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Preventing and managing bleeding complications in anticoagulated patients: A case based approach
Thrombosis Research (2008) 123, S42–S45
www.elsevier.com/locate/thromres
REGULAR ARTICLE
Preventing and managing bleeding complications in anticoagulated patients: A case based approach Mark Crowther Division of Hematology, McMaster University, 1200 Main Street West, Hamilton, Ontario, Canada L8N 4A6 Available online 1 October 2008
Abstract Bleeding is the most common complication of anticoagulant therapy. Despite the frequency of its occurrence, little evidence is available to guide the care of anticoagulated patients with, or at high risk of, bleeding. This article attempts, using a case based format, to describe common clinical scenarios encountered by clinicians who manage anticoagulated patients and who are bleeding. The paper is “case based” and narrative since there is little evidence to guide practice in this area. © 2008 Published by Elsevier Ltd.
Introduction Anticoagulation is effective for the prevention and treatment of both arterial and venous thromboembolism. Anticoagulant therapy produces bleeding complications in a roughly dose-dependent fashion; as anticoagulation is intensified (as a result of increasing doses or due to the use of multiple antithrombotic agents) the risk of bleeding further increases. The risk of bleeding varies both with the types of anticoagulant and as a result of patients characteristics. This qualitative review will focus on bleeding manifestations; their prediction, prevention and treatment and will provide anecdotally based treatment recommendations.
irregular heart rhythm. She has recently been discharged from the hospital after an admission during which she was identified to have extensive bowel angiodysplasia which caused a hemodynamically significant lower gastrointestinal bleed. At present there is no evidence of active bleeding, the hemoglobin is stable and she is taking only hydrochlorothiazide for mild hypertension. She has no prior history of stroke or transient ischemic attack, no prior history of diabetes or known cardiac disease and is healthy and active. You consider whether this patient should be started on warfarin for primary prevention of atrialfibrillation associated arterial thromboembolism?
Discussion
Case 1 A 76-year-old woman presents to the office as a result of palpitations - on examination she has an irregularly E-mail address: [email protected]. 0049-3848/$ - see front matter © 2008 Published by Elsevier Ltd. doi:10.1016/j.thromres.2008.08.015
Consensus conference recommendations suggest that patients with atrial fibrillation be considered for anticoagulant therapy to reduce their risk of systemic embolism [1]. This recommendation is based on the results of a series of methodologically rigorous large
Bleeding with warfarin randomized trials which evaluated clinically relevant outcomes, including stroke and bleeding, in a wide variety of types of patients presenting with atrial fibrillation. Various scales exist to grade the risk of atrial fibrillation associated stroke [2]. Using such scales this patients would probably be graded to have "low to low-moderate risk" atrial fibrillation and consensus statements would recommend that warfarin use be considered based on her age and the presence of hypertension. However, in considering the use of anticoagulants it is important to balance the benefits (presumed reduction in the risk of stroke) against the risks (which consist largely of bleeding). This patient had a recent major bleed requiring hospital admission. Such episodes of bleeding are associated significant mortality when they occur in patients receiving warfarin - rates may approach 20% and be associated with long-term morbidity [3]. In this patient the most responsible physician should firstly seek remediable causes of atrial fibrillation such as hyperthyroidism. If identified, treatment of these causes may end the atrial fibrillation thus eliminate the need for anticoagulant therapy. Interventional cardiology procedures may effectively treat some forms of atrial fibrillation thus eliminating the need for ongoing anticoagulation - it is important to note, however, that simple rate control is as effective as attempted rhythm control when evaluated in large studies suggesting that pharmaceutical rhythm control does not obviate the need for consideration of anticoagulation [4]. Patients with persistent, clinically important bleeding sources may be considered for elective surgical or endoscopic correction prior to the initiation of warfarin anticoagulation: in this particular patient the angiodysplasia presents an important ongoing risk for bleeding. Irrespective of the presence of anticoagulation patients with such bleeding sources may be candidates for surgical colectomy to reduce their future risk of additional hemorrhage. Colectomy would allow the safe introduction of warfarin to this patient. In the absence of specific efforts to ameliorate the risk of bleeding the likelihood that this patient will suffer major, catastrophic or life-threatening bleeding as a result of warfarin anticoagulation is sufficiently high that warfarin should not be initiated. Decision-making should occur in concert with the patient and their family and should take into account their preferences. Although aspirin is somewhat effective for the prevention of stroke it will also increase the risk of bleeding. The true riskbenefit impact of aspirin in a patient such as that presented here is unknown. My personal preference
S43 in this patient would be to initiate aspirin at a dose of 81 mg per day and advise her that this therapy is likely to increase somewhat her risk of bleeding.
