Clinical

Giving iron supplements every other day may be superior to daily divided doses

Serum hepcidin levels and iron absorption were compared in women given daily dosing of ferrous sulfate, women given alternate-day dosing, and women given two divided doses daily. Women on the alternate-day regimen and the single-day regimens had higher iron absorption and lower hepcidin levels than did the women on the split-dosing regimen; these findings need to be confirmed in patients with iron-deficiency anemia.

Immediate percutaneous coronary intervention (PCI) of the culprit lesion only in patients presenting with acute myocardial infarction and cardiogenic shock may lead to better outcomes, even in those with multivessel disease

A total of 706 patients with multivessel coronary artery disease who presented with acute MI and cardiogenic shock were randomized to either PCI of the culprit lesion only (followed by optional staged revascularization of nonculprit lesions) or to immediate multivessel PCI. Patients who received PCI of the culprit lesion only had a lower 30-day risk of death or severe renal failure leading to renal-replacement therapy than did those who underwent immediate multivessel PCI.

Citation: Thiele H et al. PCI strategies in patients with acute myocardial infarction and cardiogenic shock. N Engl J Med. 2017 Oct. doi: 10.1056/NEJMoa1710261 (epub ahead of print).

Giving iron supplements every other day may be superior to daily divided doses

Serum hepcidin levels and iron absorption were compared in women given daily dosing of ferrous sulfate, women given alternate-day dosing, and women given two divided doses daily. Women on the alternate-day regimen and the single-day regimens had higher iron absorption and lower hepcidin levels than did the women on the split-dosing regimen; these findings need to be confirmed in patients with iron-deficiency anemia.

Immediate percutaneous coronary intervention (PCI) of the culprit lesion only in patients presenting with acute myocardial infarction and cardiogenic shock may lead to better outcomes, even in those with multivessel disease

A total of 706 patients with multivessel coronary artery disease who presented with acute MI and cardiogenic shock were randomized to either PCI of the culprit lesion only (followed by optional staged revascularization of nonculprit lesions) or to immediate multivessel PCI. Patients who received PCI of the culprit lesion only had a lower 30-day risk of death or severe renal failure leading to renal-replacement therapy than did those who underwent immediate multivessel PCI.

Citation: Thiele H et al. PCI strategies in patients with acute myocardial infarction and cardiogenic shock. N Engl J Med. 2017 Oct. doi: 10.1056/NEJMoa1710261 (epub ahead of print).

Giving iron supplements every other day may be superior to daily divided doses

Serum hepcidin levels and iron absorption were compared in women given daily dosing of ferrous sulfate, women given alternate-day dosing, and women given two divided doses daily. Women on the alternate-day regimen and the single-day regimens had higher iron absorption and lower hepcidin levels than did the women on the split-dosing regimen; these findings need to be confirmed in patients with iron-deficiency anemia.

Immediate percutaneous coronary intervention (PCI) of the culprit lesion only in patients presenting with acute myocardial infarction and cardiogenic shock may lead to better outcomes, even in those with multivessel disease

A total of 706 patients with multivessel coronary artery disease who presented with acute MI and cardiogenic shock were randomized to either PCI of the culprit lesion only (followed by optional staged revascularization of nonculprit lesions) or to immediate multivessel PCI. Patients who received PCI of the culprit lesion only had a lower 30-day risk of death or severe renal failure leading to renal-replacement therapy than did those who underwent immediate multivessel PCI.

Citation: Thiele H et al. PCI strategies in patients with acute myocardial infarction and cardiogenic shock. N Engl J Med. 2017 Oct. doi: 10.1056/NEJMoa1710261 (epub ahead of print).

ORLANDO – A respiratory or urinary tract infection severe enough to land a patient in the hospital constitutes a novel independent risk factor for subsequent ischemic heart disease and ischemic stroke, according to a “big data” registry study from the United Kingdom.

“Our data show infection was just as much a risk factor or more compared with the traditional atherosclerotic cardiovascular disease risk factors,” Paul Carter, MD, said at the annual meeting of the American College of Cardiology.

Bruce Jancin/MDedge News

Dr. Carter of Aston Medical School in Birmingham, England, presented a retrospective analysis from the ACALM (Algorithm for Comorbidities Associated with Length of stay and Mortality) study of administrative data on all of the more than 1.22 million patients admitted to seven U.K. hospitals in 2000-2013. His analysis included all 34,027 adults aged 40 years or older admitted with a urinary tract or respiratory infection on their index hospitalization who had no history of ischemic heart disease or ischemic stroke.

These patients, with a mean age of 73 years, 59% of whom were women, were compared with an equal number of age- and gender-matched adults whose index hospitalization was for reasons other than ischemic heart disease, stroke, urinary tract infection (UTI), or respiratory infection – the two most common infections resulting in hospitalization in the United Kingdom.

Patients with a respiratory infection or UTI had a 9.9% incidence of new-onset ischemic heart disease and a 4.1% rate of ischemic stroke during follow-up starting upon discharge from their index hospitalization, significantly higher than the 5.9% and 1.5% rates in controls. In a multivariate logistic regression analysis adjusted for demographics, standard cardiovascular risk factors, and the top 10 causes of mortality in the United Kingdom, patients with respiratory infection or UTI as their admitting diagnosis had a 1.36-fold increased likelihood of developing ischemic heart disease post discharge and a 2.5-fold greater risk of ischemic stroke than matched controls.

Moreover, mortality following diagnosis of ischemic heart disease was 75.2% in patients whose index hospitalization was for infection, compared with 51.1% in controls who developed ischemic heart disease without a history of hospitalization for infection, for an adjusted 2.98-fold increased likelihood of death. Similarly, mortality after an ischemic stroke was 59.8% in patients with a prior severe infection, compared with 30.8% in controls, which translated to an adjusted 3.1-fold increased risk of death post stroke in patients with a prior hospitalization for infection.

In the multivariate analysis, hospitalization for infection was a stronger risk factor for subsequent ischemic stroke than was atrial fibrillation, heart failure, type 1 or type 2 diabetes, hypertension, or hyperlipidemia. The risk of ischemic heart disease in patients with an infectious disease hospitalization was similar to the risks associated with most of those recognized risk factors.

Two possible mechanisms by which infection might predispose to subsequent ischemic heart disease and stroke are via a direct effect whereby pathogens such as Chlamydia pneumoniae are taken up into arterial plaques, where they cause a local inflammatory response, or an indirect effect in which systemic inflammation primes the atherosclerotic plaque through distribution of inflammatory cytokines, according to Dr. Carter.

He said the ACALM findings are particularly intriguing when considered in the context of the 2017 results of the landmark CANTOS trial, in which canakinumab (Ilaris), a targeted anti-inflammatory agent that inhibits the interleukin-1 beta innate immunity pathway, reduced recurrent ischemic events in post-MI patients who had high systemic inflammation as evidenced by their elevated C-reactive protein level but a normal-range LDL cholesterol (N Engl J Med. 2017 Aug 27. doi: 10.1056/NEJMoa1707914).

“If atherosclerosis is an inflammatory condition, this begs the question of whether other inflammatory conditions, like infection, which induces a large systemic inflammatory response, might drive atherosclerosis,” Dr. Carter commented.

“It’s now very well understood that inflammatory mediators, cells, and processes are involved in every step from the initial endothelial dysfunction that leads to uptake of LDL, inflammatory cells, and monocytes all the way through to plaque progression and rupture, where Th1 cytokines have been implicated in causing that rupture, and ultimately in patient presentation at the hospital,” he added.

He sees the ACALM findings as hypothesis generating, serving to help lay the groundwork for future clinical trials of vaccine or anti-inflammatory antibiotic therapies.

Dr. Carter reported having no financial conflicts related to his presentation.

[email protected]

SOURCE: Carter P. ACC 2018, Abstract 1325M-0.

ORLANDO – A respiratory or urinary tract infection severe enough to land a patient in the hospital constitutes a novel independent risk factor for subsequent ischemic heart disease and ischemic stroke, according to a “big data” registry study from the United Kingdom.

“Our data show infection was just as much a risk factor or more compared with the traditional atherosclerotic cardiovascular disease risk factors,” Paul Carter, MD, said at the annual meeting of the American College of Cardiology.

