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Anesthesiology 11/2010; 113(5):1016-8. · 5.36 Impact Factor
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ABSTRACT: Platelets play a central role in primary hemostasis. Analysis of platelet function is therefore a cornerstone in the global assessment of the coagulation status in the perioperative setting, primarily in patients receiving antiplatelet medication, such as cyclooxygenase-1 inhibitors, adenosine diphosphate antagonists and glycoprotein IIb/IIIa inhibitors. In these patients, knowledge of residual platelet function is highly warranted in order to maintain an optimal and individual balance perioperatively between platelet function and inhibition - that is, bleeding and thrombosis. Traditional laboratory-based assays, such as light-transmission aggregometry and flow cytometry, are the clinical standards of platelet function testing today. Light-transmission aggregometry is one of the most widely used tests to identify and diagnose defects in platelet function. The majority of the conventional laboratory-based techniques are labor intensive, costly and time consuming, and require a high degree of experience and expertise to perform and interpret. Therefore, new automated technologies have been developed to measure platelet function more rapidly and easily, and several techniques can be used at the bedside, including whole blood aggregometry, high shear-induced platelet function assessment or viscoelastic measurement techniques. All methods assessing platelet function are summarized and their limitations are discussed in this article, emphasizing their perioperative use.
Expert Review of Medical Devices 09/2010; 7(5):625-37. · 2.63 Impact Factor
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Baillière' s Best Practice and Research in Clinical Anaesthesiology 03/2010; 24(1):vii-viii.
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ABSTRACT: Abnormal coagulation parameters can be found in 25% of trauma patients with major injuries. Furthermore, trauma patients presenting with coagulopathy on admission have worse clinical outcome. Tissue trauma and systemic hypoperfusion appear to be the primary factors responsible for the development of acute traumatic coagulopathy immediately after injury. As a result of overt activation of the protein C pathway, the acute traumatic coagulopathy is characterised by coagulopathy in conjunction with hyperfibrinolysis. This coagulopathy can then be exacerbated by subsequent physiologic and physical derangements such as consumption of coagulation factors, haemodilution, hypothermia, acidemia and inflammation, all factors being associated with ongoing haemorrhage and inadequate resuscitation or transfusion therapies. Knowledge of the different mechanisms involved in the pathogenesis of acute traumatic coagulopathy is essential for successful management of bleeding trauma patients. Therefore, early evidence suggests that treatment directed at aggressive and targeted haemostatic resuscitation can lead to reductions in mortality of severely injured patients.
Baillière' s Best Practice and Research in Clinical Anaesthesiology 03/2010; 24(1):15-25.
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Jérémie Roux,
Michel Carles,
Hidefumi Koh,
Arnaud Goolaerts, Michael T. Ganter,
Brian B. Chesebro,
Marybeth Howard,
Benjamin T. Houseman,
Walter Finkbeiner,
Kevan M. Shokat,
Agnès C. Paquet,
Michael A. Matthay,
Jean-François Pittet
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ABSTRACT: Exogenous or endogenous β2-adrenergic receptor agonists enhance alveolar epithelial fluid transport via a cAMP-dependent mechanism that protects the
lungs from alveolar flooding in acute lung injury. However, impaired alveolar fluid clearance is present in most of the patients
with acute lung injury and is associated with increased mortality, although the mechanisms responsible for this inhibition
of the alveolar epithelial fluid transport are not completely understood. Here, we found that transforming growth factor β1
(TGF-β1), a critical mediator of acute lung injury, inhibits β2-adrenergic receptor agonist-stimulated vectorial fluid and Cl− transport across primary rat and human alveolar epithelial type II cell monolayers. This inhibition is due to a reduction
in the cystic fibrosis transmembrane conductance regulator activity and biosynthesis mediated by a phosphatidylinositol 3-kinase
(PI3K)-dependent heterologous desensitization and down-regulation of the β2-adrenergic receptors. Consistent with these in vitro results, inhibition of the PI3K pathway or pretreatment with soluble chimeric TGF-β type II receptor restored β2-adrenergic receptor agonist-stimulated alveolar epithelial fluid transport in an in vivo model of acute lung injury induced by hemorrhagic shock in rats. The results demonstrate a novel role for TGF-β1 in impairing
the β- adrenergic agonist-stimulated alveolar fluid clearance in acute lung injury, an effect that could be corrected by using
PI3K inhibitors that are safe to use in humans.
