plasma‐clotting proteins

The Effect of Hypothermia on Heparin Anticoagulation as Measured by Activated Clotting Time and Factor Xa Inhibition

Use of Aprotinin in Patients Undergoing Deep Hypothermic Circulatory Arrest: A Review

Contact Info

Product

Resources

About