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At least 379 records · Page 21Linked to original sources
PubMed2003

Modified rapid deployment hemostat bandage reduces blood loss and mortality in coagulopathic pigs with severe liver injury.

BACKGROUND: Hemostasis can be difficult to achieve after blunt abdominal trauma, especially if the patient is coagulopathic. The U.S. Food and Drug Administration has recently approved a hemostatic dressing for treating bleeding after extremity trauma (RDH bandage; Marine Polymer Technologies, Cambridge, MA). It has not been evaluated for internal bleeding after trauma. We redesigned this dressing for internal use, and then tested whether this modified bandage (Miami-modified Rapid Deployment Hemostat) could achieve hemostasis when used as an adjunct to standard laparotomy pad packing in a pig model of severe liver injury with coagulopathy. METHODS: Anesthetized swine (35-45 kg) received an isovolemic 45% blood volume replacement with refrigerated Hextend (6% hetastarch). Core body temperature was maintained at 33-34 degrees C with intra-abdominal ice packs. A coagulopathic condition was documented by thromboelastography. At this point a severe liver injury was induced by the avulsion of the left lateral hepatic lobe, then the pigs were randomized to treatment with either standard abdominal packing (control) or packing plus Miami-modified Rapid Deployment Hemostat. Two series of experiments were conducted. In series one (n = 14), the abdomen was closed and the animals were observed with no resuscitation. After one hour, the abdomen was opened, the packing was removed and the presence of bleeding was noted. In series two (n = 10), the abdomen was closed and the animal resuscitated with one unit of blood plus as much lactated Ringers intravenous fluid (IVF) as required to maintain a mean arterial pressure (MAP) > 70 mm Hg. After one hour, the packing was removed, the abdomen closed, and data were collected for an additional two hours. RESULTS: Series one: 6/7 animals in the control group had continued bleeding at one hour; 1/7 animals in the treatment group had active bleeding (p = 0.0291). Series two: With control vs. Miami-modified Rapid Deployment Hemostat, the three-hour survival was zero vs. 80% (p = 0.0476). The total blood loss was 1.2 +/- 0.1 vs. 0.3 +/- 0.1 mL/kg/min (p = 0.001) and the IVF requirement was 1.6 +/- 0.3 vs. 0.6 +/- 0.3 mL/kg/min (p = 0.026). CONCLUSIONS: The Miami-modified Rapid Deployment Hemostat bandage significantly reduced mortality, blood loss, and fluid requirements when used as an adjunct to standard abdominal packing following severe liver injury in coagulopathic pigs [corrected].

Animals↗
PubMed2005

Independent contributions of hypothermia and acidosis to coagulopathy in swine.

BACKGROUND: Clinical coagulopathy occurs frequently in the presence of acidosis and hypothermia. The purpose of this study was to determine the relative contributions of acidosis and hypothermia to coagulopathy, as measured by current standard bedside and clinical laboratory analyses (i.e., bleeding time and prothrombin time). In addition, we investigated possible mechanisms of these effects using a modified prothrombin time test, thromboelastography, and thrombin kinetics analyses. An improved understanding of coagulopathy should facilitate hemorrhage control. METHODS: Twenty-four pigs were randomly allocated into normal (pH, 7.4; 39 degrees C), acidotic (pH, 7.1; 39 degrees C), hypothermic (pH, 7.4; 32 degrees C), and acidotic and hypothermic (pH, 7.1; 32 degrees C) combined groups. Acidosis was induced by the infusion of 0.2N hydrochloric acid in lactated Ringer's solution. Hypothermia was induced by using a blanket with circulating water at 4 degrees C. Development of a clinical coagulopathy was defined as a significant increase in splenic bleeding time. Measurements were compared before (pre) and 10 minutes after (post) the target condition was achieved. RESULTS: Acidosis, hypothermia, or both caused the development of coagulopathy, as indicated by 47%, 57%, and 72% increases in splenic bleeding time (p < 0.05, pre vs. post). Plasma fibrinogen concentration was decreased by 18% and 17% in the acidotic and combined groups, respectively, but not in the hypothermic group. Hypothermia caused a delay in the onset of thrombin generation, whereas acidosis primarily caused a decrease in thrombin generation rates. At 4 minutes' quench time, thrombin generation in the acidotic, hypothermic, and combined groups were 47.0%, 12.5%, and 5.7%, respectively, of the value in the control group. There were no changes in serum tumor necrosis factor-alpha and interleukin-6 in any group during the study. CONCLUSION: Acidosis and hypothermia cause a clinical coagulopathy with different thrombin generation kinetics. These results confirm the need to prevent or correct hypothermia and acidosis and indicate the need for improved techniques to monitor coagulopathy in the trauma population.