Journal of Biological Chemistry 02/2010; 285(7):4278-4290. · 4.77 Impact Factor
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Jérémie Roux,
Michel Carles,
Hidefumi Koh,
Arnaud Goolaerts, Michael T Ganter,
Brian B Chesebro,
Marybeth Howard,
Benjamin T Houseman,
Walter Finkbeiner,
Kevan M Shokat,
Agnès C Paquet,
Michael A Matthay,
Jean-François Pittet
[show abstract]
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ABSTRACT: Exogenous or endogenous beta(2)-adrenergic receptor agonists enhance alveolar epithelial fluid transport via a cAMP-dependent mechanism that protects the lungs from alveolar flooding in acute lung injury. However, impaired alveolar fluid clearance is present in most of the patients with acute lung injury and is associated with increased mortality, although the mechanisms responsible for this inhibition of the alveolar epithelial fluid transport are not completely understood. Here, we found that transforming growth factor beta1 (TGF-beta1), a critical mediator of acute lung injury, inhibits beta(2)-adrenergic receptor agonist-stimulated vectorial fluid and Cl(-) transport across primary rat and human alveolar epithelial type II cell monolayers. This inhibition is due to a reduction in the cystic fibrosis transmembrane conductance regulator activity and biosynthesis mediated by a phosphatidylinositol 3-kinase (PI3K)-dependent heterologous desensitization and down-regulation of the beta(2)-adrenergic receptors. Consistent with these in vitro results, inhibition of the PI3K pathway or pretreatment with soluble chimeric TGF-beta type II receptor restored beta(2)-adrenergic receptor agonist-stimulated alveolar epithelial fluid transport in an in vivo model of acute lung injury induced by hemorrhagic shock in rats. The results demonstrate a novel role for TGF-beta1 in impairing the beta- adrenergic agonist-stimulated alveolar fluid clearance in acute lung injury, an effect that could be corrected by using PI3K inhibitors that are safe to use in humans.
Journal of Biological Chemistry 12/2009; 285(7):4278-90. · 4.77 Impact Factor
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Arnaud Goolaerts,
Jérémie Roux, Michael T Ganter,
Vadim Shlyonsky,
Ahmed Chraibi,
Renauld Stéphane,
Frédérique Mies,
Michael A Matthay,
Robert Naeije,
Sarah Sariban-Sohraby,
Marybeth Howard,
Jean-Francois Pittet
[show abstract]
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ABSTRACT: Hypoxia and epithelial stretch that are commonly observed in patients with acute lung injury have been shown to promote the release of serotonin (5-hydroxytryptamine, 5-HT) in vitro. However, whether 5-HT contributes to the decrease of alveolar epithelial fluid transport, which is a hallmark of lung injury, is unknown. Thus, we investigated the effect of 5-HT on ion and fluid transport across the alveolar epithelium. 5-HT caused a dose-dependent inhibition of the amiloride-sensitive current across primary rat and human alveolar epithelial type II cell monolayers, but did not affect Na(+)/K(+) ATPase function. Furthermore, we found that the 5-HT induced inhibition of ion transport across the lung epithelium was receptor independent, as it was not prevented by the blockade of 5-HT2R (5-HT receptor 2), 5-HT3R (5-HT receptor 3), or by pretreatment with an intracellular calcium-chelating agent, BAPTA-AM (1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetra(acetoxymethyl) ester). In addition, the stimulation of 5-HT1R (5-HT receptor 1), 5-HT2R (5-HT receptor 2), 5-HT4R (5-HT receptor 4), and 5-HT7R (5-HT receptor 7) failed to reproduce the 5-HT effect on amiloride-sensitive sodium transport. We ascertained that 5-HT directly inhibited the function of rat alphabetagamma epithelial sodium channel (ENaC), as determined by heterologous expression of rat ENaC in Xenopus oocytes that do not express endogenous ENaC nor 5-HT receptors (5-HTR). Exposure of mice to hypoxia for 1 hour induced a 30% increase of 5-HT secretion into the distal airways of mice. Finally, the intratracheal instillation of 5-HT inhibited the amiloride-sensitive fraction of alveolar fluid clearance in mice. Together, these results indicate that 5-HT inhibits the amiloride-sensitive fraction of the alveolar epithelial fluid transport via a direct interaction with ENaC, and thus can be an endogenous inhibitor of this ion channel.
