Clinical

Click here to listen to excerpts of Dr. Parkhurst's interview with The Hospitalist

Click here to listen to excerpts of Dr. Parkhurst's interview with The Hospitalist

Click here to listen to excerpts of Dr. Parkhurst's interview with The Hospitalist

Click here to listen to excerpts of Dr. Chretien's interview with The Hospitalist

Click here to listen to excerpts of Dr. Chretien's interview with The Hospitalist

Click here to listen to excerpts of Dr. Chretien's interview with The Hospitalist

“You focus on the patient that’s in front of you. You focus on trying to solve the issues that are at hand. You deal with the logistical questions that come up between patients.”

—James Hudspeth, MD, Boston Medical Center

“At some point, a disaster is so large that it would overwhelm any system, no matter how many resources were available. ”

—Dan Hale, MD, Floating Hospital for Children at Tufts Medical Center, Boston

Dan Hale, MD, a pediatric hospitalist at the Floating Hospital for Children at Tufts Medical Center in Boston, was doing discharge paperwork when he started getting text messages he couldn’t quite interpret.

“Are you OK?” “Do you need anything?” friends were asking him. Then he heard a page for all anesthesiologists to report to the OR. Immediately, he knew something terrible must have happened. He soon learned about the bombings at the Boston Marathon. He rushed to the pediatric ED to see how he could help.

James Hudspeth, MD, a hospitalist at Boston Medical Center, was meeting with the program director for internal medicine when he read a text message that bombs had just gone off near the finish line. They went online for local news coverage; soon thereafter, a cap on admissions was lifted. Dr. Hudspeth started expediting discharges to make room for what might be coming the hospital’s way.

Sushrut Jangi, MD, a hospitalist at Beth Israel Deaconess Medical Center, was in a medical tent gathering information for an article on treating the health problems of marathoners that he was writing for The Boston Globe when he heard the blasts. Doctors and medical staff there worried about the possibility of a bomb in the tent, he said, but they were instructed to stay with their patients. Dr. Jangi had expected to work as a journalist for the day, but his doctoring skills were needed.

Hospitalists who were working in downtown Boston on April 15, when two bombs exploded 17 seconds apart, all experienced the tragedy in their own ways. But their accounts also resonate within some of the same themes.

They found themselves unsure of their roles, as most of the work inevitably fell to surgeons and trauma specialists. They described the importance of good leadership in times of crisis. And they say that hospitalists should be incorporated to a greater extent into disaster plans.

Dr. Jangi said that before the bombs went off, the medical tent was almost filled with runners who were “quite ill”—hypothermic and shaking, high sodium levels, disoriented. When the blasts occurred, the main instruction was, “Don’t leave your patients behind.” Those who were well enough were released from the tent, and the bomb-blast victims were essentially “whisked through.”

“We just kind of cleared the way and got them into ambulances as soon as possible. We just didn’t have the capacity to take care of such severe injury,” he said. “Why should we? We weren’t expecting a war zone.”

In the tent, Dr. Jangi wrote in an essay for the New England Journal of Medicine, “Many of us barely laid our hands on anyone. We had no trauma surgeons or supplies of blood products; tourniquets had already been applied; CPR had already been performed. Though some patients required bandages, sutures, and dressings, many of us watched these passing victims in a kind of idle horror, with no idea how to help.”

Dr. Hale was not involved in the treatment of bombing victims as the attending of record, but he said that he had a “bird’s-eye view” of the response in the pediatric ED. One child had shrapnel injuries and a ruptured tympanic membrane and was worked on by the team “professionally and efficiently,” Dr. Hale said.

When reports of a possible third bomb blast, at a library, came in, he saw the physician leaders go from team to team, making sure they were prepared.

“There were clear leaders communicating what to do,” said Dr. Hale, a firefighter in his hometown of Kittery in southern Maine. “As patients came in, it was extremely orderly. I saw very few clinical staff who were rattled.”

For his own part, in addition to his medical training, his training as a firefighter helped keep him calm, he said.

At Boston Medical Center, about a mile and a half from the blasts, the admissions that had been worked up over the course of the afternoon were essentially taken all at once so that there was room in the ED, said Dr. Hudspeth, who also does medical work in Haiti and was in New York on 9/11, though not as a doctor.

Focusing, he said, was “definitely a challenge.” Even though he had faith in hospital security, there was still “some notion of ‘You never know exactly what’s going to happen.’”

“You focus on the patient that’s in front of you. You focus on trying to solve the issues that are at hand. You deal with the logistical questions that come up between patients,” he said. “By and large, just put your nose to the grindstone.”

