Vascular

When I was growing up, my mother frequently told me that it was rude to interrupt. Although she was referring to conversations, she may have been onto something bigger.

In the nearly three quarters of a century since their discovery, vitamin K antagonist anticoagulant drugs have been used by millions of patients to prevent heart attack and stroke. Before these patients undergo surgery, a decision to continue or interrupt anticoagulation must be made, weighing the risks of postsurgical hemorrhage with continuation of anticoagulation against the risks of stroke or other embolic complications with interruption of anticoagulation. Bleeding after dental surgery when anticoagulation is continued is rarely or never life-threatening. On the other hand, embolic complications of interrupting anticoagulation are almost always consequential and often lead to death or disability. Although consideration may be different for other types of surgery, there is no need to interrupt lifesaving anticoagulation for dental surgery.

EVIDENCE THAT SUPPORTS CONTINUING ANTICOAGULATION

As early as 1957, there were reports of prolonged postoperative bleeding after dental extractions in patients taking anticoagulants. But there were also reports of embolic complications in patients whose anticoagulation was interrupted for dental procedures. Since then, there has been a plethora of literature in this area.

A review published in 2000 showed that of more than 950 anticoagulated patients undergoing more than 2,400 dental surgical procedures (including simple and surgical extraction, alveoplasty, and gingival surgery), only 12 (< 1.3%) required more than local measures for hemostasis (eg, fresh-frozen plasma, vitamin K), and no patient died,¹ leading to the conclusion that the bleeding risk was not significant in anticoagulated dental patients. Other studies and systematic reviews have also concluded that anticoagulation for dental procedures should not be interrupted.^2,3 In a recent review of 83 studies, only 31 (0.6%) of 5,431 patients taking warfarin suffered bleeding complications requiring more than local measures for hemostasis; there were no fatalities.⁴

The risk of embolism

There have been many reports of embolic complications in patients whose anticoagulation was interrupted for dental procedures. A 2000 review of 575 cases in 526 patients whose anticoagulation was interrupted for dental procedures showed that 5 patients (0.9%) had a serious embolic complication, and 4 died.¹ In a more recent review of 64 studies and more than 2,673 patients whose anticoagulation was interrupted for dental procedures, 22 patients (0.8%) suffered embolic complications, and 6 (0.2%) died of the complications.⁴ Of those with embolic complications, the interruption period was often not reported; however; the interruption ranged from 1 to 4 days. A 2003 systematic review by Dunn and Turpie found a 0.4% embolic complication rate when anticoagulation was interrupted for dental surgery.²

BLEEDING AFTER DENTAL SURGERY

Bleeding after dental surgery can occur with either anticoagulation continuation or interruption, and minor postoperative bleeding requiring additional local hemostatic methods occurs at about the same rate in anticoagulated patients as in those whose anticoagulation is interrupted.

In our recent literature review,⁴ about 6% of patients in whom anticoagulation was interrupted (and 7% in whom it was not interrupted) had minor bleeding requiring additional local hemostasis, and only 0.2% of patients required more than hemostatic measures (eg, vitamin K injection, plasma transfusion), the same rate found by Dunn and Turpie.² All patients who required more than local hemostatic measures presumably made a full recovery, while at least 6 who suffered postoperative embolic complications died, and the rest may have had permanent disabilities.

Although bridging therapy with low-molecular-weight heparin can decrease the time without anticoagulation for a dental procedure to only 12 hours, it can be complicated to implement, and there appears to be no benefit in terms of the rates of bleeding or embolic complications. Of the 64 anticoagulation interruption studies,⁴ 17 used heparin or low-molecular-weight heparin in conjunction with temporary warfarin interruption. In 210 instances of bridging therapy in 202 patients undergoing dental procedures, there were 2 embolic complications (1% of bridging cases) and 20 bleeding complications, with 3 (1.4%) requiring hemostasis beyond local measures.⁴

Many of the studies analyzed independently showed there was no significant difference in postoperative bleeding with:

• Anticoagulation continuation vs interruption for a few days
• Lower vs higher international normalized ratio (INR), including some over 4.0
• Surgical vs nonsurgical extraction
• Few vs many extractions.⁴

Some studies of anticoagulation and anticoagulation interruption for dental surgery had important limitations. Many of the anticoagulation studies excluded patients at high risk of bleeding, those with a high INR (> 4.0), and those with severe liver or kidney disease, and their exclusion could have lowered the incidence of bleeding complications. Many studies of anticoagulation interruption excluded patients at high risk of embolism, including patients with a previous embolic event and patients with an artificial heart valve, and this could have skewed the results lower for embolic complications.

WHY DO SOME CLINICIANS STILL RECOMMEND INTERRUPTION?

The choice seems clear: for dental surgery in anticoagulated patients, the small risk of a nonfatal bleeding complication in anticoagulated patients is outweighed by the small risk of a disabling or fatal embolic complication when anticoagulation is interrupted. Most authors have concluded that anticoagulation should be continued for dental surgery. Yet surveys of dentists and physicians have shown that many still recommend interrupting anticoagulation for dental surgery.^5,6

Medical and dental association positions

The American Academy of Neurology⁷ and the American Dental Association⁸ recommend continuing anticoagulant medications for dental surgery. The American College of Chest Physicians also recommends continuing anticoagulation but in 2012 added an option to interrupt or decrease anticoagulation for 2 to 3 days for dental surgery.⁹ Their recommendation was based partly on the results of four controlled prospective studies^10–13 comparing anticoagulated dental surgical patients with patients whose anticoagulation was interrupted. In each study, there were no embolic or bleeding complications requiring more than local methods for hemostasis in the interruption groups, leading the American College of Chest Physicians to conclude that brief anticoagulation interruption for dental surgery is safe and effective.

But the results of these studies actually argue against interrupting anticoagulation for dental surgery. In each study, rates of postoperative bleeding complications and blood loss were similar in both groups, and there were no embolic complications. The authors of each study independently concluded that anticoagulation should not be interrupted for dental surgery.

The optimal INR range for anticoagulation therapy is widely accepted as 2.0 to 3.0, and 2.5 to 3.5 for patients with a mechanical mitral valve.¹⁴ Interrupting warfarin anticoagulation for 2 or 3 days leads to a suboptimal INR. Patel et al¹⁵ studied the incidence of embolic complications (including stroke, non-central nervous system embolism, myocardial infarction, and vascular death) within 30 days in 7,082 patients taking warfarin with and without an interruption of therapy of at least 3 days (median 6 days). The observed rate of embolic events in those with temporary interruption (10.75 events per 100 patient-years) was more than double the rate in those without interruption (4.03 per 100 patient-years).¹⁵ However, this study was designed to compare rivaroxaban vs warfarin, not interrupting vs not interrupting warfarin.

A DECISION-TREE REANALYSIS

In 2010, Balevi published a decision-tree analysis that slightly favored withdrawing warfarin for dental surgery, but he stated that the analysis “can be updated in the future as more accurate and up-to-date data for each of the variables in the model become available.”¹⁶ Now that there are more accurate and up-to-date data, it is time to revisit this decision-tree analysis.

In Balevi’s analysis, major bleeding is not defined. But major bleeding after dental surgery should be defined as any bleeding requiring more than local measures for hemostasis. In calculating probabilities for the analysis, Balevi cited studies allegedly showing high incidences of major bleeding after dental extractions with warfarin continuation.^17,18 There were some minor bleeding complications necessitating additional local measures for hemostasis in these studies, but no major bleeding complications at all in the warfarin- continuation or warfarin-interruption group. There were no significant bleeding events in either study, and the differences in bleeding rates were not significantly different between the two groups. In both studies, the authors concluded that warfarin interruption for dental surgery should be reconsidered.

Similarly, Balevi accurately asserted that there has never been a reported case of fatal bleeding after a dental procedure in an anticoagulated patient, but “for the sake of creating balance,”¹⁶ his decision-tree analysis uses a fatal bleeding probability of 1%, based on an estimated 1% risk for nondental procedures (eg, colorectal surgery, major abdominal surgery). It is unclear how a 1% incidence creates “balance,” but dental surgery is unlike other types of surgery, and that is one reason there has never been a documented postdental fatal hemorrhage in an anticoagulated patient. Major vessels are unlikely to be encountered, and bleeding sites are easily accessible to local hemostatic methods.

Balevi used an embolic complication incidence of 0.059% with warfarin interruption of 3 days. Perhaps he used such a low embolic probability because of his incorrect assertion that “there has been no reported case of a dental extraction causing a cardiovascular accident in a patient whose warfarin was temporarily discontinued.”¹⁶ In fact, our group has now identified at least 22 reported cases of embolic complications after temporary interruption of warfarin therapy in patients undergoing dental surgery.⁴ These included 12 embolic complications (3 fatal) after interruption periods from 1 to 5 days.^19,20 In addition, there are numerous cases of embolic complications reported in patients whose warfarin was temporarily interrupted for other types of surgery.^21,22

The literature shows that embolic complications after temporary warfarin interruption occur at a much higher rate than 0.059%. Many documented embolic complications have occurred after relatively long warfarin interruption periods (greater than 5 days), but many have occurred with much shorter interruptions. Wysokinski et al²¹ showed that there was a 1.1% incidence of thromboembolic events, more than 18 times greater than Balevi’s incidence, in patients whose warfarin was interrupted for 4 or 5 days with or without bridging therapy. One of these patients developed an occipital infarct within 3 days after stopping warfarin without bridging (for a nondental procedure). Garcia et al²² showed that of 984 warfarin therapy interruptions of 5 days or less, there were 4 embolic complications, a rate (0.4%) more than 6 times greater than that reported by Balevi.

Even if one were to accept a 0.059% embolic risk from interruption of warfarin, that would mean for every 1,700 warfarin interruptions for dental procedures, there would be one possibly fatal embolic complication. On the other hand, if 1,700 dental surgeries were performed without warfarin interruption, based on the literature, there may be some bleeding complications, but none would be fatal. If airline flights had a 0.059% chance of crashing, far fewer people would choose to fly. (There are 87,000 airline flights in the US per day. A 0.059% crash rate would mean there would be 51 crashes per day in the United States alone.)

But regardless of whether the embolic risk is 0.059% or 1%, the question comes down to whether an anticoagulated patient should be subjected to a small but significant risk of death or permanent disability (if anticoagulation is interrupted) or to a small risk of a bleeding complication (if anticoagulation is continued), when 100% of cases up until now have apparently resulted in a full recovery.

As a result, the decision-tree analysis was fatally flawed by grossly overestimating the incidence of fatal bleeding when warfarin is continued, and by grossly underestimating the incidence of embolic complications when warfarin is interrupted.

IS WARFARIN CONTINUATION ‘TROUBLESOME’?

An oral surgeon stated, “My experience and that of many of my colleagues is that even though bleeding is never life-threatening [emphasis mine], it can be difficult to control at therapeutic levels of anticoagulation and can be troublesome, especially for elderly patients.”²³ The American College of Chest Physicians stated that postoperative bleeding after dental procedures can cause “anxiety and distress.”³ Patients with even minor postoperative bleeding can be anxious, but surely, postoperative stroke is almost always far more troublesome than postoperative bleeding, which has never been life-threatening. Although other types of surgery may be different, there is no need to interrupt lifesaving anticoagulation for innocuous dental surgery.

My mother was right—it can be rude to interrupt. Anticoagulation should not be interrupted for dental surgery.

When I was growing up, my mother frequently told me that it was rude to interrupt. Although she was referring to conversations, she may have been onto something bigger.

In the nearly three quarters of a century since their discovery, vitamin K antagonist anticoagulant drugs have been used by millions of patients to prevent heart attack and stroke. Before these patients undergo surgery, a decision to continue or interrupt anticoagulation must be made, weighing the risks of postsurgical hemorrhage with continuation of anticoagulation against the risks of stroke or other embolic complications with interruption of anticoagulation. Bleeding after dental surgery when anticoagulation is continued is rarely or never life-threatening. On the other hand, embolic complications of interrupting anticoagulation are almost always consequential and often lead to death or disability. Although consideration may be different for other types of surgery, there is no need to interrupt lifesaving anticoagulation for dental surgery.

EVIDENCE THAT SUPPORTS CONTINUING ANTICOAGULATION

As early as 1957, there were reports of prolonged postoperative bleeding after dental extractions in patients taking anticoagulants. But there were also reports of embolic complications in patients whose anticoagulation was interrupted for dental procedures. Since then, there has been a plethora of literature in this area.

A review published in 2000 showed that of more than 950 anticoagulated patients undergoing more than 2,400 dental surgical procedures (including simple and surgical extraction, alveoplasty, and gingival surgery), only 12 (< 1.3%) required more than local measures for hemostasis (eg, fresh-frozen plasma, vitamin K), and no patient died,¹ leading to the conclusion that the bleeding risk was not significant in anticoagulated dental patients. Other studies and systematic reviews have also concluded that anticoagulation for dental procedures should not be interrupted.^2,3 In a recent review of 83 studies, only 31 (0.6%) of 5,431 patients taking warfarin suffered bleeding complications requiring more than local measures for hemostasis; there were no fatalities.⁴

The risk of embolism

There have been many reports of embolic complications in patients whose anticoagulation was interrupted for dental procedures. A 2000 review of 575 cases in 526 patients whose anticoagulation was interrupted for dental procedures showed that 5 patients (0.9%) had a serious embolic complication, and 4 died.¹ In a more recent review of 64 studies and more than 2,673 patients whose anticoagulation was interrupted for dental procedures, 22 patients (0.8%) suffered embolic complications, and 6 (0.2%) died of the complications.⁴ Of those with embolic complications, the interruption period was often not reported; however; the interruption ranged from 1 to 4 days. A 2003 systematic review by Dunn and Turpie found a 0.4% embolic complication rate when anticoagulation was interrupted for dental surgery.²

BLEEDING AFTER DENTAL SURGERY

Bleeding after dental surgery can occur with either anticoagulation continuation or interruption, and minor postoperative bleeding requiring additional local hemostatic methods occurs at about the same rate in anticoagulated patients as in those whose anticoagulation is interrupted.

In our recent literature review,⁴ about 6% of patients in whom anticoagulation was interrupted (and 7% in whom it was not interrupted) had minor bleeding requiring additional local hemostasis, and only 0.2% of patients required more than hemostatic measures (eg, vitamin K injection, plasma transfusion), the same rate found by Dunn and Turpie.² All patients who required more than local hemostatic measures presumably made a full recovery, while at least 6 who suffered postoperative embolic complications died, and the rest may have had permanent disabilities.

Although bridging therapy with low-molecular-weight heparin can decrease the time without anticoagulation for a dental procedure to only 12 hours, it can be complicated to implement, and there appears to be no benefit in terms of the rates of bleeding or embolic complications. Of the 64 anticoagulation interruption studies,⁴ 17 used heparin or low-molecular-weight heparin in conjunction with temporary warfarin interruption. In 210 instances of bridging therapy in 202 patients undergoing dental procedures, there were 2 embolic complications (1% of bridging cases) and 20 bleeding complications, with 3 (1.4%) requiring hemostasis beyond local measures.⁴

Many of the studies analyzed independently showed there was no significant difference in postoperative bleeding with:

• Anticoagulation continuation vs interruption for a few days
• Lower vs higher international normalized ratio (INR), including some over 4.0
• Surgical vs nonsurgical extraction
• Few vs many extractions.⁴

Some studies of anticoagulation and anticoagulation interruption for dental surgery had important limitations. Many of the anticoagulation studies excluded patients at high risk of bleeding, those with a high INR (> 4.0), and those with severe liver or kidney disease, and their exclusion could have lowered the incidence of bleeding complications. Many studies of anticoagulation interruption excluded patients at high risk of embolism, including patients with a previous embolic event and patients with an artificial heart valve, and this could have skewed the results lower for embolic complications.

WHY DO SOME CLINICIANS STILL RECOMMEND INTERRUPTION?

The choice seems clear: for dental surgery in anticoagulated patients, the small risk of a nonfatal bleeding complication in anticoagulated patients is outweighed by the small risk of a disabling or fatal embolic complication when anticoagulation is interrupted. Most authors have concluded that anticoagulation should be continued for dental surgery. Yet surveys of dentists and physicians have shown that many still recommend interrupting anticoagulation for dental surgery.^5,6

Medical and dental association positions

The American Academy of Neurology⁷ and the American Dental Association⁸ recommend continuing anticoagulant medications for dental surgery. The American College of Chest Physicians also recommends continuing anticoagulation but in 2012 added an option to interrupt or decrease anticoagulation for 2 to 3 days for dental surgery.⁹ Their recommendation was based partly on the results of four controlled prospective studies^10–13 comparing anticoagulated dental surgical patients with patients whose anticoagulation was interrupted. In each study, there were no embolic or bleeding complications requiring more than local methods for hemostasis in the interruption groups, leading the American College of Chest Physicians to conclude that brief anticoagulation interruption for dental surgery is safe and effective.

But the results of these studies actually argue against interrupting anticoagulation for dental surgery. In each study, rates of postoperative bleeding complications and blood loss were similar in both groups, and there were no embolic complications. The authors of each study independently concluded that anticoagulation should not be interrupted for dental surgery.

The optimal INR range for anticoagulation therapy is widely accepted as 2.0 to 3.0, and 2.5 to 3.5 for patients with a mechanical mitral valve.¹⁴ Interrupting warfarin anticoagulation for 2 or 3 days leads to a suboptimal INR. Patel et al¹⁵ studied the incidence of embolic complications (including stroke, non-central nervous system embolism, myocardial infarction, and vascular death) within 30 days in 7,082 patients taking warfarin with and without an interruption of therapy of at least 3 days (median 6 days). The observed rate of embolic events in those with temporary interruption (10.75 events per 100 patient-years) was more than double the rate in those without interruption (4.03 per 100 patient-years).¹⁵ However, this study was designed to compare rivaroxaban vs warfarin, not interrupting vs not interrupting warfarin.