American Journal of Respiratory Cell and Molecular Biology 09/2009; 43(1):99-108. · 5.13 Impact Factor
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ABSTRACT: Major trauma is often associated with hemorrhage and transfusion of blood and blood products, which are all associated with adverse clinical outcome. The aim of this review is to emphasize why bleeding and coagulation has to be monitored closely in trauma patients and to discuss the rationale behind modern and future transfusion strategies.
Hemorrhage is a major cause of early death after trauma. Apart from the initial injuries, hemorrhage is significantly promoted by coagulopathy. Early identification of the underlying cause of hemorrhage with coagulation tests (routine and bedside) in conjunction with blood gas analysis allow early goal-directed treatment of coagulation disorders and anemia, thereby stopping bleeding and reducing transfusion requirements. These treatment options have to be adapted to the civilian and noncivilian sector. Transfusion of blood and its components is critical in the management of trauma hemorrhage, but is per se associated with adverse outcome. Decisions must weigh the potential benefits and harms.
Future transfusion strategies are based on early and continuous assessment of the bleeding and coagulation status of trauma patients. This allows specific and goal-directed treatment, thereby optimizing the patient's coagulation status early, minimizing the patient's exposure to blood products, reducing costs and improving the patient's outcome.
Current opinion in anaesthesiology 05/2009; 22(2):305-12.
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ABSTRACT: Recombinant activated factor VII (rFVIIa) is increasingly being given to treat massive bleeding. However, there is no clear guidance on which patients are suitable for treatment and how the effects of treatment should be monitored. The aim of this in vitro study was to assess the coagulation status of severely hemodiluted blood samples before and after treatment with therapeutic doses of rFVIIa and/or fibrinogen with 2 viscoelastic point-of-care coagulation analyzers: ROTEM (Pentapharm GmbH, Munich, Germany) and Sonoclot (Sienco Inc, Arvada, CO).
Laboratory study.
Research coagulation laboratory.
Ten healthy male volunteers without hereditary or acquired coagulation disorders.
Blood samples were obtained. After severe hemodilution with albumin 5%, therapeutic doses of rFVIIa and/or fibrinogen were added, and the coagulation status was assessed with new 1:1,000 diluted tissue factor-activated tests from ROTEM and Sonoclot.
The administration of therapeutic doses of rFVIIa to hemodiluted samples shortened the initiation phase of coagulation only. Isolated fibrinogen administration to physiologic levels improved both the initiation of coagulation as well as clot formation and strength. Combined fibrinogen and rFVIIa administration further improved both effects.
ROTEM and Sonoclot were able to monitor the effects of rFVIIa and fibrinogen administration with 1:1,000 diluted tissue factor-activated tests. The efficacy of rFVIIa was largely dependent on the presence of high levels of fibrinogen in reversing this severe dilutional coagulopathy.