Case 2 A 52-year-old woman with a mechanical mitral valve inserted as a result of rheumatic fever presents to the clinic with a history of three recent episodes of epistaxis requiring nasal packing. She is very disturbed by this bleeding and has stopped taking her warfarin about two weeks ago.
Discussion Although there is little data to guide clinicians in making decisions about the risks of thromboembolism in patients with mechanical heart valves who are not receiving warfarin it is generally felt that the risk of thromboembolism is lowest in patients with newer valves in the aortic position, higher in those with mitral valves, and highest in those with older types of mitral valves with or without concomitant atrial fibrillation or left atrial enlargement. Most experts would suggest that this patient has a significant risk of arterial embolism if anticoagulants are not resumed. As a result, counseling and recommendations should focus on ensuring that the patient is fully apprised of the risk of thromboembolism and of strategies which may reduce the risk of bleeding. Epistaxis is frequently due to the use of central heating without appropriate humidification - this results in drying of the nasal mucosa with a predisposition to epistaxis. Use of topical moisturizing agents or increased humidification are simple steps which eliminate epistaxis and thus allow conflict-free reintroduction of warfarin. Medically important epistaxis, due to structural abnormalities or arteriovenous malformations may be amenable to surgical interventions. Use of agents such as intranasal DDAVP are untested in this circumstance and may produce a systemic hypercoagulable state placing the patient at increased risk of valvular thrombosis or systemic embolization. As a result, their use cannot be recommended. In this particular patient, appropriate management consists of ensuring the patient is aware of the relative risks and benefits of various treatment options, apprising the patient of the likely clinical outcome of epistaxis (inconvenience, occasional visits to the emergency department and the potential need for surgical intervention) against the potential outcomes of inadequate anticoagulant therapy in the setting of a mitral valve (valvular thrombosis and systemic embolization with a very
S44 significant risk of long-term morbidity or death). If the patient continues to refuse warfarin therapy it may be prudent to obtain and document a second opinion with regards to her care in the case that a systemic embolism or valve thrombosis does occur. Aspirin is not known to be beneficial in this setting and it may cause or contribute to bleeding; however, its use might be considered if warfarin reinstitution is refused by the patient.
Case 3 A 56-year-old male with a recent pulmonary embolism (complicating knee replacement surgery performed three weeks ago) presents with hypotension in the setting of massive hematemesis. The patient's INR value is 4.7. Emergency endoscopy demonstrates a large duodenal ulcer with a visible vessel. Endoscopic therapy is applied and the bleeding appears to stop. What is the optimal management to prevent further bleeding?
Discussion The anticoagulant effect of warfarin should be reversed using intravenous vitamin K and coagulation factor replacement - either in the form of an appropriate amount of fresh frozen plasma (probably six to eight units) or prothrombin complex concentrate [5]. Failure to completely reverse the INR may place the patient at increased risk of recurrent bleeding: failure to administer vitamin K may result in "rebound anticoagulation" after initial correction due to the persistent anticoagulant effect of warfarin. Resumption of anticoagulation should be delayed until healing of the ulcer is documented - this is likely to take a period of weeks or months. During this time reinstitution of warfarin is likely to be associated with an unacceptable risk of recurrent bleeding and its associated morbidity and mortality, as discussed in a prior case. During the period of warfarin interruption the patient will be at high risk of recurrent deep vein thrombosis and/or pulmonary embolism. Placement of a temporary inferior vena cava filter should be strongly considered as it is likely to reduce the risk of pulmonary embolism. A filter which is removable after a period of weeks or months would be preferred as the duration of the filter placement is likely to be significant. Some filters are only approved for removal after one to two weeks; after this time removal is not recommended. It is important, however, that if healing of the ulcer is documented the patient (a) have an attempted removal of the filter and (b) resume anticoagulant
M. Crowther therapy promptly as inferior vena cava filters probably increase the risk of deep vein thrombosis with associated worsening leg symptomatology.