A DECISION-TREE REANALYSIS

In 2010, Balevi published a decision-tree analysis that slightly favored withdrawing warfarin for dental surgery, but he stated that the analysis “can be updated in the future as more accurate and up-to-date data for each of the variables in the model become available.”¹⁶ Now that there are more accurate and up-to-date data, it is time to revisit this decision-tree analysis.

In Balevi’s analysis, major bleeding is not defined. But major bleeding after dental surgery should be defined as any bleeding requiring more than local measures for hemostasis. In calculating probabilities for the analysis, Balevi cited studies allegedly showing high incidences of major bleeding after dental extractions with warfarin continuation.^17,18 There were some minor bleeding complications necessitating additional local measures for hemostasis in these studies, but no major bleeding complications at all in the warfarin- continuation or warfarin-interruption group. There were no significant bleeding events in either study, and the differences in bleeding rates were not significantly different between the two groups. In both studies, the authors concluded that warfarin interruption for dental surgery should be reconsidered.

Similarly, Balevi accurately asserted that there has never been a reported case of fatal bleeding after a dental procedure in an anticoagulated patient, but “for the sake of creating balance,”¹⁶ his decision-tree analysis uses a fatal bleeding probability of 1%, based on an estimated 1% risk for nondental procedures (eg, colorectal surgery, major abdominal surgery). It is unclear how a 1% incidence creates “balance,” but dental surgery is unlike other types of surgery, and that is one reason there has never been a documented postdental fatal hemorrhage in an anticoagulated patient. Major vessels are unlikely to be encountered, and bleeding sites are easily accessible to local hemostatic methods.

Balevi used an embolic complication incidence of 0.059% with warfarin interruption of 3 days. Perhaps he used such a low embolic probability because of his incorrect assertion that “there has been no reported case of a dental extraction causing a cardiovascular accident in a patient whose warfarin was temporarily discontinued.”¹⁶ In fact, our group has now identified at least 22 reported cases of embolic complications after temporary interruption of warfarin therapy in patients undergoing dental surgery.⁴ These included 12 embolic complications (3 fatal) after interruption periods from 1 to 5 days.^19,20 In addition, there are numerous cases of embolic complications reported in patients whose warfarin was temporarily interrupted for other types of surgery.^21,22

The literature shows that embolic complications after temporary warfarin interruption occur at a much higher rate than 0.059%. Many documented embolic complications have occurred after relatively long warfarin interruption periods (greater than 5 days), but many have occurred with much shorter interruptions. Wysokinski et al²¹ showed that there was a 1.1% incidence of thromboembolic events, more than 18 times greater than Balevi’s incidence, in patients whose warfarin was interrupted for 4 or 5 days with or without bridging therapy. One of these patients developed an occipital infarct within 3 days after stopping warfarin without bridging (for a nondental procedure). Garcia et al²² showed that of 984 warfarin therapy interruptions of 5 days or less, there were 4 embolic complications, a rate (0.4%) more than 6 times greater than that reported by Balevi.

Even if one were to accept a 0.059% embolic risk from interruption of warfarin, that would mean for every 1,700 warfarin interruptions for dental procedures, there would be one possibly fatal embolic complication. On the other hand, if 1,700 dental surgeries were performed without warfarin interruption, based on the literature, there may be some bleeding complications, but none would be fatal. If airline flights had a 0.059% chance of crashing, far fewer people would choose to fly. (There are 87,000 airline flights in the US per day. A 0.059% crash rate would mean there would be 51 crashes per day in the United States alone.)

But regardless of whether the embolic risk is 0.059% or 1%, the question comes down to whether an anticoagulated patient should be subjected to a small but significant risk of death or permanent disability (if anticoagulation is interrupted) or to a small risk of a bleeding complication (if anticoagulation is continued), when 100% of cases up until now have apparently resulted in a full recovery.

As a result, the decision-tree analysis was fatally flawed by grossly overestimating the incidence of fatal bleeding when warfarin is continued, and by grossly underestimating the incidence of embolic complications when warfarin is interrupted.

IS WARFARIN CONTINUATION ‘TROUBLESOME’?

An oral surgeon stated, “My experience and that of many of my colleagues is that even though bleeding is never life-threatening [emphasis mine], it can be difficult to control at therapeutic levels of anticoagulation and can be troublesome, especially for elderly patients.”²³ The American College of Chest Physicians stated that postoperative bleeding after dental procedures can cause “anxiety and distress.”³ Patients with even minor postoperative bleeding can be anxious, but surely, postoperative stroke is almost always far more troublesome than postoperative bleeding, which has never been life-threatening. Although other types of surgery may be different, there is no need to interrupt lifesaving anticoagulation for innocuous dental surgery.

My mother was right—it can be rude to interrupt. Anticoagulation should not be interrupted for dental surgery.

When I was growing up, my mother frequently told me that it was rude to interrupt. Although she was referring to conversations, she may have been onto something bigger.

In the nearly three quarters of a century since their discovery, vitamin K antagonist anticoagulant drugs have been used by millions of patients to prevent heart attack and stroke. Before these patients undergo surgery, a decision to continue or interrupt anticoagulation must be made, weighing the risks of postsurgical hemorrhage with continuation of anticoagulation against the risks of stroke or other embolic complications with interruption of anticoagulation. Bleeding after dental surgery when anticoagulation is continued is rarely or never life-threatening. On the other hand, embolic complications of interrupting anticoagulation are almost always consequential and often lead to death or disability. Although consideration may be different for other types of surgery, there is no need to interrupt lifesaving anticoagulation for dental surgery.

EVIDENCE THAT SUPPORTS CONTINUING ANTICOAGULATION

As early as 1957, there were reports of prolonged postoperative bleeding after dental extractions in patients taking anticoagulants. But there were also reports of embolic complications in patients whose anticoagulation was interrupted for dental procedures. Since then, there has been a plethora of literature in this area.

A review published in 2000 showed that of more than 950 anticoagulated patients undergoing more than 2,400 dental surgical procedures (including simple and surgical extraction, alveoplasty, and gingival surgery), only 12 (< 1.3%) required more than local measures for hemostasis (eg, fresh-frozen plasma, vitamin K), and no patient died,¹ leading to the conclusion that the bleeding risk was not significant in anticoagulated dental patients. Other studies and systematic reviews have also concluded that anticoagulation for dental procedures should not be interrupted.^2,3 In a recent review of 83 studies, only 31 (0.6%) of 5,431 patients taking warfarin suffered bleeding complications requiring more than local measures for hemostasis; there were no fatalities.⁴

The risk of embolism

There have been many reports of embolic complications in patients whose anticoagulation was interrupted for dental procedures. A 2000 review of 575 cases in 526 patients whose anticoagulation was interrupted for dental procedures showed that 5 patients (0.9%) had a serious embolic complication, and 4 died.¹ In a more recent review of 64 studies and more than 2,673 patients whose anticoagulation was interrupted for dental procedures, 22 patients (0.8%) suffered embolic complications, and 6 (0.2%) died of the complications.⁴ Of those with embolic complications, the interruption period was often not reported; however; the interruption ranged from 1 to 4 days. A 2003 systematic review by Dunn and Turpie found a 0.4% embolic complication rate when anticoagulation was interrupted for dental surgery.²

BLEEDING AFTER DENTAL SURGERY

Bleeding after dental surgery can occur with either anticoagulation continuation or interruption, and minor postoperative bleeding requiring additional local hemostatic methods occurs at about the same rate in anticoagulated patients as in those whose anticoagulation is interrupted.

In our recent literature review,⁴ about 6% of patients in whom anticoagulation was interrupted (and 7% in whom it was not interrupted) had minor bleeding requiring additional local hemostasis, and only 0.2% of patients required more than hemostatic measures (eg, vitamin K injection, plasma transfusion), the same rate found by Dunn and Turpie.² All patients who required more than local hemostatic measures presumably made a full recovery, while at least 6 who suffered postoperative embolic complications died, and the rest may have had permanent disabilities.

Although bridging therapy with low-molecular-weight heparin can decrease the time without anticoagulation for a dental procedure to only 12 hours, it can be complicated to implement, and there appears to be no benefit in terms of the rates of bleeding or embolic complications. Of the 64 anticoagulation interruption studies,⁴ 17 used heparin or low-molecular-weight heparin in conjunction with temporary warfarin interruption. In 210 instances of bridging therapy in 202 patients undergoing dental procedures, there were 2 embolic complications (1% of bridging cases) and 20 bleeding complications, with 3 (1.4%) requiring hemostasis beyond local measures.⁴

Many of the studies analyzed independently showed there was no significant difference in postoperative bleeding with:

• Anticoagulation continuation vs interruption for a few days
• Lower vs higher international normalized ratio (INR), including some over 4.0
• Surgical vs nonsurgical extraction
• Few vs many extractions.⁴

Some studies of anticoagulation and anticoagulation interruption for dental surgery had important limitations. Many of the anticoagulation studies excluded patients at high risk of bleeding, those with a high INR (> 4.0), and those with severe liver or kidney disease, and their exclusion could have lowered the incidence of bleeding complications. Many studies of anticoagulation interruption excluded patients at high risk of embolism, including patients with a previous embolic event and patients with an artificial heart valve, and this could have skewed the results lower for embolic complications.

WHY DO SOME CLINICIANS STILL RECOMMEND INTERRUPTION?

The choice seems clear: for dental surgery in anticoagulated patients, the small risk of a nonfatal bleeding complication in anticoagulated patients is outweighed by the small risk of a disabling or fatal embolic complication when anticoagulation is interrupted. Most authors have concluded that anticoagulation should be continued for dental surgery. Yet surveys of dentists and physicians have shown that many still recommend interrupting anticoagulation for dental surgery.^5,6

Medical and dental association positions

The American Academy of Neurology⁷ and the American Dental Association⁸ recommend continuing anticoagulant medications for dental surgery. The American College of Chest Physicians also recommends continuing anticoagulation but in 2012 added an option to interrupt or decrease anticoagulation for 2 to 3 days for dental surgery.⁹ Their recommendation was based partly on the results of four controlled prospective studies^10–13 comparing anticoagulated dental surgical patients with patients whose anticoagulation was interrupted. In each study, there were no embolic or bleeding complications requiring more than local methods for hemostasis in the interruption groups, leading the American College of Chest Physicians to conclude that brief anticoagulation interruption for dental surgery is safe and effective.

But the results of these studies actually argue against interrupting anticoagulation for dental surgery. In each study, rates of postoperative bleeding complications and blood loss were similar in both groups, and there were no embolic complications. The authors of each study independently concluded that anticoagulation should not be interrupted for dental surgery.

The optimal INR range for anticoagulation therapy is widely accepted as 2.0 to 3.0, and 2.5 to 3.5 for patients with a mechanical mitral valve.¹⁴ Interrupting warfarin anticoagulation for 2 or 3 days leads to a suboptimal INR. Patel et al¹⁵ studied the incidence of embolic complications (including stroke, non-central nervous system embolism, myocardial infarction, and vascular death) within 30 days in 7,082 patients taking warfarin with and without an interruption of therapy of at least 3 days (median 6 days). The observed rate of embolic events in those with temporary interruption (10.75 events per 100 patient-years) was more than double the rate in those without interruption (4.03 per 100 patient-years).¹⁵ However, this study was designed to compare rivaroxaban vs warfarin, not interrupting vs not interrupting warfarin.

A DECISION-TREE REANALYSIS

In 2010, Balevi published a decision-tree analysis that slightly favored withdrawing warfarin for dental surgery, but he stated that the analysis “can be updated in the future as more accurate and up-to-date data for each of the variables in the model become available.”¹⁶ Now that there are more accurate and up-to-date data, it is time to revisit this decision-tree analysis.

In Balevi’s analysis, major bleeding is not defined. But major bleeding after dental surgery should be defined as any bleeding requiring more than local measures for hemostasis. In calculating probabilities for the analysis, Balevi cited studies allegedly showing high incidences of major bleeding after dental extractions with warfarin continuation.^17,18 There were some minor bleeding complications necessitating additional local measures for hemostasis in these studies, but no major bleeding complications at all in the warfarin- continuation or warfarin-interruption group. There were no significant bleeding events in either study, and the differences in bleeding rates were not significantly different between the two groups. In both studies, the authors concluded that warfarin interruption for dental surgery should be reconsidered.

Similarly, Balevi accurately asserted that there has never been a reported case of fatal bleeding after a dental procedure in an anticoagulated patient, but “for the sake of creating balance,”¹⁶ his decision-tree analysis uses a fatal bleeding probability of 1%, based on an estimated 1% risk for nondental procedures (eg, colorectal surgery, major abdominal surgery). It is unclear how a 1% incidence creates “balance,” but dental surgery is unlike other types of surgery, and that is one reason there has never been a documented postdental fatal hemorrhage in an anticoagulated patient. Major vessels are unlikely to be encountered, and bleeding sites are easily accessible to local hemostatic methods.

Balevi used an embolic complication incidence of 0.059% with warfarin interruption of 3 days. Perhaps he used such a low embolic probability because of his incorrect assertion that “there has been no reported case of a dental extraction causing a cardiovascular accident in a patient whose warfarin was temporarily discontinued.”¹⁶ In fact, our group has now identified at least 22 reported cases of embolic complications after temporary interruption of warfarin therapy in patients undergoing dental surgery.⁴ These included 12 embolic complications (3 fatal) after interruption periods from 1 to 5 days.^19,20 In addition, there are numerous cases of embolic complications reported in patients whose warfarin was temporarily interrupted for other types of surgery.^21,22

The literature shows that embolic complications after temporary warfarin interruption occur at a much higher rate than 0.059%. Many documented embolic complications have occurred after relatively long warfarin interruption periods (greater than 5 days), but many have occurred with much shorter interruptions. Wysokinski et al²¹ showed that there was a 1.1% incidence of thromboembolic events, more than 18 times greater than Balevi’s incidence, in patients whose warfarin was interrupted for 4 or 5 days with or without bridging therapy. One of these patients developed an occipital infarct within 3 days after stopping warfarin without bridging (for a nondental procedure). Garcia et al²² showed that of 984 warfarin therapy interruptions of 5 days or less, there were 4 embolic complications, a rate (0.4%) more than 6 times greater than that reported by Balevi.

Even if one were to accept a 0.059% embolic risk from interruption of warfarin, that would mean for every 1,700 warfarin interruptions for dental procedures, there would be one possibly fatal embolic complication. On the other hand, if 1,700 dental surgeries were performed without warfarin interruption, based on the literature, there may be some bleeding complications, but none would be fatal. If airline flights had a 0.059% chance of crashing, far fewer people would choose to fly. (There are 87,000 airline flights in the US per day. A 0.059% crash rate would mean there would be 51 crashes per day in the United States alone.)

But regardless of whether the embolic risk is 0.059% or 1%, the question comes down to whether an anticoagulated patient should be subjected to a small but significant risk of death or permanent disability (if anticoagulation is interrupted) or to a small risk of a bleeding complication (if anticoagulation is continued), when 100% of cases up until now have apparently resulted in a full recovery.

As a result, the decision-tree analysis was fatally flawed by grossly overestimating the incidence of fatal bleeding when warfarin is continued, and by grossly underestimating the incidence of embolic complications when warfarin is interrupted.

IS WARFARIN CONTINUATION ‘TROUBLESOME’?

An oral surgeon stated, “My experience and that of many of my colleagues is that even though bleeding is never life-threatening [emphasis mine], it can be difficult to control at therapeutic levels of anticoagulation and can be troublesome, especially for elderly patients.”²³ The American College of Chest Physicians stated that postoperative bleeding after dental procedures can cause “anxiety and distress.”³ Patients with even minor postoperative bleeding can be anxious, but surely, postoperative stroke is almost always far more troublesome than postoperative bleeding, which has never been life-threatening. Although other types of surgery may be different, there is no need to interrupt lifesaving anticoagulation for innocuous dental surgery.

My mother was right—it can be rude to interrupt. Anticoagulation should not be interrupted for dental surgery.

CHICAGO – Preadmission and postdischarge factors were important predictors of postoperative readmission in a large cohort of surgical patients, but the hospital course had little incremental impact on either readmissions or postdischarge complications in the cohort, according to a retrospective study of Veterans Affairs data.

The findings suggest that efforts to reduce postoperative readmissions should focus on enhanced postdischarge surveillance and early intervention, Dr. Melanie S. Morris of the University of Alabama at Birmingham reported at the annual meeting of the American Surgical Association.

Dr. Morris

To assess the relative contributions of patient factors, operative characteristics, and postoperative hospital course on readmissions, she and her colleagues evaluated 243,956 general, vascular, and orthopedic surgery patients in 121 VA hospitals. The overall readmission rate among the cohort was 11.1%, and for general, vascular, and orthopedic surgeries, the rates were 12.9%, 15.4%, and 7.6%, respectively; the average postoperative length of stay was 6.9 days, and 6.1% of patients experienced a predischarge complication.

Almost all readmissions occurred within 2 weeks of discharge, and for general surgery patients, most occurred within 1 week. The readmission rate for vascular surgery patients remained high beyond the 2-week mark.

An examination of the reasons for readmission showed that wound complications were the most common reason for readmission, and this was particularly true for vascular surgery patients, in whom 44% of readmissions were for wound complications, Dr. Morris said.

Gastrointestinal complications including ileus and obstruction were also common, accounting for nearly 28% of readmissions among general surgery patients, she said.

Importantly, when including preoperative data (such as demographics, comorbidities, social and behavioral factors, labs and vital signs, and planned procedure type), the variability in readmissions could only be explained 8.6% of the time, she said.

“Adding in operative data, such as procedure complexity and intraoperative blood transfusions, as well as postoperative course, added very little to our predictive ability. Including both of those groups, we could only explain 10% of the variation in readmission,” she said.

