"Palliative care is not about death and dying or just pain management," said Sarah Friebert, MD, at a morning breakout session on Tuesday at HM12. Rather, she said, palliative care is a method of holistic care delivery for individuals with chronic, complex, and/or life-threatening conditions.

"There is a role for [palliative] subspecialty care" beyond just "good care," said Dr. Friebert. It is a model of shared management with other caregivers that is similar to other models of chronic disease. Additionally, palliative care has evolved to embrace an integrated model, such that palliation is longitudinally woven together with care for curing, dying, and bereavement.

Families continue to have many unmet needs, and hospitalists should provide them with clear and honest communication. Involving the palliative care team early on in the course of the illness is important to facilitate effective care.

Takeaways

• Palliative care is not code for "hospice."
• Other care (providers and treatment) does not need to be given up.
• Early integration of the palliative care team is essential.
• Consider using triggers to prompt referral to palliative care.

Dr. Shen is medical director of hospital medicine and assistant professor of pediatrics at UTMB Austin Pediatrics and Dell Children's Medical Center of Central Texas.

"Palliative care is not about death and dying or just pain management," said Sarah Friebert, MD, at a morning breakout session on Tuesday at HM12. Rather, she said, palliative care is a method of holistic care delivery for individuals with chronic, complex, and/or life-threatening conditions.

"There is a role for [palliative] subspecialty care" beyond just "good care," said Dr. Friebert. It is a model of shared management with other caregivers that is similar to other models of chronic disease. Additionally, palliative care has evolved to embrace an integrated model, such that palliation is longitudinally woven together with care for curing, dying, and bereavement.

Families continue to have many unmet needs, and hospitalists should provide them with clear and honest communication. Involving the palliative care team early on in the course of the illness is important to facilitate effective care.

Takeaways

• Palliative care is not code for "hospice."
• Other care (providers and treatment) does not need to be given up.
• Early integration of the palliative care team is essential.
• Consider using triggers to prompt referral to palliative care.

Dr. Shen is medical director of hospital medicine and assistant professor of pediatrics at UTMB Austin Pediatrics and Dell Children's Medical Center of Central Texas.

"Palliative care is not about death and dying or just pain management," said Sarah Friebert, MD, at a morning breakout session on Tuesday at HM12. Rather, she said, palliative care is a method of holistic care delivery for individuals with chronic, complex, and/or life-threatening conditions.

"There is a role for [palliative] subspecialty care" beyond just "good care," said Dr. Friebert. It is a model of shared management with other caregivers that is similar to other models of chronic disease. Additionally, palliative care has evolved to embrace an integrated model, such that palliation is longitudinally woven together with care for curing, dying, and bereavement.

Families continue to have many unmet needs, and hospitalists should provide them with clear and honest communication. Involving the palliative care team early on in the course of the illness is important to facilitate effective care.

Takeaways

• Palliative care is not code for "hospice."
• Other care (providers and treatment) does not need to be given up.
• Early integration of the palliative care team is essential.
• Consider using triggers to prompt referral to palliative care.

Dr. Shen is medical director of hospital medicine and assistant professor of pediatrics at UTMB Austin Pediatrics and Dell Children's Medical Center of Central Texas.

Shalini Chandra, MD, MS, Gregory Harlan, MD, FAAP, MPH, Brian Donovan, MD, MMM, FACP, SFHM, and Judy Shumway, DO, MPH, led a standing-room only morning breakout session on Monday at HM12 that focused on the challenges and opportunities of scheduling and rounding.

Dr. Harlan, a hospitalist at IPC, introduced the topic of innovative scheduling by placing the issue in a framework easily understood by hospitalists: quality improvement. He advocated identifying the salient problems faced by each individual group and then applying changes that make sense to each facility and group.

Dr. Chandra, a hospitalist at Johns Hopkins Bayview Medical Center, further elaborated on this by explaining how the PDSA (plan, do, study, act) approach can be used to initiate and assess the changes implemented in scheduling. Metrics such as hospitalist morale, patient satisfaction, length of stay, and time of discharge, can be used to assess the effect of each scheduling change.

Dr. Donovan, medical director of IPC, described a “zone” approach to scheduling. This rounding scheme assigns a hospitalist to a geographic unit, allowing for greater accessibility and higher efficiency. Closer relationships with multidisciplinary personnel can be achieved with this model.

Takeaways

• Test your scheduling changes with PDSA methods of quality improvement.
• Multidisciplinary rounds are critical to success.
• "Zone" rounding allows the development of physician leaders in each zone, and enable more efficiency.
• Engaging stakeholders in the success of physician scheduling is critical; this may enable more support and resources for these changes from administration.

Dr. Chang is a pediatric hospitalist with the University of San Diego Medical Center and  Rady Children's Hospital, San Diego.

Shalini Chandra, MD, MS, Gregory Harlan, MD, FAAP, MPH, Brian Donovan, MD, MMM, FACP, SFHM, and Judy Shumway, DO, MPH, led a standing-room only morning breakout session on Monday at HM12 that focused on the challenges and opportunities of scheduling and rounding.

Dr. Harlan, a hospitalist at IPC, introduced the topic of innovative scheduling by placing the issue in a framework easily understood by hospitalists: quality improvement. He advocated identifying the salient problems faced by each individual group and then applying changes that make sense to each facility and group.

Dr. Chandra, a hospitalist at Johns Hopkins Bayview Medical Center, further elaborated on this by explaining how the PDSA (plan, do, study, act) approach can be used to initiate and assess the changes implemented in scheduling. Metrics such as hospitalist morale, patient satisfaction, length of stay, and time of discharge, can be used to assess the effect of each scheduling change.

Dr. Donovan, medical director of IPC, described a “zone” approach to scheduling. This rounding scheme assigns a hospitalist to a geographic unit, allowing for greater accessibility and higher efficiency. Closer relationships with multidisciplinary personnel can be achieved with this model.

Takeaways

• Test your scheduling changes with PDSA methods of quality improvement.
• Multidisciplinary rounds are critical to success.
• "Zone" rounding allows the development of physician leaders in each zone, and enable more efficiency.
• Engaging stakeholders in the success of physician scheduling is critical; this may enable more support and resources for these changes from administration.

Dr. Chang is a pediatric hospitalist with the University of San Diego Medical Center and  Rady Children's Hospital, San Diego.

Shalini Chandra, MD, MS, Gregory Harlan, MD, FAAP, MPH, Brian Donovan, MD, MMM, FACP, SFHM, and Judy Shumway, DO, MPH, led a standing-room only morning breakout session on Monday at HM12 that focused on the challenges and opportunities of scheduling and rounding.