Case four A 92-year-old woman receiving warfarin for prevention of stroke in the setting of atrial fibrillation, a prior transient ischemic attack, known enlarged left atrium and moderate valvular disease secondary to rheumatic fever presents with a hypotension and melena stool. She has been previously quite well except as noted above. The melena stool began approximately 1 week ago. On initial examination or hemoglobin is 8.6 g per liter with a mean corpuscular volume of 62 fL (normal 85 to 100 fL).
Discussion This patient has several risk factors for stroke and the use of warfarin for long-term primary prophylaxis of stroke would be strongly recommended by consensus conferences. However, the patient has evidence of both acute bleeding (in the form of melena stool) and chronic blood loss (in the form of microcytic anemia). It is probable that she has a gastrointestinal malignancy as the cause of her presentation. This patient should have her warfarin interrupted, should have their INR corrected as noted above and should be promptly evaluated for colonic malignancy. While awaiting surgery anticoagulants are contraindicated however surgery should be expedited to minimize the risk of stroke. If surgery is performed then reinstitution of warfarin anticoagulation is indicated immediately upon hemostasis being assured. Reinstitution of warfarin before surgical correction of the malignancy is likely to be associated with bleeding which may be associated with significant morbidity and/or mortality. Alternate strategies such as the use of aspirin and/or low-dose unfractionated heparin have been proposed however their safety (as indicated by their relative propensity to cause bleeding, compared with warfarin) and efficacy (as indicated by their ability to prevent stroke) in this setting have not been evaluated in methodologically rigorous studies.
Case five A 24 year old male presents is transported to your tertiary care hospital from a peripheral centre. 5 days prior he had been in a motor vehicle accident and had suffered a splenic laceration – 24 hours before he had a cardiopulmonary arrest ultimately proven to be due to saddle pulmonary embolism. He
Bleeding with warfarin received thrombolytic therapy and is transferred for further care. Twelve hours after arrival he develops hypotension (systolic BP 65 mmHg) and passes voluminous bright red blood per rectum. His APTT is 97 seconds.
Discussion A standardized approach to the management of life threatening bleeding has recently been published [5]. This patient requires urgent hemodynamic support with vasopressors until adequate fluid, colloid and red cell resuscitation can be provided. In the absence of evidence of dilutional coagulopathy plasma has no role in the management of this case as it does not reverse the anticoagulant effect of heparin. Protamine should be administered; although an estimated dose can be arrived at using a variety of formulae in this case a dose of 50 mg will probably reverse the anticoagulant of heparin within minutes of its administration. To evaluate correction, the APTT should be checked 5 to 10 minutes after protamine is administered and if the aAPTT is persistently prolonged additional protamine should be administered. The source of the bleeding should be sought using endoscopic, radiological or surgical techniques (whichever can be arranged most quickly) – bleeding should not be attributed to the heparin therapy rather the mechanical cause must be identified and corrected. Given the proximity to the pulmonary embolism a temporary IVC filter should be placed – however this should only be done after required life saving therapies have been administered (for example, placement of the filter should not delay heparin reversal or evaluation of the source of blood loss, both of which are more immediately life-preserving than the filter). Anticoagulation should be reinstituted as soon as the bleeding source has been identified and corrected and once hemostasis is ensured – the filter should then be removed as quickly as possible to avoid complications associated with prolonged IVC interruption and to increase the likelihood of filter removal. Currently only about 20% of “temporary” filters are actually removed. [6]
Summary Preventing and managing bleeding in patients who are receiving anticoagulant therapy should consist of
S45 an initial assessment of the risk of bleeding prior to the initiation of anticoagulation, an assessment of the relative risks of clinically apparent bleeding and thromboembolism in the individual patient with the passage of time, and appropriate (oftentimes emergent) management of bleeding complications. Fundamental principles include considering the important mortality and morbidity risk associated with bleeding in patients receiving anticoagulation and a careful consideration of measures which may ameliorate the risk of bleeding in an individual patient.