Including postdischarge data such as complications and emergency department utilization in the model increased predictive ability to 18%.

R² and C-statistics comparing the sequentially built model showed that demographics and comorbidities contributed the most to predicting readmission risk, Dr. Morris said.

Modeling based on readmission reason and specialty improved predictive ability. For example, almost 12% of readmissions for wound complications among vascular surgery patients were predictable.

“Our best predictive ability was for orthopedic patients who were readmitted with pneumonia. We were able to predict that 14% of the time,” she said.

The findings were derived by merging VA Surgical Quality Improvement Program data from inpatient operations performed between 2007 and 2014 and involving at least a 2-day postoperative hospital stay, with clinical data including laboratory findings, vitals, prior health care utilization, and postoperative complications.

“We then grouped our variables of interest into the following categories: preoperative, operative, postoperative but predischarge, and postdischarge,” she explained, noting that logistic models predicting 30-day readmission were constructed by sequentially adding groups into the model. Models were compared by way of adjusted R² and C-statistics.

Assuming postoperative readmissions are preventable suggests that they are linked to the quality of care during the index hospitalization. The current findings demonstrate the challenges in predicting readmissions, and are important given that hospitals with higher-than-expected readmission rates for certain diagnoses and procedures are fined by the Centers for Medicare & Medicaid Services; 54% of hospitals were fined in 2015, she said.

“Readmission is difficult to predict at the time of discharge despite exhaustive statistical modeling with very granular clinical patient-level detail. Preoperative patient factors and postdischarge complications contribute the most to predictive models. Efforts to decrease readmissions should focus on modifiable patient-level factors, transitions of care, and minimizing postoperative complications,” she concluded.

Dr. Morris reported having no disclosures.

The complete manuscript of this presentation is anticipated to be published in Annals of Surgery pending editorial review.

[email protected]

CHICAGO – Preadmission and postdischarge factors were important predictors of postoperative readmission in a large cohort of surgical patients, but the hospital course had little incremental impact on either readmissions or postdischarge complications in the cohort, according to a retrospective study of Veterans Affairs data.

The findings suggest that efforts to reduce postoperative readmissions should focus on enhanced postdischarge surveillance and early intervention, Dr. Melanie S. Morris of the University of Alabama at Birmingham reported at the annual meeting of the American Surgical Association.

Dr. Morris

To assess the relative contributions of patient factors, operative characteristics, and postoperative hospital course on readmissions, she and her colleagues evaluated 243,956 general, vascular, and orthopedic surgery patients in 121 VA hospitals. The overall readmission rate among the cohort was 11.1%, and for general, vascular, and orthopedic surgeries, the rates were 12.9%, 15.4%, and 7.6%, respectively; the average postoperative length of stay was 6.9 days, and 6.1% of patients experienced a predischarge complication.

Almost all readmissions occurred within 2 weeks of discharge, and for general surgery patients, most occurred within 1 week. The readmission rate for vascular surgery patients remained high beyond the 2-week mark.

An examination of the reasons for readmission showed that wound complications were the most common reason for readmission, and this was particularly true for vascular surgery patients, in whom 44% of readmissions were for wound complications, Dr. Morris said.

Gastrointestinal complications including ileus and obstruction were also common, accounting for nearly 28% of readmissions among general surgery patients, she said.

Importantly, when including preoperative data (such as demographics, comorbidities, social and behavioral factors, labs and vital signs, and planned procedure type), the variability in readmissions could only be explained 8.6% of the time, she said.

“Adding in operative data, such as procedure complexity and intraoperative blood transfusions, as well as postoperative course, added very little to our predictive ability. Including both of those groups, we could only explain 10% of the variation in readmission,” she said.

Including postdischarge data such as complications and emergency department utilization in the model increased predictive ability to 18%.

R² and C-statistics comparing the sequentially built model showed that demographics and comorbidities contributed the most to predicting readmission risk, Dr. Morris said.

Modeling based on readmission reason and specialty improved predictive ability. For example, almost 12% of readmissions for wound complications among vascular surgery patients were predictable.

“Our best predictive ability was for orthopedic patients who were readmitted with pneumonia. We were able to predict that 14% of the time,” she said.

The findings were derived by merging VA Surgical Quality Improvement Program data from inpatient operations performed between 2007 and 2014 and involving at least a 2-day postoperative hospital stay, with clinical data including laboratory findings, vitals, prior health care utilization, and postoperative complications.

“We then grouped our variables of interest into the following categories: preoperative, operative, postoperative but predischarge, and postdischarge,” she explained, noting that logistic models predicting 30-day readmission were constructed by sequentially adding groups into the model. Models were compared by way of adjusted R² and C-statistics.

Assuming postoperative readmissions are preventable suggests that they are linked to the quality of care during the index hospitalization. The current findings demonstrate the challenges in predicting readmissions, and are important given that hospitals with higher-than-expected readmission rates for certain diagnoses and procedures are fined by the Centers for Medicare & Medicaid Services; 54% of hospitals were fined in 2015, she said.

“Readmission is difficult to predict at the time of discharge despite exhaustive statistical modeling with very granular clinical patient-level detail. Preoperative patient factors and postdischarge complications contribute the most to predictive models. Efforts to decrease readmissions should focus on modifiable patient-level factors, transitions of care, and minimizing postoperative complications,” she concluded.

Dr. Morris reported having no disclosures.

The complete manuscript of this presentation is anticipated to be published in Annals of Surgery pending editorial review.

[email protected]

CHICAGO – Preadmission and postdischarge factors were important predictors of postoperative readmission in a large cohort of surgical patients, but the hospital course had little incremental impact on either readmissions or postdischarge complications in the cohort, according to a retrospective study of Veterans Affairs data.

The findings suggest that efforts to reduce postoperative readmissions should focus on enhanced postdischarge surveillance and early intervention, Dr. Melanie S. Morris of the University of Alabama at Birmingham reported at the annual meeting of the American Surgical Association.

Dr. Morris

To assess the relative contributions of patient factors, operative characteristics, and postoperative hospital course on readmissions, she and her colleagues evaluated 243,956 general, vascular, and orthopedic surgery patients in 121 VA hospitals. The overall readmission rate among the cohort was 11.1%, and for general, vascular, and orthopedic surgeries, the rates were 12.9%, 15.4%, and 7.6%, respectively; the average postoperative length of stay was 6.9 days, and 6.1% of patients experienced a predischarge complication.

Almost all readmissions occurred within 2 weeks of discharge, and for general surgery patients, most occurred within 1 week. The readmission rate for vascular surgery patients remained high beyond the 2-week mark.

An examination of the reasons for readmission showed that wound complications were the most common reason for readmission, and this was particularly true for vascular surgery patients, in whom 44% of readmissions were for wound complications, Dr. Morris said.

Gastrointestinal complications including ileus and obstruction were also common, accounting for nearly 28% of readmissions among general surgery patients, she said.

Importantly, when including preoperative data (such as demographics, comorbidities, social and behavioral factors, labs and vital signs, and planned procedure type), the variability in readmissions could only be explained 8.6% of the time, she said.

“Adding in operative data, such as procedure complexity and intraoperative blood transfusions, as well as postoperative course, added very little to our predictive ability. Including both of those groups, we could only explain 10% of the variation in readmission,” she said.

Including postdischarge data such as complications and emergency department utilization in the model increased predictive ability to 18%.

R² and C-statistics comparing the sequentially built model showed that demographics and comorbidities contributed the most to predicting readmission risk, Dr. Morris said.

Modeling based on readmission reason and specialty improved predictive ability. For example, almost 12% of readmissions for wound complications among vascular surgery patients were predictable.

“Our best predictive ability was for orthopedic patients who were readmitted with pneumonia. We were able to predict that 14% of the time,” she said.

The findings were derived by merging VA Surgical Quality Improvement Program data from inpatient operations performed between 2007 and 2014 and involving at least a 2-day postoperative hospital stay, with clinical data including laboratory findings, vitals, prior health care utilization, and postoperative complications.

“We then grouped our variables of interest into the following categories: preoperative, operative, postoperative but predischarge, and postdischarge,” she explained, noting that logistic models predicting 30-day readmission were constructed by sequentially adding groups into the model. Models were compared by way of adjusted R² and C-statistics.

Assuming postoperative readmissions are preventable suggests that they are linked to the quality of care during the index hospitalization. The current findings demonstrate the challenges in predicting readmissions, and are important given that hospitals with higher-than-expected readmission rates for certain diagnoses and procedures are fined by the Centers for Medicare & Medicaid Services; 54% of hospitals were fined in 2015, she said.

“Readmission is difficult to predict at the time of discharge despite exhaustive statistical modeling with very granular clinical patient-level detail. Preoperative patient factors and postdischarge complications contribute the most to predictive models. Efforts to decrease readmissions should focus on modifiable patient-level factors, transitions of care, and minimizing postoperative complications,” she concluded.

Dr. Morris reported having no disclosures.

The complete manuscript of this presentation is anticipated to be published in Annals of Surgery pending editorial review.

[email protected]

A single-center experience using the da Vinci robotic system to perform vascular procedures demonstrated the safety and feasibility of this technique in different areas of vascular surgery.

Dr. Petr Štádler and his colleagues at the No Homolce Hospital in Prague reported on 310 robotic-assisted vascular procedures performed between November 2005 and May 2014 with the aid of the da Vinci system. They concluded that robotic-assisted vascular procedures added to the speed and relative simplicity of construction of vascular anastomoses.

The patient cohort had procedures consisting of 224 robotic occlusive disease treatments (group 1), 65 robotic aorto-illiac aneurysm surgeries (group II), and 21 other robotic procedures (group III) as reported online in the European Journal of Vascular and Endovascular Surgery (2016. doi: 10.1016/j.ejvs.2016.02.016).

A total of 298 cases (96.1%) were successfully completed robotically, with conversion required in 10 cases; 2 patients were inoperable. The overall 30-day mortality rate was 0.3% for the entire cohort, and only two (0.6%) late prosthetic infections were seen. The median operating time was 204 min, the median anastomosis time was 29 min, and median blood loss was 571 mL.

In comparing groups I and II, group I required an operative time of 194 min, compared with 253 min in group II. Mean aortic cross-clamp time was 37 min in group I and 93 min in group II, while the mean blood loss was greater in group II (1,210 mL) as compared with group 1 (320 mL).

“The robotic system provides a real opportunity for minimally invasive surgery in the field of vascular surgery ... with all its advantages. Robotic AAA [abdominal aortic aneurysm] and aortofemoral bypass represent the standard operations in vascular surgery and they are not only possible, but safe and effective,” said Dr. Štádler and his colleagues. They added, however, that “further randomized studies are needed to ensure its benefits and the cost-effectiveness of robotic vascular surgery, compared with open and laparoscopic repair.”

Dr, Štádler and his colleagues reported that they had no disclosures.

[email protected]

A single-center experience using the da Vinci robotic system to perform vascular procedures demonstrated the safety and feasibility of this technique in different areas of vascular surgery.

Dr. Petr Štádler and his colleagues at the No Homolce Hospital in Prague reported on 310 robotic-assisted vascular procedures performed between November 2005 and May 2014 with the aid of the da Vinci system. They concluded that robotic-assisted vascular procedures added to the speed and relative simplicity of construction of vascular anastomoses.

The patient cohort had procedures consisting of 224 robotic occlusive disease treatments (group 1), 65 robotic aorto-illiac aneurysm surgeries (group II), and 21 other robotic procedures (group III) as reported online in the European Journal of Vascular and Endovascular Surgery (2016. doi: 10.1016/j.ejvs.2016.02.016).

A total of 298 cases (96.1%) were successfully completed robotically, with conversion required in 10 cases; 2 patients were inoperable. The overall 30-day mortality rate was 0.3% for the entire cohort, and only two (0.6%) late prosthetic infections were seen. The median operating time was 204 min, the median anastomosis time was 29 min, and median blood loss was 571 mL.

In comparing groups I and II, group I required an operative time of 194 min, compared with 253 min in group II. Mean aortic cross-clamp time was 37 min in group I and 93 min in group II, while the mean blood loss was greater in group II (1,210 mL) as compared with group 1 (320 mL).

“The robotic system provides a real opportunity for minimally invasive surgery in the field of vascular surgery ... with all its advantages. Robotic AAA [abdominal aortic aneurysm] and aortofemoral bypass represent the standard operations in vascular surgery and they are not only possible, but safe and effective,” said Dr. Štádler and his colleagues. They added, however, that “further randomized studies are needed to ensure its benefits and the cost-effectiveness of robotic vascular surgery, compared with open and laparoscopic repair.”

Dr, Štádler and his colleagues reported that they had no disclosures.

[email protected]

A single-center experience using the da Vinci robotic system to perform vascular procedures demonstrated the safety and feasibility of this technique in different areas of vascular surgery.

Dr. Petr Štádler and his colleagues at the No Homolce Hospital in Prague reported on 310 robotic-assisted vascular procedures performed between November 2005 and May 2014 with the aid of the da Vinci system. They concluded that robotic-assisted vascular procedures added to the speed and relative simplicity of construction of vascular anastomoses.

The patient cohort had procedures consisting of 224 robotic occlusive disease treatments (group 1), 65 robotic aorto-illiac aneurysm surgeries (group II), and 21 other robotic procedures (group III) as reported online in the European Journal of Vascular and Endovascular Surgery (2016. doi: 10.1016/j.ejvs.2016.02.016).

A total of 298 cases (96.1%) were successfully completed robotically, with conversion required in 10 cases; 2 patients were inoperable. The overall 30-day mortality rate was 0.3% for the entire cohort, and only two (0.6%) late prosthetic infections were seen. The median operating time was 204 min, the median anastomosis time was 29 min, and median blood loss was 571 mL.

In comparing groups I and II, group I required an operative time of 194 min, compared with 253 min in group II. Mean aortic cross-clamp time was 37 min in group I and 93 min in group II, while the mean blood loss was greater in group II (1,210 mL) as compared with group 1 (320 mL).

“The robotic system provides a real opportunity for minimally invasive surgery in the field of vascular surgery ... with all its advantages. Robotic AAA [abdominal aortic aneurysm] and aortofemoral bypass represent the standard operations in vascular surgery and they are not only possible, but safe and effective,” said Dr. Štádler and his colleagues. They added, however, that “further randomized studies are needed to ensure its benefits and the cost-effectiveness of robotic vascular surgery, compared with open and laparoscopic repair.”

Dr, Štádler and his colleagues reported that they had no disclosures.

[email protected]

We have tools to predict bleeding risk, but their predictive value is modest, and the estimated risk of bleeding is often outweighed by the benefits of anticoagulant therapy.

Anticoagulant therapy is commonly prescribed for conditions that disproportionately affect the elderly, including atrial fibrillation, venous thromboembolism, and valvular heart disease. Though anticoagulants are highly effective in preventing clots, they also significantly increase the risk of bleeding. Since older age is a risk factor for bleeding as well as thrombosis, it is essential to weigh the risks and benefits of anticoagulants for each patient.

WHAT KINDS OF BLEEDING DEVELOP IN PATIENTS ON ANTICOAGULANTS?

Patients taking anticoagulants have roughly double the risk of bleeding compared with patients not on anticoagulants.¹ Bleeding rates tend to be slightly higher in patients taking anticoagulants for venous thromboembolism than in those taking them for atrial fibrillation. The average yearly risk of a “major” anticoagulant-associated bleeding event (eg, requiring transfusion or intervention or occurring in a critical anatomic site) is about 2% to 3%, with most of the bleeding being gastrointestinal.²

Intracranial hemorrhage is by far the most deadly complication of anticoagulant therapy: it causes 90% of deaths and disability from warfarin-associated hemorrhage and is associated with a death rate over 50%; however, it is much less common than gastrointestinal bleeding.³ Anticoagulant therapy increases the risk of intracranial hemorrhage by only 0.2% per year.¹

RISK-PREDICTION TOOLS HAVE LIMITATIONS

Not all patients have the same risk of bleeding when taking anticoagulants. Many factors in addition to advanced age have been associated with increased bleeding risk, including coexisting medical conditions (such as malignancy, prior stroke or bleeding event, and renal insufficiency), medications (particularly aspirin, nonsteroidal anti-inflammatory drugs, and other antiplatelet drugs), and the timing and intensity of anticoagulation therapy.⁴

Scoring tools have been developed to identify patients at higher risk of bleeding (Table 1).^4–9 The various schemes incorporate many of the same variables, such as older age, renal impairment, and history of bleeding, but some include additional risk factors while others are more parsimonious. They also differ in how individual risk factors are weighted to generate a final risk score.

In terms of predictive ability, none of the available risk schemes appears to be vastly superior, and their ability to predict hemorrhage is modest at best. There is also no universal or well-established threshold at which the risk of bleeding is so high that one would not consider anticoagulants. In fact, a “high-risk” patient may have an aggregate bleeding rate of only 4% to 6% per year. Using risk schemes such as ATRIA,⁵ HEMORR₂HAGES,⁶ and HAS-BLED⁷ may be more useful because they provide an estimate of bleeding risk for each point on the scale.

Moreover, the current tools to predict bleeding risk have several other limitations. They were developed in patients already taking anticoagulants and so probably underestimate the actual risk of hemorrhage, as people who could not take anticoagulants were excluded, most likely because they were at high risk of bleeding. Therefore, bleeding risk tools probably apply best to a patient for whom anticoagulation can be considered.

Some clinical variables are necessarily broad. For example, “prior bleeding” is a risk factor included in several risk scores, but does not distinguish between massive variceal bleeding and minor hemorrhoidal bleeding.

Risk scores do not effectively predict intracranial hemorrhage.

Finally, these risk tools were developed in patients taking vitamin K antagonists, and it is not yet established that they can effectively predict hemorrhage related to other, newer anticoagulants.