The doctors said that hospitalists had an unclear role in the response effort and hope to have their roles clarified so that they can better put to use their expertise in internal medicine. If hospitalists are monitoring general medical issues, that will help take some of the pressure off the trauma team.

“We know the [general] medicine stuff very well—that is our bread and butter,” said Dr. Hudspeth, who added that steps are being taken as part of Boston Medical Center’s post-response analysis to determine hospitalists’ role in future disaster responses.

They also said they felt fortunate that the bombings had occurred where they did, with so many hospitals close to the scene. It kept the system from becoming overwhelmed. Even so, “at some point, a disaster is so large that it would overwhelm any system, no matter how many resources were available,” Dr. Hale added.

Dr. Jangi said that he thinks his residency training helped him when he found himself having to provide care in a high-pressure situation in the medical tent.

“During residency, there are a lot of situations where you’re responsible for making a decision on your feet,” he said. “That’s a skill that you’re not really exposed to until you do it and that type of fast decision-making. I felt myself drawing on that. Not that I resuscitated anyone in the tent, but I felt more comfortable with uncertainty, with doing your duty in a situation of uncertainty. And I don’t know—maybe if I hadn’t gone through that, I would have just run out of there.”

He said the experience has helped make him more committed as a doctor.

“It makes it easier to remember what my duty is more, and it just gives me more empathy for suffering in general—I feel that very strongly,” he said. “It’s possible that this experience could have numbed me, but it didn’t. It’s made me more acute to the idea of people suffering.”

Tom Collins is a freelance writer in South Florida.

Reference

1. Under the Medical Tent at the Boston Marathon. N Engl J Med. 2013;368:1953-1955.

“You focus on the patient that’s in front of you. You focus on trying to solve the issues that are at hand. You deal with the logistical questions that come up between patients.”

—James Hudspeth, MD, Boston Medical Center

“At some point, a disaster is so large that it would overwhelm any system, no matter how many resources were available. ”

—Dan Hale, MD, Floating Hospital for Children at Tufts Medical Center, Boston

Dan Hale, MD, a pediatric hospitalist at the Floating Hospital for Children at Tufts Medical Center in Boston, was doing discharge paperwork when he started getting text messages he couldn’t quite interpret.

“Are you OK?” “Do you need anything?” friends were asking him. Then he heard a page for all anesthesiologists to report to the OR. Immediately, he knew something terrible must have happened. He soon learned about the bombings at the Boston Marathon. He rushed to the pediatric ED to see how he could help.

James Hudspeth, MD, a hospitalist at Boston Medical Center, was meeting with the program director for internal medicine when he read a text message that bombs had just gone off near the finish line. They went online for local news coverage; soon thereafter, a cap on admissions was lifted. Dr. Hudspeth started expediting discharges to make room for what might be coming the hospital’s way.

Sushrut Jangi, MD, a hospitalist at Beth Israel Deaconess Medical Center, was in a medical tent gathering information for an article on treating the health problems of marathoners that he was writing for The Boston Globe when he heard the blasts. Doctors and medical staff there worried about the possibility of a bomb in the tent, he said, but they were instructed to stay with their patients. Dr. Jangi had expected to work as a journalist for the day, but his doctoring skills were needed.

Hospitalists who were working in downtown Boston on April 15, when two bombs exploded 17 seconds apart, all experienced the tragedy in their own ways. But their accounts also resonate within some of the same themes.

They found themselves unsure of their roles, as most of the work inevitably fell to surgeons and trauma specialists. They described the importance of good leadership in times of crisis. And they say that hospitalists should be incorporated to a greater extent into disaster plans.

Dr. Jangi said that before the bombs went off, the medical tent was almost filled with runners who were “quite ill”—hypothermic and shaking, high sodium levels, disoriented. When the blasts occurred, the main instruction was, “Don’t leave your patients behind.” Those who were well enough were released from the tent, and the bomb-blast victims were essentially “whisked through.”

“We just kind of cleared the way and got them into ambulances as soon as possible. We just didn’t have the capacity to take care of such severe injury,” he said. “Why should we? We weren’t expecting a war zone.”

In the tent, Dr. Jangi wrote in an essay for the New England Journal of Medicine, “Many of us barely laid our hands on anyone. We had no trauma surgeons or supplies of blood products; tourniquets had already been applied; CPR had already been performed. Though some patients required bandages, sutures, and dressings, many of us watched these passing victims in a kind of idle horror, with no idea how to help.”

Dr. Hale was not involved in the treatment of bombing victims as the attending of record, but he said that he had a “bird’s-eye view” of the response in the pediatric ED. One child had shrapnel injuries and a ruptured tympanic membrane and was worked on by the team “professionally and efficiently,” Dr. Hale said.