Conflicts of interest Dr Crowther has received an honorarium for serving on an advisory board for a manufacturer of a prothrombin complex concentrate.
Acknowledgements Dr Crowther is a career investigator of the Heart and Stroke Foundation of Canada.
References [1] Singer DE, Albers GW, Dalen JE, Go AS, Halperin JL, Manning WJ, et al. Antithrombotic therapy in atrial fibrillation: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest Sep 2004;126(3 Suppl):429S–56S. [2] Gage BF, Waterman AD, Shannon W, Boechler M, Rich MW, Radford MJ. Validation of clinical classification schemes for predicting stroke: results from the National Registry of Atrial Fibrillation. JAMA Jun 13 2001;285(22):2864–70. [3] Linkins LA, Choi PT, Douketis JD. Clinical impact of bleeding in patients taking oral anticoagulant therapy for venous thromboembolism: a meta-analysis.[see comment]. Ann Intern Med Dec 2 2003;139(11):893–900. [4] de Denus S, Sanoski CA, Carlsson J, Opolski G, Spinler SA. Rate vs rhythm control in patients with atrial fibrillation: a meta-analysis. Arch Intern Med 2005 Feb 14;165(3):258–62. [5] Crowther MA, Warkentin TE. Bleeding risk and the management of bleeding complications in patients undergoing anticoagulant therapy: focus on new anticoagulant agents. Blood Feb 2009;28. [6] Karmy-Jones R, Jurkovich GJ, Velmahos GC, Burdick T, Spaniolas K, Todd SR, et al. Practice patterns and outcomes of retrievable vena cava filters in trauma patients: an AAST multicenter study. J Trauma Jan 2007;62(1):17–24.
www.elsevier.com/locate/thromres
REGULAR ARTICLE
Preventing and managing bleeding complications in anticoagulated patients: A case based approach Mark Crowther Division of Hematology, McMaster University, 1200 Main Street West, Hamilton, Ontario, Canada L8N 4A6 Available online 1 October 2008
Abstract Bleeding is the most common complication of anticoagulant therapy. Despite the frequency of its occurrence, little evidence is available to guide the care of anticoagulated patients with, or at high risk of, bleeding. This article attempts, using a case based format, to describe common clinical scenarios encountered by clinicians who manage anticoagulated patients and who are bleeding. The paper is “case based” and narrative since there is little evidence to guide practice in this area. © 2008 Published by Elsevier Ltd.
Introduction Anticoagulation is effective for the prevention and treatment of both arterial and venous thromboembolism. Anticoagulant therapy produces bleeding complications in a roughly dose-dependent fashion; as anticoagulation is intensified (as a result of increasing doses or due to the use of multiple antithrombotic agents) the risk of bleeding further increases. The risk of bleeding varies both with the types of anticoagulant and as a result of patients characteristics. This qualitative review will focus on bleeding manifestations; their prediction, prevention and treatment and will provide anecdotally based treatment recommendations.
irregular heart rhythm. She has recently been discharged from the hospital after an admission during which she was identified to have extensive bowel angiodysplasia which caused a hemodynamically significant lower gastrointestinal bleed. At present there is no evidence of active bleeding, the hemoglobin is stable and she is taking only hydrochlorothiazide for mild hypertension. She has no prior history of stroke or transient ischemic attack, no prior history of diabetes or known cardiac disease and is healthy and active. You consider whether this patient should be started on warfarin for primary prevention of atrialfibrillation associated arterial thromboembolism?