WHEN DOES BLEEDING RISK OUTWEIGH ANTICOAGULATION BENEFIT?

For patients with atrial fibrillation, the net clinical benefit of anticoagulation (strokes prevented minus bleeding events induced) increases as the risk of stroke rises. Updated guidelines for managing atrial fibrillation now recommend anticoagulation for most patients.¹⁰

For most older patients with atrial fibrillation, the decision to anticoagulate may not change even if a bleeding risk tool indicates a high bleeding risk.¹¹ For example, a patient with a history of ischemic stroke will generally derive more benefit than harm from anticoagulants. The primary exception is in patients with prior lobar intracranial hemorrhage, because of the high risk of rebleeding and the worse outcomes associated with intracranial hemorrhage.¹² As a general rule, most patients with atrial fibrillation and an additional risk factor for stroke should be considered for anticoagulant therapy unless they have a history of lobar intracranial hemorrhage.

Anticoagulation may be deferred if the patient is at the lower end of the stroke risk spectrum and if the bleeding risk is calculated to be high. However, as noted before, current bleeding risk tools probably do not capture the experiences of patients at the extremes of high bleeding risk, so clinical judgment continues to be important. In addition, forgoing anticoagulation could be reasonable even in patients at high risk for recurrent stroke if their life expectancy is limited, if anticoagulation is unacceptably burdensome, or if it is not within their goals and preferences.

WHAT ABOUT FALL RISK?

Fall risk commonly deters clinicians from prescribing anticoagulants because of the fear of causing intracranial hemorrhage. In particular, falls increase the risk for subdural hematoma, which has a death rate comparable to that of ischemic stroke.¹³

Studies have had difficulty quantifying the exact risk associated with falls because these patients are less likely to be prescribed anticoagulants. One decision analysis estimated that a person would have to fall about 300 times per year before the risk of intracranial hemorrhage outweighed the benefits from stroke reduction.¹⁴ Studies have found that patients at high risk of falls have a higher risk of intracranial hemorrhage, but that this risk is counterbalanced by an even greater risk of ischemic stroke.¹⁵

Therefore, if the baseline risk of ischemic stroke is high, anticoagulation is still favored.

WHEN SHOULD I USE A BLEEDING RISK TOOL?

Despite their limitations, bleeding risk tools are useful in clinical practice when estimates of bleeding risk affect clinical behavior. They are most helpful for patients at the lower end of the stroke or thromboembolism risk spectrum, where the decision to anticoagulate is strongly influenced by bleeding risk. Risk tools may also be helpful when counseling patients about their bleeding risk off and on anticoagulants.

Finally, recognizing that a patient is at high bleeding risk may lead the clinician to consider closer monitoring of anticoagulants or to implement strategies to reduce the risk.

We have tools to predict bleeding risk, but their predictive value is modest, and the estimated risk of bleeding is often outweighed by the benefits of anticoagulant therapy.

Anticoagulant therapy is commonly prescribed for conditions that disproportionately affect the elderly, including atrial fibrillation, venous thromboembolism, and valvular heart disease. Though anticoagulants are highly effective in preventing clots, they also significantly increase the risk of bleeding. Since older age is a risk factor for bleeding as well as thrombosis, it is essential to weigh the risks and benefits of anticoagulants for each patient.

WHAT KINDS OF BLEEDING DEVELOP IN PATIENTS ON ANTICOAGULANTS?

Patients taking anticoagulants have roughly double the risk of bleeding compared with patients not on anticoagulants.¹ Bleeding rates tend to be slightly higher in patients taking anticoagulants for venous thromboembolism than in those taking them for atrial fibrillation. The average yearly risk of a “major” anticoagulant-associated bleeding event (eg, requiring transfusion or intervention or occurring in a critical anatomic site) is about 2% to 3%, with most of the bleeding being gastrointestinal.²

Intracranial hemorrhage is by far the most deadly complication of anticoagulant therapy: it causes 90% of deaths and disability from warfarin-associated hemorrhage and is associated with a death rate over 50%; however, it is much less common than gastrointestinal bleeding.³ Anticoagulant therapy increases the risk of intracranial hemorrhage by only 0.2% per year.¹

RISK-PREDICTION TOOLS HAVE LIMITATIONS

Not all patients have the same risk of bleeding when taking anticoagulants. Many factors in addition to advanced age have been associated with increased bleeding risk, including coexisting medical conditions (such as malignancy, prior stroke or bleeding event, and renal insufficiency), medications (particularly aspirin, nonsteroidal anti-inflammatory drugs, and other antiplatelet drugs), and the timing and intensity of anticoagulation therapy.⁴

Scoring tools have been developed to identify patients at higher risk of bleeding (Table 1).^4–9 The various schemes incorporate many of the same variables, such as older age, renal impairment, and history of bleeding, but some include additional risk factors while others are more parsimonious. They also differ in how individual risk factors are weighted to generate a final risk score.

In terms of predictive ability, none of the available risk schemes appears to be vastly superior, and their ability to predict hemorrhage is modest at best. There is also no universal or well-established threshold at which the risk of bleeding is so high that one would not consider anticoagulants. In fact, a “high-risk” patient may have an aggregate bleeding rate of only 4% to 6% per year. Using risk schemes such as ATRIA,⁵ HEMORR₂HAGES,⁶ and HAS-BLED⁷ may be more useful because they provide an estimate of bleeding risk for each point on the scale.

Moreover, the current tools to predict bleeding risk have several other limitations. They were developed in patients already taking anticoagulants and so probably underestimate the actual risk of hemorrhage, as people who could not take anticoagulants were excluded, most likely because they were at high risk of bleeding. Therefore, bleeding risk tools probably apply best to a patient for whom anticoagulation can be considered.

Some clinical variables are necessarily broad. For example, “prior bleeding” is a risk factor included in several risk scores, but does not distinguish between massive variceal bleeding and minor hemorrhoidal bleeding.

Risk scores do not effectively predict intracranial hemorrhage.

Finally, these risk tools were developed in patients taking vitamin K antagonists, and it is not yet established that they can effectively predict hemorrhage related to other, newer anticoagulants.

WHEN DOES BLEEDING RISK OUTWEIGH ANTICOAGULATION BENEFIT?

For patients with atrial fibrillation, the net clinical benefit of anticoagulation (strokes prevented minus bleeding events induced) increases as the risk of stroke rises. Updated guidelines for managing atrial fibrillation now recommend anticoagulation for most patients.¹⁰

For most older patients with atrial fibrillation, the decision to anticoagulate may not change even if a bleeding risk tool indicates a high bleeding risk.¹¹ For example, a patient with a history of ischemic stroke will generally derive more benefit than harm from anticoagulants. The primary exception is in patients with prior lobar intracranial hemorrhage, because of the high risk of rebleeding and the worse outcomes associated with intracranial hemorrhage.¹² As a general rule, most patients with atrial fibrillation and an additional risk factor for stroke should be considered for anticoagulant therapy unless they have a history of lobar intracranial hemorrhage.

Anticoagulation may be deferred if the patient is at the lower end of the stroke risk spectrum and if the bleeding risk is calculated to be high. However, as noted before, current bleeding risk tools probably do not capture the experiences of patients at the extremes of high bleeding risk, so clinical judgment continues to be important. In addition, forgoing anticoagulation could be reasonable even in patients at high risk for recurrent stroke if their life expectancy is limited, if anticoagulation is unacceptably burdensome, or if it is not within their goals and preferences.

WHAT ABOUT FALL RISK?

Fall risk commonly deters clinicians from prescribing anticoagulants because of the fear of causing intracranial hemorrhage. In particular, falls increase the risk for subdural hematoma, which has a death rate comparable to that of ischemic stroke.¹³

Studies have had difficulty quantifying the exact risk associated with falls because these patients are less likely to be prescribed anticoagulants. One decision analysis estimated that a person would have to fall about 300 times per year before the risk of intracranial hemorrhage outweighed the benefits from stroke reduction.¹⁴ Studies have found that patients at high risk of falls have a higher risk of intracranial hemorrhage, but that this risk is counterbalanced by an even greater risk of ischemic stroke.¹⁵

Therefore, if the baseline risk of ischemic stroke is high, anticoagulation is still favored.

WHEN SHOULD I USE A BLEEDING RISK TOOL?

Despite their limitations, bleeding risk tools are useful in clinical practice when estimates of bleeding risk affect clinical behavior. They are most helpful for patients at the lower end of the stroke or thromboembolism risk spectrum, where the decision to anticoagulate is strongly influenced by bleeding risk. Risk tools may also be helpful when counseling patients about their bleeding risk off and on anticoagulants.

Finally, recognizing that a patient is at high bleeding risk may lead the clinician to consider closer monitoring of anticoagulants or to implement strategies to reduce the risk.

We have tools to predict bleeding risk, but their predictive value is modest, and the estimated risk of bleeding is often outweighed by the benefits of anticoagulant therapy.

Anticoagulant therapy is commonly prescribed for conditions that disproportionately affect the elderly, including atrial fibrillation, venous thromboembolism, and valvular heart disease. Though anticoagulants are highly effective in preventing clots, they also significantly increase the risk of bleeding. Since older age is a risk factor for bleeding as well as thrombosis, it is essential to weigh the risks and benefits of anticoagulants for each patient.

WHAT KINDS OF BLEEDING DEVELOP IN PATIENTS ON ANTICOAGULANTS?

Patients taking anticoagulants have roughly double the risk of bleeding compared with patients not on anticoagulants.¹ Bleeding rates tend to be slightly higher in patients taking anticoagulants for venous thromboembolism than in those taking them for atrial fibrillation. The average yearly risk of a “major” anticoagulant-associated bleeding event (eg, requiring transfusion or intervention or occurring in a critical anatomic site) is about 2% to 3%, with most of the bleeding being gastrointestinal.²

Intracranial hemorrhage is by far the most deadly complication of anticoagulant therapy: it causes 90% of deaths and disability from warfarin-associated hemorrhage and is associated with a death rate over 50%; however, it is much less common than gastrointestinal bleeding.³ Anticoagulant therapy increases the risk of intracranial hemorrhage by only 0.2% per year.¹

RISK-PREDICTION TOOLS HAVE LIMITATIONS

Not all patients have the same risk of bleeding when taking anticoagulants. Many factors in addition to advanced age have been associated with increased bleeding risk, including coexisting medical conditions (such as malignancy, prior stroke or bleeding event, and renal insufficiency), medications (particularly aspirin, nonsteroidal anti-inflammatory drugs, and other antiplatelet drugs), and the timing and intensity of anticoagulation therapy.⁴

Scoring tools have been developed to identify patients at higher risk of bleeding (Table 1).^4–9 The various schemes incorporate many of the same variables, such as older age, renal impairment, and history of bleeding, but some include additional risk factors while others are more parsimonious. They also differ in how individual risk factors are weighted to generate a final risk score.

In terms of predictive ability, none of the available risk schemes appears to be vastly superior, and their ability to predict hemorrhage is modest at best. There is also no universal or well-established threshold at which the risk of bleeding is so high that one would not consider anticoagulants. In fact, a “high-risk” patient may have an aggregate bleeding rate of only 4% to 6% per year. Using risk schemes such as ATRIA,⁵ HEMORR₂HAGES,⁶ and HAS-BLED⁷ may be more useful because they provide an estimate of bleeding risk for each point on the scale.

Moreover, the current tools to predict bleeding risk have several other limitations. They were developed in patients already taking anticoagulants and so probably underestimate the actual risk of hemorrhage, as people who could not take anticoagulants were excluded, most likely because they were at high risk of bleeding. Therefore, bleeding risk tools probably apply best to a patient for whom anticoagulation can be considered.

Some clinical variables are necessarily broad. For example, “prior bleeding” is a risk factor included in several risk scores, but does not distinguish between massive variceal bleeding and minor hemorrhoidal bleeding.

Risk scores do not effectively predict intracranial hemorrhage.

Finally, these risk tools were developed in patients taking vitamin K antagonists, and it is not yet established that they can effectively predict hemorrhage related to other, newer anticoagulants.

WHEN DOES BLEEDING RISK OUTWEIGH ANTICOAGULATION BENEFIT?

For patients with atrial fibrillation, the net clinical benefit of anticoagulation (strokes prevented minus bleeding events induced) increases as the risk of stroke rises. Updated guidelines for managing atrial fibrillation now recommend anticoagulation for most patients.¹⁰

For most older patients with atrial fibrillation, the decision to anticoagulate may not change even if a bleeding risk tool indicates a high bleeding risk.¹¹ For example, a patient with a history of ischemic stroke will generally derive more benefit than harm from anticoagulants. The primary exception is in patients with prior lobar intracranial hemorrhage, because of the high risk of rebleeding and the worse outcomes associated with intracranial hemorrhage.¹² As a general rule, most patients with atrial fibrillation and an additional risk factor for stroke should be considered for anticoagulant therapy unless they have a history of lobar intracranial hemorrhage.

Anticoagulation may be deferred if the patient is at the lower end of the stroke risk spectrum and if the bleeding risk is calculated to be high. However, as noted before, current bleeding risk tools probably do not capture the experiences of patients at the extremes of high bleeding risk, so clinical judgment continues to be important. In addition, forgoing anticoagulation could be reasonable even in patients at high risk for recurrent stroke if their life expectancy is limited, if anticoagulation is unacceptably burdensome, or if it is not within their goals and preferences.

WHAT ABOUT FALL RISK?

Fall risk commonly deters clinicians from prescribing anticoagulants because of the fear of causing intracranial hemorrhage. In particular, falls increase the risk for subdural hematoma, which has a death rate comparable to that of ischemic stroke.¹³

Studies have had difficulty quantifying the exact risk associated with falls because these patients are less likely to be prescribed anticoagulants. One decision analysis estimated that a person would have to fall about 300 times per year before the risk of intracranial hemorrhage outweighed the benefits from stroke reduction.¹⁴ Studies have found that patients at high risk of falls have a higher risk of intracranial hemorrhage, but that this risk is counterbalanced by an even greater risk of ischemic stroke.¹⁵

Therefore, if the baseline risk of ischemic stroke is high, anticoagulation is still favored.

WHEN SHOULD I USE A BLEEDING RISK TOOL?

Despite their limitations, bleeding risk tools are useful in clinical practice when estimates of bleeding risk affect clinical behavior. They are most helpful for patients at the lower end of the stroke or thromboembolism risk spectrum, where the decision to anticoagulate is strongly influenced by bleeding risk. Risk tools may also be helpful when counseling patients about their bleeding risk off and on anticoagulants.

Finally, recognizing that a patient is at high bleeding risk may lead the clinician to consider closer monitoring of anticoagulants or to implement strategies to reduce the risk.

Quinn and Fang, in this issue of the Journal discuss efforts to predict bleeding complications associated with anticoagulant therapy in elderly patients. They note, as others have suggested, that we may fear the risk of severe anticoagulant-associated bleeding more than is warranted based on the data. The level of that fear and the risk of bleeding depend on the specific need for anticoagulant therapy in a given patient and on the risk of serious adverse outcomes from thrombosis that the anticoagulation is supposed to prevent. All prediction models are based on an “average” patient with certain characteristics. But of course none of our patients are average.

The studies Quinn and Fang discuss focus on vitamin K antagonist therapy. There is probably not enough practice-based or trial-based evidence yet to evaluate the risks associated with the new generation of anticoagulants.

All prediction models have limitations. The recent discussion on establishing a risk-based strategy to guide institution of lipid-lowering therapy highlights the challenges inherent in trying to base therapeutic decisions on predictive models. But however imperfect, models are still widely used to predict fracture risk in patients being considered for bone antiresorptive therapy and to predict the need for anticoagulation therapy or further diagnostic testing in patients with potential deep vein thrombosis or atrial fibrillation.

The decision to start anticoagulation in an elderly patient is often informed by the possibility of an easily recognized and feared risk factor for bleeding complications—falling. Falls are certainly important and are a major contributor to subdural hematoma and complicated hip fracture. But there are more common causes of severe bleeding complications that are less easily predicted by functional assessment of the patient. Nonetheless, fall risk can be lessened by prescribing exercise programs such as tai chi to improve balance, limiting the use of drugs associated with falls in the elderly, perhaps correcting hyponatremia, and testing for orthostatic hypotension as part of the physical examination. (Mild compression stockings and medication adjustment may reduce orthostasis.) Some of these interventions are easily accomplished, and probably should be done with all of our elderly and frail patients.

As we build more risk calculators into our electronic medical records, we must continue to consider their limitations as well as their specific utility. To paraphrase Yogi Berra, making predictions is tough, especially about the future.

Quinn and Fang, in this issue of the Journal discuss efforts to predict bleeding complications associated with anticoagulant therapy in elderly patients. They note, as others have suggested, that we may fear the risk of severe anticoagulant-associated bleeding more than is warranted based on the data. The level of that fear and the risk of bleeding depend on the specific need for anticoagulant therapy in a given patient and on the risk of serious adverse outcomes from thrombosis that the anticoagulation is supposed to prevent. All prediction models are based on an “average” patient with certain characteristics. But of course none of our patients are average.

The studies Quinn and Fang discuss focus on vitamin K antagonist therapy. There is probably not enough practice-based or trial-based evidence yet to evaluate the risks associated with the new generation of anticoagulants.

All prediction models have limitations. The recent discussion on establishing a risk-based strategy to guide institution of lipid-lowering therapy highlights the challenges inherent in trying to base therapeutic decisions on predictive models. But however imperfect, models are still widely used to predict fracture risk in patients being considered for bone antiresorptive therapy and to predict the need for anticoagulation therapy or further diagnostic testing in patients with potential deep vein thrombosis or atrial fibrillation.