Dr. Harlan, a hospitalist at IPC, introduced the topic of innovative scheduling by placing the issue in a framework easily understood by hospitalists: quality improvement. He advocated identifying the salient problems faced by each individual group and then applying changes that make sense to each facility and group.

Dr. Chandra, a hospitalist at Johns Hopkins Bayview Medical Center, further elaborated on this by explaining how the PDSA (plan, do, study, act) approach can be used to initiate and assess the changes implemented in scheduling. Metrics such as hospitalist morale, patient satisfaction, length of stay, and time of discharge, can be used to assess the effect of each scheduling change.

Dr. Donovan, medical director of IPC, described a “zone” approach to scheduling. This rounding scheme assigns a hospitalist to a geographic unit, allowing for greater accessibility and higher efficiency. Closer relationships with multidisciplinary personnel can be achieved with this model.

Takeaways

• Test your scheduling changes with PDSA methods of quality improvement.
• Multidisciplinary rounds are critical to success.
• "Zone" rounding allows the development of physician leaders in each zone, and enable more efficiency.
• Engaging stakeholders in the success of physician scheduling is critical; this may enable more support and resources for these changes from administration.

Dr. Chang is a pediatric hospitalist with the University of San Diego Medical Center and  Rady Children's Hospital, San Diego.

Three longtime hospitalists were announced today as new members of the Society of Hospital Medicine's 2012-13 Board of Directors.

Jeff Glasheen, MD, SFHM, Nasim Afsar, MD, SFHM, and Brian Harte, MD, SFHM, are newly elected members of the board. Each will serve a three-year term. Dr. Glasheen is director of the hospitalist service at the University of Colorado Denver, and former physician editor of The Hospitalist. Dr. Afsar is director of quality for HM and neurosurgery at Ronald Reagan UCLA Medical Center in Los Angeles. Dr. Harte is chief operating officer of Hillcrest Hospital in Ohio and chairman of hospital medicine at The Cleveland Clinic.

The board voted Eric Howell, MD, SFHM, as president-elect. Burke T. Kealey, MD, SFHM, is board treasurer and Erin Stucky Fisher, MD, MHM, is board secretary.

The other board members are: Shaun Frost, MD, SFHM, president; Joseph M. Li, MD, SFHM, past president; Lakshmi Halasyamani, MD, SFHM; Robert Harrington Jr., MD, SFHM; Janet Nagamine, MD, SFHM; and Eric M. Siegal, MD, SFHM.

Three longtime hospitalists were announced today as new members of the Society of Hospital Medicine's 2012-13 Board of Directors.

Jeff Glasheen, MD, SFHM, Nasim Afsar, MD, SFHM, and Brian Harte, MD, SFHM, are newly elected members of the board. Each will serve a three-year term. Dr. Glasheen is director of the hospitalist service at the University of Colorado Denver, and former physician editor of The Hospitalist. Dr. Afsar is director of quality for HM and neurosurgery at Ronald Reagan UCLA Medical Center in Los Angeles. Dr. Harte is chief operating officer of Hillcrest Hospital in Ohio and chairman of hospital medicine at The Cleveland Clinic.

The board voted Eric Howell, MD, SFHM, as president-elect. Burke T. Kealey, MD, SFHM, is board treasurer and Erin Stucky Fisher, MD, MHM, is board secretary.

The other board members are: Shaun Frost, MD, SFHM, president; Joseph M. Li, MD, SFHM, past president; Lakshmi Halasyamani, MD, SFHM; Robert Harrington Jr., MD, SFHM; Janet Nagamine, MD, SFHM; and Eric M. Siegal, MD, SFHM.

Three longtime hospitalists were announced today as new members of the Society of Hospital Medicine's 2012-13 Board of Directors.

Jeff Glasheen, MD, SFHM, Nasim Afsar, MD, SFHM, and Brian Harte, MD, SFHM, are newly elected members of the board. Each will serve a three-year term. Dr. Glasheen is director of the hospitalist service at the University of Colorado Denver, and former physician editor of The Hospitalist. Dr. Afsar is director of quality for HM and neurosurgery at Ronald Reagan UCLA Medical Center in Los Angeles. Dr. Harte is chief operating officer of Hillcrest Hospital in Ohio and chairman of hospital medicine at The Cleveland Clinic.

The board voted Eric Howell, MD, SFHM, as president-elect. Burke T. Kealey, MD, SFHM, is board treasurer and Erin Stucky Fisher, MD, MHM, is board secretary.

The other board members are: Shaun Frost, MD, SFHM, president; Joseph M. Li, MD, SFHM, past president; Lakshmi Halasyamani, MD, SFHM; Robert Harrington Jr., MD, SFHM; Janet Nagamine, MD, SFHM; and Eric M. Siegal, MD, SFHM.

The topic was of strong interest, as demonstrated by the standing-room-only group of hospitalists attending Monday afternoon's presentation at HM12 in San Diego on the brand new antithrombic therapy from ACCP. I doubt giving away a new IPAD 3 would have brought a bigger audience. However, no one left disappointed, leaving with valuable new information which could be used at the bedside.

The excellent, evidence-based rapid fire presentation by Catherine Curley took us as a tour guide through key aspects of the new guidelines. The methodology improvements were extremely important. She used the more-controversial topics as examples: treatment of submassive PE, use of catheter directed thrombolysis in patients with acute DVT, and the recommended VTE prophylaxis. She even threw in some anatomy lessons for us clinicians.

Key Takeaways:

1. Major innovations in the methodology in the AT9. Focus on the absolute effects allow the provider to weight the benefit and risk of therapy easily, rigorous conflict of interests review of the editors, re-analysis of many older studies, and simplified recommendations with emphasis on summary of finding tables as opposed to texts
.
2. A strong focus on patient-centered outcomes. This is the first major guideline I have seen that recommends specifically focusing on the patients preferences.

Dr. Holder is medical director of hospitalist services and chief medical information officer at Decatur (Ill.) Memorial Hospital.

The topic was of strong interest, as demonstrated by the standing-room-only group of hospitalists attending Monday afternoon's presentation at HM12 in San Diego on the brand new antithrombic therapy from ACCP. I doubt giving away a new IPAD 3 would have brought a bigger audience. However, no one left disappointed, leaving with valuable new information which could be used at the bedside.

The excellent, evidence-based rapid fire presentation by Catherine Curley took us as a tour guide through key aspects of the new guidelines. The methodology improvements were extremely important. She used the more-controversial topics as examples: treatment of submassive PE, use of catheter directed thrombolysis in patients with acute DVT, and the recommended VTE prophylaxis. She even threw in some anatomy lessons for us clinicians.