Bruce Jancin/MDedge News

Dr. Carter of Aston Medical School in Birmingham, England, presented a retrospective analysis from the ACALM (Algorithm for Comorbidities Associated with Length of stay and Mortality) study of administrative data on all of the more than 1.22 million patients admitted to seven U.K. hospitals in 2000-2013. His analysis included all 34,027 adults aged 40 years or older admitted with a urinary tract or respiratory infection on their index hospitalization who had no history of ischemic heart disease or ischemic stroke.

These patients, with a mean age of 73 years, 59% of whom were women, were compared with an equal number of age- and gender-matched adults whose index hospitalization was for reasons other than ischemic heart disease, stroke, urinary tract infection (UTI), or respiratory infection – the two most common infections resulting in hospitalization in the United Kingdom.

Patients with a respiratory infection or UTI had a 9.9% incidence of new-onset ischemic heart disease and a 4.1% rate of ischemic stroke during follow-up starting upon discharge from their index hospitalization, significantly higher than the 5.9% and 1.5% rates in controls. In a multivariate logistic regression analysis adjusted for demographics, standard cardiovascular risk factors, and the top 10 causes of mortality in the United Kingdom, patients with respiratory infection or UTI as their admitting diagnosis had a 1.36-fold increased likelihood of developing ischemic heart disease post discharge and a 2.5-fold greater risk of ischemic stroke than matched controls.

Moreover, mortality following diagnosis of ischemic heart disease was 75.2% in patients whose index hospitalization was for infection, compared with 51.1% in controls who developed ischemic heart disease without a history of hospitalization for infection, for an adjusted 2.98-fold increased likelihood of death. Similarly, mortality after an ischemic stroke was 59.8% in patients with a prior severe infection, compared with 30.8% in controls, which translated to an adjusted 3.1-fold increased risk of death post stroke in patients with a prior hospitalization for infection.

In the multivariate analysis, hospitalization for infection was a stronger risk factor for subsequent ischemic stroke than was atrial fibrillation, heart failure, type 1 or type 2 diabetes, hypertension, or hyperlipidemia. The risk of ischemic heart disease in patients with an infectious disease hospitalization was similar to the risks associated with most of those recognized risk factors.

Two possible mechanisms by which infection might predispose to subsequent ischemic heart disease and stroke are via a direct effect whereby pathogens such as Chlamydia pneumoniae are taken up into arterial plaques, where they cause a local inflammatory response, or an indirect effect in which systemic inflammation primes the atherosclerotic plaque through distribution of inflammatory cytokines, according to Dr. Carter.

He said the ACALM findings are particularly intriguing when considered in the context of the 2017 results of the landmark CANTOS trial, in which canakinumab (Ilaris), a targeted anti-inflammatory agent that inhibits the interleukin-1 beta innate immunity pathway, reduced recurrent ischemic events in post-MI patients who had high systemic inflammation as evidenced by their elevated C-reactive protein level but a normal-range LDL cholesterol (N Engl J Med. 2017 Aug 27. doi: 10.1056/NEJMoa1707914).

“If atherosclerosis is an inflammatory condition, this begs the question of whether other inflammatory conditions, like infection, which induces a large systemic inflammatory response, might drive atherosclerosis,” Dr. Carter commented.

“It’s now very well understood that inflammatory mediators, cells, and processes are involved in every step from the initial endothelial dysfunction that leads to uptake of LDL, inflammatory cells, and monocytes all the way through to plaque progression and rupture, where Th1 cytokines have been implicated in causing that rupture, and ultimately in patient presentation at the hospital,” he added.

He sees the ACALM findings as hypothesis generating, serving to help lay the groundwork for future clinical trials of vaccine or anti-inflammatory antibiotic therapies.

Dr. Carter reported having no financial conflicts related to his presentation.

[email protected]

SOURCE: Carter P. ACC 2018, Abstract 1325M-0.

ORLANDO – A respiratory or urinary tract infection severe enough to land a patient in the hospital constitutes a novel independent risk factor for subsequent ischemic heart disease and ischemic stroke, according to a “big data” registry study from the United Kingdom.

“Our data show infection was just as much a risk factor or more compared with the traditional atherosclerotic cardiovascular disease risk factors,” Paul Carter, MD, said at the annual meeting of the American College of Cardiology.

Bruce Jancin/MDedge News

Dr. Carter of Aston Medical School in Birmingham, England, presented a retrospective analysis from the ACALM (Algorithm for Comorbidities Associated with Length of stay and Mortality) study of administrative data on all of the more than 1.22 million patients admitted to seven U.K. hospitals in 2000-2013. His analysis included all 34,027 adults aged 40 years or older admitted with a urinary tract or respiratory infection on their index hospitalization who had no history of ischemic heart disease or ischemic stroke.

These patients, with a mean age of 73 years, 59% of whom were women, were compared with an equal number of age- and gender-matched adults whose index hospitalization was for reasons other than ischemic heart disease, stroke, urinary tract infection (UTI), or respiratory infection – the two most common infections resulting in hospitalization in the United Kingdom.

Patients with a respiratory infection or UTI had a 9.9% incidence of new-onset ischemic heart disease and a 4.1% rate of ischemic stroke during follow-up starting upon discharge from their index hospitalization, significantly higher than the 5.9% and 1.5% rates in controls. In a multivariate logistic regression analysis adjusted for demographics, standard cardiovascular risk factors, and the top 10 causes of mortality in the United Kingdom, patients with respiratory infection or UTI as their admitting diagnosis had a 1.36-fold increased likelihood of developing ischemic heart disease post discharge and a 2.5-fold greater risk of ischemic stroke than matched controls.

Moreover, mortality following diagnosis of ischemic heart disease was 75.2% in patients whose index hospitalization was for infection, compared with 51.1% in controls who developed ischemic heart disease without a history of hospitalization for infection, for an adjusted 2.98-fold increased likelihood of death. Similarly, mortality after an ischemic stroke was 59.8% in patients with a prior severe infection, compared with 30.8% in controls, which translated to an adjusted 3.1-fold increased risk of death post stroke in patients with a prior hospitalization for infection.

In the multivariate analysis, hospitalization for infection was a stronger risk factor for subsequent ischemic stroke than was atrial fibrillation, heart failure, type 1 or type 2 diabetes, hypertension, or hyperlipidemia. The risk of ischemic heart disease in patients with an infectious disease hospitalization was similar to the risks associated with most of those recognized risk factors.

Two possible mechanisms by which infection might predispose to subsequent ischemic heart disease and stroke are via a direct effect whereby pathogens such as Chlamydia pneumoniae are taken up into arterial plaques, where they cause a local inflammatory response, or an indirect effect in which systemic inflammation primes the atherosclerotic plaque through distribution of inflammatory cytokines, according to Dr. Carter.

He said the ACALM findings are particularly intriguing when considered in the context of the 2017 results of the landmark CANTOS trial, in which canakinumab (Ilaris), a targeted anti-inflammatory agent that inhibits the interleukin-1 beta innate immunity pathway, reduced recurrent ischemic events in post-MI patients who had high systemic inflammation as evidenced by their elevated C-reactive protein level but a normal-range LDL cholesterol (N Engl J Med. 2017 Aug 27. doi: 10.1056/NEJMoa1707914).

“If atherosclerosis is an inflammatory condition, this begs the question of whether other inflammatory conditions, like infection, which induces a large systemic inflammatory response, might drive atherosclerosis,” Dr. Carter commented.

“It’s now very well understood that inflammatory mediators, cells, and processes are involved in every step from the initial endothelial dysfunction that leads to uptake of LDL, inflammatory cells, and monocytes all the way through to plaque progression and rupture, where Th1 cytokines have been implicated in causing that rupture, and ultimately in patient presentation at the hospital,” he added.

He sees the ACALM findings as hypothesis generating, serving to help lay the groundwork for future clinical trials of vaccine or anti-inflammatory antibiotic therapies.

Dr. Carter reported having no financial conflicts related to his presentation.

[email protected]

SOURCE: Carter P. ACC 2018, Abstract 1325M-0.

Clinical question: How does using procalcitonin levels for adults with acute respiratory infections (ARIs) affect patient outcomes?

Background: While the ARI diagnosis encompasses bacterial, viral, and inflammatory etiologies, as many as 75% of ARIs are treated with antibiotics. Procalcitonin is a biomarker released by tissues in response to bacterial infections. Its production is also inhibited by interferon-gamma, a cytokine released in response to viral infections, therefore, making procalcitonin a biomarker of particular interest to support the use of antibiotic therapy in the treatment of ARIs.

Study design: Cochrane Review.