Acidosis↗
PubMed2006

Prehospital HBOC-201 after traumatic brain injury and hemorrhagic shock in swine.

BACKGROUND: Data are limited on the actions of hemoglobin based oxygen carriers (HBOCs) after traumatic brain injury (TBI). This study evaluates neurotoxicity, vasoactivity, cardiac toxicity, and inflammatory activity of HBOC-201 (Biopure, Cambridge, Mass.) resuscitation in a TBI model. METHODS: Swine received TBI and hemorrhage. After 30 minutes, resuscitation was initiated with 10 mL/kg normal saline (NS), followed by either HBOC-201 (6 mL/kg, n = 10) or NS control (n = 10). Supplemental NS was administered to both groups to maintain mean arterial pressure (MAP) >60 mm Hg until 60 minutes, and to maintain cerebral perfusion pressure (CPP) >70 mm Hg from 60 to 300 minutes. The control group received mannitol (1 g/kg) and blood (10 mL/kg) at 90 minutes and half (n = 5) received CPP directed phenylephrine (PE) therapy after 120 minutes. Serum cytokines were measured with ELISA and coagulation was evaluated with thromboelastography. Brains were harvested for neuropathology. RESULTS: With HBOC administration, MAP, CPP, and brain tissue PO2 were restored within 30 minutes and maintained until 300 minutes. Clot strength and fibrin formation were maintained and 9/10 successfully extubated. In contrast, with control, MAP and brain tissue PO2 did not correct until 120 minutes, after mannitol, transfusion and 40% more crystalloid. Furthermore, without PE, CPP did not reach target and 0/5 could be extubated. Lactate, heart rate, cardiac output, mixed venous oxygenation, muscle oxygenation, serum cytokines, and histology did not differ between groups. CONCLUSIONS: After TBI, a single HBOC-201 bolus with minimal supplements provided rapid resuscitation, while maintaining CPP and improving brain oxygenation, without causing cardiac dysfunction, coagulopathy, cytokine release, or brain structural changes.

Analysis of Variance↗
PubMed2003

Adverse outcome of human islet-allogeneic blood interaction.

BACKGROUND: A report of inflammatory damage when islets come into contact with allogeneic blood prompted us to confirm the finding. METHODS: Fresh handpicked human islets were incubated in blood group matched, nonsensitized allogeneic blood. Destruction was quantified by assaying the supernatants for proinsulin release and by blood clot histology. The effect on global hemostasis was assessed by thromboelastography (TEG), and heparin-bonded tubing was used to assess the effect on blood cellular counts. In separate experiments, islets were incubated in allogeneic blood with heparin or Reopro (monoclonal anti-GpIIbIIIa). Islets were also incubated in serum, and cryosections were stained for C1q, C4, C3, C5b-9, immunoglobulin (Ig)M, and IgG binding using immunohistochemistry. RESULTS: Histologic assessment showed severe destruction in 37% of islets in contact with allogeneic blood versus none in controls and a sevenfold increase in proinsulin release from controls (n = 6)(P < 0.005). TEG (n = 11) showed accelerated coagulation in the presence of islets (P < 0.001). Analysis of blood cellular counts (n = 3) showed consumption of platelets, neutrophils, and monocytes in the presence of islets (P < 0.001). Inhibition of coagulation with heparin (n = 3) or inhibition of platelet aggregation with Reopro (n = 3), separately or together (n = 3), did not make a substantial improvement in the destruction in terms of histology or proinsulin release. Immunohistochemical staining (n = 4) revealed C1q, C4, C3, and C5b-9 deposition along with IgG binding. IgM binding was weak if anything. CONCLUSION: This study confirms and extends the finding that human islet-allogeneic blood interaction results in significant destruction of islet tissue with activation of the coagulation cascade and platelet, neutrophil, and monocyte consumption. There was evidence for activation of complement by the classical pathway along with IgG binding.