The decision to start anticoagulation in an elderly patient is often informed by the possibility of an easily recognized and feared risk factor for bleeding complications—falling. Falls are certainly important and are a major contributor to subdural hematoma and complicated hip fracture. But there are more common causes of severe bleeding complications that are less easily predicted by functional assessment of the patient. Nonetheless, fall risk can be lessened by prescribing exercise programs such as tai chi to improve balance, limiting the use of drugs associated with falls in the elderly, perhaps correcting hyponatremia, and testing for orthostatic hypotension as part of the physical examination. (Mild compression stockings and medication adjustment may reduce orthostasis.) Some of these interventions are easily accomplished, and probably should be done with all of our elderly and frail patients.

As we build more risk calculators into our electronic medical records, we must continue to consider their limitations as well as their specific utility. To paraphrase Yogi Berra, making predictions is tough, especially about the future.

Quinn and Fang, in this issue of the Journal discuss efforts to predict bleeding complications associated with anticoagulant therapy in elderly patients. They note, as others have suggested, that we may fear the risk of severe anticoagulant-associated bleeding more than is warranted based on the data. The level of that fear and the risk of bleeding depend on the specific need for anticoagulant therapy in a given patient and on the risk of serious adverse outcomes from thrombosis that the anticoagulation is supposed to prevent. All prediction models are based on an “average” patient with certain characteristics. But of course none of our patients are average.

The studies Quinn and Fang discuss focus on vitamin K antagonist therapy. There is probably not enough practice-based or trial-based evidence yet to evaluate the risks associated with the new generation of anticoagulants.

All prediction models have limitations. The recent discussion on establishing a risk-based strategy to guide institution of lipid-lowering therapy highlights the challenges inherent in trying to base therapeutic decisions on predictive models. But however imperfect, models are still widely used to predict fracture risk in patients being considered for bone antiresorptive therapy and to predict the need for anticoagulation therapy or further diagnostic testing in patients with potential deep vein thrombosis or atrial fibrillation.

The decision to start anticoagulation in an elderly patient is often informed by the possibility of an easily recognized and feared risk factor for bleeding complications—falling. Falls are certainly important and are a major contributor to subdural hematoma and complicated hip fracture. But there are more common causes of severe bleeding complications that are less easily predicted by functional assessment of the patient. Nonetheless, fall risk can be lessened by prescribing exercise programs such as tai chi to improve balance, limiting the use of drugs associated with falls in the elderly, perhaps correcting hyponatremia, and testing for orthostatic hypotension as part of the physical examination. (Mild compression stockings and medication adjustment may reduce orthostasis.) Some of these interventions are easily accomplished, and probably should be done with all of our elderly and frail patients.

As we build more risk calculators into our electronic medical records, we must continue to consider their limitations as well as their specific utility. To paraphrase Yogi Berra, making predictions is tough, especially about the future.

VANCOUVER – The relationship between hospitals’ procedural volume and patient outcomes that has been observed for many cardiovascular interventions and other surgeries does not hold for endovascular mechanical thrombectomy procedures for acute ischemic stroke, according to an analysis of cases during 2008-2011 in the Nationwide Inpatient Sample.

In-hospital mortality and rates for any complications were not associated with high or low endovascular mechanical thrombectomy (EMT) volume at hospitals across the United States in the analysis of 13,502 adult patients hospitalized with a primary diagnosis of acute ischemic stroke and treated with EMT, neurology resident Dr. Abhishek Lunagariya of the University of Florida, Gainesville, reported at the annual meeting of the American Academy of Neurology.

A smaller prior study of 2,749 EMTs done in 296 hospitals in 2008 showed lower mortality in high-volume hospitals that performed 10 or more of the procedures per year (J Stroke Cerebrovasc Dis. 2013 Nov; 22[8]:1263-9).

Of the 13,502 EMTs in the study, 25% occurred at low-volume hospitals performing less than 10 per year. Low-volume hospitals had higher in-hospital mortality than did higher-volume centers performing 10 or more of the procedures per year in an unadjusted comparison (26% vs. 21%). A comparison of a combined endpoint for any complications (in-hospital mortality, intracerebral hemorrhage, and vascular complications) was also significantly in favor of high-volume hospitals (34% vs. 30%).

However, in a multivariate hierarchical model, low-volume hospitals were not associated with higher in-hospital mortality (odds ratio, 0.95; 95% confidence interval, 0.74-1.23) or rate of any complications (OR, 0.96; 95% CI, 0.76-1.21). These analyses were adjusted for age, gender, ethnicity, primary payer, median household income, hospital region/teaching status/location/bed size, Charlson Comorbidity Index, calendar year, and use of intravenous tissue plasminogen activator.

Dr. Lunagariya noted that he and his associates could not adjust the comparisons for National Institutes of Health Stroke Scale scores because they are not recorded in the National Inpatient Sample. They also could not examine what happened to patients after discharge.

Dr. Lunagariya suggested a variety of possible reasons that might help to explain the lack of an association between hospital procedure volume and outcomes after adjustment: the availability of better thrombectomy devices since the smaller 2008 study, lesser operator variability, favorable patient selection, and an increased skill set of operators working at low-volume hospitals.

One audience member noted that some endovascular interventionalists will operate at both high-volume and low-volume hospitals and could account for some of the findings. That indeed might be happening more often and needs to happen more often, Dr. Lunagariya said in an interview, in order to combat the “common belief” that it would be better to wait for a patient to undergo the procedure at a high- rather than low-volume hospital. Patients who receive initial care for stroke at a low-volume hospital but are not stable enough or do not have enough time to be transferred could benefit from EMT if an interventionalist who performs EMT drove there instead, he said.

With even newer devices now available that are thought to be easier to use, Dr. Lunagariya suggested that the similarity in outcomes at low- and higher-volume centers may not change in updated analyses of more recent EMT procedures for ischemic stroke.

The investigators received no funding for the study, and they reported having no financial disclosures.

[email protected]

VANCOUVER – The relationship between hospitals’ procedural volume and patient outcomes that has been observed for many cardiovascular interventions and other surgeries does not hold for endovascular mechanical thrombectomy procedures for acute ischemic stroke, according to an analysis of cases during 2008-2011 in the Nationwide Inpatient Sample.

In-hospital mortality and rates for any complications were not associated with high or low endovascular mechanical thrombectomy (EMT) volume at hospitals across the United States in the analysis of 13,502 adult patients hospitalized with a primary diagnosis of acute ischemic stroke and treated with EMT, neurology resident Dr. Abhishek Lunagariya of the University of Florida, Gainesville, reported at the annual meeting of the American Academy of Neurology.

A smaller prior study of 2,749 EMTs done in 296 hospitals in 2008 showed lower mortality in high-volume hospitals that performed 10 or more of the procedures per year (J Stroke Cerebrovasc Dis. 2013 Nov; 22[8]:1263-9).

Of the 13,502 EMTs in the study, 25% occurred at low-volume hospitals performing less than 10 per year. Low-volume hospitals had higher in-hospital mortality than did higher-volume centers performing 10 or more of the procedures per year in an unadjusted comparison (26% vs. 21%). A comparison of a combined endpoint for any complications (in-hospital mortality, intracerebral hemorrhage, and vascular complications) was also significantly in favor of high-volume hospitals (34% vs. 30%).

However, in a multivariate hierarchical model, low-volume hospitals were not associated with higher in-hospital mortality (odds ratio, 0.95; 95% confidence interval, 0.74-1.23) or rate of any complications (OR, 0.96; 95% CI, 0.76-1.21). These analyses were adjusted for age, gender, ethnicity, primary payer, median household income, hospital region/teaching status/location/bed size, Charlson Comorbidity Index, calendar year, and use of intravenous tissue plasminogen activator.

Dr. Lunagariya noted that he and his associates could not adjust the comparisons for National Institutes of Health Stroke Scale scores because they are not recorded in the National Inpatient Sample. They also could not examine what happened to patients after discharge.

Dr. Lunagariya suggested a variety of possible reasons that might help to explain the lack of an association between hospital procedure volume and outcomes after adjustment: the availability of better thrombectomy devices since the smaller 2008 study, lesser operator variability, favorable patient selection, and an increased skill set of operators working at low-volume hospitals.

One audience member noted that some endovascular interventionalists will operate at both high-volume and low-volume hospitals and could account for some of the findings. That indeed might be happening more often and needs to happen more often, Dr. Lunagariya said in an interview, in order to combat the “common belief” that it would be better to wait for a patient to undergo the procedure at a high- rather than low-volume hospital. Patients who receive initial care for stroke at a low-volume hospital but are not stable enough or do not have enough time to be transferred could benefit from EMT if an interventionalist who performs EMT drove there instead, he said.

With even newer devices now available that are thought to be easier to use, Dr. Lunagariya suggested that the similarity in outcomes at low- and higher-volume centers may not change in updated analyses of more recent EMT procedures for ischemic stroke.

The investigators received no funding for the study, and they reported having no financial disclosures.

[email protected]

VANCOUVER – The relationship between hospitals’ procedural volume and patient outcomes that has been observed for many cardiovascular interventions and other surgeries does not hold for endovascular mechanical thrombectomy procedures for acute ischemic stroke, according to an analysis of cases during 2008-2011 in the Nationwide Inpatient Sample.

In-hospital mortality and rates for any complications were not associated with high or low endovascular mechanical thrombectomy (EMT) volume at hospitals across the United States in the analysis of 13,502 adult patients hospitalized with a primary diagnosis of acute ischemic stroke and treated with EMT, neurology resident Dr. Abhishek Lunagariya of the University of Florida, Gainesville, reported at the annual meeting of the American Academy of Neurology.

A smaller prior study of 2,749 EMTs done in 296 hospitals in 2008 showed lower mortality in high-volume hospitals that performed 10 or more of the procedures per year (J Stroke Cerebrovasc Dis. 2013 Nov; 22[8]:1263-9).

Of the 13,502 EMTs in the study, 25% occurred at low-volume hospitals performing less than 10 per year. Low-volume hospitals had higher in-hospital mortality than did higher-volume centers performing 10 or more of the procedures per year in an unadjusted comparison (26% vs. 21%). A comparison of a combined endpoint for any complications (in-hospital mortality, intracerebral hemorrhage, and vascular complications) was also significantly in favor of high-volume hospitals (34% vs. 30%).

However, in a multivariate hierarchical model, low-volume hospitals were not associated with higher in-hospital mortality (odds ratio, 0.95; 95% confidence interval, 0.74-1.23) or rate of any complications (OR, 0.96; 95% CI, 0.76-1.21). These analyses were adjusted for age, gender, ethnicity, primary payer, median household income, hospital region/teaching status/location/bed size, Charlson Comorbidity Index, calendar year, and use of intravenous tissue plasminogen activator.

Dr. Lunagariya noted that he and his associates could not adjust the comparisons for National Institutes of Health Stroke Scale scores because they are not recorded in the National Inpatient Sample. They also could not examine what happened to patients after discharge.

Dr. Lunagariya suggested a variety of possible reasons that might help to explain the lack of an association between hospital procedure volume and outcomes after adjustment: the availability of better thrombectomy devices since the smaller 2008 study, lesser operator variability, favorable patient selection, and an increased skill set of operators working at low-volume hospitals.

One audience member noted that some endovascular interventionalists will operate at both high-volume and low-volume hospitals and could account for some of the findings. That indeed might be happening more often and needs to happen more often, Dr. Lunagariya said in an interview, in order to combat the “common belief” that it would be better to wait for a patient to undergo the procedure at a high- rather than low-volume hospital. Patients who receive initial care for stroke at a low-volume hospital but are not stable enough or do not have enough time to be transferred could benefit from EMT if an interventionalist who performs EMT drove there instead, he said.

With even newer devices now available that are thought to be easier to use, Dr. Lunagariya suggested that the similarity in outcomes at low- and higher-volume centers may not change in updated analyses of more recent EMT procedures for ischemic stroke.

The investigators received no funding for the study, and they reported having no financial disclosures.

[email protected]

The incidental finding of high systolic pulmonary artery pressure on echocardiography is common. What we should do about it varies according to clinical presentation, comorbidities, and results of other tests, including assessment of the right ventricle. Thus, the optimal approach ranges from no further investigation to right heart catheterization and, in some cases, referral to a pulmonary hypertension center.

THE TWO MEASUREMENTS COMPARED

Although it raises concern, the finding of high systolic pulmonary artery pressure is not enough to diagnose pulmonary hypertension. In fact, several other conditions are associated with high systolic pulmonary artery pressure on echocardiography (Table 1). The diagnosis must be confirmed with right heart catheterization.¹

Echocardiography provides an estimate of the systolic pulmonary artery pressure that is calculated from other values, whereas right heart catheterization gives a direct measurement of the mean pulmonary artery pressure, which is necessary for diagnosing pulmonary hypertension. The two values are correlated, but the differences are noteworthy.

WHAT IS PULMONARY HYPERTENSION?

Pulmonary hypertension is defined by a resting mean pulmonary artery pressure 25 mm Hg or greater during right heart catheterization.¹ The large number of conditions associated with pulmonary hypertension can be divided into five groups²:

• Group 1, pulmonary artery hypertension
• Group 2, pulmonary hypertension associated with left heart disease
• Group 3, pulmonary hypertension due to chronic lung disease or hypoxia
• Group 4, chronic thromboembolic pulmonary hypertension
• Group 5, pulmonary hypertension due to unclear multifactorial mechanisms.²

Pulmonary artery hypertension (group 1) is a syndrome characterized by a restricted flow of small pulmonary arteries that can be idiopathic, heritable, or induced by anorexigens, connective tissue disease, congenital heart disease, portal hypertension, human immunodeficiency virus (HIV), or schistosomiasis.^2,3 In spite of significant advances in therapy in the last 3 decades, pulmonary artery hypertension continues to lead to right heart failure and death,⁴ and the diagnosis has adverse prognostic implications. Therefore, it is essential to be attentive when reviewing the echocardiogram, since an elevated systolic pulmonary artery pressure may be an important clue to pulmonary hypertension.

ESTIMATED PRESSURE: HOW HIGH IS TOO HIGH?

There is no consensus on the optimal cutoff of echocardiographic systolic pulmonary artery pressure to trigger a further evaluation for pulmonary hypertension.

A retrospective evaluation of nearly 16,000 normal echocardiograms found that the 95% upper limit for systolic pulmonary artery pressure was 37 mm Hg.⁵

European guidelines⁶ propose that pulmonary hypertension is unlikely if the estimated systolic pulmonary artery pressure is 36 mm Hg or lower, possible if it is 37 to 50 mm Hg, and likely if it is higher than 50 mm Hg.⁶

The 2009 consensus document of the American College of Cardiology Foundation and American Heart Association³ recommends a systolic pulmonary artery pressure greater than 40 mm Hg as the threshold to suggest further evaluation in a patient with unexplained dyspnea.

Converting the systolic pulmonary artery pressure to the mean pressure

Although not validated to use with echocardiography, the most accurate estimate of mean pulmonary artery pressure was shown in one study⁷ to be obtained with the equation:

0.61 × systolic pulmonary artery pressure
+ 2 mm Hg

Using this formula, a systolic pulmonary artery pressure of 37 mm Hg would correspond to a mean pulmonary artery pressure of 24.6 mm Hg. A systolic pulmonary artery pressure of 40 mm Hg would correspond to a mean pulmonary artery pressure of 26.4 mm Hg.

Estimated systolic pulmonary artery pressure depends on several variables

Systolic pulmonary artery pressure is estimated using the simplified Bernoulli equation⁸:

4 × tricuspid regurgitation jet velocity² (m/s)
+ right atrial pressure (mm Hg)

Tricuspid regurgitation is present in over 75% of the normal population. The regurgitation velocity across the tricuspid valve must be measured to estimate the pressure gradient between the right ventricle and the right atrium. The right atrial pressure is estimated from the diameter of the inferior vena cava and the degree of inspiratory collapse with the sniff test. As the right atrial pressure increases, the inferior vena cava dilates and inspiratory collapse decreases.⁸ If there is no gradient across the right ventricular outflow tract or pulmonary valve, the right ventricular systolic pressure is equal to the systolic pulmonary artery pressure.

Since tricuspid regurgitation velocity is squared and then multiplied by 4, small deviations of this measurement lead to markedly different systolic pulmonary artery pressure values. To avoid this problem, the tricuspid regurgitation velocity needs to be looked at in multiple echocardiographic views to find the best alignment with the flow and an adequate envelope.

Many causes of high estimated systolic pulmonary artery pressure

Table 1 shows conditions associated with a high estimated systolic pulmonary artery pressure. Echocardiographic limitations, constitutional factors, and high cardiac output states can lead to an apparent elevation in systolic pulmonary artery pressure, which is not confirmed later during right heart catheterization.

Systolic pulmonary artery pressure increases with age and body mass index as a result of worsening left ventricular diastolic dysfunction.⁸ In fact, an estimated pressure greater than 40 mm Hg is found⁵ in 6% of people over age 50 and in 5% of people with a body mass index greater than 30 kg/m². It can also be high in conditions in which there is an increase in cardiac output, such as pregnancy, anemia (sickle cell disease, thalassemia), cirrhosis, and arteriovenous fistula.

The estimated systolic value often differs from the measured value

Studies have compared the systolic pulmonary artery pressure measured during right heart catheterization with the estimated value on echocardiography.^9,10 These studies noted a reasonable degree of agreement between the tests but a substantial variability.