Setting: Medical wards, intensive care units, primary care clinics, and emergency departments across 12 countries.

Synopsis: The review included 26 randomized control trials of 6,708 immunocompetent adults with ARIs who received antibiotics either based on procalcitonin-guided antibiotic therapy or routine care. Primary endpoints evaluated included all-cause mortality and treatment failure at 30 days. Secondary endpoints were antibiotic use, antibiotic-related side effects, and length of hospital stay. There were significantly fewer deaths in the procalcitonin-guided group than in the control group (286/8.6% vs. 336/10%; adjusted odds ratio, 0.83; 95% confidence interval, 0.70-0.99; P = .037). Treatment failure was not statistically different between the procalcitonin-guided participants and the controls. Of the secondary endpoints, antibiotic use and antibiotic-related side effects were lower in the procalcitonin-guided group (5.7 days vs. 8.1 days; P less than .001; and 16.3% vs. 22.1%; P less than .001). Each of the RCTs had varying algorithms for the use of procalcitonin-guided therapy, so no specific treatment guidelines can be gleaned from this review.

Bottom line: Procalcitonin-guided algorithms are associated with lower mortality, lower antibiotic exposure, and lower antibiotic-related side effects. However, more research is needed to determine best practice algorithms for using procalcitonin levels to guide treatment decisions.

Citation: Schuetz P et al. Procalcitonin to initiate or discontinue antibiotics in acute respiratory tract infections. Cochrane Database Syst Rev. 2017 Oct 12. doi: 10.1002/14651858.cd007498.pub3.

Clinical question: How does using procalcitonin levels for adults with acute respiratory infections (ARIs) affect patient outcomes?

Background: While the ARI diagnosis encompasses bacterial, viral, and inflammatory etiologies, as many as 75% of ARIs are treated with antibiotics. Procalcitonin is a biomarker released by tissues in response to bacterial infections. Its production is also inhibited by interferon-gamma, a cytokine released in response to viral infections, therefore, making procalcitonin a biomarker of particular interest to support the use of antibiotic therapy in the treatment of ARIs.

Study design: Cochrane Review.

Setting: Medical wards, intensive care units, primary care clinics, and emergency departments across 12 countries.

Synopsis: The review included 26 randomized control trials of 6,708 immunocompetent adults with ARIs who received antibiotics either based on procalcitonin-guided antibiotic therapy or routine care. Primary endpoints evaluated included all-cause mortality and treatment failure at 30 days. Secondary endpoints were antibiotic use, antibiotic-related side effects, and length of hospital stay. There were significantly fewer deaths in the procalcitonin-guided group than in the control group (286/8.6% vs. 336/10%; adjusted odds ratio, 0.83; 95% confidence interval, 0.70-0.99; P = .037). Treatment failure was not statistically different between the procalcitonin-guided participants and the controls. Of the secondary endpoints, antibiotic use and antibiotic-related side effects were lower in the procalcitonin-guided group (5.7 days vs. 8.1 days; P less than .001; and 16.3% vs. 22.1%; P less than .001). Each of the RCTs had varying algorithms for the use of procalcitonin-guided therapy, so no specific treatment guidelines can be gleaned from this review.

Bottom line: Procalcitonin-guided algorithms are associated with lower mortality, lower antibiotic exposure, and lower antibiotic-related side effects. However, more research is needed to determine best practice algorithms for using procalcitonin levels to guide treatment decisions.

Citation: Schuetz P et al. Procalcitonin to initiate or discontinue antibiotics in acute respiratory tract infections. Cochrane Database Syst Rev. 2017 Oct 12. doi: 10.1002/14651858.cd007498.pub3.

Clinical question: How does using procalcitonin levels for adults with acute respiratory infections (ARIs) affect patient outcomes?

Background: While the ARI diagnosis encompasses bacterial, viral, and inflammatory etiologies, as many as 75% of ARIs are treated with antibiotics. Procalcitonin is a biomarker released by tissues in response to bacterial infections. Its production is also inhibited by interferon-gamma, a cytokine released in response to viral infections, therefore, making procalcitonin a biomarker of particular interest to support the use of antibiotic therapy in the treatment of ARIs.

Study design: Cochrane Review.

Setting: Medical wards, intensive care units, primary care clinics, and emergency departments across 12 countries.

Synopsis: The review included 26 randomized control trials of 6,708 immunocompetent adults with ARIs who received antibiotics either based on procalcitonin-guided antibiotic therapy or routine care. Primary endpoints evaluated included all-cause mortality and treatment failure at 30 days. Secondary endpoints were antibiotic use, antibiotic-related side effects, and length of hospital stay. There were significantly fewer deaths in the procalcitonin-guided group than in the control group (286/8.6% vs. 336/10%; adjusted odds ratio, 0.83; 95% confidence interval, 0.70-0.99; P = .037). Treatment failure was not statistically different between the procalcitonin-guided participants and the controls. Of the secondary endpoints, antibiotic use and antibiotic-related side effects were lower in the procalcitonin-guided group (5.7 days vs. 8.1 days; P less than .001; and 16.3% vs. 22.1%; P less than .001). Each of the RCTs had varying algorithms for the use of procalcitonin-guided therapy, so no specific treatment guidelines can be gleaned from this review.

Bottom line: Procalcitonin-guided algorithms are associated with lower mortality, lower antibiotic exposure, and lower antibiotic-related side effects. However, more research is needed to determine best practice algorithms for using procalcitonin levels to guide treatment decisions.

Citation: Schuetz P et al. Procalcitonin to initiate or discontinue antibiotics in acute respiratory tract infections. Cochrane Database Syst Rev. 2017 Oct 12. doi: 10.1002/14651858.cd007498.pub3.

SAN DIEGO – The “holy grail” of thrombosis prevention is the ability to determine the risk of recurrence with or without continuation of anticoagulant treatment, according to Philip S. Wells, MD.

“Very little data exists for the comparison of active treatment to placebo in the acute and long-term phases of treatment,” he said at the biennial summit of the Thrombosis & Hemostasis Societies of North America. “With low molecular weight heparin, vitamin K antagonists, and direct-acting oral anticoagulants, the relative risk reduction is about 90% in the acute phase and 80%-85% in the extended phase. After discontinuing anticoagulants, the absolute risk of recurrence varies depending on VTE category.”

Dr. Wells, chair and chief of the department of medicine at The Ottawa Hospital and the University of Ottawa, said that after 3 months of anticoagulation the chance of recurrence in postsurgical VTE patients is less than 1% per year. After 3 months of anticoagulant use in nonsurgical patients with provoked risk factors, it is around 4%. This includes medical patients, trauma victims, pregnant women, and patients wearing a plaster cast.

In patients who survive an unprovoked VTE, after 3-6 months of anticoagulant therapy their overall recurrence risk is 10% in the first year and 30% after 5 years. The risk of recurrence is 50% higher if a patient experiences a second unprovoked VTE, and the risk of fatality is 50% higher if the initial event was a pulmonary embolism (PE), he said.

According to the ongoing prospective Austrian Study on Recurrent Venous Thromboembolism, the risk of recurrent VTE is 20% in men and 6% in women (N Engl J Med. 2004 Jun 17;350[25]:2558-63). A multicenter prospective study in Canada yielded similar results. It found that the risk of recurrent VTE is 19% in men versus 9% in women (CMAJ 2008;179[5]:417-26).

That Canadian prospective study, led by Marc Rodger, MD, described the development of the HERDOO2 clinical decision rule for determining a patient’s risk for a recurrent VTE. This includes hyperpigmentation, edema, or redness in either leg (signs of postthrombotic syndrome), D-dimer level of 250 mcg/L or greater while on warfarin, body mass index of 30 kg/m² or greater, and age of 65 years or older.

If patients have zero or one risk factor, the annual risk of VTE after 6 months of treatment is 1.6%, while two or more risk factors bumps the annual risk of VTE to 14.1%, according to the researchers.

Doug Brunk/MDedge News

In a separate study of 319 patients with two negative D-dimer results who did not restart anticoagulation therapy, the rate of recurrent VTE was 6.7% per patient-year (Ann Intern Med 2015;162:27-34). It was 9.7% per patient-year in men, compared with 5.4% per patient-year in women.

Dr. Wells emphasized the importance of shared decision-making with the patient when devising a strategy for long-term anticoagulation following a VTE. “We don’t have a lot of good tools, but [trying to elicit] patient preference is the right thing to try and do,” he said. “Physicians should present an unbiased perspective to patients regarding their treatment, including the benefits and harms, effect on quality of life, and cost.”