Abciximab↗
PubMed2003

A novel therapeutic approach combining human plasma-derived Factors VIIa and X for haemophiliacs with inhibitors: evidence of a higher thrombin generation rate in vitro and more sustained haemostatic activity in vivo than obtained with Factor VIIa alone.

BACKGROUND AND OBJECTIVES: Therapy with recombinant Factor VIIa (rFVIIa) for haemophiliacs with inhibitors still has some unresolved problems, such as the requirement for frequent infusions of rFVIIa every 2-3 h to sustain haemostatic activity for an extended time-period and that the therapeutic dose of rFVIIa is not always predictable. In the present study, we searched for an effective combination of plasma-derived FVIIa with other blood coagulation factors, and demonstrated that a therapeutic approach combining plasma-derived FVIIa and Factor X (FX) was more useful for treating haemophiliacs with inhibitors than FVIIa alone. MATERIALS AND METHODS: The haemostatic effects of FVIIa and FX were evaluated in vitro and in vivo. In in vitro experiments we assessed the following: the ability to enhance the thrombin generation rate in a reconstituted blood coagulation model without Factor VIII (FVIII) or Factor IX (FIX); the ability to correct the activated partial prothrombin time (APTT) of FVIII-depleted plasma or FIX-depleted plasma; and the ability to correct the clotting time of haemophilia-like whole blood using thromboelastography (TEG). In in vivo experiments, the haemostatic activity of the combination treatment of FVIIa and FX was determined by measuring the bleeding time and TEG using a monkey haemophilia B model produced by the injection of anti-human FIX polyclonal antibodies. The degree of thrombogenicity of the combination was evaluated using the rabbit stasis model. RESULTS: The addition of FX to FVIIa dramatically enhanced the thrombin generation rate in the reconstituted blood coagulation model and corrected the prolonged APTTs of FVIII- and FIX-depleted plasmas to levels achieved by the replacement therapies. In contrast, the addition of prothrombin to FVIIa did not show such enhancing activity. Furthermore, FVIIa-induced whole blood clotting times in the FVIII- and FIX-inhibited states were also shortened by the addition of FX in a concentration-dependent manner. Finally, the co-administration of FVIIa (80 microg/kg) and FX (800 microg/kg) in a monkey haemophilia B model resulted in a more robust and persistent haemostatic effect on the secondary bleeding time and whole-blood clotting time of TEG than that of FVIIa alone. The results of rabbit stasis tests for evaluating the risk of thrombogenicity showed that the combination of FVIIa and FX was less thrombogenic than FEIBA. CONCLUSIONS: The present study demonstrated that the combination of FVIIa and FX appeared to have a higher and more sustainable haemostatic potential than FVIIa alone, and less thrombogenicity than FEIBA. A therapeutic approach combining FVIIa and FX could be a promising and novel approach to compensate for the disadvantages of rFVIIa and FEIBA for haemophiliacs with inhibitors.

Animals↗
PubMed2005

Spinal anaesthesia despite combined clopidogrel and aspirin therapy in a patient awaiting lung transplantation: effects of platelet transfusion on clotting tests.

The risk of central neuraxial blockade in patients treated with newer antiplatelet drugs is unclear. We report the case of a woman awaiting lung transplantation who presented for emergency groin surgery. She had recently undergone a coronary artery stent implantation and was treated with both clopidogrel and aspirin. Despite this dual antiplatelet therapy, uneventful spinal anaesthesia was administered following platelet transfusion. While thromboelastography was of no help in assessing the degree of anticoagulation, the effects of platelet transfusion were reflected by adenosine diphosphate and epinephrine aggregometry. Thus, in selected patients, platelet transfusion may be appropriate to enable central neuraxial blockade when deemed necessary.

Anesthesia, Spinal↗
PubMed2006

Basic aspects of bypassing agents.