Discussion
Case 1 A 76-year-old woman presents to the office as a result of palpitations - on examination she has an irregularly E-mail address: [email protected]. 0049-3848/$ - see front matter © 2008 Published by Elsevier Ltd. doi:10.1016/j.thromres.2008.08.015
Consensus conference recommendations suggest that patients with atrial fibrillation be considered for anticoagulant therapy to reduce their risk of systemic embolism [1]. This recommendation is based on the results of a series of methodologically rigorous large
Bleeding with warfarin randomized trials which evaluated clinically relevant outcomes, including stroke and bleeding, in a wide variety of types of patients presenting with atrial fibrillation. Various scales exist to grade the risk of atrial fibrillation associated stroke [2]. Using such scales this patients would probably be graded to have "low to low-moderate risk" atrial fibrillation and consensus statements would recommend that warfarin use be considered based on her age and the presence of hypertension. However, in considering the use of anticoagulants it is important to balance the benefits (presumed reduction in the risk of stroke) against the risks (which consist largely of bleeding). This patient had a recent major bleed requiring hospital admission. Such episodes of bleeding are associated significant mortality when they occur in patients receiving warfarin - rates may approach 20% and be associated with long-term morbidity [3]. In this patient the most responsible physician should firstly seek remediable causes of atrial fibrillation such as hyperthyroidism. If identified, treatment of these causes may end the atrial fibrillation thus eliminate the need for anticoagulant therapy. Interventional cardiology procedures may effectively treat some forms of atrial fibrillation thus eliminating the need for ongoing anticoagulation - it is important to note, however, that simple rate control is as effective as attempted rhythm control when evaluated in large studies suggesting that pharmaceutical rhythm control does not obviate the need for consideration of anticoagulation [4]. Patients with persistent, clinically important bleeding sources may be considered for elective surgical or endoscopic correction prior to the initiation of warfarin anticoagulation: in this particular patient the angiodysplasia presents an important ongoing risk for bleeding. Irrespective of the presence of anticoagulation patients with such bleeding sources may be candidates for surgical colectomy to reduce their future risk of additional hemorrhage. Colectomy would allow the safe introduction of warfarin to this patient. In the absence of specific efforts to ameliorate the risk of bleeding the likelihood that this patient will suffer major, catastrophic or life-threatening bleeding as a result of warfarin anticoagulation is sufficiently high that warfarin should not be initiated. Decision-making should occur in concert with the patient and their family and should take into account their preferences. Although aspirin is somewhat effective for the prevention of stroke it will also increase the risk of bleeding. The true riskbenefit impact of aspirin in a patient such as that presented here is unknown. My personal preference
S43 in this patient would be to initiate aspirin at a dose of 81 mg per day and advise her that this therapy is likely to increase somewhat her risk of bleeding.
Case 2 A 52-year-old woman with a mechanical mitral valve inserted as a result of rheumatic fever presents to the clinic with a history of three recent episodes of epistaxis requiring nasal packing. She is very disturbed by this bleeding and has stopped taking her warfarin about two weeks ago.
Discussion Although there is little data to guide clinicians in making decisions about the risks of thromboembolism in patients with mechanical heart valves who are not receiving warfarin it is generally felt that the risk of thromboembolism is lowest in patients with newer valves in the aortic position, higher in those with mitral valves, and highest in those with older types of mitral valves with or without concomitant atrial fibrillation or left atrial enlargement. Most experts would suggest that this patient has a significant risk of arterial embolism if anticoagulants are not resumed. As a result, counseling and recommendations should focus on ensuring that the patient is fully apprised of the risk of thromboembolism and of strategies which may reduce the risk of bleeding. Epistaxis is frequently due to the use of central heating without appropriate humidification - this results in drying of the nasal mucosa with a predisposition to epistaxis. Use of topical moisturizing agents or increased humidification are simple steps which eliminate epistaxis and thus allow conflict-free reintroduction of warfarin. Medically important epistaxis, due to structural abnormalities or arteriovenous malformations may be amenable to surgical interventions. Use of agents such as intranasal DDAVP are untested in this circumstance and may produce a systemic hypercoagulable state placing the patient at increased risk of valvular thrombosis or systemic embolization. As a result, their use cannot be recommended. In this particular patient, appropriate management consists of ensuring the patient is aware of the relative risks and benefits of various treatment options, apprising the patient of the likely clinical outcome of epistaxis (inconvenience, occasional visits to the emergency department and the potential need for surgical intervention) against the potential outcomes of inadequate anticoagulant therapy in the setting of a mitral valve (valvular thrombosis and systemic embolization with a very
S44 significant risk of long-term morbidity or death). If the patient continues to refuse warfarin therapy it may be prudent to obtain and document a second opinion with regards to her care in the case that a systemic embolism or valve thrombosis does occur. Aspirin is not known to be beneficial in this setting and it may cause or contribute to bleeding; however, its use might be considered if warfarin reinstitution is refused by the patient.