Dr. Wells also shared his current clinical approach. In women with an unprovoked VTE, he applies the HERDOO2 rule. If there’s a low recurrence risk, he discontinues the anticoagulant. If there’s a non-low recurrence risk he continues with the anticoagulant unless there’s a high risk for bleeding. Men with an unprovoked VTE receive indefinite anticoagulant therapy, but if the index event is a deep vein thrombosis (DVT), Dr. Wells applies a bleeding risk tool to help him determine management going forward. If the patient has a high risk of bleeding, he does not use an anticoagulant.

“If there is a high risk of bleeding it’s best of stay off anticoagulant therapy,” he said. “If there is an intermediate risk of bleeding and the index event was a DVT, the patient could stay off anticoagulants. I think we have a long way to go to developing tools that actually enable us to reach these points with each patient in discussions we have with them about continuing anticoagulants.”

Dr. Wells reported having received research support from BMS/Pfizer and honoraria from Bayer AG, Janssen, Pfizer, and Daiichi Sankyo. He is a member of the scientific advisory board for Bayer AG and Pfizer.

[email protected]

SAN DIEGO – The “holy grail” of thrombosis prevention is the ability to determine the risk of recurrence with or without continuation of anticoagulant treatment, according to Philip S. Wells, MD.

“Very little data exists for the comparison of active treatment to placebo in the acute and long-term phases of treatment,” he said at the biennial summit of the Thrombosis & Hemostasis Societies of North America. “With low molecular weight heparin, vitamin K antagonists, and direct-acting oral anticoagulants, the relative risk reduction is about 90% in the acute phase and 80%-85% in the extended phase. After discontinuing anticoagulants, the absolute risk of recurrence varies depending on VTE category.”

Dr. Wells, chair and chief of the department of medicine at The Ottawa Hospital and the University of Ottawa, said that after 3 months of anticoagulation the chance of recurrence in postsurgical VTE patients is less than 1% per year. After 3 months of anticoagulant use in nonsurgical patients with provoked risk factors, it is around 4%. This includes medical patients, trauma victims, pregnant women, and patients wearing a plaster cast.

In patients who survive an unprovoked VTE, after 3-6 months of anticoagulant therapy their overall recurrence risk is 10% in the first year and 30% after 5 years. The risk of recurrence is 50% higher if a patient experiences a second unprovoked VTE, and the risk of fatality is 50% higher if the initial event was a pulmonary embolism (PE), he said.

According to the ongoing prospective Austrian Study on Recurrent Venous Thromboembolism, the risk of recurrent VTE is 20% in men and 6% in women (N Engl J Med. 2004 Jun 17;350[25]:2558-63). A multicenter prospective study in Canada yielded similar results. It found that the risk of recurrent VTE is 19% in men versus 9% in women (CMAJ 2008;179[5]:417-26).

That Canadian prospective study, led by Marc Rodger, MD, described the development of the HERDOO2 clinical decision rule for determining a patient’s risk for a recurrent VTE. This includes hyperpigmentation, edema, or redness in either leg (signs of postthrombotic syndrome), D-dimer level of 250 mcg/L or greater while on warfarin, body mass index of 30 kg/m² or greater, and age of 65 years or older.

If patients have zero or one risk factor, the annual risk of VTE after 6 months of treatment is 1.6%, while two or more risk factors bumps the annual risk of VTE to 14.1%, according to the researchers.

Doug Brunk/MDedge News

In a separate study of 319 patients with two negative D-dimer results who did not restart anticoagulation therapy, the rate of recurrent VTE was 6.7% per patient-year (Ann Intern Med 2015;162:27-34). It was 9.7% per patient-year in men, compared with 5.4% per patient-year in women.

Dr. Wells emphasized the importance of shared decision-making with the patient when devising a strategy for long-term anticoagulation following a VTE. “We don’t have a lot of good tools, but [trying to elicit] patient preference is the right thing to try and do,” he said. “Physicians should present an unbiased perspective to patients regarding their treatment, including the benefits and harms, effect on quality of life, and cost.”

Dr. Wells also shared his current clinical approach. In women with an unprovoked VTE, he applies the HERDOO2 rule. If there’s a low recurrence risk, he discontinues the anticoagulant. If there’s a non-low recurrence risk he continues with the anticoagulant unless there’s a high risk for bleeding. Men with an unprovoked VTE receive indefinite anticoagulant therapy, but if the index event is a deep vein thrombosis (DVT), Dr. Wells applies a bleeding risk tool to help him determine management going forward. If the patient has a high risk of bleeding, he does not use an anticoagulant.

“If there is a high risk of bleeding it’s best of stay off anticoagulant therapy,” he said. “If there is an intermediate risk of bleeding and the index event was a DVT, the patient could stay off anticoagulants. I think we have a long way to go to developing tools that actually enable us to reach these points with each patient in discussions we have with them about continuing anticoagulants.”

Dr. Wells reported having received research support from BMS/Pfizer and honoraria from Bayer AG, Janssen, Pfizer, and Daiichi Sankyo. He is a member of the scientific advisory board for Bayer AG and Pfizer.

[email protected]

SAN DIEGO – The “holy grail” of thrombosis prevention is the ability to determine the risk of recurrence with or without continuation of anticoagulant treatment, according to Philip S. Wells, MD.

“Very little data exists for the comparison of active treatment to placebo in the acute and long-term phases of treatment,” he said at the biennial summit of the Thrombosis & Hemostasis Societies of North America. “With low molecular weight heparin, vitamin K antagonists, and direct-acting oral anticoagulants, the relative risk reduction is about 90% in the acute phase and 80%-85% in the extended phase. After discontinuing anticoagulants, the absolute risk of recurrence varies depending on VTE category.”

Dr. Wells, chair and chief of the department of medicine at The Ottawa Hospital and the University of Ottawa, said that after 3 months of anticoagulation the chance of recurrence in postsurgical VTE patients is less than 1% per year. After 3 months of anticoagulant use in nonsurgical patients with provoked risk factors, it is around 4%. This includes medical patients, trauma victims, pregnant women, and patients wearing a plaster cast.

In patients who survive an unprovoked VTE, after 3-6 months of anticoagulant therapy their overall recurrence risk is 10% in the first year and 30% after 5 years. The risk of recurrence is 50% higher if a patient experiences a second unprovoked VTE, and the risk of fatality is 50% higher if the initial event was a pulmonary embolism (PE), he said.

According to the ongoing prospective Austrian Study on Recurrent Venous Thromboembolism, the risk of recurrent VTE is 20% in men and 6% in women (N Engl J Med. 2004 Jun 17;350[25]:2558-63). A multicenter prospective study in Canada yielded similar results. It found that the risk of recurrent VTE is 19% in men versus 9% in women (CMAJ 2008;179[5]:417-26).

That Canadian prospective study, led by Marc Rodger, MD, described the development of the HERDOO2 clinical decision rule for determining a patient’s risk for a recurrent VTE. This includes hyperpigmentation, edema, or redness in either leg (signs of postthrombotic syndrome), D-dimer level of 250 mcg/L or greater while on warfarin, body mass index of 30 kg/m² or greater, and age of 65 years or older.

If patients have zero or one risk factor, the annual risk of VTE after 6 months of treatment is 1.6%, while two or more risk factors bumps the annual risk of VTE to 14.1%, according to the researchers.

Doug Brunk/MDedge News

In a separate study of 319 patients with two negative D-dimer results who did not restart anticoagulation therapy, the rate of recurrent VTE was 6.7% per patient-year (Ann Intern Med 2015;162:27-34). It was 9.7% per patient-year in men, compared with 5.4% per patient-year in women.

Dr. Wells emphasized the importance of shared decision-making with the patient when devising a strategy for long-term anticoagulation following a VTE. “We don’t have a lot of good tools, but [trying to elicit] patient preference is the right thing to try and do,” he said. “Physicians should present an unbiased perspective to patients regarding their treatment, including the benefits and harms, effect on quality of life, and cost.”

Dr. Wells also shared his current clinical approach. In women with an unprovoked VTE, he applies the HERDOO2 rule. If there’s a low recurrence risk, he discontinues the anticoagulant. If there’s a non-low recurrence risk he continues with the anticoagulant unless there’s a high risk for bleeding. Men with an unprovoked VTE receive indefinite anticoagulant therapy, but if the index event is a deep vein thrombosis (DVT), Dr. Wells applies a bleeding risk tool to help him determine management going forward. If the patient has a high risk of bleeding, he does not use an anticoagulant.