Journal of cardiothoracic and vascular anesthesia 11/2008; 22(5):675-80. · 1.06 Impact Factor
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Michael T Ganter,
Jérémie Roux,
George Su,
Susan V Lynch,
Clifford S Deutschman,
Yoram G Weiss,
Sarah C Christiaans,
Byron Myazawa,
Eric Kipnis,
Jeanine P Wiener-Kronish,
Marybeth Howard,
Jean-François Pittet
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ABSTRACT: Pseudomonas aeruginosa is an opportunistic pathogen that can cause severe pneumonia associated with airspace flooding with protein-rich edema in critically ill patients. The type III secretion system is a major virulence factor and contributes to dissemination of P. aeruginosa. However, it is still unknown which particular bacterial toxin and which cellular pathways are responsible for the increase in lung endothelial permeability induced by P. aeruginosa. Thus, the first objective of this study was to determine the mechanisms by which this species causes an increase in lung endothelial permeability. The results showed that ExoS and ExoT, two of the four known P. aeruginosa type III cytotoxins, were primarily responsible for bacterium-induced increases in protein permeability across the lung endothelium via an inhibition of Rac1 and an activation of the RhoA signaling pathway. In addition, inhibition of the alphavbeta5 integrin, a central regulator of lung vascular permeability, prevented these P. aeruginosa-mediated increases in albumin flux due to endothelial permeability. Finally, prior activation of the stress protein response or adenoviral gene transfer of the inducible heat shock protein Hsp72 also inhibited the damaging effects of P. aeruginosa on the barrier function of lung endothelium. Taken together, these results demonstrate the critical role of the RhoA/alphavbeta5 integrin pathway in mediating P. aeruginosa-induced lung vascular permeability. In addition, activation of the stress protein response with pharmacologic inhibitors of Hsp90 may protect lungs against P. aeruginosa-induced permeability changes.
American Journal of Respiratory Cell and Molecular Biology 09/2008; 40(1):108-18. · 5.13 Impact Factor
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ABSTRACT: Perioperative monitoring of blood coagulation is critical to better understand causes of hemorrhage, to guide hemostatic therapies, and to predict the risk of bleeding during the consecutive anesthetic or surgical procedures. Point-of-care (POC) coagulation monitoring devices assessing the viscoelastic properties of whole blood, i.e., thrombelastography, rotation thrombelastometry, and Sonoclot analysis, may overcome several limitations of routine coagulation tests in the perioperative setting. The advantage of these techniques is that they have the potential to measure the clotting process, starting with fibrin formation and continue through to clot retraction and fibrinolysis at the bedside, with minimal delays. Furthermore, the coagulation status of patients is assessed in whole blood, allowing the plasmatic coagulation system to interact with platelets and red cells, and thereby providing useful additional information on platelet function. Viscoelastic POC coagulation devices are increasingly being used in clinical practice, especially in the management of patients undergoing cardiac and liver surgery. Furthermore, they provide useful information in a large variety of clinical scenarios, e.g., massive hemorrhage, assessment of hypo- and hypercoagulable states, guiding pro- and anticoagulant therapies, and in diagnosing of a surgical bleeding. A surgical etiology of bleeding has to be considered when viscoelastic test results are normal. In summary, viscoelastic POC coagulation devices may help identify the cause of bleeding and guide pro- and anticoagulant therapies. To ensure optimal accuracy and performance, standardized procedures for blood sampling and handling, strict quality controls and trained personnel are required.
Anesthesia and analgesia 06/2008; 106(5):1366-75. · 3.08 Impact Factor
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ABSTRACT: Coagulopathy is present at admission in 25% of trauma patients, is associated with shock and a 5-fold increase in mortality. The coagulopathy has recently been associated with systemic activation of the protein C pathway. This study was designed to characterize the thrombotic, coagulant and fibrinolytic derangements of trauma-induced shock.