Case 3 A 56-year-old male with a recent pulmonary embolism (complicating knee replacement surgery performed three weeks ago) presents with hypotension in the setting of massive hematemesis. The patient's INR value is 4.7. Emergency endoscopy demonstrates a large duodenal ulcer with a visible vessel. Endoscopic therapy is applied and the bleeding appears to stop. What is the optimal management to prevent further bleeding?
Discussion The anticoagulant effect of warfarin should be reversed using intravenous vitamin K and coagulation factor replacement - either in the form of an appropriate amount of fresh frozen plasma (probably six to eight units) or prothrombin complex concentrate [5]. Failure to completely reverse the INR may place the patient at increased risk of recurrent bleeding: failure to administer vitamin K may result in "rebound anticoagulation" after initial correction due to the persistent anticoagulant effect of warfarin. Resumption of anticoagulation should be delayed until healing of the ulcer is documented - this is likely to take a period of weeks or months. During this time reinstitution of warfarin is likely to be associated with an unacceptable risk of recurrent bleeding and its associated morbidity and mortality, as discussed in a prior case. During the period of warfarin interruption the patient will be at high risk of recurrent deep vein thrombosis and/or pulmonary embolism. Placement of a temporary inferior vena cava filter should be strongly considered as it is likely to reduce the risk of pulmonary embolism. A filter which is removable after a period of weeks or months would be preferred as the duration of the filter placement is likely to be significant. Some filters are only approved for removal after one to two weeks; after this time removal is not recommended. It is important, however, that if healing of the ulcer is documented the patient (a) have an attempted removal of the filter and (b) resume anticoagulant
M. Crowther therapy promptly as inferior vena cava filters probably increase the risk of deep vein thrombosis with associated worsening leg symptomatology.
Case four A 92-year-old woman receiving warfarin for prevention of stroke in the setting of atrial fibrillation, a prior transient ischemic attack, known enlarged left atrium and moderate valvular disease secondary to rheumatic fever presents with a hypotension and melena stool. She has been previously quite well except as noted above. The melena stool began approximately 1 week ago. On initial examination or hemoglobin is 8.6 g per liter with a mean corpuscular volume of 62 fL (normal 85 to 100 fL).
Discussion This patient has several risk factors for stroke and the use of warfarin for long-term primary prophylaxis of stroke would be strongly recommended by consensus conferences. However, the patient has evidence of both acute bleeding (in the form of melena stool) and chronic blood loss (in the form of microcytic anemia). It is probable that she has a gastrointestinal malignancy as the cause of her presentation. This patient should have her warfarin interrupted, should have their INR corrected as noted above and should be promptly evaluated for colonic malignancy. While awaiting surgery anticoagulants are contraindicated however surgery should be expedited to minimize the risk of stroke. If surgery is performed then reinstitution of warfarin anticoagulation is indicated immediately upon hemostasis being assured. Reinstitution of warfarin before surgical correction of the malignancy is likely to be associated with bleeding which may be associated with significant morbidity and/or mortality. Alternate strategies such as the use of aspirin and/or low-dose unfractionated heparin have been proposed however their safety (as indicated by their relative propensity to cause bleeding, compared with warfarin) and efficacy (as indicated by their ability to prevent stroke) in this setting have not been evaluated in methodologically rigorous studies.