“If there is a high risk of bleeding it’s best of stay off anticoagulant therapy,” he said. “If there is an intermediate risk of bleeding and the index event was a DVT, the patient could stay off anticoagulants. I think we have a long way to go to developing tools that actually enable us to reach these points with each patient in discussions we have with them about continuing anticoagulants.”

Dr. Wells reported having received research support from BMS/Pfizer and honoraria from Bayer AG, Janssen, Pfizer, and Daiichi Sankyo. He is a member of the scientific advisory board for Bayer AG and Pfizer.

[email protected]

Clinical question: Does switching from a brand name ARB to its generic lead to more ED visits and hospitalizations?

Background: Once a brand name drug’s patent expires, its generic form is commercialized and patients may be switched to the generic version. The drug equivalence of the generic vs. the brand name product may be substantial enough to affect clinically what is happening to the patient. Very few studies exist on the impact of the differences between brand-name and generic ARBs; those that do exist show conflicting results on clinical outcomes for the patient.

Study design: Observational retrospective interrupted time–series analysis.

Setting: Quebec Integrated Chronic Disease Surveillance System in Quebec.

Synopsis: The study analyzed 136,177 patients older than 66 years old with multiple comorbidities during the transition from brand-name to generic versions of losartan, valsartan, and candesartan. The authors compared ER visits or hospitalization of the brand-name users for 24 months before and 12 months after being transitioned from a brand-name ARB to a generic. All three groups were found to have higher rates of adverse events after switching to generics (8% for losartan, 11.7% for valsartan, and 16.6% for candesartan). The study was limited as the authors did not have access to the reason for the ER visits/admissions or the ability to determine which generic version was used (e.g., losartan has eight generic versions). The study highlights the need for further evaluation by risk and survival analysis to control confounders when switching to a generic formulation.

Bottom line: Switching patients from a brand-name to a generic ARB may lead to more ED consultations and hospital admissions.

Citation: Leclerc J et al. Impact of the commercialization of three generic angiotensin II receptor blockers on adverse events in Quebec Canada. Circ Cardiovasc Qual Outcomes. 2017 Oct 3. pii 10e003891. doi: 10.1161/circoutcomes.117.003891.

Dr. Smith is assistant professor of medicine in the Division of Hospital Medicine, Emory University, Atlanta.

Clinical question: Does switching from a brand name ARB to its generic lead to more ED visits and hospitalizations?

Background: Once a brand name drug’s patent expires, its generic form is commercialized and patients may be switched to the generic version. The drug equivalence of the generic vs. the brand name product may be substantial enough to affect clinically what is happening to the patient. Very few studies exist on the impact of the differences between brand-name and generic ARBs; those that do exist show conflicting results on clinical outcomes for the patient.

Study design: Observational retrospective interrupted time–series analysis.

Setting: Quebec Integrated Chronic Disease Surveillance System in Quebec.

Synopsis: The study analyzed 136,177 patients older than 66 years old with multiple comorbidities during the transition from brand-name to generic versions of losartan, valsartan, and candesartan. The authors compared ER visits or hospitalization of the brand-name users for 24 months before and 12 months after being transitioned from a brand-name ARB to a generic. All three groups were found to have higher rates of adverse events after switching to generics (8% for losartan, 11.7% for valsartan, and 16.6% for candesartan). The study was limited as the authors did not have access to the reason for the ER visits/admissions or the ability to determine which generic version was used (e.g., losartan has eight generic versions). The study highlights the need for further evaluation by risk and survival analysis to control confounders when switching to a generic formulation.

Bottom line: Switching patients from a brand-name to a generic ARB may lead to more ED consultations and hospital admissions.

Citation: Leclerc J et al. Impact of the commercialization of three generic angiotensin II receptor blockers on adverse events in Quebec Canada. Circ Cardiovasc Qual Outcomes. 2017 Oct 3. pii 10e003891. doi: 10.1161/circoutcomes.117.003891.

Dr. Smith is assistant professor of medicine in the Division of Hospital Medicine, Emory University, Atlanta.

Clinical question: Does switching from a brand name ARB to its generic lead to more ED visits and hospitalizations?

Background: Once a brand name drug’s patent expires, its generic form is commercialized and patients may be switched to the generic version. The drug equivalence of the generic vs. the brand name product may be substantial enough to affect clinically what is happening to the patient. Very few studies exist on the impact of the differences between brand-name and generic ARBs; those that do exist show conflicting results on clinical outcomes for the patient.

Study design: Observational retrospective interrupted time–series analysis.

Setting: Quebec Integrated Chronic Disease Surveillance System in Quebec.

Synopsis: The study analyzed 136,177 patients older than 66 years old with multiple comorbidities during the transition from brand-name to generic versions of losartan, valsartan, and candesartan. The authors compared ER visits or hospitalization of the brand-name users for 24 months before and 12 months after being transitioned from a brand-name ARB to a generic. All three groups were found to have higher rates of adverse events after switching to generics (8% for losartan, 11.7% for valsartan, and 16.6% for candesartan). The study was limited as the authors did not have access to the reason for the ER visits/admissions or the ability to determine which generic version was used (e.g., losartan has eight generic versions). The study highlights the need for further evaluation by risk and survival analysis to control confounders when switching to a generic formulation.

Bottom line: Switching patients from a brand-name to a generic ARB may lead to more ED consultations and hospital admissions.

Citation: Leclerc J et al. Impact of the commercialization of three generic angiotensin II receptor blockers on adverse events in Quebec Canada. Circ Cardiovasc Qual Outcomes. 2017 Oct 3. pii 10e003891. doi: 10.1161/circoutcomes.117.003891.

Dr. Smith is assistant professor of medicine in the Division of Hospital Medicine, Emory University, Atlanta.

Background: Patients with saddle PEs can differ in terms of their clinical presentation and may present as hemodynamically stable or unstable. There have been few studies to quantify the presentation, management, and outcome of patients who present with saddle PEs.

Study design: Retrospective cohort study.

Setting: Quaternary care hospital in Minnesota.

Synopsis: Using a localized database, 187 consecutive patients with saddle PEs were matched with 187 nonsaddle PEs using age and the simplified Pulmonary Embolism Severity Index (sPESI). Saddle PE patients had no significant in-hospital mortality differences versus nonsaddle PEs. However, they were more likely to present with massive and submassive hemodynamics (80% vs. 52%; P less than .05), RV dilatation (84% vs. 67%; P less than .001), and troponin elevation (71% vs. 40%; P less than .001). Patients with saddle PEs were more likely to receive thrombolytics, inferior vena cava filter placement, and require mechanical ventilation. They also had increased risk of decompensation after 6 hours (12 patients vs. 6 patients). Limitations of this study include some selection bias and use of a single-center study. Regardless, hospitalists should consider close monitoring for patients with saddle PEs upon admission, independent of hemodynamics given risk of decompensation regardless of presenting vitals.

Bottom line: Saddle PEs have an increased risk of late decompensation, clot burden, and presentation with massive and submassive hemodynamics but not an increased risk of mortality when compared with nonsaddle PEs.

Citation: Alkinj B et al. Saddle vs. nonsaddle pulmonary embolism: Clinical presentation, hemodynamics, management, and outcomes. Mayo Clin Proc. 2017 Oct;92(10):1511-8.

Dr. O’Donnell is assistant professor of medicine in the division of hospital medicine, Emory University, Atlanta.

Background: Patients with saddle PEs can differ in terms of their clinical presentation and may present as hemodynamically stable or unstable. There have been few studies to quantify the presentation, management, and outcome of patients who present with saddle PEs.

Study design: Retrospective cohort study.

Setting: Quaternary care hospital in Minnesota.

Synopsis: Using a localized database, 187 consecutive patients with saddle PEs were matched with 187 nonsaddle PEs using age and the simplified Pulmonary Embolism Severity Index (sPESI). Saddle PE patients had no significant in-hospital mortality differences versus nonsaddle PEs. However, they were more likely to present with massive and submassive hemodynamics (80% vs. 52%; P less than .05), RV dilatation (84% vs. 67%; P less than .001), and troponin elevation (71% vs. 40%; P less than .001). Patients with saddle PEs were more likely to receive thrombolytics, inferior vena cava filter placement, and require mechanical ventilation. They also had increased risk of decompensation after 6 hours (12 patients vs. 6 patients). Limitations of this study include some selection bias and use of a single-center study. Regardless, hospitalists should consider close monitoring for patients with saddle PEs upon admission, independent of hemodynamics given risk of decompensation regardless of presenting vitals.