Both underestimation and overestimation of the systolic pulmonary artery pressure by echocardiography were common, with 95% limits of agreement ranging from minus 40 mm Hg to plus 40 mm Hg.^9,10 A difference of plus or minus 10 mm Hg in systolic pulmonary artery pressure between echocardiography and catheterization was observed in 48% to 51% of patients with pulmonary hypertension, particularly in those with higher systolic pulmonary artery pressure.^9,10

An important reason for overestimation of systolic pulmonary artery pressure is the inaccurate estimation of the right atrial pressure by echocardiography.^9,10 Indeed, this factor may account for half of the cases in which the systolic pulmonary artery pressure is overestimated.¹⁰ Although the traditional methods to estimate the right atrial pressure have been revisited,^8,11 this estimation is less reliable for intermediate pressure values, for patients on mechanical ventilation, and for young athletes.⁸

Other explanations for the variability between measured and estimated systolic pulmonary artery pressure include suboptimal alignment between the Doppler beam and the regurgitant jet, severe tricuspid regurgitation, arrhythmias, and limitations inherent to the simplified Bernoulli equation.¹² The estimated value is particularly inaccurate in patients with advanced lung disease, possibly owing to lung hyperinflation and alteration in the thoracic cavity and position of the heart—all factors that limit visualization and measurement of the tricuspid regurgitant jet.¹³

OTHER SIGNS OF PULMONARY HYPERTENSION ON ECHOCARDIOGRAPHY

Echocardiography provides information that is useful in assessing the accuracy of the estimated systolic pulmonary artery pressure, particularly right ventricular size and function.

As pulmonary hypertension progresses, the right ventricle dilates, and its function is compromised. Therefore, it is important to determine the right ventricular size and function by using objective echocardiographic findings such as right ventricular diameters (basal, mid, apical) and area, right ventricular fractional area change, tricuspid annular plane systolic excursion, myocardial performance index, and the pulsed tissue Doppler tricuspid annular peak systolic excursion velocity.⁸

Other echocardiographic features that suggest pulmonary hypertension include a dilated right atrial area, flattening of the interventricular septum, notching of the right ventricular outflow tract flow, and dilation of the main pulmonary artery. Interestingly, left ventricular diastolic dysfunction of the impaired relaxation type (grade I) is commonly observed in pulmonary hypertension¹⁴; however, more advanced degrees of diastolic dysfunction, ie, pseudonormalization (grade II) or restrictive left ventricular filling (grade III),¹⁵ particularly when associated with a left atrial enlargement, suggest pulmonary hypertension associated with left heart disease and not pulmonary artery hypertension.

WHAT TO DO IF ECHOCARDIOGRAPHY INDICATES PULMONARY HYPERTENSION

Adapted in part from the diagnostic approach to pulmonary hypertension recommended by the Fifth World Symposium on Pulmonary Hypertension (reference 6).

An algorithm showing the approach to an elevated systolic pulmonary artery pressure on echocardiography is presented in Figure 1.

In the appropriate clinical setting, if the systolic pulmonary artery pressure is 40 mm Hg or greater or if other echocardiographic variables suggest pulmonary hypertension, our practice is to proceed with right heart catheterization.

Clinical variables that suggest pulmonary hypertension include progressive dyspnea, chest pain, presyncope-syncope, lower extremity edema, hepatomegaly, jugular vein distention, hepatojugular reflux, sternal heave, loud second heart sound (P2), murmur of tricuspid or pulmonary regurgitation, and right ventricular third heart sound.¹⁶ These are of particular interest when associated with conditions known to cause pulmonary hypertension,²such as connective tissue disease, portal hypertension, congenital heart disease, HIV infection, and certain drugs and toxins.

Other tests that raise suspicion of pulmonary hypertension are an electrocardiogram suggesting a dilated right atrium or ventricle, an elevated brain natriuretic peptide level, a low carbon monoxide diffusing capacity on pulmonary function testing, and an enlarged pulmonary artery diameter on imaging.

Given the high prevalence of pulmonary hypertension, the Fifth World Symposium on Pulmonary Hypertension recommended first considering heart or parenchymal lung disease when an echocardiogram suggests pulmonary hypertension.⁶ If there are signs of severe pulmonary hypertension or right ventricular dysfunction, referral to a center specializing in pulmonary hypertension is recommended. Referral is also appropriate when there is no major heart or lung disease and the echocardiogram shows an elevated systolic pulmonary artery pressure, particularly when the clinical presentation or results of other testing suggest pulmonary hypertension.

TAKE-HOME POINTS

In the appropriate context, a high systolic pulmonary artery pressure on echocardiography suggests pulmonary hypertension, but right heart catheterization is needed to confirm the diagnosis. Estimating the systolic pulmonary artery pressure with echocardiography has limitations, including false-positive results, predominantly when the pretest probability of pulmonary hypertension is low.

The incidental finding of high systolic pulmonary artery pressure on echocardiography is common. What we should do about it varies according to clinical presentation, comorbidities, and results of other tests, including assessment of the right ventricle. Thus, the optimal approach ranges from no further investigation to right heart catheterization and, in some cases, referral to a pulmonary hypertension center.

THE TWO MEASUREMENTS COMPARED

Although it raises concern, the finding of high systolic pulmonary artery pressure is not enough to diagnose pulmonary hypertension. In fact, several other conditions are associated with high systolic pulmonary artery pressure on echocardiography (Table 1). The diagnosis must be confirmed with right heart catheterization.¹

Echocardiography provides an estimate of the systolic pulmonary artery pressure that is calculated from other values, whereas right heart catheterization gives a direct measurement of the mean pulmonary artery pressure, which is necessary for diagnosing pulmonary hypertension. The two values are correlated, but the differences are noteworthy.

WHAT IS PULMONARY HYPERTENSION?

Pulmonary hypertension is defined by a resting mean pulmonary artery pressure 25 mm Hg or greater during right heart catheterization.¹ The large number of conditions associated with pulmonary hypertension can be divided into five groups²:

• Group 1, pulmonary artery hypertension
• Group 2, pulmonary hypertension associated with left heart disease
• Group 3, pulmonary hypertension due to chronic lung disease or hypoxia
• Group 4, chronic thromboembolic pulmonary hypertension
• Group 5, pulmonary hypertension due to unclear multifactorial mechanisms.²

Pulmonary artery hypertension (group 1) is a syndrome characterized by a restricted flow of small pulmonary arteries that can be idiopathic, heritable, or induced by anorexigens, connective tissue disease, congenital heart disease, portal hypertension, human immunodeficiency virus (HIV), or schistosomiasis.^2,3 In spite of significant advances in therapy in the last 3 decades, pulmonary artery hypertension continues to lead to right heart failure and death,⁴ and the diagnosis has adverse prognostic implications. Therefore, it is essential to be attentive when reviewing the echocardiogram, since an elevated systolic pulmonary artery pressure may be an important clue to pulmonary hypertension.

ESTIMATED PRESSURE: HOW HIGH IS TOO HIGH?

There is no consensus on the optimal cutoff of echocardiographic systolic pulmonary artery pressure to trigger a further evaluation for pulmonary hypertension.

A retrospective evaluation of nearly 16,000 normal echocardiograms found that the 95% upper limit for systolic pulmonary artery pressure was 37 mm Hg.⁵

European guidelines⁶ propose that pulmonary hypertension is unlikely if the estimated systolic pulmonary artery pressure is 36 mm Hg or lower, possible if it is 37 to 50 mm Hg, and likely if it is higher than 50 mm Hg.⁶

The 2009 consensus document of the American College of Cardiology Foundation and American Heart Association³ recommends a systolic pulmonary artery pressure greater than 40 mm Hg as the threshold to suggest further evaluation in a patient with unexplained dyspnea.

Converting the systolic pulmonary artery pressure to the mean pressure

Although not validated to use with echocardiography, the most accurate estimate of mean pulmonary artery pressure was shown in one study⁷ to be obtained with the equation:

0.61 × systolic pulmonary artery pressure
+ 2 mm Hg

Using this formula, a systolic pulmonary artery pressure of 37 mm Hg would correspond to a mean pulmonary artery pressure of 24.6 mm Hg. A systolic pulmonary artery pressure of 40 mm Hg would correspond to a mean pulmonary artery pressure of 26.4 mm Hg.

Estimated systolic pulmonary artery pressure depends on several variables

Systolic pulmonary artery pressure is estimated using the simplified Bernoulli equation⁸:

4 × tricuspid regurgitation jet velocity² (m/s)
+ right atrial pressure (mm Hg)

Tricuspid regurgitation is present in over 75% of the normal population. The regurgitation velocity across the tricuspid valve must be measured to estimate the pressure gradient between the right ventricle and the right atrium. The right atrial pressure is estimated from the diameter of the inferior vena cava and the degree of inspiratory collapse with the sniff test. As the right atrial pressure increases, the inferior vena cava dilates and inspiratory collapse decreases.⁸ If there is no gradient across the right ventricular outflow tract or pulmonary valve, the right ventricular systolic pressure is equal to the systolic pulmonary artery pressure.

Since tricuspid regurgitation velocity is squared and then multiplied by 4, small deviations of this measurement lead to markedly different systolic pulmonary artery pressure values. To avoid this problem, the tricuspid regurgitation velocity needs to be looked at in multiple echocardiographic views to find the best alignment with the flow and an adequate envelope.

Many causes of high estimated systolic pulmonary artery pressure

Table 1 shows conditions associated with a high estimated systolic pulmonary artery pressure. Echocardiographic limitations, constitutional factors, and high cardiac output states can lead to an apparent elevation in systolic pulmonary artery pressure, which is not confirmed later during right heart catheterization.

Systolic pulmonary artery pressure increases with age and body mass index as a result of worsening left ventricular diastolic dysfunction.⁸ In fact, an estimated pressure greater than 40 mm Hg is found⁵ in 6% of people over age 50 and in 5% of people with a body mass index greater than 30 kg/m². It can also be high in conditions in which there is an increase in cardiac output, such as pregnancy, anemia (sickle cell disease, thalassemia), cirrhosis, and arteriovenous fistula.

The estimated systolic value often differs from the measured value

Studies have compared the systolic pulmonary artery pressure measured during right heart catheterization with the estimated value on echocardiography.^9,10 These studies noted a reasonable degree of agreement between the tests but a substantial variability.

Both underestimation and overestimation of the systolic pulmonary artery pressure by echocardiography were common, with 95% limits of agreement ranging from minus 40 mm Hg to plus 40 mm Hg.^9,10 A difference of plus or minus 10 mm Hg in systolic pulmonary artery pressure between echocardiography and catheterization was observed in 48% to 51% of patients with pulmonary hypertension, particularly in those with higher systolic pulmonary artery pressure.^9,10

An important reason for overestimation of systolic pulmonary artery pressure is the inaccurate estimation of the right atrial pressure by echocardiography.^9,10 Indeed, this factor may account for half of the cases in which the systolic pulmonary artery pressure is overestimated.¹⁰ Although the traditional methods to estimate the right atrial pressure have been revisited,^8,11 this estimation is less reliable for intermediate pressure values, for patients on mechanical ventilation, and for young athletes.⁸

Other explanations for the variability between measured and estimated systolic pulmonary artery pressure include suboptimal alignment between the Doppler beam and the regurgitant jet, severe tricuspid regurgitation, arrhythmias, and limitations inherent to the simplified Bernoulli equation.¹² The estimated value is particularly inaccurate in patients with advanced lung disease, possibly owing to lung hyperinflation and alteration in the thoracic cavity and position of the heart—all factors that limit visualization and measurement of the tricuspid regurgitant jet.¹³

OTHER SIGNS OF PULMONARY HYPERTENSION ON ECHOCARDIOGRAPHY

Echocardiography provides information that is useful in assessing the accuracy of the estimated systolic pulmonary artery pressure, particularly right ventricular size and function.

As pulmonary hypertension progresses, the right ventricle dilates, and its function is compromised. Therefore, it is important to determine the right ventricular size and function by using objective echocardiographic findings such as right ventricular diameters (basal, mid, apical) and area, right ventricular fractional area change, tricuspid annular plane systolic excursion, myocardial performance index, and the pulsed tissue Doppler tricuspid annular peak systolic excursion velocity.⁸

Other echocardiographic features that suggest pulmonary hypertension include a dilated right atrial area, flattening of the interventricular septum, notching of the right ventricular outflow tract flow, and dilation of the main pulmonary artery. Interestingly, left ventricular diastolic dysfunction of the impaired relaxation type (grade I) is commonly observed in pulmonary hypertension¹⁴; however, more advanced degrees of diastolic dysfunction, ie, pseudonormalization (grade II) or restrictive left ventricular filling (grade III),¹⁵ particularly when associated with a left atrial enlargement, suggest pulmonary hypertension associated with left heart disease and not pulmonary artery hypertension.

WHAT TO DO IF ECHOCARDIOGRAPHY INDICATES PULMONARY HYPERTENSION

Adapted in part from the diagnostic approach to pulmonary hypertension recommended by the Fifth World Symposium on Pulmonary Hypertension (reference 6).

An algorithm showing the approach to an elevated systolic pulmonary artery pressure on echocardiography is presented in Figure 1.

In the appropriate clinical setting, if the systolic pulmonary artery pressure is 40 mm Hg or greater or if other echocardiographic variables suggest pulmonary hypertension, our practice is to proceed with right heart catheterization.

Clinical variables that suggest pulmonary hypertension include progressive dyspnea, chest pain, presyncope-syncope, lower extremity edema, hepatomegaly, jugular vein distention, hepatojugular reflux, sternal heave, loud second heart sound (P2), murmur of tricuspid or pulmonary regurgitation, and right ventricular third heart sound.¹⁶ These are of particular interest when associated with conditions known to cause pulmonary hypertension,²such as connective tissue disease, portal hypertension, congenital heart disease, HIV infection, and certain drugs and toxins.

Other tests that raise suspicion of pulmonary hypertension are an electrocardiogram suggesting a dilated right atrium or ventricle, an elevated brain natriuretic peptide level, a low carbon monoxide diffusing capacity on pulmonary function testing, and an enlarged pulmonary artery diameter on imaging.

Given the high prevalence of pulmonary hypertension, the Fifth World Symposium on Pulmonary Hypertension recommended first considering heart or parenchymal lung disease when an echocardiogram suggests pulmonary hypertension.⁶ If there are signs of severe pulmonary hypertension or right ventricular dysfunction, referral to a center specializing in pulmonary hypertension is recommended. Referral is also appropriate when there is no major heart or lung disease and the echocardiogram shows an elevated systolic pulmonary artery pressure, particularly when the clinical presentation or results of other testing suggest pulmonary hypertension.

TAKE-HOME POINTS

In the appropriate context, a high systolic pulmonary artery pressure on echocardiography suggests pulmonary hypertension, but right heart catheterization is needed to confirm the diagnosis. Estimating the systolic pulmonary artery pressure with echocardiography has limitations, including false-positive results, predominantly when the pretest probability of pulmonary hypertension is low.

The incidental finding of high systolic pulmonary artery pressure on echocardiography is common. What we should do about it varies according to clinical presentation, comorbidities, and results of other tests, including assessment of the right ventricle. Thus, the optimal approach ranges from no further investigation to right heart catheterization and, in some cases, referral to a pulmonary hypertension center.

THE TWO MEASUREMENTS COMPARED

Although it raises concern, the finding of high systolic pulmonary artery pressure is not enough to diagnose pulmonary hypertension. In fact, several other conditions are associated with high systolic pulmonary artery pressure on echocardiography (Table 1). The diagnosis must be confirmed with right heart catheterization.¹

Echocardiography provides an estimate of the systolic pulmonary artery pressure that is calculated from other values, whereas right heart catheterization gives a direct measurement of the mean pulmonary artery pressure, which is necessary for diagnosing pulmonary hypertension. The two values are correlated, but the differences are noteworthy.

WHAT IS PULMONARY HYPERTENSION?

Pulmonary hypertension is defined by a resting mean pulmonary artery pressure 25 mm Hg or greater during right heart catheterization.¹ The large number of conditions associated with pulmonary hypertension can be divided into five groups²:

• Group 1, pulmonary artery hypertension
• Group 2, pulmonary hypertension associated with left heart disease
• Group 3, pulmonary hypertension due to chronic lung disease or hypoxia
• Group 4, chronic thromboembolic pulmonary hypertension
• Group 5, pulmonary hypertension due to unclear multifactorial mechanisms.²

Pulmonary artery hypertension (group 1) is a syndrome characterized by a restricted flow of small pulmonary arteries that can be idiopathic, heritable, or induced by anorexigens, connective tissue disease, congenital heart disease, portal hypertension, human immunodeficiency virus (HIV), or schistosomiasis.^2,3 In spite of significant advances in therapy in the last 3 decades, pulmonary artery hypertension continues to lead to right heart failure and death,⁴ and the diagnosis has adverse prognostic implications. Therefore, it is essential to be attentive when reviewing the echocardiogram, since an elevated systolic pulmonary artery pressure may be an important clue to pulmonary hypertension.

ESTIMATED PRESSURE: HOW HIGH IS TOO HIGH?

There is no consensus on the optimal cutoff of echocardiographic systolic pulmonary artery pressure to trigger a further evaluation for pulmonary hypertension.

A retrospective evaluation of nearly 16,000 normal echocardiograms found that the 95% upper limit for systolic pulmonary artery pressure was 37 mm Hg.⁵

European guidelines⁶ propose that pulmonary hypertension is unlikely if the estimated systolic pulmonary artery pressure is 36 mm Hg or lower, possible if it is 37 to 50 mm Hg, and likely if it is higher than 50 mm Hg.⁶

The 2009 consensus document of the American College of Cardiology Foundation and American Heart Association³ recommends a systolic pulmonary artery pressure greater than 40 mm Hg as the threshold to suggest further evaluation in a patient with unexplained dyspnea.

Converting the systolic pulmonary artery pressure to the mean pressure

Although not validated to use with echocardiography, the most accurate estimate of mean pulmonary artery pressure was shown in one study⁷ to be obtained with the equation:

0.61 × systolic pulmonary artery pressure
+ 2 mm Hg

Using this formula, a systolic pulmonary artery pressure of 37 mm Hg would correspond to a mean pulmonary artery pressure of 24.6 mm Hg. A systolic pulmonary artery pressure of 40 mm Hg would correspond to a mean pulmonary artery pressure of 26.4 mm Hg.