Key Takeaways:

1. Major innovations in the methodology in the AT9. Focus on the absolute effects allow the provider to weight the benefit and risk of therapy easily, rigorous conflict of interests review of the editors, re-analysis of many older studies, and simplified recommendations with emphasis on summary of finding tables as opposed to texts
.
2. A strong focus on patient-centered outcomes. This is the first major guideline I have seen that recommends specifically focusing on the patients preferences.

Dr. Holder is medical director of hospitalist services and chief medical information officer at Decatur (Ill.) Memorial Hospital.

The topic was of strong interest, as demonstrated by the standing-room-only group of hospitalists attending Monday afternoon's presentation at HM12 in San Diego on the brand new antithrombic therapy from ACCP. I doubt giving away a new IPAD 3 would have brought a bigger audience. However, no one left disappointed, leaving with valuable new information which could be used at the bedside.

The excellent, evidence-based rapid fire presentation by Catherine Curley took us as a tour guide through key aspects of the new guidelines. The methodology improvements were extremely important. She used the more-controversial topics as examples: treatment of submassive PE, use of catheter directed thrombolysis in patients with acute DVT, and the recommended VTE prophylaxis. She even threw in some anatomy lessons for us clinicians.

Key Takeaways:

1. Major innovations in the methodology in the AT9. Focus on the absolute effects allow the provider to weight the benefit and risk of therapy easily, rigorous conflict of interests review of the editors, re-analysis of many older studies, and simplified recommendations with emphasis on summary of finding tables as opposed to texts
.
2. A strong focus on patient-centered outcomes. This is the first major guideline I have seen that recommends specifically focusing on the patients preferences.

Dr. Holder is medical director of hospitalist services and chief medical information officer at Decatur (Ill.) Memorial Hospital.

Daniel Brotman, MD, FACP, FHM, of Johns Hopkins Hospital in Baltimore, addressed questions all hospitalists wonder about:

1. Is warfarin still the best anticoagulant in afib? 2. Should DVT prevention extend beyond hospitalization? 3. What is the best evidence for LMWH bridging in valve patients? 4. When should anticoagulation be started in stroke patients with afib?

Warfarin, Dr. Brotman explained, has many disadvantages, and new oral anticoagulants (dabigatran, apixaban, rivaoxaban) offer many advantages with lower side-effect profiles. All of the new agents appear to have either better efficacy or trend toward better efficacy, none require monitoring, and all have lower rate of ICH.

Prices are higher for new agents, but are competitive with other drugs currently on market for other diseases. Use dabigatran with caution in patients with renal failure, and realize that there is no antidote for any of these drugs. Dabigatran is acidic and causes GI upset, thus a higher rate of GI bleeding. Stop any of these 5 days prior to planned proceduers; longer if patients are at high risk of bleeding.

Evidence from RCTs in hospitalized surgical patients suggest that VTE prophylaxis should be continued in patients undergoing hip surgery and surgery for abdominal or pelvic malignancy. Patients admitted for acute medical illness do not benefit from VTE prophylaxis beyond acute hospitlaization, even if immobilized, unless they have solid tumors with additional risk factors (hormone use, prior VTE, etc.) and are at low risk for bleeding. Chronically immobilized patients do not benefit from VTE prophylaxis beyond the acute hospitalization.

Bridging-aortic valves have an equivalent CHAD2 score of about 2, so there really is no need to bridge pre-op. Mitral valves have a CHADS2 score of about 4-5, so they always need to be bridged. No head-to-head trials of bridging with LMWH exist, but it's still worth considering if no contraindications because it is much more cost-effective than inpatient admission for IV UFH.

Oral anticoag can be started within 1-2 weeks of stroke onset. The larger the stroke, the greater the risk of hemorrhagic transformation with early anticoagulation, so the smaller the stroke, the safer to start early. VTE prophylaxis important regardless.

Key Takeaways:

• We'll be using the new oral anticoagulants in place of warfarin in the coming years, although there is no safe anticoagulant. Be cautious and aware of the side effect profiles of each.
• Don't sweat VTE prophylaxis in chronically immobilized patients unless they are acutely hospitalized.
• VTE prophylaxis is critical in stroke patients, but the larger the stroke in afib patients, the longer the wait to start oral anticoagulation.

Dr. Foxley is medical director of Inpatient Management, Inc., at the The Nebraska Medical Center Hospitals in Omaha

Daniel Brotman, MD, FACP, FHM, of Johns Hopkins Hospital in Baltimore, addressed questions all hospitalists wonder about:

1. Is warfarin still the best anticoagulant in afib? 2. Should DVT prevention extend beyond hospitalization? 3. What is the best evidence for LMWH bridging in valve patients? 4. When should anticoagulation be started in stroke patients with afib?

Warfarin, Dr. Brotman explained, has many disadvantages, and new oral anticoagulants (dabigatran, apixaban, rivaoxaban) offer many advantages with lower side-effect profiles. All of the new agents appear to have either better efficacy or trend toward better efficacy, none require monitoring, and all have lower rate of ICH.

Prices are higher for new agents, but are competitive with other drugs currently on market for other diseases. Use dabigatran with caution in patients with renal failure, and realize that there is no antidote for any of these drugs. Dabigatran is acidic and causes GI upset, thus a higher rate of GI bleeding. Stop any of these 5 days prior to planned proceduers; longer if patients are at high risk of bleeding.

Evidence from RCTs in hospitalized surgical patients suggest that VTE prophylaxis should be continued in patients undergoing hip surgery and surgery for abdominal or pelvic malignancy. Patients admitted for acute medical illness do not benefit from VTE prophylaxis beyond acute hospitlaization, even if immobilized, unless they have solid tumors with additional risk factors (hormone use, prior VTE, etc.) and are at low risk for bleeding. Chronically immobilized patients do not benefit from VTE prophylaxis beyond the acute hospitalization.

Bridging-aortic valves have an equivalent CHAD2 score of about 2, so there really is no need to bridge pre-op. Mitral valves have a CHADS2 score of about 4-5, so they always need to be bridged. No head-to-head trials of bridging with LMWH exist, but it's still worth considering if no contraindications because it is much more cost-effective than inpatient admission for IV UFH.

Oral anticoag can be started within 1-2 weeks of stroke onset. The larger the stroke, the greater the risk of hemorrhagic transformation with early anticoagulation, so the smaller the stroke, the safer to start early. VTE prophylaxis important regardless.

Key Takeaways:

• We'll be using the new oral anticoagulants in place of warfarin in the coming years, although there is no safe anticoagulant. Be cautious and aware of the side effect profiles of each.
• Don't sweat VTE prophylaxis in chronically immobilized patients unless they are acutely hospitalized.
• VTE prophylaxis is critical in stroke patients, but the larger the stroke in afib patients, the longer the wait to start oral anticoagulation.