Bottom line: Saddle PEs have an increased risk of late decompensation, clot burden, and presentation with massive and submassive hemodynamics but not an increased risk of mortality when compared with nonsaddle PEs.

Citation: Alkinj B et al. Saddle vs. nonsaddle pulmonary embolism: Clinical presentation, hemodynamics, management, and outcomes. Mayo Clin Proc. 2017 Oct;92(10):1511-8.

Dr. O’Donnell is assistant professor of medicine in the division of hospital medicine, Emory University, Atlanta.

Background: Patients with saddle PEs can differ in terms of their clinical presentation and may present as hemodynamically stable or unstable. There have been few studies to quantify the presentation, management, and outcome of patients who present with saddle PEs.

Study design: Retrospective cohort study.

Setting: Quaternary care hospital in Minnesota.

Synopsis: Using a localized database, 187 consecutive patients with saddle PEs were matched with 187 nonsaddle PEs using age and the simplified Pulmonary Embolism Severity Index (sPESI). Saddle PE patients had no significant in-hospital mortality differences versus nonsaddle PEs. However, they were more likely to present with massive and submassive hemodynamics (80% vs. 52%; P less than .05), RV dilatation (84% vs. 67%; P less than .001), and troponin elevation (71% vs. 40%; P less than .001). Patients with saddle PEs were more likely to receive thrombolytics, inferior vena cava filter placement, and require mechanical ventilation. They also had increased risk of decompensation after 6 hours (12 patients vs. 6 patients). Limitations of this study include some selection bias and use of a single-center study. Regardless, hospitalists should consider close monitoring for patients with saddle PEs upon admission, independent of hemodynamics given risk of decompensation regardless of presenting vitals.

Bottom line: Saddle PEs have an increased risk of late decompensation, clot burden, and presentation with massive and submassive hemodynamics but not an increased risk of mortality when compared with nonsaddle PEs.

Citation: Alkinj B et al. Saddle vs. nonsaddle pulmonary embolism: Clinical presentation, hemodynamics, management, and outcomes. Mayo Clin Proc. 2017 Oct;92(10):1511-8.

Dr. O’Donnell is assistant professor of medicine in the division of hospital medicine, Emory University, Atlanta.

Sepsis and critical care issues are in the spotlight at HM18, and these hot topics were the focus of the Monday education session, “He-Who-Shall-Not-Be-Named: Updates in Sepsis and Critical Care.”

Patricia Kritek, MD, EdM, of the University of Washington, Seattle, led an interactive and engaging session, educating attendees about the current research in sepsis and critical care areas so they would feel comfortable implementing the latest evidence into practice in the ICU.

The session focused on “what’s new” in critical care and sepsis from the literature published in the past year.

According to the National Center for Health Statistics at the Centers for Disease Control and Prevention, sepsis or septicemia patients averaged a 75% longer length of stay and were more than eight times likely to die, compared with patients hospitalized for other conditions.

“There has been a lot of discussion about steroids in sepsis that is potentially practice changing,” Dr. Kritek said in an interview. To tackle the always-tricky topic of steroids and sepsis, Dr. Kritek selected a trio of studies for review and discussion. In the first, vitamin C was potentially as effective as hydrocortisone and thiamine for the treatment of severe sepsis and septic shock (CHEST. 2017;151[6]:1229‐38). Another study addressed adjunctive glucocorticoid therapy for septic shock patients, and a third examined the use of hydrocortisone plus fludrocortisone for adults with septic shock.

The trials not involving vitamin C were published in the New England Journal of Medicine this year, conducted in Australia (2018;378:797‐808) and France (2018;378:809‐18), and included 3,658 and 1,241 adult sepsis patients, respectively. The studies were similar in size and design. Based on these two studies, hydrocortisone appears to shorten septic shock duration, and treatment with hydrocortisone and possibly fludrocortisone could be helpful for the more seriously ill patients, said Dr. Kritek. As for the value of vitamin C and thiamine, “the jury is still out,” she noted.

 

Sepsis and critical care issues are in the spotlight at HM18, and these hot topics were the focus of the Monday education session, “He-Who-Shall-Not-Be-Named: Updates in Sepsis and Critical Care.”

Patricia Kritek, MD, EdM, of the University of Washington, Seattle, led an interactive and engaging session, educating attendees about the current research in sepsis and critical care areas so they would feel comfortable implementing the latest evidence into practice in the ICU.

The session focused on “what’s new” in critical care and sepsis from the literature published in the past year.

According to the National Center for Health Statistics at the Centers for Disease Control and Prevention, sepsis or septicemia patients averaged a 75% longer length of stay and were more than eight times likely to die, compared with patients hospitalized for other conditions.

“There has been a lot of discussion about steroids in sepsis that is potentially practice changing,” Dr. Kritek said in an interview. To tackle the always-tricky topic of steroids and sepsis, Dr. Kritek selected a trio of studies for review and discussion. In the first, vitamin C was potentially as effective as hydrocortisone and thiamine for the treatment of severe sepsis and septic shock (CHEST. 2017;151[6]:1229‐38). Another study addressed adjunctive glucocorticoid therapy for septic shock patients, and a third examined the use of hydrocortisone plus fludrocortisone for adults with septic shock.

The trials not involving vitamin C were published in the New England Journal of Medicine this year, conducted in Australia (2018;378:797‐808) and France (2018;378:809‐18), and included 3,658 and 1,241 adult sepsis patients, respectively. The studies were similar in size and design. Based on these two studies, hydrocortisone appears to shorten septic shock duration, and treatment with hydrocortisone and possibly fludrocortisone could be helpful for the more seriously ill patients, said Dr. Kritek. As for the value of vitamin C and thiamine, “the jury is still out,” she noted.

 

Sepsis and critical care issues are in the spotlight at HM18, and these hot topics were the focus of the Monday education session, “He-Who-Shall-Not-Be-Named: Updates in Sepsis and Critical Care.”

Patricia Kritek, MD, EdM, of the University of Washington, Seattle, led an interactive and engaging session, educating attendees about the current research in sepsis and critical care areas so they would feel comfortable implementing the latest evidence into practice in the ICU.

The session focused on “what’s new” in critical care and sepsis from the literature published in the past year.

According to the National Center for Health Statistics at the Centers for Disease Control and Prevention, sepsis or septicemia patients averaged a 75% longer length of stay and were more than eight times likely to die, compared with patients hospitalized for other conditions.

“There has been a lot of discussion about steroids in sepsis that is potentially practice changing,” Dr. Kritek said in an interview. To tackle the always-tricky topic of steroids and sepsis, Dr. Kritek selected a trio of studies for review and discussion. In the first, vitamin C was potentially as effective as hydrocortisone and thiamine for the treatment of severe sepsis and septic shock (CHEST. 2017;151[6]:1229‐38). Another study addressed adjunctive glucocorticoid therapy for septic shock patients, and a third examined the use of hydrocortisone plus fludrocortisone for adults with septic shock.

The trials not involving vitamin C were published in the New England Journal of Medicine this year, conducted in Australia (2018;378:797‐808) and France (2018;378:809‐18), and included 3,658 and 1,241 adult sepsis patients, respectively. The studies were similar in size and design. Based on these two studies, hydrocortisone appears to shorten septic shock duration, and treatment with hydrocortisone and possibly fludrocortisone could be helpful for the more seriously ill patients, said Dr. Kritek. As for the value of vitamin C and thiamine, “the jury is still out,” she noted.

 

Hospitalists are on the front lines of diagnosis and management of patients with cancer, the second-leading cause of death in the United States. The session on Oncology Emergencies addressed the enormous number of clinical issues that must be considered within this patient population. The goal of the presentation was to ensure that attendees feel comfortable with the initial management of sick cancer patients and have the confidence to identify who needs an expedited work-up and how to complete one quickly and safely.

“The real challenge in managing sick cancer patients lies in the data-free zones,” presenter Benjamin L. Schlechter, MD, of Beth Israel Deaconess Medical Center in Boston, said in an interview. “I think the oncologic emergency we forget to talk about most often is the early diagnostic period,” he noted. The focus of Dr. Schlechter’s Monday talk was on this time frame and the process of getting patients with an advanced malignancy from diagnosis to treatment safely, which remains a clinical challenge.

