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DOI: 10.1055/s-0028-1092870
© Thieme Medical Publishers
Hemostasis and Thrombosis in Critically Ill Patients
Publication History
Publication Date:
27 October 2008 (online)
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A large number of critically ill patients will develop hemostasis and thrombosis issues during their clinical course. These problems may vary from excessive blood loss due to a myriad of causes; to widespread intravascular fibrin formation and consequent multiple organ dysfunction as a result of systemic inflammation; to the development of venous thromboembolic complications. Some patients will present with simultaneous bleeding and thrombotic complications, which will render the appropriate treatment even more complex. Both anticoagulant and prohemostatic drugs belong to the most frequently prescribed agents for patients in the intensive care unit (ICU).[1] [2] In addition, in critically ill patients, coagulation abnormalities often occur. A variety of changes, such as thrombocytopenia, prolonged global coagulation tests, reduced levels of coagulation inhibitors, or high levels of fibrin split products, may reflect various disease mechanisms. Also, some patients may have a marked coagulopathy that is not readily revealed by routine coagulation tests. In all cases, a proper differential diagnosis is required, as various underlying causes may require totally different therapeutic approaches. In this issue of Seminars in Thrombosis and Hemostasis, various topics regarding the diagnostic and therapeutic management of hemostasis and thrombosis issues in critically ill patients are discussed.
Thrombocytopenia is frequently seen in patients in the ICU and has a broad differential diagnosis. Thrombocytopenia seems to be a highly relevant finding, as it has a strong prognostic value and may point to various underlying disorders where each may require a specific therapeutic strategy. The diagnostic workup of thrombocytopenia in critically ill patients and the management of each of the underlying causes is discussed in the article by Levi and Löwenberg.[3]
A specific and often confusing cause of thrombocytopenia is heparin-induced thrombocytopenia. This complication of heparin treatment is relatively often seen in the ICU and is discussed by Selleng and colleagues in this issue.[4] The authors provide a series of very practical algorithms that may be helpful for clinicians in the (differential) diagnosis of this disease and may guide proper treatment.
Several major surgical procedures may be complicated by excessive blood loss, which will cause significant morbidity, increase the risk of reoperations, and may even affect mortality. Levy and Tanaka discuss the various prohemostatic agents that may be helpful a adjunctive treatment in these complex clinical situations.[5] These authors conclude that based on current needs to reduce perioperative blood loss, hemostatic agents offer important therapeutic options to manage critically ill surgical patients in the perioperative setting but also that further investigations into the safety of these agents should be conducted.
In the diagnostic workup of critically ill patients, speed may be of utmost importance. In patients with excessive bleeding or rapidly deranging coagulation, waiting for even 1 hour for coagulation laboratory results may be inadequate, as the clinical picture may change very rapidly, and more immediate monitoring may be required. Bedside coagulation tests by point of care devices has recently been developed and is gaining increasing attention. The various tests and their accuracy as well as other issues related to point of care testing in critically ill patients are discussed by Dempfle and Borggrefe in this issue.[6] The authors conclude that indeed point of care coagulation assays in critical care medicine may be necessary if centralized laboratory facilities are not able to provide coagulation diagnostics within a satisfactory time frame. There are marked differences in the diagnostic and therapeutic approach for bleeding and thrombosis in critically ill children compared with that in adults in the ICU. Kenet and colleagues discuss the management of these issues in critically ill children.[7] In their excellent review, these authors provide practical guidance based on new insights into the pathogenesis of various coagulation disorders and thrombotic complications in children.