Bypassing agents consist of activated prothrombin complex concentrates (aPCC) and recombinant factor VIIa (rFVIIa). Their main utilization is for prevention and treatment of bleeding complications, which may occur in inhibitor-developing haemophiliacs, although new indications for rFVIIa (e.g. trauma-related and cerebral bleeds) are now under evaluation in clinical trials. The mechanisms of action for these agents are still not fully understood. The relative complexity of the composition of aPCC suggests the possibility of multiple modes of action for achieving haemostasis. Among those possibilities, the contributions of activated factor X and prothrombin have been demonstrated in recent years both in vitro and in animal models for the only aPCC which remains on the market. rFVIIa also exhibits a complex mode of action, improving coagulation through both tissue factor-dependent and -independent pathways. The various mechanisms that occur at the cellular surfaces, particularly on the outer leaflet of the platelet membrane, primarily contribute to Xase complex formation and thrombin generation. The ways in which these agents affect the complex kinetics of fibrin formation at the site of vascular damage need further clarification, although significant progress has been achieved in the last 10 years. In addition, the ex vivo monitoring that would reflect achievement of haemostasis in vivo is still not standardized, although several attempts using thromboelastography, thrombin generation and the kinetics of fibrin formation have been initiated.

Blood Coagulation↗
PubMed2006

Coagulation patterns following haemoglobin-based oxygen carrier resuscitation in severe uncontrolled haemorrhagic shock in swine.

Massive blood loss due to penetrating trauma and internal organ damage can cause severe haemorrhagic shock (HS), leading to a severely compromised haemostatic balance. This study evaluated the effect of bovine polymerized haemoglobin (Hb) (Hb-based oxygen carrier, HBOC) resuscitation on haemostasis in a swine model of uncontrolled HS. Following liver injury/HS, swine received HBOC (n= 8), Hextend (HEX) (n= 8) or no resuscitation (NON) (n= 8). Fluids were infused to increase mean arterial pressure above 60 mmHg and to reduce heart rate to baseline. At 4 h, the animals were eligible for blood transfusions. Prothrombin time (PT), activated partial thromboplastin time, fibrinogen, thromboelastography (TEG) and platelet function analyser closure time (PFA-CT) were compared by using mixed statistical model. At 4 h, blood loss (% estimated blood volume) was comparable for HBOC (65.5 +/- 18.5%) and HEX (80.8 +/- 14.4%) and less for NON (58.7 +/- 10.1%; P < 0.05). Resuscitation-induced dilutional coagulopathy was observed with HBOC and HEX, as indicated by reduced haematocrit, platelets and fibrinogen (P < 0.05). At 4 h, PT was higher in HEX than in HBOC groups (P < 0.01). In the early hospital phase, a trend to increased TEG reaction time and PFA-CT indicates that dilutional effects persist in HBOC and HEX groups. PFA-CT returned to baseline later with HBOC than with HEX (48 vs. 24 h) following blood transfusion. At 4 h, all surviving HEX animals (n= 3) required transfusion, in contrast to no HBOC (n= 7) or NON (n= 1) animals. In this severe uncontrolled HS model, successful resuscitation with HBOC produced haemodilutional coagulopathy less than or similar to that produced by resuscitation with HEX.

Abdominal Injuries↗
PubMed1995

Perioperative autotransfusion and functional coagulation analysis in total hip replacement.

Functional coagulation analyses like Sonoclot and thromboelastography have not been evaluated during perioperative autotransfusion. We have prospectively studied three different transfusion regimes in 45 patients undergoing total hip arthroplasty. Blood losses were replaced either with heterologous erythrocyte concentrate (group I), intra- and postoperative autotransfusion of blood salvaged with cellsaver technique (group II) or predonated autologous erythrocyte concentrates together with salvaged blood (group III). Routine and functional coagulation analyses with a Sonoclot were performed preoperatively, 6 hours postoperatively (6 h), day 1-5 and 10. An early postoperative hypo- and late postoperative hypercoagulative phase could be detected with Sonoclot signs of platelet function and fibrin deposition in all groups. Sonoclot coagulation analyses better correlated to both blood loss and dextran dosage than APTT and platelet count in the routine coagulation analyses. Functional coagulation analysis has a potential use in individualizing plasmasubstitution and thromboprophylaxis regimes during autotransfusion in THR.

Blood Coagulation↗
PubMed1981

Sodium valproate, platelet dysfunction, and bleeding.

The antiepileptic drug sodium valproate (VPA) can provoke a thrombocytopenia or platelet dysfunction, with or without hemorrhages. These unwanted side effects are probably infrequent or, at least, have little clinical importance except in patients undergoing surgery. Thromboelastography appears to be a reliable screening test. As hematological abnormalities are often dose related, VPA dosages greater than 40 mg/kg/day are not advised.