This was a prospective cohort study of major trauma patients admitted to a single trauma center. Blood was drawn within 10 minutes of arrival for analysis of partial thromboplastin and prothrombin times, prothrombin fragments 1 + 2 (PF1 + 2), fibrinogen, factor VII, thrombomodulin, protein C, plasminogen activator inhibitor-1 (PAI-1), thrombin activatable fibrinolysis inhibitor (TAFI), tissue plasminogen activator (tPA), and D-dimers. Base deficit was used as a measure of tissue hypoperfusion.
Two hundred eight patients were studied. Systemic hypoperfusion was associated with anticoagulation and hyperfibrinolysis. Coagulation was activated and thrombin generation was related to injury severity, but acidosis did not affect Factor VII or PF1 + 2 levels. Hypoperfusion-induced increase in soluble thrombomodulin levels was associated with reduced fibrinogen utilization, reduction in protein C and an increase in TAFI. Hypoperfusion also resulted in hyperfibrinolysis, with raised tPA and D-Dimers, associated with the observed reduction in PAI-1 and not alterations in TAFI.
Acute coagulopathy of trauma is associated with systemic hypoperfusion and is characterized by anticoagulation and hyperfibrinolysis. There was no evidence of coagulation factor loss or dysfunction at this time point. Soluble thrombomodulin levels correlate with thrombomodulin activity. Thrombin binding to thrombomodulin contributes to hyperfibrinolysis via activated protein C consumption of PAI-1.
The Journal of trauma 06/2008; 64(5):1211-7; discussion 1217. · 2.48 Impact Factor
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ABSTRACT: The aim of this study was to compare the following approaches to assess left ventricular preload by transesophageal echocardiography (TEE): left ventricular end-diastolic volume index (LVEDVI) determined by using the method of disc summation (LVEDVI(Md)) and left ventricular end-diastolic area index (LVEDAI) were compared with LVEDVI assessed by the modified Simpson formula (LVEDVI(Si)). Global end-diastolic volume index (GEDVI) and stroke volume index (SVI) measured by the PiCCO(plus) system (Pulsion Medical Systems, Munich, Germany) were used as TEE-independent reference variables.
Prospective observational study.
Community hospital.
Twenty-two patients undergoing elective cardiac surgery.
After the induction of anesthesia, hemodynamic assessment by TEE and the PiCCO(plus) system was made 20 (T(1)) and 10 minutes (T(2)) before and 10 (T(3)) and 20 minutes (T(4)) after a fluid trial. At each time point, LVEDVI(Md), LVEDAI, LVEDVI(Si), GEDVI, and SVI were determined.
The fluid trial resulted in a significant increase of all preload variables measured at T(3). At T(4), all preload variables but LVEDVI(Md) showed a significant decrease. The mean bias +/- 2 SD for percent changes (Delta) of LVEDVI(Md) - DeltaLVEDVI(Si) was 1.5% +/- 59.0% and for DeltaLVEDAI - Delta LVEDVI(Si) 0.9% +/- 23.6%. The correlation between LVEDVI(Md) and LVEDVI(Si) was significantly weaker than between LVEDAI and LVEDVI(Si) (p < 0.001). Comparing TEE measurements with GEDVI and SVI, strong correlations were observed for LVEDAI and LVEDVI(Si) only.
The method of disc summation cannot be recommended for preload assessment during a fluid challenge in cardiac surgery patients. By contrast, single-plane area measurements provided reliable information when compared with the application of the modified Simpson formula.