When reports of a possible third bomb blast, at a library, came in, he saw the physician leaders go from team to team, making sure they were prepared.

“There were clear leaders communicating what to do,” said Dr. Hale, a firefighter in his hometown of Kittery in southern Maine. “As patients came in, it was extremely orderly. I saw very few clinical staff who were rattled.”

For his own part, in addition to his medical training, his training as a firefighter helped keep him calm, he said.

At Boston Medical Center, about a mile and a half from the blasts, the admissions that had been worked up over the course of the afternoon were essentially taken all at once so that there was room in the ED, said Dr. Hudspeth, who also does medical work in Haiti and was in New York on 9/11, though not as a doctor.

Focusing, he said, was “definitely a challenge.” Even though he had faith in hospital security, there was still “some notion of ‘You never know exactly what’s going to happen.’”

“You focus on the patient that’s in front of you. You focus on trying to solve the issues that are at hand. You deal with the logistical questions that come up between patients,” he said. “By and large, just put your nose to the grindstone.”

The doctors said that hospitalists had an unclear role in the response effort and hope to have their roles clarified so that they can better put to use their expertise in internal medicine. If hospitalists are monitoring general medical issues, that will help take some of the pressure off the trauma team.

“We know the [general] medicine stuff very well—that is our bread and butter,” said Dr. Hudspeth, who added that steps are being taken as part of Boston Medical Center’s post-response analysis to determine hospitalists’ role in future disaster responses.

They also said they felt fortunate that the bombings had occurred where they did, with so many hospitals close to the scene. It kept the system from becoming overwhelmed. Even so, “at some point, a disaster is so large that it would overwhelm any system, no matter how many resources were available,” Dr. Hale added.

Dr. Jangi said that he thinks his residency training helped him when he found himself having to provide care in a high-pressure situation in the medical tent.

“During residency, there are a lot of situations where you’re responsible for making a decision on your feet,” he said. “That’s a skill that you’re not really exposed to until you do it and that type of fast decision-making. I felt myself drawing on that. Not that I resuscitated anyone in the tent, but I felt more comfortable with uncertainty, with doing your duty in a situation of uncertainty. And I don’t know—maybe if I hadn’t gone through that, I would have just run out of there.”

He said the experience has helped make him more committed as a doctor.

“It makes it easier to remember what my duty is more, and it just gives me more empathy for suffering in general—I feel that very strongly,” he said. “It’s possible that this experience could have numbed me, but it didn’t. It’s made me more acute to the idea of people suffering.”

Tom Collins is a freelance writer in South Florida.

Reference

1. Under the Medical Tent at the Boston Marathon. N Engl J Med. 2013;368:1953-1955.

“You focus on the patient that’s in front of you. You focus on trying to solve the issues that are at hand. You deal with the logistical questions that come up between patients.”

—James Hudspeth, MD, Boston Medical Center

“At some point, a disaster is so large that it would overwhelm any system, no matter how many resources were available. ”

—Dan Hale, MD, Floating Hospital for Children at Tufts Medical Center, Boston

Dan Hale, MD, a pediatric hospitalist at the Floating Hospital for Children at Tufts Medical Center in Boston, was doing discharge paperwork when he started getting text messages he couldn’t quite interpret.

“Are you OK?” “Do you need anything?” friends were asking him. Then he heard a page for all anesthesiologists to report to the OR. Immediately, he knew something terrible must have happened. He soon learned about the bombings at the Boston Marathon. He rushed to the pediatric ED to see how he could help.

James Hudspeth, MD, a hospitalist at Boston Medical Center, was meeting with the program director for internal medicine when he read a text message that bombs had just gone off near the finish line. They went online for local news coverage; soon thereafter, a cap on admissions was lifted. Dr. Hudspeth started expediting discharges to make room for what might be coming the hospital’s way.

Sushrut Jangi, MD, a hospitalist at Beth Israel Deaconess Medical Center, was in a medical tent gathering information for an article on treating the health problems of marathoners that he was writing for The Boston Globe when he heard the blasts. Doctors and medical staff there worried about the possibility of a bomb in the tent, he said, but they were instructed to stay with their patients. Dr. Jangi had expected to work as a journalist for the day, but his doctoring skills were needed.

Hospitalists who were working in downtown Boston on April 15, when two bombs exploded 17 seconds apart, all experienced the tragedy in their own ways. But their accounts also resonate within some of the same themes.

They found themselves unsure of their roles, as most of the work inevitably fell to surgeons and trauma specialists. They described the importance of good leadership in times of crisis. And they say that hospitalists should be incorporated to a greater extent into disaster plans.