“These patients often present with vague symptoms that do not point to any particular diagnosis,” stated Dr. Schlechter. “Once we identify that a patient has a symptomatic new malignancy, it is critical to determine who needs a rapid work-up as an inpatient on a hospital medicine service and who can be managed as an outpatient.”

Dr. Schlechter explained that there are no randomized trials to guide diagnostic work-up of malignancy or even define an expedited work-up. On the other hand, there are extensive data on treatment of newly diagnosed cancers. Clinical trials that guide first-line cancer therapy have clear eligibility criteria, which should inform hospitalists’ work-ups. “These include torso imaging, biopsy of a metastatic site, and assessment of liver and kidney function,” Dr. Schlechter continued. “The reason kidney and liver function are so critical is that patients who have organ dysfunction cannot receive effective chemotherapy.”

During the presentation, Dr. Schlechter reminded attendees that two-thirds of all cancers are cured, and there are clear data showing that chemotherapy in the first-line setting improves quality and length of life in virtually all cases. He underscored how critical it is to get patients treated before they develop organ dysfunction. “We can also use fairly basic clinical and laboratory assessment to determine who has a hyperaggressive malignancy and who doesn’t,” he added. “If LDH [lactate dehydrogenase] or uric acid are elevated, something really dangerous is happening. If the transaminases and alkaline phosphatase are rising, liver function is in danger. If the kidneys are failing, we need to act quickly.”

Dr. Schlechter closed by saying, “There are huge challenges in studying this time frame in a patient’s illness, which is why the initial work-up of cancer remains a high-risk period.”

Hospitalists are on the front lines of diagnosis and management of patients with cancer, the second-leading cause of death in the United States. The session on Oncology Emergencies addressed the enormous number of clinical issues that must be considered within this patient population. The goal of the presentation was to ensure that attendees feel comfortable with the initial management of sick cancer patients and have the confidence to identify who needs an expedited work-up and how to complete one quickly and safely.

“The real challenge in managing sick cancer patients lies in the data-free zones,” presenter Benjamin L. Schlechter, MD, of Beth Israel Deaconess Medical Center in Boston, said in an interview. “I think the oncologic emergency we forget to talk about most often is the early diagnostic period,” he noted. The focus of Dr. Schlechter’s Monday talk was on this time frame and the process of getting patients with an advanced malignancy from diagnosis to treatment safely, which remains a clinical challenge.

“These patients often present with vague symptoms that do not point to any particular diagnosis,” stated Dr. Schlechter. “Once we identify that a patient has a symptomatic new malignancy, it is critical to determine who needs a rapid work-up as an inpatient on a hospital medicine service and who can be managed as an outpatient.”

Dr. Schlechter explained that there are no randomized trials to guide diagnostic work-up of malignancy or even define an expedited work-up. On the other hand, there are extensive data on treatment of newly diagnosed cancers. Clinical trials that guide first-line cancer therapy have clear eligibility criteria, which should inform hospitalists’ work-ups. “These include torso imaging, biopsy of a metastatic site, and assessment of liver and kidney function,” Dr. Schlechter continued. “The reason kidney and liver function are so critical is that patients who have organ dysfunction cannot receive effective chemotherapy.”

During the presentation, Dr. Schlechter reminded attendees that two-thirds of all cancers are cured, and there are clear data showing that chemotherapy in the first-line setting improves quality and length of life in virtually all cases. He underscored how critical it is to get patients treated before they develop organ dysfunction. “We can also use fairly basic clinical and laboratory assessment to determine who has a hyperaggressive malignancy and who doesn’t,” he added. “If LDH [lactate dehydrogenase] or uric acid are elevated, something really dangerous is happening. If the transaminases and alkaline phosphatase are rising, liver function is in danger. If the kidneys are failing, we need to act quickly.”

Dr. Schlechter closed by saying, “There are huge challenges in studying this time frame in a patient’s illness, which is why the initial work-up of cancer remains a high-risk period.”

Hospitalists are on the front lines of diagnosis and management of patients with cancer, the second-leading cause of death in the United States. The session on Oncology Emergencies addressed the enormous number of clinical issues that must be considered within this patient population. The goal of the presentation was to ensure that attendees feel comfortable with the initial management of sick cancer patients and have the confidence to identify who needs an expedited work-up and how to complete one quickly and safely.

“The real challenge in managing sick cancer patients lies in the data-free zones,” presenter Benjamin L. Schlechter, MD, of Beth Israel Deaconess Medical Center in Boston, said in an interview. “I think the oncologic emergency we forget to talk about most often is the early diagnostic period,” he noted. The focus of Dr. Schlechter’s Monday talk was on this time frame and the process of getting patients with an advanced malignancy from diagnosis to treatment safely, which remains a clinical challenge.

“These patients often present with vague symptoms that do not point to any particular diagnosis,” stated Dr. Schlechter. “Once we identify that a patient has a symptomatic new malignancy, it is critical to determine who needs a rapid work-up as an inpatient on a hospital medicine service and who can be managed as an outpatient.”

Dr. Schlechter explained that there are no randomized trials to guide diagnostic work-up of malignancy or even define an expedited work-up. On the other hand, there are extensive data on treatment of newly diagnosed cancers. Clinical trials that guide first-line cancer therapy have clear eligibility criteria, which should inform hospitalists’ work-ups. “These include torso imaging, biopsy of a metastatic site, and assessment of liver and kidney function,” Dr. Schlechter continued. “The reason kidney and liver function are so critical is that patients who have organ dysfunction cannot receive effective chemotherapy.”

During the presentation, Dr. Schlechter reminded attendees that two-thirds of all cancers are cured, and there are clear data showing that chemotherapy in the first-line setting improves quality and length of life in virtually all cases. He underscored how critical it is to get patients treated before they develop organ dysfunction. “We can also use fairly basic clinical and laboratory assessment to determine who has a hyperaggressive malignancy and who doesn’t,” he added. “If LDH [lactate dehydrogenase] or uric acid are elevated, something really dangerous is happening. If the transaminases and alkaline phosphatase are rising, liver function is in danger. If the kidneys are failing, we need to act quickly.”

Dr. Schlechter closed by saying, “There are huge challenges in studying this time frame in a patient’s illness, which is why the initial work-up of cancer remains a high-risk period.”

Background: ABM is a diagnosis with high morbidity and mortality. Early antimicrobial and corticosteroid therapy is beneficial. Current practice tends to defer LP prior to imaging when there is potential risk of herniation. Sweden’s guidelines for getting a CT scan prior to LP differ substantially from the Infectious Disease Society of America (IDSA), which recommends obtaining CT in patients with immunocompromised state, history of CNS disease, or impaired mental status.

Study design: Prospective cohort study.

Setting: 815 adult patients (older than 16 years old) in Sweden with confirmed acute bacterial meningitis.

Synopsis: The authors looked at adherence to guidelines for when to obtain a CT prior to LP, as well as compared mortality and neurologic outcomes when an LP was performed promptly versus when delayed for prior neuroimaging. CT neuroimaging was required in much smaller populations under Swedish guidelines (7%), compared with IDSA (65%), with improved mortality and outcomes in patients managed with the Swedish guidelines. Mortality was lower in patients who had a prompt LP than for those who got CT prior to the LP (4% vs. 10%). This mortality benefit was seen even in patients with immunocompromised state or altered mental status, confirming that earlier administration of appropriate therapy is associated with lower mortality. A major limitation is that the study included patients with confirmed meningitis rather than more clinically relevant cases of suspected bacterial meningitis.

Bottom line: Patients with suspected bacterial meningitis should have appropriate antimicrobial and corticosteroid therapy started as soon as possible, regardless of the decision to obtain CT scan prior to performing lumbar puncture.

Citation: Glimaker M et al. Lumbar puncture performed promptly or after neuroimaging in acute bacterial meningitis in adults: a prospective national cohort study evaluating different guidelines. Clin Infect Dis. 2017 Sep 9. doi: 10.1093/cid/cix806 (epub ahead of print).

Dr. Maleque is assistant professor of medicine in the division of hospital medicine, Emory University, Atlanta.

Background: ABM is a diagnosis with high morbidity and mortality. Early antimicrobial and corticosteroid therapy is beneficial. Current practice tends to defer LP prior to imaging when there is potential risk of herniation. Sweden’s guidelines for getting a CT scan prior to LP differ substantially from the Infectious Disease Society of America (IDSA), which recommends obtaining CT in patients with immunocompromised state, history of CNS disease, or impaired mental status.