Journal of cardiothoracic and vascular anesthesia 05/2008; 22(2):236-42. · 1.06 Impact Factor
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Michael T Ganter,
Jérémie Roux,
Byron Miyazawa,
Marybeth Howard,
James A Frank,
George Su,
Dean Sheppard,
Shelia M Violette,
Paul H Weinreb,
Gerald S Horan,
Michael A Matthay,
Jean-François Pittet
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ABSTRACT: Interleukin (IL)-1beta has previously been shown to be among the most biologically active cytokines in the lungs of patients with acute lung injury (ALI). Furthermore, there is experimental evidence that lung vascular permeability increases after short-term exposure to IL-1 protein, although the exact mechanism is unknown. Therefore, the objective of this study was to determine the mechanisms of IL-1beta-mediated increase in lung vascular permeability and pulmonary edema following transient overexpression of this cytokine in the lungs by adenoviral gene transfer. Lung vascular permeability increased with intrapulmonary IL-1beta production with a maximal effect 7 days after instillation of the adenovirus. Furthermore, inhibition of the alphavbeta6 integrin and/or transforming growth factor-beta attenuated the IL-1beta-induced ALI. The results of in vitro studies indicated that IL-1beta caused the activation of transforming growth factor-beta via RhoA/alphavbeta6 integrin-dependent mechanisms and the inhibition of the alphavbeta6 integrin and/or transforming growth factor-beta signaling completely blocked the IL-1beta-mediated protein permeability across alveolar epithelial cell monolayers. In addition, IL-1beta increased protein permeability across lung endothelial cell monolayers via RhoA- and alphavbeta5 integrin-dependent mechanisms. The final series of in vivo experiments demonstrated that pretreatment with blocking antibodies to both the alphavbeta5 and alphavbeta6 integrins had an additive protective effect against IL-1beta-induced ALI. In summary, these results demonstrate a critical role for the alphavbeta5/beta6 integrins in mediating the IL-1beta-induced ALI and indicate that these integrins could be a potentially attractive therapeutic target in ALI.
Circulation Research 05/2008; 102(7):804-12. · 9.49 Impact Factor
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ABSTRACT: To measure plasma levels of angiopoietin-1 (Ang-1), angiopoietin-2 (Ang-2), and vascular endothelial growth factor (VEGF) early after trauma and to determine their clinical significance.
Angiopoietins and VEGF play a central role in the physiology and pathophysiology of endothelial cells. Ang-2 has recently been shown to have pathogenetic significance in sepsis and acute lung injury. Little is known about the role of angiopoietins and VEGF early after trauma.
Blood specimens from consecutive major trauma patients were obtained immediately upon arrival in the emergency department and plasma samples assayed for Ang-1, Ang-2, VEGF, markers of endothelial activation, protein C pathway, fibrinolytic system, and complement. Base deficit was used as a measure of tissue hypoperfusion. Data were collected prospectively.
Blood samples were obtained from 208 adult trauma patients within 30 minutes after injury before any significant fluid resuscitation. Plasma levels of Ang-2, but not Ang-1 and VEGF were increased and correlated independently with severity of injury and tissue hypoperfusion. Furthermore, plasma levels of Ang-2 correlated with markers of endothelial activation, coagulation abnormalities, and activation of the complement cascade and were associated with worse clinical outcome.
Ang-2 is released early after trauma with the degree proportional to both injury severity and systemic hypoperfusion. High levels of Ang-2 were associated with an activated endothelium, coagulation abnormalities, complement activation, and worse clinical outcome. These data indicate that Ang-2 is a marker and possibly a direct mediator of endothelial activation and dysfunction after severe trauma.
Annals of Surgery 03/2008; 247(2):320-6. · 7.49 Impact Factor
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ABSTRACT: Early coagulopathy after traumatic brain injury (TBI) is thought to be the result of injury-mediated local release of tissue factor, although the precise mechanisms that cause hypoperfusion and early systemic coagulopathy in TBI patients are unknown. We have previously reported that early systemic coagulopathy after trauma is present only when tissue injury is associated with severe hypoperfusion leading to the activation of the protein C pathway. However, the role of hypoperfusion as an important mechanism for the development of coagulopathy early after TBI is unclear. The objective of the present study was to determine the importance of hypoperfusion and protein C activation in causing early coagulopathy in TBI patients.