Dr. Foxley is medical director of Inpatient Management, Inc., at the The Nebraska Medical Center Hospitals in Omaha

Daniel Brotman, MD, FACP, FHM, of Johns Hopkins Hospital in Baltimore, addressed questions all hospitalists wonder about:

1. Is warfarin still the best anticoagulant in afib? 2. Should DVT prevention extend beyond hospitalization? 3. What is the best evidence for LMWH bridging in valve patients? 4. When should anticoagulation be started in stroke patients with afib?

Warfarin, Dr. Brotman explained, has many disadvantages, and new oral anticoagulants (dabigatran, apixaban, rivaoxaban) offer many advantages with lower side-effect profiles. All of the new agents appear to have either better efficacy or trend toward better efficacy, none require monitoring, and all have lower rate of ICH.

Prices are higher for new agents, but are competitive with other drugs currently on market for other diseases. Use dabigatran with caution in patients with renal failure, and realize that there is no antidote for any of these drugs. Dabigatran is acidic and causes GI upset, thus a higher rate of GI bleeding. Stop any of these 5 days prior to planned proceduers; longer if patients are at high risk of bleeding.

Evidence from RCTs in hospitalized surgical patients suggest that VTE prophylaxis should be continued in patients undergoing hip surgery and surgery for abdominal or pelvic malignancy. Patients admitted for acute medical illness do not benefit from VTE prophylaxis beyond acute hospitlaization, even if immobilized, unless they have solid tumors with additional risk factors (hormone use, prior VTE, etc.) and are at low risk for bleeding. Chronically immobilized patients do not benefit from VTE prophylaxis beyond the acute hospitalization.

Bridging-aortic valves have an equivalent CHAD2 score of about 2, so there really is no need to bridge pre-op. Mitral valves have a CHADS2 score of about 4-5, so they always need to be bridged. No head-to-head trials of bridging with LMWH exist, but it's still worth considering if no contraindications because it is much more cost-effective than inpatient admission for IV UFH.

Oral anticoag can be started within 1-2 weeks of stroke onset. The larger the stroke, the greater the risk of hemorrhagic transformation with early anticoagulation, so the smaller the stroke, the safer to start early. VTE prophylaxis important regardless.

Key Takeaways:

• We'll be using the new oral anticoagulants in place of warfarin in the coming years, although there is no safe anticoagulant. Be cautious and aware of the side effect profiles of each.
• Don't sweat VTE prophylaxis in chronically immobilized patients unless they are acutely hospitalized.
• VTE prophylaxis is critical in stroke patients, but the larger the stroke in afib patients, the longer the wait to start oral anticoagulation.

Dr. Foxley is medical director of Inpatient Management, Inc., at the The Nebraska Medical Center Hospitals in Omaha

CHICAGO – An investigational fully human monoclonal antibody slashed low-density lipoprotein cholesterol levels by up to 72% in a phase II clinical trial in dyslipidemic patients not at goal despite already being on a statin.

The study results for the monoclonal antibody known for now as SAR236553/REGN727 caused head-swiveling and double-takes at the annual meeting of the American College of Cardiology.

Bruce Jancin/IMNG Medical Media

"We need to understand: This is a ‘wow.’ It could be a game changer in the future," commented scientific session program committee cochair Dr. Rick A. Nishimura, professor of medicine at the Mayo Clinic, Rochester, Minn. He was referring to the randomized, double-blind, placebo-controlled, 12-week phase II study presented by James M. McKenney, Pharm.D. The trial involved 183 patients with an LDL cholesterol level above the target of 100 mg/dL despite an average of 7 years of statin therapy. The participants remained on atorvastatin at 10, 20, or 40 mg/day as background therapy while being randomized to 12 weeks of subcutaneously administered SAR236553/REGN727 at one of five dosing regimens or to placebo.

At the most effective dosing schedule – 150 mg once every 2 weeks – LDL dropped by a mean of 72% at 12 weeks, from a baseline of 124 mg/dL. Within the first 2 weeks the LDL level had already fallen by 60%.

A clear dose-response relationship was evident, with dosing at 50 and 100 mg once every 2 weeks eliciting mean 40% and 64% LDL reductions, respectively, reported Dr. McKenney, chief executive officer at National Clinical Research, Richmond, Va.

"This is monumental clearance of LDL. It’s just unheard of, especially considering the statin these patients were on should already have produced about a 40% decrease in LDL," he said. "If the drug pans out, if it continues to show efficacy and especially if it shows safety, we may be moving into a new era in the treatment of lipid disorders and, more importantly, in the reduction of heart disease in this country."

At the optimal dosing regimen of SAR236553/REGN727, an agent Dr. McKenney referred to as "553" for the sake of brevity, patients also had mean reductions of 27% in lipoprotein(a), 56% in apolipoprotein B, and 63% in non-HDL (non-high-density lipoprotein) cholesterol, along with a nonsignificant trend for lower triglycerides.

The monoclonal antibody is highly specific for proprotein convertase subtilisin/kexin type 9 serine protease (PCSK9). This protein plays a pivotal role in the degradation of LDL receptors, thereby interfering with cholesterol uptake by the liver.

Treatment with 553 was well tolerated; the most common side effect was mild, transient, injection site reactions. Importantly, given that patients were already on statin therapy, there were no increases in hepatic or muscle-related enzymes.

The one significant adverse event was a case of biopsy-confirmed leukocytoclastic vasculitis occurring 9 days after a patient received a first 300-mg injection of 553. The reaction took the form of a rash on the arms, legs, and abdomen, with no other organ involvement. It responded quickly to drug withdrawal and initiation of prednisone. No other cases of leukocytoclastic vasculitis occurred in any other 553-treated patients, including those who participated in three just-published phase I studies (N. Engl. J. Med. 2012;366:1108-18).

No antidrug antibodies were detected shortly after the patient developed leukocytoclastic vasculitis; however, low-level titers were found at week 20. The patient remained negative for antinuclear antibodies through 6 months of follow-up blood tests.

Leukocytoclastic vasculitis is a rare, generally benign disease with an incidence of 40-60 cases per million persons per year. Medications are identified as the cause of about 20% of cases, with antibiotics and NSAIDs being among the most common offenders. Leukocytoclastic vasculitis is listed as a possible adverse event in the product labeling for most monoclonal antibody therapies, Dr. McKenney noted.

Large phase III clinical trials will begin enrollment later this year. They will focus on patients at high cardiovascular risk, including those with familial hypercholesterolemia and/or prior vascular events who aren’t at goal despite statin therapy.

Coinvestigator Dr. Dean J. Kereiakes said in an interview that one of the most intriguing observations in the phase II study was that mean LDL levels were still on their way down when 553 was stopped after 12 weeks.