Study design: Prospective cohort study.

Setting: 815 adult patients (older than 16 years old) in Sweden with confirmed acute bacterial meningitis.

Synopsis: The authors looked at adherence to guidelines for when to obtain a CT prior to LP, as well as compared mortality and neurologic outcomes when an LP was performed promptly versus when delayed for prior neuroimaging. CT neuroimaging was required in much smaller populations under Swedish guidelines (7%), compared with IDSA (65%), with improved mortality and outcomes in patients managed with the Swedish guidelines. Mortality was lower in patients who had a prompt LP than for those who got CT prior to the LP (4% vs. 10%). This mortality benefit was seen even in patients with immunocompromised state or altered mental status, confirming that earlier administration of appropriate therapy is associated with lower mortality. A major limitation is that the study included patients with confirmed meningitis rather than more clinically relevant cases of suspected bacterial meningitis.

Bottom line: Patients with suspected bacterial meningitis should have appropriate antimicrobial and corticosteroid therapy started as soon as possible, regardless of the decision to obtain CT scan prior to performing lumbar puncture.

Citation: Glimaker M et al. Lumbar puncture performed promptly or after neuroimaging in acute bacterial meningitis in adults: a prospective national cohort study evaluating different guidelines. Clin Infect Dis. 2017 Sep 9. doi: 10.1093/cid/cix806 (epub ahead of print).

Dr. Maleque is assistant professor of medicine in the division of hospital medicine, Emory University, Atlanta.

Background: ABM is a diagnosis with high morbidity and mortality. Early antimicrobial and corticosteroid therapy is beneficial. Current practice tends to defer LP prior to imaging when there is potential risk of herniation. Sweden’s guidelines for getting a CT scan prior to LP differ substantially from the Infectious Disease Society of America (IDSA), which recommends obtaining CT in patients with immunocompromised state, history of CNS disease, or impaired mental status.

Study design: Prospective cohort study.

Setting: 815 adult patients (older than 16 years old) in Sweden with confirmed acute bacterial meningitis.

Synopsis: The authors looked at adherence to guidelines for when to obtain a CT prior to LP, as well as compared mortality and neurologic outcomes when an LP was performed promptly versus when delayed for prior neuroimaging. CT neuroimaging was required in much smaller populations under Swedish guidelines (7%), compared with IDSA (65%), with improved mortality and outcomes in patients managed with the Swedish guidelines. Mortality was lower in patients who had a prompt LP than for those who got CT prior to the LP (4% vs. 10%). This mortality benefit was seen even in patients with immunocompromised state or altered mental status, confirming that earlier administration of appropriate therapy is associated with lower mortality. A major limitation is that the study included patients with confirmed meningitis rather than more clinically relevant cases of suspected bacterial meningitis.

Bottom line: Patients with suspected bacterial meningitis should have appropriate antimicrobial and corticosteroid therapy started as soon as possible, regardless of the decision to obtain CT scan prior to performing lumbar puncture.

Citation: Glimaker M et al. Lumbar puncture performed promptly or after neuroimaging in acute bacterial meningitis in adults: a prospective national cohort study evaluating different guidelines. Clin Infect Dis. 2017 Sep 9. doi: 10.1093/cid/cix806 (epub ahead of print).

Dr. Maleque is assistant professor of medicine in the division of hospital medicine, Emory University, Atlanta.

“Zero harm” refers to the concept of not having any patients harmed as a result of their interactions with a health care system. For example, no laboratory results are misread or overlooked, no medication errors occur, a patient is not misdiagnosed, and a patient does not fall or get an infection.

As clinicians work to improve quality and safety for patients, some have been able to reach the ideal concept of zero harm.

“But the goal of zero harm should become everyone’s new mantra and, to get there, health care providers need to add new dimensions to their typical quality improvement and patient safety efforts,” said Karyn D. Baum, MD, MSEd, MHA, associate chief medical officer, University of Minnesota, Minneapolis, who will speak during the session “Aiming for Zero Preventable Harm.”

Dr. Baum said the interactive lecture, which she will present with MaryEllen Pfeiffer, DO, SFHM, director of patient safety, WellSpan Health, York, Pa., is designed to review the concept of zero harm. The duo will discuss what this goal entails and explain the skills and concepts that providers need to implement at their sites.

Many of these, which are needed to achieve zero harm, are similar to those already employed in quality improvement efforts, such as employing a plan-do-study-act cycle. To achieve zero harm, however, providers must relentlessly execute all of these efforts. In addition, newer concepts, such as more hospital board involvement in safety, need to be woven into previous concepts for health systems to reach this goal.

“When looking to achieve zero patient harm, look through the lens of operations and care delivery; it will become clear what changes need to be made in order to reach that goal,” Dr. Baum said.

Dr. Baum is a speaker for Boehringer Ingelheim on transitions of care and a consultant for Excelsior HealthCare Group.

Aiming for Zero Preventable Harm
Tues., 2:50-3:50 p.m.
Crystal Ballroom G1/A&B

“Zero harm” refers to the concept of not having any patients harmed as a result of their interactions with a health care system. For example, no laboratory results are misread or overlooked, no medication errors occur, a patient is not misdiagnosed, and a patient does not fall or get an infection.

As clinicians work to improve quality and safety for patients, some have been able to reach the ideal concept of zero harm.

“But the goal of zero harm should become everyone’s new mantra and, to get there, health care providers need to add new dimensions to their typical quality improvement and patient safety efforts,” said Karyn D. Baum, MD, MSEd, MHA, associate chief medical officer, University of Minnesota, Minneapolis, who will speak during the session “Aiming for Zero Preventable Harm.”

Dr. Baum said the interactive lecture, which she will present with MaryEllen Pfeiffer, DO, SFHM, director of patient safety, WellSpan Health, York, Pa., is designed to review the concept of zero harm. The duo will discuss what this goal entails and explain the skills and concepts that providers need to implement at their sites.

Many of these, which are needed to achieve zero harm, are similar to those already employed in quality improvement efforts, such as employing a plan-do-study-act cycle. To achieve zero harm, however, providers must relentlessly execute all of these efforts. In addition, newer concepts, such as more hospital board involvement in safety, need to be woven into previous concepts for health systems to reach this goal.

“When looking to achieve zero patient harm, look through the lens of operations and care delivery; it will become clear what changes need to be made in order to reach that goal,” Dr. Baum said.

Dr. Baum is a speaker for Boehringer Ingelheim on transitions of care and a consultant for Excelsior HealthCare Group.

Aiming for Zero Preventable Harm
Tues., 2:50-3:50 p.m.
Crystal Ballroom G1/A&B

“Zero harm” refers to the concept of not having any patients harmed as a result of their interactions with a health care system. For example, no laboratory results are misread or overlooked, no medication errors occur, a patient is not misdiagnosed, and a patient does not fall or get an infection.

As clinicians work to improve quality and safety for patients, some have been able to reach the ideal concept of zero harm.

“But the goal of zero harm should become everyone’s new mantra and, to get there, health care providers need to add new dimensions to their typical quality improvement and patient safety efforts,” said Karyn D. Baum, MD, MSEd, MHA, associate chief medical officer, University of Minnesota, Minneapolis, who will speak during the session “Aiming for Zero Preventable Harm.”

Dr. Baum said the interactive lecture, which she will present with MaryEllen Pfeiffer, DO, SFHM, director of patient safety, WellSpan Health, York, Pa., is designed to review the concept of zero harm. The duo will discuss what this goal entails and explain the skills and concepts that providers need to implement at their sites.

Many of these, which are needed to achieve zero harm, are similar to those already employed in quality improvement efforts, such as employing a plan-do-study-act cycle. To achieve zero harm, however, providers must relentlessly execute all of these efforts. In addition, newer concepts, such as more hospital board involvement in safety, need to be woven into previous concepts for health systems to reach this goal.

“When looking to achieve zero patient harm, look through the lens of operations and care delivery; it will become clear what changes need to be made in order to reach that goal,” Dr. Baum said.

Dr. Baum is a speaker for Boehringer Ingelheim on transitions of care and a consultant for Excelsior HealthCare Group.

Aiming for Zero Preventable Harm
Tues., 2:50-3:50 p.m.
Crystal Ballroom G1/A&B