We performed a prospective cohort study including patients with isolated brain injury admitted to a single trauma center. Blood was drawn on average 32 minutes after injury. Plasma samples were assayed for protein C and thrombomodulin by standard laboratory techniques. Routine coagulation measures (prothrombin time, partial thromboplastin time) and arterial blood gas analysis were performed concurrently. Severe hypoperfusion was evidenced by the presence of an arterial base deficit greater than 6.
Thirty-nine TBI patients were included in the study during a 15-month period. TBI patients without concurrent hypoperfusion (n = 28) did not develop an early coagulopathy after trauma, no matter the severity of injury. In contrast, patients with TBI who also had severe hypoperfusion (BD >6) (n = 11) were coagulopathic early after injury. Indeed, these patients had higher prothrombin time and partial thromboplastin time, compared with those with TBI and a BD <6 (17.6 +/- 3.6 vs. 14.3 +/- 2.3, p < 0.005; and 43.13 +/- 18.3 vs. 27.4 +/- 3.8, p < 0.0001). Unactivated protein C levels were lower in the TBI group with BD >6 (56 +/- 32 vs. 85 +/- 35, p = 0.03) and thrombomodulin levels were significantly higher (48 +/- 26 vs. 35 +/- 10, p = 0.04). Without hypoperfusion, there was no effect of increasing brain injury on protein C pathway or fibrinolysis pathway mediators.
TBI alone does not cause early coagulopathy, but must be coupled with hypoperfusion to lead to coagulation derangements, associated with the activation of the protein C pathway. This novel finding has significant implications for the treatment of coagulopathy after severe brain injury.
The Journal of trauma 01/2008; 63(6):1254-61; discussion 1261-2. · 2.48 Impact Factor
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ABSTRACT: To continuously measure arterial blood gases (ABGs), to calculate the percentage of anticipated changes over time, and to develop recommendations for sampling frequencies of arterial blood gases in patients undergoing thoracoscopic surgery.
Prospective, observational clinical trial.
University hospital.
43 consecutive elective patients undergoing thoracoscopic surgery with one-lung ventilation.
A Paratrend 7 probe for continuous arterial partial pressure of oxygen and arterial partial pressure of carbon dioxide measurement was introduced through a radial artery cannula in the awake patient before surgery. Data were collected throughout the procedure until patients left the operating room. Afterward, time courses of arterial blood gas values were transformed into frequency space by fast Fourier transform analysis, and the expected deviations in arterial blood gases were calculated over time.
Forty-three consecutive patients undergoing thoracoscopic surgery were included, and arterial blood gas values were measured during a total of 141.5 h. Critical arterial partial pressure of oxygen values <or=60 mmHg were recorded in 16 patients for a total of 4.5 hours. Fourier amplitude spectra showed comparable characteristics of arterial partial pressure of oxygen and arterial partial pressure of carbon dioxide time courses in all patients. It takes only 5, 10, or 20 minutes for the arterial partial pressure of oxygen to change 10%, 20%, or 40%, respectively (95% confidence).
Current standards to monitor arterial blood gases are not sufficient to detect and prevent hypoxemic events during thoracoscopic surgery with one-lung ventilation. Intermittent arterial blood gas analyses must be performed more frequently, up to every 10 minutes, to detect changes of 20% in arterial partial pressure of oxygen.
Journal of Clinical Anesthesia 12/2007; 19(8):569-75. · 1.21 Impact Factor
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ABSTRACT: In vivo data for the kaolin-based ACT test from the Sonoclot Analyzer (SkACT, Sienco Inc, Arvada, CO) are lacking. The aim of this study was to compare SkACT with an established kaolin-based ACT from Hemochron (HkACT) and anti-Xa activity in patients undergoing cardiopulmonary bypass (CPB).
Prospective observational study.
Community hospital.
Fifty patients scheduled for elective cardiac surgery.