"We didn’t hit the nadir. The LDL hadn’t plateaued. If we had taken patients out to 18-20 weeks, we might have seen an even greater delta," according to Dr. Kereiakes of Christ Hospital, Cincinnati.

He sees the target population for 553 as being the large number of patients who can’t reach their LDL target despite maximum doses of currently approved medications, as well as those who can’t do so because they can’t tolerate maximum doses of those drugs.

"I’d say probably more than one-third of my patients are on combination therapy for lipid lowering," the cardiologist said.

With 553, it will also become possible to take to its logical conclusion the hypothesis that a lower LDL is better for preventing atherosclerosis.

"The average LDL in a newborn is 35 mg/dL, and they have clean vasculature. There aren’t even the lipid streaks that occur as the first step in the atherosclerotic process," he noted.

In phase III, the monoclonal antibody will be self-administered subcutaneously using a fixed-dose pen, much like the insulin-sensitizing agent exenatide (Byetta or Bydureon).

Discussant Dr. Karol E. Watson said 553 "has a lot of potential and certainly does offer up some hope." But she zeroed in on the fact that as a monoclonal antibody – even a fully human one – it has the potential for autoimmunity.

"That is something that clearly would limit the usefulness of this molecule. I’d want to see more data on that," added Dr. Watson, codirector of the University of California, Los Angeles, program in preventive cardiology.

Her fellow panelist Dr. Christie M. Ballantyne was particularly intrigued by the fact that C-reactive protein levels did not change significantly during the phase II study.

A clinical trial with 553 could settle the question of whether the clinical benefits of statin therapy are due solely to LDL lowering, or if the concomitant decrease in CRP is also essential, said Dr. Ballantyne, professor of medicine at Baylor College of Medicine, Houston.

The study was sponsored by Sanofi and Regeneron. Dr. McKenney reported that he has received research grants from both companies to conduct clinical trials of 553. He also serves as a consultant to Sanofi, which is developing 553, and to numerous other pharmaceutical companies with an interest in lipid-altering agents. Dr. Kereiakes reported having no financial conflicts.

CHICAGO – An investigational fully human monoclonal antibody slashed low-density lipoprotein cholesterol levels by up to 72% in a phase II clinical trial in dyslipidemic patients not at goal despite already being on a statin.

The study results for the monoclonal antibody known for now as SAR236553/REGN727 caused head-swiveling and double-takes at the annual meeting of the American College of Cardiology.

Bruce Jancin/IMNG Medical Media

"We need to understand: This is a ‘wow.’ It could be a game changer in the future," commented scientific session program committee cochair Dr. Rick A. Nishimura, professor of medicine at the Mayo Clinic, Rochester, Minn. He was referring to the randomized, double-blind, placebo-controlled, 12-week phase II study presented by James M. McKenney, Pharm.D. The trial involved 183 patients with an LDL cholesterol level above the target of 100 mg/dL despite an average of 7 years of statin therapy. The participants remained on atorvastatin at 10, 20, or 40 mg/day as background therapy while being randomized to 12 weeks of subcutaneously administered SAR236553/REGN727 at one of five dosing regimens or to placebo.

At the most effective dosing schedule – 150 mg once every 2 weeks – LDL dropped by a mean of 72% at 12 weeks, from a baseline of 124 mg/dL. Within the first 2 weeks the LDL level had already fallen by 60%.

A clear dose-response relationship was evident, with dosing at 50 and 100 mg once every 2 weeks eliciting mean 40% and 64% LDL reductions, respectively, reported Dr. McKenney, chief executive officer at National Clinical Research, Richmond, Va.

"This is monumental clearance of LDL. It’s just unheard of, especially considering the statin these patients were on should already have produced about a 40% decrease in LDL," he said. "If the drug pans out, if it continues to show efficacy and especially if it shows safety, we may be moving into a new era in the treatment of lipid disorders and, more importantly, in the reduction of heart disease in this country."

At the optimal dosing regimen of SAR236553/REGN727, an agent Dr. McKenney referred to as "553" for the sake of brevity, patients also had mean reductions of 27% in lipoprotein(a), 56% in apolipoprotein B, and 63% in non-HDL (non-high-density lipoprotein) cholesterol, along with a nonsignificant trend for lower triglycerides.

The monoclonal antibody is highly specific for proprotein convertase subtilisin/kexin type 9 serine protease (PCSK9). This protein plays a pivotal role in the degradation of LDL receptors, thereby interfering with cholesterol uptake by the liver.

Treatment with 553 was well tolerated; the most common side effect was mild, transient, injection site reactions. Importantly, given that patients were already on statin therapy, there were no increases in hepatic or muscle-related enzymes.

The one significant adverse event was a case of biopsy-confirmed leukocytoclastic vasculitis occurring 9 days after a patient received a first 300-mg injection of 553. The reaction took the form of a rash on the arms, legs, and abdomen, with no other organ involvement. It responded quickly to drug withdrawal and initiation of prednisone. No other cases of leukocytoclastic vasculitis occurred in any other 553-treated patients, including those who participated in three just-published phase I studies (N. Engl. J. Med. 2012;366:1108-18).

No antidrug antibodies were detected shortly after the patient developed leukocytoclastic vasculitis; however, low-level titers were found at week 20. The patient remained negative for antinuclear antibodies through 6 months of follow-up blood tests.

Leukocytoclastic vasculitis is a rare, generally benign disease with an incidence of 40-60 cases per million persons per year. Medications are identified as the cause of about 20% of cases, with antibiotics and NSAIDs being among the most common offenders. Leukocytoclastic vasculitis is listed as a possible adverse event in the product labeling for most monoclonal antibody therapies, Dr. McKenney noted.

Large phase III clinical trials will begin enrollment later this year. They will focus on patients at high cardiovascular risk, including those with familial hypercholesterolemia and/or prior vascular events who aren’t at goal despite statin therapy.

Coinvestigator Dr. Dean J. Kereiakes said in an interview that one of the most intriguing observations in the phase II study was that mean LDL levels were still on their way down when 553 was stopped after 12 weeks.

"We didn’t hit the nadir. The LDL hadn’t plateaued. If we had taken patients out to 18-20 weeks, we might have seen an even greater delta," according to Dr. Kereiakes of Christ Hospital, Cincinnati.

He sees the target population for 553 as being the large number of patients who can’t reach their LDL target despite maximum doses of currently approved medications, as well as those who can’t do so because they can’t tolerate maximum doses of those drugs.

"I’d say probably more than one-third of my patients are on combination therapy for lipid lowering," the cardiologist said.

With 553, it will also become possible to take to its logical conclusion the hypothesis that a lower LDL is better for preventing atherosclerosis.