Blood Platelet Disorders↗
PubMed1977

Conjugated equine oestrogens and blood clotting: a follow-up report.

A follow-up study of blood clotting and platelet aggregation was performed on 21 women who had received long-term hormone replacement treatment with conjugated equine oestrogens. The prothrombin time and factor VII and X values were significantly accelerated after three months, but there was no further increase with continual administration for 18 months. After 12 to 18 months' treatment, however, thrombin-induced platelet aggregation (Chandler's tube) was also significantly accelerated, which suggested a widening spectrum of effect. No overall acceleration of "intrinsic" clotting (partial thromboplastin time and thromboelastography) was found during the study, but the relatively small numbers may have been responsible. Further efforts are therefore required to find formulations and doses of oestrogens which, while relieving menopausal symptoms, cause less acceleration of blood clotting and platelet aggregation.

Blood Coagulation↗
PubMed2006

Does calcium cause the different effects of Gelofusine and Haemaccel on coagulation?

BACKGROUND: Gelofusine (which does not contain calcium) has a greater effect on coagulation than Haemaccel (which contains 6.25 mmol/l of calcium). This in vitro study was performed to assess whether calcium might be the cause of the different effects on coagulation. METHODS: Three solutions were compared; (a) Gelofusine, (b) Gelofusine with calcium added to 6.25 mmol/l, and (c) Haemaccel. Thromboelastography (Sonoclot) was used to examine whole blood coagulation, with time to peak clot weight as the primary outcome measure. RESULTS: There was no significant difference between the Gelofusine containing solutions. Both Gelofusine solutions gave a greater impairment of coagulation than the Haemaccel solution. CONCLUSIONS: The different effect of Gelofusine on coagulation compared with Haemaccel does not seem to be related to the different calcium contents of the solutions.

Blood Coagulation↗
PubMed1967

Hypofibrinogenaemia in metastatic carcinoma of the prostate: suppression of systemic fibrinolysis by haparin.

In a patient with generalized prostatic carcinoma and hypofibrinogenaemia heparin infusion on four occasions abolished systemic fibrinolysis as determined by euglobulin clot lysis time, bovine fibrin plate assay, thromboelastography, and immunoelectrophoretic demonstration of fibrinogen split products. The pathogenesis of hypofibrinogenaemia in cases of prostatic carcinoma and the possibility of a direct heparin effect on fibrinolysis are discussed. Despite the lack of histological evidence for intravascular coagulation, the findings are considered additional evidence for the view that fibrinolysis in this syndrome may be secondary to intravascular coagulation.

Afibrinogenemia↗
PubMed1973

Experimental hypercalcaemia and whole blood clotting.

Experimental hypercalcaemia was induced in rats by (1) transplantation of the solid Walker 256 tumour, and (2) intraperitoneal injections of calcium gluconate. Whole blood clotting was studied by means of thromboelastography and whole blood clotting times in polystyrene and glass test tubes. At serum calcium levels between 10.3 and 11.5 m-equiv/l a slight delay in clot formation was found which was reversible by the addition of EDTA to whole blood. Acute, calcium-gluconate-induced hypercalcaemia, however, leads to a significant shortening of the clotting time in the polystyrene tube and to a lesser degree in the glass tube. Maximal factor XII activation in vitro with ellagic acid levels the difference of clotting times again. From these experiments it is concluded that acute hypercalcaemia induces a hypercoagulable state, possibly by partial contact activation, and thus may favour thrombus formation in vivo.

Animals↗
PubMed1995

Hyperfibrinolysis during intracranial surgery: effect of high dose aprotinin.

A patient undergoing intracranial surgery developed disseminated intravascular coagulation with life threatening peroperative bleeding. Thromboelastography established the diagnosis of hyperfibrinolysis, usually a fatal complication of a neurosurgical operation. With the administration of a high dose regimen of aprotinin (Trasylol) the haemorrhage was controlled and the hyperfibrinolytic state reversed. Evaluation of blood samples from the jugular bulb suggested that there was a pronounced local release of tissue plasminogen activator into the circulation.

Aged↗
PubMed1997

Haemostatic changes during surgery for primary brain tumours.