In recent years, the role of natural anticoagulant pathways, such as antithrombin or the protein C system, in the pathogenesis and management of sepsis and other diseases associated with a systemic inflammatory state has attracted considerable attention. It has been shown that natural anticoagulants possess a crucial position at the crossroads of inflammatory and coagulation pathways, and this has set the stage for the application of anticoagulant factor concentrates as a treatment modality in critically ill patients. Levi and van der Poll discuss the pathogenetic importance of natural anticoagulants and the efficacy and safety of anticoagulant concentrates in clinical trials.[8]
As critical illness seems to be a major risk factor for the development of venous thromboembolism, adequate thromboprophylaxis is indicated for patients in the ICU. Crowther and Cook discuss the incidence, clinical presentation, and consequences of venous thrombosis and pulmonary embolism in critically ill patients.[9] In addition, they review the efficacy of preventive strategies, including (low molecular weight) heparin and mechanical devices. They conclude that venous thromboembolism is a common and largely unrecognized complication of critical illness and is associated with adverse patient outcomes. Evidence about the effectiveness of thromboprophylaxis in the critically ill is limited but suggests efficacy similar to that seen outside the ICU.
Finally, Hofstra and colleagues discuss recently obtained insights into the role of bronchoalveolar hemostasis in the pathogenesis of acute lung injury, including pneumonia and adult respiratory distress syndrome.[10] Interestingly, these results seem to lead to new treatment strategies for patients with acute lung injury, as supported by experimental studies.[11] [12] Ongoing clinical trials on the effects of natural inhibitors of coagulation in patients with acute lung injury will provide further knowledge on the optimal strategy to treat activation of pulmonary coagulation and fibrin formation.
Taken together, the various articles in this issue of Seminars in Thrombosis and Hemostasis provide a nice overview of different topics regarding the pathogenesis and management of coagulation abnormalities in critically ill patients. It is gratifying to see how many new insights have been gained during the past years and how quickly some of these findings have been translated into new treatment strategies, most of which are now being evaluated in clinical trials. I would like to thank the authors of the articles in this issue for their excellent contributions.
REFERENCES
- 1 Levi M, Opal S M. Coagulation abnormalities in critically ill patients. Crit Care. 2006; 10 222-228
- 2 Mannucci P M, Levi M. Prevention and treatment of major blood loss. N Engl J Med. 2007; 356 2301-2311
- 3 Levi M, Löwenberg E C. Thrombocytopenia in critically ill patients. Semin Thromb Hemost. 2008; 34 417-424
- 4 Selleng K, Selleng S, Greinacher A. Heparin-induced thrombocytopenia in intensive care patients. Semin Thromb Hemost. 2008; 34 425-438
- 5 Levy J H, Tanaka K A. Prohemostatic agents to prevent perioperative blood loss. Semin Thromb Hemost. 2008; 34 439-444
- 6 Dempfle C E, Borggrefe M. Point of care coagulation tests in critically ill patients. Semin Thromb Hemost. 2008; 34 445-450
- 7 Kenet G, Strauss T, Kaplinsky C, Paret G. Hemostasis and thrombosis in critically ill children. Semin Thromb Hemost. 2008; 34 451-458
- 8 Levi M, van der Poll T. The role of natural anticoagulants in the pathogenesis and management of systemic activation of coagulation and inflammation in critically ill patients. Semin Thromb Hemost. 2008; 34 459-468
- 9 Crowther M, Cook D. Preventing venous thromboembolism in critically ill patients. Semin Thromb Hemost. 2008; 34 469-474
- 10 Hofstra J J, Haitsma J J, Juffermans N P, Levi M, Schultz M J. The role of bronchoalveolar hemostasis in the pathogenesis of acute lung injury. Semin Thromb Hemost. 2008; 34 475-484
- 11 Choi G, Vlaar A P, Schouten M et al.. Natural anticoagulants limit lipopolysaccharide-induced pulmonary coagulation but not inflammation. Eur Respir J. 2007; 30 423-428
- 12 Choi G, Hofstra J J, Roelofs J J et al.. Antithrombin inhibits bronchoalveolar activation of coagulation and limits lung injury during Streptococcus pneumoniae pneumonia in rats. Crit Care Med. 2008; 36 204-210