Estimated systolic pulmonary artery pressure depends on several variables

Systolic pulmonary artery pressure is estimated using the simplified Bernoulli equation⁸:

4 × tricuspid regurgitation jet velocity² (m/s)
+ right atrial pressure (mm Hg)

Tricuspid regurgitation is present in over 75% of the normal population. The regurgitation velocity across the tricuspid valve must be measured to estimate the pressure gradient between the right ventricle and the right atrium. The right atrial pressure is estimated from the diameter of the inferior vena cava and the degree of inspiratory collapse with the sniff test. As the right atrial pressure increases, the inferior vena cava dilates and inspiratory collapse decreases.⁸ If there is no gradient across the right ventricular outflow tract or pulmonary valve, the right ventricular systolic pressure is equal to the systolic pulmonary artery pressure.

Since tricuspid regurgitation velocity is squared and then multiplied by 4, small deviations of this measurement lead to markedly different systolic pulmonary artery pressure values. To avoid this problem, the tricuspid regurgitation velocity needs to be looked at in multiple echocardiographic views to find the best alignment with the flow and an adequate envelope.

Many causes of high estimated systolic pulmonary artery pressure

Table 1 shows conditions associated with a high estimated systolic pulmonary artery pressure. Echocardiographic limitations, constitutional factors, and high cardiac output states can lead to an apparent elevation in systolic pulmonary artery pressure, which is not confirmed later during right heart catheterization.

Systolic pulmonary artery pressure increases with age and body mass index as a result of worsening left ventricular diastolic dysfunction.⁸ In fact, an estimated pressure greater than 40 mm Hg is found⁵ in 6% of people over age 50 and in 5% of people with a body mass index greater than 30 kg/m². It can also be high in conditions in which there is an increase in cardiac output, such as pregnancy, anemia (sickle cell disease, thalassemia), cirrhosis, and arteriovenous fistula.

The estimated systolic value often differs from the measured value

Studies have compared the systolic pulmonary artery pressure measured during right heart catheterization with the estimated value on echocardiography.^9,10 These studies noted a reasonable degree of agreement between the tests but a substantial variability.

Both underestimation and overestimation of the systolic pulmonary artery pressure by echocardiography were common, with 95% limits of agreement ranging from minus 40 mm Hg to plus 40 mm Hg.^9,10 A difference of plus or minus 10 mm Hg in systolic pulmonary artery pressure between echocardiography and catheterization was observed in 48% to 51% of patients with pulmonary hypertension, particularly in those with higher systolic pulmonary artery pressure.^9,10

An important reason for overestimation of systolic pulmonary artery pressure is the inaccurate estimation of the right atrial pressure by echocardiography.^9,10 Indeed, this factor may account for half of the cases in which the systolic pulmonary artery pressure is overestimated.¹⁰ Although the traditional methods to estimate the right atrial pressure have been revisited,^8,11 this estimation is less reliable for intermediate pressure values, for patients on mechanical ventilation, and for young athletes.⁸

Other explanations for the variability between measured and estimated systolic pulmonary artery pressure include suboptimal alignment between the Doppler beam and the regurgitant jet, severe tricuspid regurgitation, arrhythmias, and limitations inherent to the simplified Bernoulli equation.¹² The estimated value is particularly inaccurate in patients with advanced lung disease, possibly owing to lung hyperinflation and alteration in the thoracic cavity and position of the heart—all factors that limit visualization and measurement of the tricuspid regurgitant jet.¹³

OTHER SIGNS OF PULMONARY HYPERTENSION ON ECHOCARDIOGRAPHY

Echocardiography provides information that is useful in assessing the accuracy of the estimated systolic pulmonary artery pressure, particularly right ventricular size and function.

As pulmonary hypertension progresses, the right ventricle dilates, and its function is compromised. Therefore, it is important to determine the right ventricular size and function by using objective echocardiographic findings such as right ventricular diameters (basal, mid, apical) and area, right ventricular fractional area change, tricuspid annular plane systolic excursion, myocardial performance index, and the pulsed tissue Doppler tricuspid annular peak systolic excursion velocity.⁸

Other echocardiographic features that suggest pulmonary hypertension include a dilated right atrial area, flattening of the interventricular septum, notching of the right ventricular outflow tract flow, and dilation of the main pulmonary artery. Interestingly, left ventricular diastolic dysfunction of the impaired relaxation type (grade I) is commonly observed in pulmonary hypertension¹⁴; however, more advanced degrees of diastolic dysfunction, ie, pseudonormalization (grade II) or restrictive left ventricular filling (grade III),¹⁵ particularly when associated with a left atrial enlargement, suggest pulmonary hypertension associated with left heart disease and not pulmonary artery hypertension.

WHAT TO DO IF ECHOCARDIOGRAPHY INDICATES PULMONARY HYPERTENSION

Adapted in part from the diagnostic approach to pulmonary hypertension recommended by the Fifth World Symposium on Pulmonary Hypertension (reference 6).

An algorithm showing the approach to an elevated systolic pulmonary artery pressure on echocardiography is presented in Figure 1.

In the appropriate clinical setting, if the systolic pulmonary artery pressure is 40 mm Hg or greater or if other echocardiographic variables suggest pulmonary hypertension, our practice is to proceed with right heart catheterization.

Clinical variables that suggest pulmonary hypertension include progressive dyspnea, chest pain, presyncope-syncope, lower extremity edema, hepatomegaly, jugular vein distention, hepatojugular reflux, sternal heave, loud second heart sound (P2), murmur of tricuspid or pulmonary regurgitation, and right ventricular third heart sound.¹⁶ These are of particular interest when associated with conditions known to cause pulmonary hypertension,²such as connective tissue disease, portal hypertension, congenital heart disease, HIV infection, and certain drugs and toxins.

Other tests that raise suspicion of pulmonary hypertension are an electrocardiogram suggesting a dilated right atrium or ventricle, an elevated brain natriuretic peptide level, a low carbon monoxide diffusing capacity on pulmonary function testing, and an enlarged pulmonary artery diameter on imaging.

Given the high prevalence of pulmonary hypertension, the Fifth World Symposium on Pulmonary Hypertension recommended first considering heart or parenchymal lung disease when an echocardiogram suggests pulmonary hypertension.⁶ If there are signs of severe pulmonary hypertension or right ventricular dysfunction, referral to a center specializing in pulmonary hypertension is recommended. Referral is also appropriate when there is no major heart or lung disease and the echocardiogram shows an elevated systolic pulmonary artery pressure, particularly when the clinical presentation or results of other testing suggest pulmonary hypertension.

TAKE-HOME POINTS

In the appropriate context, a high systolic pulmonary artery pressure on echocardiography suggests pulmonary hypertension, but right heart catheterization is needed to confirm the diagnosis. Estimating the systolic pulmonary artery pressure with echocardiography has limitations, including false-positive results, predominantly when the pretest probability of pulmonary hypertension is low.

A 50-year-old man presented with a painful rash over his extremities for the past 2 days (Figure 1). He said he had been in his usual state of health until the day he woke up with the rash. The rash was initially limited to his upper and lower extremities, but the next day he noticed similar lesions over his cheek and hard palate. He was a smoker and was known to have hepatitis C virus infection. He denied recent trauma, fever, or chills. He said he had snorted cocaine about 24 hours before the rash first appeared.

On examination, his vital signs were normal. He had an extensive retiform rash involving the upper and lower extremities, earlobes, right cheek, and hard palate. Otherwise, the physical examination was normal.

Initial laboratory evaluation showed:

• Hemoglobin 11.5 g/dL (reference range 14.0–17.5)
• White blood cell count 2.1 × 10⁹/L (4.5–11.0)
• Platelet count 168 × 10⁹/L (150–350)
• Absolute neutrophil count 0.9 × 10⁹/L (≥ 1.5)
• Urine toxicology screen positive for cocaine.

He was admitted to the hospital and was started on intravenous vancomycin and piperacillin-sulbactam for a presumed infectious cause of the rash.

One day later, testing for myeloperoxidase-specific antineutrophil cytoplasmic antibodies (p-ANCA) was strongly positive. Skin biopsy revealed leukocytoclastic vasculitis with small-vessel thrombosis. These findings, along with the timing of the appearance of the rash after his cocaine use,  led to a diagnosis of levamisole-adulterated cocaine-induced vasculitis.

LEVAMISOLE AND VASCULITIS

Levamisole used to be used as an antihelminthic and as an adjuvant chemotherapeutic agent, but it is also added to cocaine to increase its euphoric and psychotropic effects.¹ It has been withdrawn from the market for human use because of toxic side effects including agranulocytosis, vasculitis, and autoantibody positivity.

Levamisole-adulterated cocaine has been known to induce ANCA-associated vasculitis.² Symptoms of levamisole-induced vasculitis usually start a few hours to a few days after the last dose of cocaine. Almost all patients with this condition present with a characteristic retiform purpuric rash, which has a predilection for the ears, nose, cheeks, and extremities. It also causes neutropenia and agranulocytosis (as well as autoantibodies, including antinuclear antibodies and antiphospholipid antibodies).

The characteristic lesions tend to be in a stellate pattern with erythematous borders. They often but not always have a central necrotic area. The location of the rash and the fact that it resolves after discontinuation of the offending agent help distinguish this condition from other types of vasculitis. Usually, antibodies against myeloperoxidase are present.³

Leukopenia does not typically occur in patients with primary vasculitis syndromes. The literature is mixed on the presence or absence of specific ANCAs.

Inflammatory and noninflammatory vasculopathic disorders that can present similarly include disseminated intravascular coagulation, antiphospholipid syndrome, warfarin-induced skin necrosis, paroxysmal nocturnal hemoglobinuria, cryoglobulinemia, vasculitis, and calciphylaxis.

Treatment is mainly supportive, but emollients and steroids⁴ have been reported to alleviate the symptoms. Surgical debridement is rarely needed unless skin necrosis is extensive.

Levamisole-induced vasculitis is a diagnosis of exclusion but should be strongly considered when the rash is associated with recent cocaine use, retiform purpura, or bullae with skin involvement, leukopenia, and positive ANCA in high titers.³ If cocaine use is discontinued, the syndrome is expected to resolve.

A 50-year-old man presented with a painful rash over his extremities for the past 2 days (Figure 1). He said he had been in his usual state of health until the day he woke up with the rash. The rash was initially limited to his upper and lower extremities, but the next day he noticed similar lesions over his cheek and hard palate. He was a smoker and was known to have hepatitis C virus infection. He denied recent trauma, fever, or chills. He said he had snorted cocaine about 24 hours before the rash first appeared.

On examination, his vital signs were normal. He had an extensive retiform rash involving the upper and lower extremities, earlobes, right cheek, and hard palate. Otherwise, the physical examination was normal.

Initial laboratory evaluation showed:

• Hemoglobin 11.5 g/dL (reference range 14.0–17.5)
• White blood cell count 2.1 × 10⁹/L (4.5–11.0)
• Platelet count 168 × 10⁹/L (150–350)
• Absolute neutrophil count 0.9 × 10⁹/L (≥ 1.5)
• Urine toxicology screen positive for cocaine.

He was admitted to the hospital and was started on intravenous vancomycin and piperacillin-sulbactam for a presumed infectious cause of the rash.

One day later, testing for myeloperoxidase-specific antineutrophil cytoplasmic antibodies (p-ANCA) was strongly positive. Skin biopsy revealed leukocytoclastic vasculitis with small-vessel thrombosis. These findings, along with the timing of the appearance of the rash after his cocaine use,  led to a diagnosis of levamisole-adulterated cocaine-induced vasculitis.

LEVAMISOLE AND VASCULITIS

Levamisole used to be used as an antihelminthic and as an adjuvant chemotherapeutic agent, but it is also added to cocaine to increase its euphoric and psychotropic effects.¹ It has been withdrawn from the market for human use because of toxic side effects including agranulocytosis, vasculitis, and autoantibody positivity.

Levamisole-adulterated cocaine has been known to induce ANCA-associated vasculitis.² Symptoms of levamisole-induced vasculitis usually start a few hours to a few days after the last dose of cocaine. Almost all patients with this condition present with a characteristic retiform purpuric rash, which has a predilection for the ears, nose, cheeks, and extremities. It also causes neutropenia and agranulocytosis (as well as autoantibodies, including antinuclear antibodies and antiphospholipid antibodies).

The characteristic lesions tend to be in a stellate pattern with erythematous borders. They often but not always have a central necrotic area. The location of the rash and the fact that it resolves after discontinuation of the offending agent help distinguish this condition from other types of vasculitis. Usually, antibodies against myeloperoxidase are present.³

Leukopenia does not typically occur in patients with primary vasculitis syndromes. The literature is mixed on the presence or absence of specific ANCAs.

Inflammatory and noninflammatory vasculopathic disorders that can present similarly include disseminated intravascular coagulation, antiphospholipid syndrome, warfarin-induced skin necrosis, paroxysmal nocturnal hemoglobinuria, cryoglobulinemia, vasculitis, and calciphylaxis.

Treatment is mainly supportive, but emollients and steroids⁴ have been reported to alleviate the symptoms. Surgical debridement is rarely needed unless skin necrosis is extensive.

Levamisole-induced vasculitis is a diagnosis of exclusion but should be strongly considered when the rash is associated with recent cocaine use, retiform purpura, or bullae with skin involvement, leukopenia, and positive ANCA in high titers.³ If cocaine use is discontinued, the syndrome is expected to resolve.

A 50-year-old man presented with a painful rash over his extremities for the past 2 days (Figure 1). He said he had been in his usual state of health until the day he woke up with the rash. The rash was initially limited to his upper and lower extremities, but the next day he noticed similar lesions over his cheek and hard palate. He was a smoker and was known to have hepatitis C virus infection. He denied recent trauma, fever, or chills. He said he had snorted cocaine about 24 hours before the rash first appeared.

On examination, his vital signs were normal. He had an extensive retiform rash involving the upper and lower extremities, earlobes, right cheek, and hard palate. Otherwise, the physical examination was normal.

Initial laboratory evaluation showed:

• Hemoglobin 11.5 g/dL (reference range 14.0–17.5)
• White blood cell count 2.1 × 10⁹/L (4.5–11.0)
• Platelet count 168 × 10⁹/L (150–350)
• Absolute neutrophil count 0.9 × 10⁹/L (≥ 1.5)
• Urine toxicology screen positive for cocaine.

He was admitted to the hospital and was started on intravenous vancomycin and piperacillin-sulbactam for a presumed infectious cause of the rash.

One day later, testing for myeloperoxidase-specific antineutrophil cytoplasmic antibodies (p-ANCA) was strongly positive. Skin biopsy revealed leukocytoclastic vasculitis with small-vessel thrombosis. These findings, along with the timing of the appearance of the rash after his cocaine use,  led to a diagnosis of levamisole-adulterated cocaine-induced vasculitis.

LEVAMISOLE AND VASCULITIS

Levamisole used to be used as an antihelminthic and as an adjuvant chemotherapeutic agent, but it is also added to cocaine to increase its euphoric and psychotropic effects.¹ It has been withdrawn from the market for human use because of toxic side effects including agranulocytosis, vasculitis, and autoantibody positivity.

Levamisole-adulterated cocaine has been known to induce ANCA-associated vasculitis.² Symptoms of levamisole-induced vasculitis usually start a few hours to a few days after the last dose of cocaine. Almost all patients with this condition present with a characteristic retiform purpuric rash, which has a predilection for the ears, nose, cheeks, and extremities. It also causes neutropenia and agranulocytosis (as well as autoantibodies, including antinuclear antibodies and antiphospholipid antibodies).

The characteristic lesions tend to be in a stellate pattern with erythematous borders. They often but not always have a central necrotic area. The location of the rash and the fact that it resolves after discontinuation of the offending agent help distinguish this condition from other types of vasculitis. Usually, antibodies against myeloperoxidase are present.³

Leukopenia does not typically occur in patients with primary vasculitis syndromes. The literature is mixed on the presence or absence of specific ANCAs.

Inflammatory and noninflammatory vasculopathic disorders that can present similarly include disseminated intravascular coagulation, antiphospholipid syndrome, warfarin-induced skin necrosis, paroxysmal nocturnal hemoglobinuria, cryoglobulinemia, vasculitis, and calciphylaxis.

Treatment is mainly supportive, but emollients and steroids⁴ have been reported to alleviate the symptoms. Surgical debridement is rarely needed unless skin necrosis is extensive.

Levamisole-induced vasculitis is a diagnosis of exclusion but should be strongly considered when the rash is associated with recent cocaine use, retiform purpura, or bullae with skin involvement, leukopenia, and positive ANCA in high titers.³ If cocaine use is discontinued, the syndrome is expected to resolve.

Even though there was a steady rate of patients with critical limb ischemia (CLI) admitted to hospitals from 2003 to 2011, surgical revascularization decreased and endovascular treatment increased significantly, with concomitant decreases in in-hospital mortality and major amputation, according to the results of an analysis of the Nationwide Inpatient Sample of 642,433 patients hospitalized with CLI.

In addition, despite multiple adjustments, endovascular revascularization was associated with reduced in-hospital mortality, compared with surgical revascularization over the same period, according to a report online in the Journal of the American College of Cardiology.

©Ingram Publishing/Thinkstock

The annual in-hospital mortality rate decreased from 5.4% in 2003 to 3.4% in 2011 (P less than .001), and the major amputation rate dropped from 16.7% to 10.8%. There also was a significant decrease in length-of-stay (LOS) from 10 days to 8.4 days over the same period (P less than .001); however this did not translate to a significant difference in the cost of hospitalization, according to Dr. Shikhar Agarwal and colleagues at the Cleveland Clinic [doi:10.1016/j.jacc.2016.02.040].