"The average LDL in a newborn is 35 mg/dL, and they have clean vasculature. There aren’t even the lipid streaks that occur as the first step in the atherosclerotic process," he noted.

In phase III, the monoclonal antibody will be self-administered subcutaneously using a fixed-dose pen, much like the insulin-sensitizing agent exenatide (Byetta or Bydureon).

Discussant Dr. Karol E. Watson said 553 "has a lot of potential and certainly does offer up some hope." But she zeroed in on the fact that as a monoclonal antibody – even a fully human one – it has the potential for autoimmunity.

"That is something that clearly would limit the usefulness of this molecule. I’d want to see more data on that," added Dr. Watson, codirector of the University of California, Los Angeles, program in preventive cardiology.

Her fellow panelist Dr. Christie M. Ballantyne was particularly intrigued by the fact that C-reactive protein levels did not change significantly during the phase II study.

A clinical trial with 553 could settle the question of whether the clinical benefits of statin therapy are due solely to LDL lowering, or if the concomitant decrease in CRP is also essential, said Dr. Ballantyne, professor of medicine at Baylor College of Medicine, Houston.

The study was sponsored by Sanofi and Regeneron. Dr. McKenney reported that he has received research grants from both companies to conduct clinical trials of 553. He also serves as a consultant to Sanofi, which is developing 553, and to numerous other pharmaceutical companies with an interest in lipid-altering agents. Dr. Kereiakes reported having no financial conflicts.

CHICAGO – An investigational fully human monoclonal antibody slashed low-density lipoprotein cholesterol levels by up to 72% in a phase II clinical trial in dyslipidemic patients not at goal despite already being on a statin.

The study results for the monoclonal antibody known for now as SAR236553/REGN727 caused head-swiveling and double-takes at the annual meeting of the American College of Cardiology.

Bruce Jancin/IMNG Medical Media

"We need to understand: This is a ‘wow.’ It could be a game changer in the future," commented scientific session program committee cochair Dr. Rick A. Nishimura, professor of medicine at the Mayo Clinic, Rochester, Minn. He was referring to the randomized, double-blind, placebo-controlled, 12-week phase II study presented by James M. McKenney, Pharm.D. The trial involved 183 patients with an LDL cholesterol level above the target of 100 mg/dL despite an average of 7 years of statin therapy. The participants remained on atorvastatin at 10, 20, or 40 mg/day as background therapy while being randomized to 12 weeks of subcutaneously administered SAR236553/REGN727 at one of five dosing regimens or to placebo.

At the most effective dosing schedule – 150 mg once every 2 weeks – LDL dropped by a mean of 72% at 12 weeks, from a baseline of 124 mg/dL. Within the first 2 weeks the LDL level had already fallen by 60%.

A clear dose-response relationship was evident, with dosing at 50 and 100 mg once every 2 weeks eliciting mean 40% and 64% LDL reductions, respectively, reported Dr. McKenney, chief executive officer at National Clinical Research, Richmond, Va.

"This is monumental clearance of LDL. It’s just unheard of, especially considering the statin these patients were on should already have produced about a 40% decrease in LDL," he said. "If the drug pans out, if it continues to show efficacy and especially if it shows safety, we may be moving into a new era in the treatment of lipid disorders and, more importantly, in the reduction of heart disease in this country."

At the optimal dosing regimen of SAR236553/REGN727, an agent Dr. McKenney referred to as "553" for the sake of brevity, patients also had mean reductions of 27% in lipoprotein(a), 56% in apolipoprotein B, and 63% in non-HDL (non-high-density lipoprotein) cholesterol, along with a nonsignificant trend for lower triglycerides.

The monoclonal antibody is highly specific for proprotein convertase subtilisin/kexin type 9 serine protease (PCSK9). This protein plays a pivotal role in the degradation of LDL receptors, thereby interfering with cholesterol uptake by the liver.

Treatment with 553 was well tolerated; the most common side effect was mild, transient, injection site reactions. Importantly, given that patients were already on statin therapy, there were no increases in hepatic or muscle-related enzymes.

The one significant adverse event was a case of biopsy-confirmed leukocytoclastic vasculitis occurring 9 days after a patient received a first 300-mg injection of 553. The reaction took the form of a rash on the arms, legs, and abdomen, with no other organ involvement. It responded quickly to drug withdrawal and initiation of prednisone. No other cases of leukocytoclastic vasculitis occurred in any other 553-treated patients, including those who participated in three just-published phase I studies (N. Engl. J. Med. 2012;366:1108-18).

No antidrug antibodies were detected shortly after the patient developed leukocytoclastic vasculitis; however, low-level titers were found at week 20. The patient remained negative for antinuclear antibodies through 6 months of follow-up blood tests.

Leukocytoclastic vasculitis is a rare, generally benign disease with an incidence of 40-60 cases per million persons per year. Medications are identified as the cause of about 20% of cases, with antibiotics and NSAIDs being among the most common offenders. Leukocytoclastic vasculitis is listed as a possible adverse event in the product labeling for most monoclonal antibody therapies, Dr. McKenney noted.

Large phase III clinical trials will begin enrollment later this year. They will focus on patients at high cardiovascular risk, including those with familial hypercholesterolemia and/or prior vascular events who aren’t at goal despite statin therapy.

Coinvestigator Dr. Dean J. Kereiakes said in an interview that one of the most intriguing observations in the phase II study was that mean LDL levels were still on their way down when 553 was stopped after 12 weeks.

"We didn’t hit the nadir. The LDL hadn’t plateaued. If we had taken patients out to 18-20 weeks, we might have seen an even greater delta," according to Dr. Kereiakes of Christ Hospital, Cincinnati.

He sees the target population for 553 as being the large number of patients who can’t reach their LDL target despite maximum doses of currently approved medications, as well as those who can’t do so because they can’t tolerate maximum doses of those drugs.

"I’d say probably more than one-third of my patients are on combination therapy for lipid lowering," the cardiologist said.

With 553, it will also become possible to take to its logical conclusion the hypothesis that a lower LDL is better for preventing atherosclerosis.

"The average LDL in a newborn is 35 mg/dL, and they have clean vasculature. There aren’t even the lipid streaks that occur as the first step in the atherosclerotic process," he noted.

In phase III, the monoclonal antibody will be self-administered subcutaneously using a fixed-dose pen, much like the insulin-sensitizing agent exenatide (Byetta or Bydureon).

Discussant Dr. Karol E. Watson said 553 "has a lot of potential and certainly does offer up some hope." But she zeroed in on the fact that as a monoclonal antibody – even a fully human one – it has the potential for autoimmunity.