Case five A 24 year old male presents is transported to your tertiary care hospital from a peripheral centre. 5 days prior he had been in a motor vehicle accident and had suffered a splenic laceration – 24 hours before he had a cardiopulmonary arrest ultimately proven to be due to saddle pulmonary embolism. He
Bleeding with warfarin received thrombolytic therapy and is transferred for further care. Twelve hours after arrival he develops hypotension (systolic BP 65 mmHg) and passes voluminous bright red blood per rectum. His APTT is 97 seconds.
Discussion A standardized approach to the management of life threatening bleeding has recently been published [5]. This patient requires urgent hemodynamic support with vasopressors until adequate fluid, colloid and red cell resuscitation can be provided. In the absence of evidence of dilutional coagulopathy plasma has no role in the management of this case as it does not reverse the anticoagulant effect of heparin. Protamine should be administered; although an estimated dose can be arrived at using a variety of formulae in this case a dose of 50 mg will probably reverse the anticoagulant of heparin within minutes of its administration. To evaluate correction, the APTT should be checked 5 to 10 minutes after protamine is administered and if the aAPTT is persistently prolonged additional protamine should be administered. The source of the bleeding should be sought using endoscopic, radiological or surgical techniques (whichever can be arranged most quickly) – bleeding should not be attributed to the heparin therapy rather the mechanical cause must be identified and corrected. Given the proximity to the pulmonary embolism a temporary IVC filter should be placed – however this should only be done after required life saving therapies have been administered (for example, placement of the filter should not delay heparin reversal or evaluation of the source of blood loss, both of which are more immediately life-preserving than the filter). Anticoagulation should be reinstituted as soon as the bleeding source has been identified and corrected and once hemostasis is ensured – the filter should then be removed as quickly as possible to avoid complications associated with prolonged IVC interruption and to increase the likelihood of filter removal. Currently only about 20% of “temporary” filters are actually removed. [6]
Summary Preventing and managing bleeding in patients who are receiving anticoagulant therapy should consist of
S45 an initial assessment of the risk of bleeding prior to the initiation of anticoagulation, an assessment of the relative risks of clinically apparent bleeding and thromboembolism in the individual patient with the passage of time, and appropriate (oftentimes emergent) management of bleeding complications. Fundamental principles include considering the important mortality and morbidity risk associated with bleeding in patients receiving anticoagulation and a careful consideration of measures which may ameliorate the risk of bleeding in an individual patient.
Conflicts of interest Dr Crowther has received an honorarium for serving on an advisory board for a manufacturer of a prothrombin complex concentrate.
Acknowledgements Dr Crowther is a career investigator of the Heart and Stroke Foundation of Canada.
References [1] Singer DE, Albers GW, Dalen JE, Go AS, Halperin JL, Manning WJ, et al. Antithrombotic therapy in atrial fibrillation: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest Sep 2004;126(3 Suppl):429S–56S. [2] Gage BF, Waterman AD, Shannon W, Boechler M, Rich MW, Radford MJ. Validation of clinical classification schemes for predicting stroke: results from the National Registry of Atrial Fibrillation. JAMA Jun 13 2001;285(22):2864–70. [3] Linkins LA, Choi PT, Douketis JD. Clinical impact of bleeding in patients taking oral anticoagulant therapy for venous thromboembolism: a meta-analysis.[see comment]. Ann Intern Med Dec 2 2003;139(11):893–900. [4] de Denus S, Sanoski CA, Carlsson J, Opolski G, Spinler SA. Rate vs rhythm control in patients with atrial fibrillation: a meta-analysis. Arch Intern Med 2005 Feb 14;165(3):258–62. [5] Crowther MA, Warkentin TE. Bleeding risk and the management of bleeding complications in patients undergoing anticoagulant therapy: focus on new anticoagulant agents. Blood Feb 2009;28. [6] Karmy-Jones R, Jurkovich GJ, Velmahos GC, Burdick T, Spaniolas K, Todd SR, et al. Practice patterns and outcomes of retrievable vena cava filters in trauma patients: an AAST multicenter study. J Trauma Jan 2007;62(1):17–24.