Blood samples were taken before CPB at baseline (T0) and after heparinization (T1 and T2), on CPB after administration of aprotinin (5, 15, 30, 60 minutes; T3-T6), and at the end after protamine infusion (T7).
A total of 375 blood samples were analyzed. ACT measurements were comparable for SkACT and HkACT at each measurement time point. Overall bias +/- standard deviation between SkACT and HkACT was -19 +/- 75 seconds (-2.4% +/- 11.7%). Mean bias between SkACT and HkACT at each time point ranged from -35 to 3 seconds (-4.5% to 2.6%) and showed no statistical significance over time. Heparin sensitivity of SkACT and HkACT, defined as (ACT(Tx)-ACT(T0))/(anti-Xa(Tx)-anti-Xa(T0)), significantly increased for measurements during CPB (p < 0.001) but without significant difference between the 2 methods. Test variability was comparable for both ACT measurement techniques. Overall test variability was 7.5% +/- 7.4% for SkACT and 7.8% +/- 11% for HkACT.
Accuracy and performance of SkACT and HkACT were comparable for heparin monitoring in patients undergoing CPB for elective cardiac surgery. However, both tests were affected significantly after initiating CPB and aprotinin infusion.
Journal of Cardiothoracic and Vascular Anesthesia 08/2007; 21(4):524-8. · 1.64 Impact Factor
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ABSTRACT: Complement activation has been reported after major trauma. However, little is known about the clinical relevance and the mechanisms of complement activation early after trauma. Therefore, the aim of this study was to measure complement activation, to identify the roles of injury severity and hypoperfusion, to determine the predominant activated pathway, and to identify the clinical significance of early complement activation in trauma patients. A total of 208 adult trauma patients were enrolled in this prospective single-center cohort study of major trauma patients. Blood samples were obtained within 30 min after injury before any significant fluid resuscitation. Complement (C5b-9) was activated early after trauma, correlated with injury severity and tissue hypoperfusion, and was associated with increased mortality rate and with the development of organ failure such as acute lung injury and acute renal failure. The alternative pathway seems to be the predominant activated complement pathway early after trauma. However, the classical and/or the lectin pathway initiated complement activation because of the correlation between plasma levels of C4d and C3a/C5b-9. Finally, in patients with low C3a levels, C5b-9 levels correlated with plasma levels of prothrombin fragments 1 + 2, a marker of thrombin generation, suggesting additional C3-independent complement activation by thrombin after severe trauma. In summary, complement activation via its amplification by the alternative pathway is observed early after trauma and correlates with injury severity, tissue hypoperfusion, and worse clinical outcomes. Besides complement activation by the classical and/or lectin pathways, there is an independent association between thrombin generation and complement activation.
Shock 08/2007; 28(1):29-34. · 2.85 Impact Factor
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ABSTRACT: Several less invasive cardiac output monitoring techniques are now commercially available and have the potential to replace the pulmonary artery catheter under certain clinical circumstances. The aim of this review is to give a synopsis of the currently available cardiac output measurement methods. This information should help in selecting the appropriate technique in a particular clinical setting.
An overview is given of the currently available techniques for cardiac output monitoring. Recent validation studies demonstrate that pulse wave analysis may be used reliably as an alternative to the pulmonary artery catheter in different clinical settings. The use of transesophageal echocardiography and Doppler measurements is limited due to high operator dependency, the partial carbon dioxide rebreathing technique should be applied in a precisely defined clinical setting to mechanically ventilated patients only, and pulsed dye densitometry as well as the bioimpedance technique are currently primarily applied in an investigational setting.
Less invasive cardiac output monitoring techniques may replace the pulmonary artery catheter in different clinical settings considering the specific properties of these techniques. The pulmonary artery catheter, however, may still be recommended for cardiac output measurement in specific clinical situations when monitoring of pulmonary artery pressures is desirable.
Current opinion in critical care 07/2007; 13(3):308-17. · 2.67 Impact Factor