"That is something that clearly would limit the usefulness of this molecule. I’d want to see more data on that," added Dr. Watson, codirector of the University of California, Los Angeles, program in preventive cardiology.

Her fellow panelist Dr. Christie M. Ballantyne was particularly intrigued by the fact that C-reactive protein levels did not change significantly during the phase II study.

A clinical trial with 553 could settle the question of whether the clinical benefits of statin therapy are due solely to LDL lowering, or if the concomitant decrease in CRP is also essential, said Dr. Ballantyne, professor of medicine at Baylor College of Medicine, Houston.

The study was sponsored by Sanofi and Regeneron. Dr. McKenney reported that he has received research grants from both companies to conduct clinical trials of 553. He also serves as a consultant to Sanofi, which is developing 553, and to numerous other pharmaceutical companies with an interest in lipid-altering agents. Dr. Kereiakes reported having no financial conflicts.

In this, the second installment of a two-part series on how physicians can demonstrate meaningful use of their electronic health record to earn federal incentives, Dr. Skolnik and Dr. Notte talk about what it will take for providers to complete 5 of 10 menu measures, of which at least one must be a public health measure.

To download the podcast, right-click here.

To read the related column, click here.

To listen via this Web page, click on the player below:

In this, the second installment of a two-part series on how physicians can demonstrate meaningful use of their electronic health record to earn federal incentives, Dr. Skolnik and Dr. Notte talk about what it will take for providers to complete 5 of 10 menu measures, of which at least one must be a public health measure.

To download the podcast, right-click here.

To read the related column, click here.

To listen via this Web page, click on the player below:

In this, the second installment of a two-part series on how physicians can demonstrate meaningful use of their electronic health record to earn federal incentives, Dr. Skolnik and Dr. Notte talk about what it will take for providers to complete 5 of 10 menu measures, of which at least one must be a public health measure.

To download the podcast, right-click here.

To read the related column, click here.

To listen via this Web page, click on the player below:

Most would agree that "we are seeing more thrombosis over time" in children over the past decade, and although we don't know why, it is likely due to multifactorial causes, said Leslie Raffini, MD, MSCE, director of the Hemostasis and Thrombosis Center at Children's Hospital of Philadelphia, in a session on Monday at HM12.

Central venous catheters remain a significant risk factor for venous thromboembolism (VTE) and our knowledge of inherited risk factors has expanded in recent years. While it is likely that inherited risk factors increase the risk of thrombosis in children, the question of testing has engendered debate, due in large part to the lack of clear benefit of that information in the majority of situations.

"The decision to test should be made on an individual basis, after counseling," said Dr. Raffini. "Results should be interpreted by an experienced physician with adolescent females most likely to benefit from the testing. There are no recommendations for what to do with pediatric patients" despite the fact that this is an important cause of morbidity in high-risk patients.

Dr. Raffini describes efforts at Children's Hospital of Philadelphia that led to a VTE prophylaxis guideline. Successful implementation of the guideline required significant multidisciplinary collaboration, and an analysis of outcomes is underway.

Takeaways

• The decision to test for inherited risk factors should be individualized.
• Adolescent females are most likely to benefit from testing for inherited risk factors.
• Implementation of guidelines requires intentional multidisciplinary collaboration.

Most would agree that "we are seeing more thrombosis over time" in children over the past decade, and although we don't know why, it is likely due to multifactorial causes, said Leslie Raffini, MD, MSCE, director of the Hemostasis and Thrombosis Center at Children's Hospital of Philadelphia, in a session on Monday at HM12.

Central venous catheters remain a significant risk factor for venous thromboembolism (VTE) and our knowledge of inherited risk factors has expanded in recent years. While it is likely that inherited risk factors increase the risk of thrombosis in children, the question of testing has engendered debate, due in large part to the lack of clear benefit of that information in the majority of situations.

"The decision to test should be made on an individual basis, after counseling," said Dr. Raffini. "Results should be interpreted by an experienced physician with adolescent females most likely to benefit from the testing. There are no recommendations for what to do with pediatric patients" despite the fact that this is an important cause of morbidity in high-risk patients.

Dr. Raffini describes efforts at Children's Hospital of Philadelphia that led to a VTE prophylaxis guideline. Successful implementation of the guideline required significant multidisciplinary collaboration, and an analysis of outcomes is underway.

Takeaways

• The decision to test for inherited risk factors should be individualized.
• Adolescent females are most likely to benefit from testing for inherited risk factors.
• Implementation of guidelines requires intentional multidisciplinary collaboration.

Most would agree that "we are seeing more thrombosis over time" in children over the past decade, and although we don't know why, it is likely due to multifactorial causes, said Leslie Raffini, MD, MSCE, director of the Hemostasis and Thrombosis Center at Children's Hospital of Philadelphia, in a session on Monday at HM12.

Central venous catheters remain a significant risk factor for venous thromboembolism (VTE) and our knowledge of inherited risk factors has expanded in recent years. While it is likely that inherited risk factors increase the risk of thrombosis in children, the question of testing has engendered debate, due in large part to the lack of clear benefit of that information in the majority of situations.

"The decision to test should be made on an individual basis, after counseling," said Dr. Raffini. "Results should be interpreted by an experienced physician with adolescent females most likely to benefit from the testing. There are no recommendations for what to do with pediatric patients" despite the fact that this is an important cause of morbidity in high-risk patients.

Dr. Raffini describes efforts at Children's Hospital of Philadelphia that led to a VTE prophylaxis guideline. Successful implementation of the guideline required significant multidisciplinary collaboration, and an analysis of outcomes is underway.

Takeaways

• The decision to test for inherited risk factors should be individualized.
• Adolescent females are most likely to benefit from testing for inherited risk factors.
• Implementation of guidelines requires intentional multidisciplinary collaboration.

Vineet Arora, MD, FHM, has had extensive experience in patient handoffs, and highlighted the importance of handoffs for the transfer of patient information in a Monday afternoon breakout session at HM12. Safe and successful handoffs include several steps for the transfer of information, said Dr. Arora. These steps include pre-handoff, the arrival of the incoming physician, dialogue, and post-handoff.

Effective handoffs strategies include standardized information, updated information, limited interruptions, and specific structure including read-backs. Face-to-face handoffs are ideal.

Takeaways

• Beware of egocentric heuristic, the assumption that the receiving physician has the exact same information and fund of knowledge as the initial or sending physician.
• Checklists can be helpful but can have flaws when not used appropriately.
• "If-then" and "to do" lists are the most retained form of information from handoffs.
• Prioritize the most-ill patients during handoffs.
• Assess receiver understanding.
• Beware of too much information during handoffs.
• Programatic changes, such as protected handoff time and space, can support proper handoffs.