Dr. Jangi said that before the bombs went off, the medical tent was almost filled with runners who were “quite ill”—hypothermic and shaking, high sodium levels, disoriented. When the blasts occurred, the main instruction was, “Don’t leave your patients behind.” Those who were well enough were released from the tent, and the bomb-blast victims were essentially “whisked through.”

“We just kind of cleared the way and got them into ambulances as soon as possible. We just didn’t have the capacity to take care of such severe injury,” he said. “Why should we? We weren’t expecting a war zone.”

In the tent, Dr. Jangi wrote in an essay for the New England Journal of Medicine, “Many of us barely laid our hands on anyone. We had no trauma surgeons or supplies of blood products; tourniquets had already been applied; CPR had already been performed. Though some patients required bandages, sutures, and dressings, many of us watched these passing victims in a kind of idle horror, with no idea how to help.”

Dr. Hale was not involved in the treatment of bombing victims as the attending of record, but he said that he had a “bird’s-eye view” of the response in the pediatric ED. One child had shrapnel injuries and a ruptured tympanic membrane and was worked on by the team “professionally and efficiently,” Dr. Hale said.

When reports of a possible third bomb blast, at a library, came in, he saw the physician leaders go from team to team, making sure they were prepared.

“There were clear leaders communicating what to do,” said Dr. Hale, a firefighter in his hometown of Kittery in southern Maine. “As patients came in, it was extremely orderly. I saw very few clinical staff who were rattled.”

For his own part, in addition to his medical training, his training as a firefighter helped keep him calm, he said.

At Boston Medical Center, about a mile and a half from the blasts, the admissions that had been worked up over the course of the afternoon were essentially taken all at once so that there was room in the ED, said Dr. Hudspeth, who also does medical work in Haiti and was in New York on 9/11, though not as a doctor.

Focusing, he said, was “definitely a challenge.” Even though he had faith in hospital security, there was still “some notion of ‘You never know exactly what’s going to happen.’”

“You focus on the patient that’s in front of you. You focus on trying to solve the issues that are at hand. You deal with the logistical questions that come up between patients,” he said. “By and large, just put your nose to the grindstone.”

The doctors said that hospitalists had an unclear role in the response effort and hope to have their roles clarified so that they can better put to use their expertise in internal medicine. If hospitalists are monitoring general medical issues, that will help take some of the pressure off the trauma team.

“We know the [general] medicine stuff very well—that is our bread and butter,” said Dr. Hudspeth, who added that steps are being taken as part of Boston Medical Center’s post-response analysis to determine hospitalists’ role in future disaster responses.

They also said they felt fortunate that the bombings had occurred where they did, with so many hospitals close to the scene. It kept the system from becoming overwhelmed. Even so, “at some point, a disaster is so large that it would overwhelm any system, no matter how many resources were available,” Dr. Hale added.

Dr. Jangi said that he thinks his residency training helped him when he found himself having to provide care in a high-pressure situation in the medical tent.

“During residency, there are a lot of situations where you’re responsible for making a decision on your feet,” he said. “That’s a skill that you’re not really exposed to until you do it and that type of fast decision-making. I felt myself drawing on that. Not that I resuscitated anyone in the tent, but I felt more comfortable with uncertainty, with doing your duty in a situation of uncertainty. And I don’t know—maybe if I hadn’t gone through that, I would have just run out of there.”

He said the experience has helped make him more committed as a doctor.

“It makes it easier to remember what my duty is more, and it just gives me more empathy for suffering in general—I feel that very strongly,” he said. “It’s possible that this experience could have numbed me, but it didn’t. It’s made me more acute to the idea of people suffering.”

Tom Collins is a freelance writer in South Florida.

Reference

1. Under the Medical Tent at the Boston Marathon. N Engl J Med. 2013;368:1953-1955.

What I’d like to highlight is how pediatric hospitalists can follow their adult hospitalist brothers and sisters into the role of being leaders … in how to handle challenges that their hospitals face.

—Weijen Chang, MD, SFHM, FAAP

Next month, readers of The Hospitalist will see a new face alongside the monthly “Pediatric HM Literature” column. Weijen Chang, MD, SFHM, FAAP, has been selected its new pediatric editor. Next month Dr. Chang takes over for Mark Shen, MD, SFHM, the magazine's pediatric editor since 2010.

Dr. Chang attended Duke University’s medicine-pediatrics residency program in Durham, N.C., after graduating from New York Medical College in Valhalla, N.Y. He serves as health sciences associate clinical professor of medicine and pediatrics at the University of California at San Diego (UCSD) School of Medicine, and serves as a hospitalist at both UCSD Medical Center and Rady Children’s Hospital, just across town from UCSD.