Significant predictive factors of in-hospital mortality after multivariate regression analysis were female sex, older age, emergent admission, a primary indication of septicemia, heart failure, and respiratory disease, as well any stump complications present during admission. In contrast, any form of revascularization was associated with significantly reduced in-hospital mortality.

A comparison of revascularization methods showed that surgical revascularization significantly decreased from 13.9% in 2003 to 8.8% in 2011, while endovascular revascularization increased from 5.1% to 11%. Also, endovascular revascularization was associated with a significant decrease in in-hospital mortality compared with surgical revascularization over the study period (2.34% vs. 2.73%, respectively; odds ratio = .69). Major amputation rates were not significantly different between the two treatments (6.5% vs. 5.7%; OR = .99).

Length of stay was significantly lower with endovascular treatment compared with surgical (8.7 vs. 10.7 days) as were costs ($31,679 vs. $32,485, respectively).

Women had a higher rate of in-hospital mortality, but a lower rate of major amputation. Although race was not seen as a factor in predicting in-hospital mortality, blacks and other nonwhite races had significantly higher rates of amputation and lower rates of revascularization, compared with whites.

Approximately half of the patients assessed were admitted for primary CLI-related diagnoses. The other, non–CLI-related conditions – such as acute MI, cerebrovascular events, respiratory disease, heart failure, and acute kidney disease – have all been independently associated with increased in-hospital mortality and may be confounding, according to the authors. These are still relevant because CLI patients have an overall elevated cardiovascular risk in multiple vascular beds.

In terms of limitations, the authors noted the possibility of selection bias in the database, the rise of standalone outpatient centers in more recent years, which might funnel off select patients, and the lack of anatomical information in the NIS database, which precludes a determination of the appropriateness of treatment choice. Also, the type and invasiveness of the endovascular therapy cannot be determined. “It is possible that simple lesions were preferentially treated with endovascular therapy, whereas more complex lesions were treated by surgical techniques, leading to obvious differences in outcomes. Alternatively, it may be likely that the findings underestimate the impact of endovascular therapy, as sicker patients with higher comorbidities and poor targets were more likely to undergo endovascular revascularization,” the researchers pointed out.

“Despite similar rates of major amputation, endovascular revascularization was associated with reduced in-hospital mortality, mean LOS, and mean cost of hospitalization. Although the results are encouraging, there remain significant disparities and gaps that must be addressed,” Dr. Agarwal and his colleagues concluded.

The authors reported that they had no relevant disclosures.

[email protected]

Even though there was a steady rate of patients with critical limb ischemia (CLI) admitted to hospitals from 2003 to 2011, surgical revascularization decreased and endovascular treatment increased significantly, with concomitant decreases in in-hospital mortality and major amputation, according to the results of an analysis of the Nationwide Inpatient Sample of 642,433 patients hospitalized with CLI.

In addition, despite multiple adjustments, endovascular revascularization was associated with reduced in-hospital mortality, compared with surgical revascularization over the same period, according to a report online in the Journal of the American College of Cardiology.

©Ingram Publishing/Thinkstock

The annual in-hospital mortality rate decreased from 5.4% in 2003 to 3.4% in 2011 (P less than .001), and the major amputation rate dropped from 16.7% to 10.8%. There also was a significant decrease in length-of-stay (LOS) from 10 days to 8.4 days over the same period (P less than .001); however this did not translate to a significant difference in the cost of hospitalization, according to Dr. Shikhar Agarwal and colleagues at the Cleveland Clinic [doi:10.1016/j.jacc.2016.02.040].

Significant predictive factors of in-hospital mortality after multivariate regression analysis were female sex, older age, emergent admission, a primary indication of septicemia, heart failure, and respiratory disease, as well any stump complications present during admission. In contrast, any form of revascularization was associated with significantly reduced in-hospital mortality.

A comparison of revascularization methods showed that surgical revascularization significantly decreased from 13.9% in 2003 to 8.8% in 2011, while endovascular revascularization increased from 5.1% to 11%. Also, endovascular revascularization was associated with a significant decrease in in-hospital mortality compared with surgical revascularization over the study period (2.34% vs. 2.73%, respectively; odds ratio = .69). Major amputation rates were not significantly different between the two treatments (6.5% vs. 5.7%; OR = .99).

Length of stay was significantly lower with endovascular treatment compared with surgical (8.7 vs. 10.7 days) as were costs ($31,679 vs. $32,485, respectively).

Women had a higher rate of in-hospital mortality, but a lower rate of major amputation. Although race was not seen as a factor in predicting in-hospital mortality, blacks and other nonwhite races had significantly higher rates of amputation and lower rates of revascularization, compared with whites.

Approximately half of the patients assessed were admitted for primary CLI-related diagnoses. The other, non–CLI-related conditions – such as acute MI, cerebrovascular events, respiratory disease, heart failure, and acute kidney disease – have all been independently associated with increased in-hospital mortality and may be confounding, according to the authors. These are still relevant because CLI patients have an overall elevated cardiovascular risk in multiple vascular beds.

In terms of limitations, the authors noted the possibility of selection bias in the database, the rise of standalone outpatient centers in more recent years, which might funnel off select patients, and the lack of anatomical information in the NIS database, which precludes a determination of the appropriateness of treatment choice. Also, the type and invasiveness of the endovascular therapy cannot be determined. “It is possible that simple lesions were preferentially treated with endovascular therapy, whereas more complex lesions were treated by surgical techniques, leading to obvious differences in outcomes. Alternatively, it may be likely that the findings underestimate the impact of endovascular therapy, as sicker patients with higher comorbidities and poor targets were more likely to undergo endovascular revascularization,” the researchers pointed out.

“Despite similar rates of major amputation, endovascular revascularization was associated with reduced in-hospital mortality, mean LOS, and mean cost of hospitalization. Although the results are encouraging, there remain significant disparities and gaps that must be addressed,” Dr. Agarwal and his colleagues concluded.

The authors reported that they had no relevant disclosures.

[email protected]

Even though there was a steady rate of patients with critical limb ischemia (CLI) admitted to hospitals from 2003 to 2011, surgical revascularization decreased and endovascular treatment increased significantly, with concomitant decreases in in-hospital mortality and major amputation, according to the results of an analysis of the Nationwide Inpatient Sample of 642,433 patients hospitalized with CLI.

In addition, despite multiple adjustments, endovascular revascularization was associated with reduced in-hospital mortality, compared with surgical revascularization over the same period, according to a report online in the Journal of the American College of Cardiology.

©Ingram Publishing/Thinkstock

The annual in-hospital mortality rate decreased from 5.4% in 2003 to 3.4% in 2011 (P less than .001), and the major amputation rate dropped from 16.7% to 10.8%. There also was a significant decrease in length-of-stay (LOS) from 10 days to 8.4 days over the same period (P less than .001); however this did not translate to a significant difference in the cost of hospitalization, according to Dr. Shikhar Agarwal and colleagues at the Cleveland Clinic [doi:10.1016/j.jacc.2016.02.040].

Significant predictive factors of in-hospital mortality after multivariate regression analysis were female sex, older age, emergent admission, a primary indication of septicemia, heart failure, and respiratory disease, as well any stump complications present during admission. In contrast, any form of revascularization was associated with significantly reduced in-hospital mortality.

A comparison of revascularization methods showed that surgical revascularization significantly decreased from 13.9% in 2003 to 8.8% in 2011, while endovascular revascularization increased from 5.1% to 11%. Also, endovascular revascularization was associated with a significant decrease in in-hospital mortality compared with surgical revascularization over the study period (2.34% vs. 2.73%, respectively; odds ratio = .69). Major amputation rates were not significantly different between the two treatments (6.5% vs. 5.7%; OR = .99).

Length of stay was significantly lower with endovascular treatment compared with surgical (8.7 vs. 10.7 days) as were costs ($31,679 vs. $32,485, respectively).

Women had a higher rate of in-hospital mortality, but a lower rate of major amputation. Although race was not seen as a factor in predicting in-hospital mortality, blacks and other nonwhite races had significantly higher rates of amputation and lower rates of revascularization, compared with whites.

Approximately half of the patients assessed were admitted for primary CLI-related diagnoses. The other, non–CLI-related conditions – such as acute MI, cerebrovascular events, respiratory disease, heart failure, and acute kidney disease – have all been independently associated with increased in-hospital mortality and may be confounding, according to the authors. These are still relevant because CLI patients have an overall elevated cardiovascular risk in multiple vascular beds.

In terms of limitations, the authors noted the possibility of selection bias in the database, the rise of standalone outpatient centers in more recent years, which might funnel off select patients, and the lack of anatomical information in the NIS database, which precludes a determination of the appropriateness of treatment choice. Also, the type and invasiveness of the endovascular therapy cannot be determined. “It is possible that simple lesions were preferentially treated with endovascular therapy, whereas more complex lesions were treated by surgical techniques, leading to obvious differences in outcomes. Alternatively, it may be likely that the findings underestimate the impact of endovascular therapy, as sicker patients with higher comorbidities and poor targets were more likely to undergo endovascular revascularization,” the researchers pointed out.

“Despite similar rates of major amputation, endovascular revascularization was associated with reduced in-hospital mortality, mean LOS, and mean cost of hospitalization. Although the results are encouraging, there remain significant disparities and gaps that must be addressed,” Dr. Agarwal and his colleagues concluded.

The authors reported that they had no relevant disclosures.

[email protected]

Immunizing surgical patients against seasonal influenza before they are discharged from the hospital appears safe and is a sound strategy for expanding vaccine coverage, especially among people at high risk, according to a report published online March 14 in Annals of Internal Medicine.

All health care contacts, including hospitalizations, are considered excellent opportunities for influenza vaccination, and current recommendations advise that eligible inpatients receive the immunization before discharge. However, surgical patients don’t often get the flu vaccine before they leave the hospital, likely because of concerns that potential adverse effects like fever and myalgia could be falsely attributed to surgical complications. This would lead to unnecessary patient evaluations and could interfere with postsurgical care, said Sara Y. Tartof, Ph.D., and her associates in the department of research and evaluation, Kaiser Permanente Southern California, Pasadena.

©CAP53/iStockphoto.com

“Although this concern is understandable, few clinical data support it,” they noted.

“To provide clinical evidence that would either substantiate or refute” these concerns about perioperative flu vaccination, the investigators analyzed data in the electronic health records for 81,647 surgeries. All the study participants were deemed eligible for flu vaccination. They were socioeconomically and ethnically diverse, ranged in age from 6 months to 106 years, and underwent surgery at 14 hospitals during three consecutive flu seasons. Operations included general, cardiac, eye, dermatologic, ENT, neurologic, ob.gyn., oral/maxillofacial, orthopedic, plastic, podiatric, urologic, and vascular procedures.

Patients received a flu vaccine in 6,420 hospital stays for surgery – only 15% of 42,777 eligible hospitalizations – usually on the day of discharge. (The remaining 38,870 patients either had been vaccinated before hospital admission or were vaccinated more than a week after discharge and were not included in further analyses.)

Compared with eligible patients who didn’t receive a flu vaccine during hospitalization for surgery, those who did showed no increased risk for subsequent inpatient visits, ED visits, or clinical work-ups for infection. Patients who received the flu vaccine before discharge showed a minimally increased risk for outpatient visits during the week following hospitalization, but this was considered unlikely “to translate into substantial clinical impact,” especially when balanced against the benefit of immunization, Dr. Tartof and her associates said (Ann Intern Med. 2016 Mar 14. doi: 10.7326/M15-1667).

Giving the flu vaccine during a surgical hospitalization “is an opportunity to protect a high-risk population,” because surgery patients tend to be of an age, and to have comorbid conditions, that raise their risk for flu complications. In addition, previous research has reported that 39%-46% of adults hospitalized for influenza-related disease in a given year had been hospitalized during the preceding autumn, indicating that recent hospitalization also raises the risk for flu complications, the investigators said.

“Our data support the rationale for increasing vaccination rates among surgical inpatients,” they said.

This study was funded by the U.S. Centers for Disease Control and Prevention through the Vaccine Safety Datalink program. Dr. Tartof reported receiving grants from Merck outside of this work; two of her associates reported receiving grants from Novartis and GlaxoSmithKline outside of this work.

Immunizing surgical patients against seasonal influenza before they are discharged from the hospital appears safe and is a sound strategy for expanding vaccine coverage, especially among people at high risk, according to a report published online March 14 in Annals of Internal Medicine.

All health care contacts, including hospitalizations, are considered excellent opportunities for influenza vaccination, and current recommendations advise that eligible inpatients receive the immunization before discharge. However, surgical patients don’t often get the flu vaccine before they leave the hospital, likely because of concerns that potential adverse effects like fever and myalgia could be falsely attributed to surgical complications. This would lead to unnecessary patient evaluations and could interfere with postsurgical care, said Sara Y. Tartof, Ph.D., and her associates in the department of research and evaluation, Kaiser Permanente Southern California, Pasadena.

©CAP53/iStockphoto.com

“Although this concern is understandable, few clinical data support it,” they noted.

“To provide clinical evidence that would either substantiate or refute” these concerns about perioperative flu vaccination, the investigators analyzed data in the electronic health records for 81,647 surgeries. All the study participants were deemed eligible for flu vaccination. They were socioeconomically and ethnically diverse, ranged in age from 6 months to 106 years, and underwent surgery at 14 hospitals during three consecutive flu seasons. Operations included general, cardiac, eye, dermatologic, ENT, neurologic, ob.gyn., oral/maxillofacial, orthopedic, plastic, podiatric, urologic, and vascular procedures.

Patients received a flu vaccine in 6,420 hospital stays for surgery – only 15% of 42,777 eligible hospitalizations – usually on the day of discharge. (The remaining 38,870 patients either had been vaccinated before hospital admission or were vaccinated more than a week after discharge and were not included in further analyses.)

Compared with eligible patients who didn’t receive a flu vaccine during hospitalization for surgery, those who did showed no increased risk for subsequent inpatient visits, ED visits, or clinical work-ups for infection. Patients who received the flu vaccine before discharge showed a minimally increased risk for outpatient visits during the week following hospitalization, but this was considered unlikely “to translate into substantial clinical impact,” especially when balanced against the benefit of immunization, Dr. Tartof and her associates said (Ann Intern Med. 2016 Mar 14. doi: 10.7326/M15-1667).

Giving the flu vaccine during a surgical hospitalization “is an opportunity to protect a high-risk population,” because surgery patients tend to be of an age, and to have comorbid conditions, that raise their risk for flu complications. In addition, previous research has reported that 39%-46% of adults hospitalized for influenza-related disease in a given year had been hospitalized during the preceding autumn, indicating that recent hospitalization also raises the risk for flu complications, the investigators said.

“Our data support the rationale for increasing vaccination rates among surgical inpatients,” they said.

This study was funded by the U.S. Centers for Disease Control and Prevention through the Vaccine Safety Datalink program. Dr. Tartof reported receiving grants from Merck outside of this work; two of her associates reported receiving grants from Novartis and GlaxoSmithKline outside of this work.

Immunizing surgical patients against seasonal influenza before they are discharged from the hospital appears safe and is a sound strategy for expanding vaccine coverage, especially among people at high risk, according to a report published online March 14 in Annals of Internal Medicine.

All health care contacts, including hospitalizations, are considered excellent opportunities for influenza vaccination, and current recommendations advise that eligible inpatients receive the immunization before discharge. However, surgical patients don’t often get the flu vaccine before they leave the hospital, likely because of concerns that potential adverse effects like fever and myalgia could be falsely attributed to surgical complications. This would lead to unnecessary patient evaluations and could interfere with postsurgical care, said Sara Y. Tartof, Ph.D., and her associates in the department of research and evaluation, Kaiser Permanente Southern California, Pasadena.

©CAP53/iStockphoto.com

“Although this concern is understandable, few clinical data support it,” they noted.

“To provide clinical evidence that would either substantiate or refute” these concerns about perioperative flu vaccination, the investigators analyzed data in the electronic health records for 81,647 surgeries. All the study participants were deemed eligible for flu vaccination. They were socioeconomically and ethnically diverse, ranged in age from 6 months to 106 years, and underwent surgery at 14 hospitals during three consecutive flu seasons. Operations included general, cardiac, eye, dermatologic, ENT, neurologic, ob.gyn., oral/maxillofacial, orthopedic, plastic, podiatric, urologic, and vascular procedures.

Patients received a flu vaccine in 6,420 hospital stays for surgery – only 15% of 42,777 eligible hospitalizations – usually on the day of discharge. (The remaining 38,870 patients either had been vaccinated before hospital admission or were vaccinated more than a week after discharge and were not included in further analyses.)

Compared with eligible patients who didn’t receive a flu vaccine during hospitalization for surgery, those who did showed no increased risk for subsequent inpatient visits, ED visits, or clinical work-ups for infection. Patients who received the flu vaccine before discharge showed a minimally increased risk for outpatient visits during the week following hospitalization, but this was considered unlikely “to translate into substantial clinical impact,” especially when balanced against the benefit of immunization, Dr. Tartof and her associates said (Ann Intern Med. 2016 Mar 14. doi: 10.7326/M15-1667).

Giving the flu vaccine during a surgical hospitalization “is an opportunity to protect a high-risk population,” because surgery patients tend to be of an age, and to have comorbid conditions, that raise their risk for flu complications. In addition, previous research has reported that 39%-46% of adults hospitalized for influenza-related disease in a given year had been hospitalized during the preceding autumn, indicating that recent hospitalization also raises the risk for flu complications, the investigators said.

“Our data support the rationale for increasing vaccination rates among surgical inpatients,” they said.

This study was funded by the U.S. Centers for Disease Control and Prevention through the Vaccine Safety Datalink program. Dr. Tartof reported receiving grants from Merck outside of this work; two of her associates reported receiving grants from Novartis and GlaxoSmithKline outside of this work.