OBJECTIVE: Primary brain tumours may be associated with coagulation disorders which can pose intraoperative and postoperative management difficulties. The aim was to evaluate the coagulation profile of patients with brain tumours undergoing surgery using thromboelastography (TEG) in combination with simple laboratory tests. METHODS: Fifty adult patients with primary brain tumours larger than 4 cm in maximum diameter and no history of coagulation disorders were studied in a prospective, observational manner over a one year period. Preoperative, intraoperative, and postoperative measurements included haemoglobin concentration, platelet count, prothrombin and partial thromboplastin times, fibrin(ogen) degradation product concentration, D-dimer concentration, and TEG. RESULTS: Eleven patients (22%) had abnormal intraoperative TEGs, of whom six (12%) subsequently developed haematomas requiring surgical evacuation. The coagulopathy seemed to be hyperfibrinolysis in two cases (4%) and disseminated intravascular coagulation in four (8%). There was no preoperative difference in reaction time (R time) for clot formation between the non-haematoma and haematoma groups(mean 11.44 (SD 3.42) v 12.33 (2.50) min, P=0.46). However, when other preoperative indices were compared, in the non-haematoma group, K time (time to reach a clot amplitude of 20 mm) was shorter (6.72 (2.15) v 10.56 (3.50) min, P=0.001), rate of clot growth (å) was faster (43.67 degrees (7.53) v 27.11 degrees (5.42), P<0.0001) and maximum amplitude of clot strength (MA) was greater (52.64 (7.85) v 40.33 (6.59) mm, P<0.001). Intraoperatively, R time was significantly shortened in the non-haematoma group, (7.67 (1.78) min, P<0.0001) unlike the haematoma group (10.67 (1.58) minutes, P=0.11). CONCLUSIONS: Although these results indicate a general hypercoagulability during brain tumour surgery, in certain cases, a predisposition towards hypocoagulability may exist even before surgery, detectable only when the physical characteristics of clot formation are studied by TEG. Judicious replacement of clotting factors, platelets, and antifibrinolytic agents should be considered intraoperatively if the TEG is abnormal, without waiting for laboratory test results.

Adolescent↗
PubMed1999

Clinical utility of available methods for determining platelet function.

Determination of platelet function has become increasingly important as new antiplatelet drugs are being developed. Objective means to monitor the pharmacological effects of these agents, in order to maximize efficacy and minimize toxicity, is needed. The available methods for determination of platelet function at the current time are reviewed, including platelet aggregometry, the PFA-100, flow cytometry, platelet contractile force, the rapid platelet function assay, the clot signature analyzer, Sonoclot, and thromboelastography. The principle, advantages, disadvantages, and clinical utility of each method is presented. The uses of the various methods of determining platelet function reported in the literature are summarized, in an effort to provide information regarding the applicability of those different methods.

Humans↗
PubMed1974

Correction of the haemostatic defect in haemophiliacs without apparent correction of the coagulation defect.

The evaluation of microhaematuria may be considered as a measure of the haemostatic defect of haemophiliacs in nonhaemorrhagic periods. In order to study the relationship between coagulation disorder and haemostatic defect we have administered small amounts (1 U and 3 U/kg) of AHG and of factor IX (1U/kg) to 12 haemophiliacs (20 A and 2 B) and we have examined the effects on coagulation and microhaematuria. Microhaematuria was determined by the measurement of urinary radioactivity/24 h, after infusion of autologous RBC labelled with 51-Cr, for 11 consecutive days (4 days before and 7 after the administration). Coagulation was investigated by thromboelastography, PTT, Quick's time, PCI, factor VIII and IX activity assays, fibrinogen assay, and euglobulin lysis time. During the period of investigation, the patients remained in bed. In controls, factor VIII administration did not affect microhaematuria. On the other hand, in all haemophiliacs, factor VIII and IX administration significantly reduced microhaematuria, although the administered dose was not able to modify the coagulation defect. In all subjects the reduction of microhaematuria lasted at least 5 days. The correction of the haemostatic defect, without improvement of the clotting disorder, and its persistence for several days suggest that factor VIII is involved in the composition of the vascular wall and in its functional integrity. Moreover, on the basis of these results it is possible to carry out a rational prophylaxis of the haemorrhagic episodes using small doses of factor VIII, be determining the duration of the correction of the haemostatic defect for each subject.

Blood Coagulation↗