Vineet Arora, MD, FHM, has had extensive experience in patient handoffs, and highlighted the importance of handoffs for the transfer of patient information in a Monday afternoon breakout session at HM12. Safe and successful handoffs include several steps for the transfer of information, said Dr. Arora. These steps include pre-handoff, the arrival of the incoming physician, dialogue, and post-handoff.

Effective handoffs strategies include standardized information, updated information, limited interruptions, and specific structure including read-backs. Face-to-face handoffs are ideal.

Takeaways

• Beware of egocentric heuristic, the assumption that the receiving physician has the exact same information and fund of knowledge as the initial or sending physician.
• Checklists can be helpful but can have flaws when not used appropriately.
• "If-then" and "to do" lists are the most retained form of information from handoffs.
• Prioritize the most-ill patients during handoffs.
• Assess receiver understanding.
• Beware of too much information during handoffs.
• Programatic changes, such as protected handoff time and space, can support proper handoffs.

Vineet Arora, MD, FHM, has had extensive experience in patient handoffs, and highlighted the importance of handoffs for the transfer of patient information in a Monday afternoon breakout session at HM12. Safe and successful handoffs include several steps for the transfer of information, said Dr. Arora. These steps include pre-handoff, the arrival of the incoming physician, dialogue, and post-handoff.

Effective handoffs strategies include standardized information, updated information, limited interruptions, and specific structure including read-backs. Face-to-face handoffs are ideal.

Takeaways

• Beware of egocentric heuristic, the assumption that the receiving physician has the exact same information and fund of knowledge as the initial or sending physician.
• Checklists can be helpful but can have flaws when not used appropriately.
• "If-then" and "to do" lists are the most retained form of information from handoffs.
• Prioritize the most-ill patients during handoffs.
• Assess receiver understanding.
• Beware of too much information during handoffs.
• Programatic changes, such as protected handoff time and space, can support proper handoffs.

The etiologic agents for complicated pneumonias and osteomyelitis have changed recently, according to presenters Drs. William and Creech, who assisted pediatric hospitalists in updated diagnosis and intervention strategies.

The increase in complicated pneumonias and empyemas is mostly due to the increase in Streptococcus pneumoniae serotype 19a. After introduction of the PCV-7 vaccine, incidence of serotype 19a infections increased to 98% of infections. Serotype 19a is now included in the PCV-13 vaccine, approved by the FDA in 2011. There are multiple interventions available for empyemas including chest tube alone, chest tube with fibrinolysis, and VATS. Current research is being done to assess efficacy for these measures.

Osteomyelitis may be caused by direct inoculation, spread from local infection, or hematogenous spread. S. Aureus is causative agent in 80-90% of patients. MRSA infection has a more complicated course. Based on patient response and inflammatory markers, a short course of intravenous antibiotics followed by oral antibiotics may be appropriate.

Key Takeaways:

1. Surgical intervention for empyemas is patient specific and depends on clinical status, effusion, status, presence of loculations, and expertise of consultants.

2. Hematogenous spread is the most common cause of osteomyelitis in children.

3. MRI is diagnostic modality of choice for osteomyelitis.

4. Bone aspiration and blood cultures are very helpful in treatment of osteomyelitis.

5. Clindamycin can be considered for first line osteomyelitis treatment if it is not a life threatening infection, a limb threatening infection, or a high likelihood of bacteremia. Beta lactam coverage should be considered in toddlers due to Kingella.

Dr. Hale is a pediatric hospitalist at Floating Hospital for Children at Tufts Medical Center in Boston.

The etiologic agents for complicated pneumonias and osteomyelitis have changed recently, according to presenters Drs. William and Creech, who assisted pediatric hospitalists in updated diagnosis and intervention strategies.

The increase in complicated pneumonias and empyemas is mostly due to the increase in Streptococcus pneumoniae serotype 19a. After introduction of the PCV-7 vaccine, incidence of serotype 19a infections increased to 98% of infections. Serotype 19a is now included in the PCV-13 vaccine, approved by the FDA in 2011. There are multiple interventions available for empyemas including chest tube alone, chest tube with fibrinolysis, and VATS. Current research is being done to assess efficacy for these measures.

Osteomyelitis may be caused by direct inoculation, spread from local infection, or hematogenous spread. S. Aureus is causative agent in 80-90% of patients. MRSA infection has a more complicated course. Based on patient response and inflammatory markers, a short course of intravenous antibiotics followed by oral antibiotics may be appropriate.

Key Takeaways:

1. Surgical intervention for empyemas is patient specific and depends on clinical status, effusion, status, presence of loculations, and expertise of consultants.

2. Hematogenous spread is the most common cause of osteomyelitis in children.

3. MRI is diagnostic modality of choice for osteomyelitis.

4. Bone aspiration and blood cultures are very helpful in treatment of osteomyelitis.

5. Clindamycin can be considered for first line osteomyelitis treatment if it is not a life threatening infection, a limb threatening infection, or a high likelihood of bacteremia. Beta lactam coverage should be considered in toddlers due to Kingella.

Dr. Hale is a pediatric hospitalist at Floating Hospital for Children at Tufts Medical Center in Boston.

The etiologic agents for complicated pneumonias and osteomyelitis have changed recently, according to presenters Drs. William and Creech, who assisted pediatric hospitalists in updated diagnosis and intervention strategies.

The increase in complicated pneumonias and empyemas is mostly due to the increase in Streptococcus pneumoniae serotype 19a. After introduction of the PCV-7 vaccine, incidence of serotype 19a infections increased to 98% of infections. Serotype 19a is now included in the PCV-13 vaccine, approved by the FDA in 2011. There are multiple interventions available for empyemas including chest tube alone, chest tube with fibrinolysis, and VATS. Current research is being done to assess efficacy for these measures.

Osteomyelitis may be caused by direct inoculation, spread from local infection, or hematogenous spread. S. Aureus is causative agent in 80-90% of patients. MRSA infection has a more complicated course. Based on patient response and inflammatory markers, a short course of intravenous antibiotics followed by oral antibiotics may be appropriate.

Key Takeaways:

1. Surgical intervention for empyemas is patient specific and depends on clinical status, effusion, status, presence of loculations, and expertise of consultants.

2. Hematogenous spread is the most common cause of osteomyelitis in children.

3. MRI is diagnostic modality of choice for osteomyelitis.

4. Bone aspiration and blood cultures are very helpful in treatment of osteomyelitis.

5. Clindamycin can be considered for first line osteomyelitis treatment if it is not a life threatening infection, a limb threatening infection, or a high likelihood of bacteremia. Beta lactam coverage should be considered in toddlers due to Kingella.

Dr. Hale is a pediatric hospitalist at Floating Hospital for Children at Tufts Medical Center in Boston.