As pediatric editor, Dr. Chang hopes to help grow the field of pediatric hospital medicine, just as adult HM has grown over the last decade.

“In the past 10 years of HM being in existence, I think adult hospitalists have gone from being a fill-in-type player to really being leaders in their institutions,” he says, “and I think pediatric hospitalists are beginning to fill that role. What I’d like to highlight is how pediatric hospitalists can follow their adult hospitalist brothers and sisters into the role of being leaders … in how to handle challenges that their hospitals face.”

Danielle Scheurer, MD, MSCR, SFHM, The Hospitalist’s physician editor, echoed Dr. Change’s enthusiasm. “We are thrilled to have Weijen Chang as our new pediatric editor,” Dr. Scheurer says. “He is a long-time member of Team Hospitalist, active SHM member, and a respected mentor in the pediatric hospitalist community. He will bring insight and depth to the pediatric HM community. We are lucky to be able to recruit him to this position.”

Dr. Chang says he’s looking forward to his new role and new contacts he will be making. He recently joined SHM’s Pediatrics Committee, and will continue engagement with Team Hospitalist, the magazine’s editorial advisory board.

“I’m really excited to get the chance to contact other pediatric hospitalists around the country to gauge opinions about various issues that we face,” Dr. Chang says. “For me, the most exciting part is having an excuse to call people to see what’s going on in their institutions. As hospitalists, we’re so focused on what happens within our walls that we don’t get to see what’s happening elsewhere.”

Michael O’Neal is a freelance writer in New York.

What I’d like to highlight is how pediatric hospitalists can follow their adult hospitalist brothers and sisters into the role of being leaders … in how to handle challenges that their hospitals face.

—Weijen Chang, MD, SFHM, FAAP

Next month, readers of The Hospitalist will see a new face alongside the monthly “Pediatric HM Literature” column. Weijen Chang, MD, SFHM, FAAP, has been selected its new pediatric editor. Next month Dr. Chang takes over for Mark Shen, MD, SFHM, the magazine's pediatric editor since 2010.

Dr. Chang attended Duke University’s medicine-pediatrics residency program in Durham, N.C., after graduating from New York Medical College in Valhalla, N.Y. He serves as health sciences associate clinical professor of medicine and pediatrics at the University of California at San Diego (UCSD) School of Medicine, and serves as a hospitalist at both UCSD Medical Center and Rady Children’s Hospital, just across town from UCSD.

As pediatric editor, Dr. Chang hopes to help grow the field of pediatric hospital medicine, just as adult HM has grown over the last decade.

“In the past 10 years of HM being in existence, I think adult hospitalists have gone from being a fill-in-type player to really being leaders in their institutions,” he says, “and I think pediatric hospitalists are beginning to fill that role. What I’d like to highlight is how pediatric hospitalists can follow their adult hospitalist brothers and sisters into the role of being leaders … in how to handle challenges that their hospitals face.”

Danielle Scheurer, MD, MSCR, SFHM, The Hospitalist’s physician editor, echoed Dr. Change’s enthusiasm. “We are thrilled to have Weijen Chang as our new pediatric editor,” Dr. Scheurer says. “He is a long-time member of Team Hospitalist, active SHM member, and a respected mentor in the pediatric hospitalist community. He will bring insight and depth to the pediatric HM community. We are lucky to be able to recruit him to this position.”

Dr. Chang says he’s looking forward to his new role and new contacts he will be making. He recently joined SHM’s Pediatrics Committee, and will continue engagement with Team Hospitalist, the magazine’s editorial advisory board.

“I’m really excited to get the chance to contact other pediatric hospitalists around the country to gauge opinions about various issues that we face,” Dr. Chang says. “For me, the most exciting part is having an excuse to call people to see what’s going on in their institutions. As hospitalists, we’re so focused on what happens within our walls that we don’t get to see what’s happening elsewhere.”

Michael O’Neal is a freelance writer in New York.

What I’d like to highlight is how pediatric hospitalists can follow their adult hospitalist brothers and sisters into the role of being leaders … in how to handle challenges that their hospitals face.

—Weijen Chang, MD, SFHM, FAAP

Next month, readers of The Hospitalist will see a new face alongside the monthly “Pediatric HM Literature” column. Weijen Chang, MD, SFHM, FAAP, has been selected its new pediatric editor. Next month Dr. Chang takes over for Mark Shen, MD, SFHM, the magazine's pediatric editor since 2010.

Dr. Chang attended Duke University’s medicine-pediatrics residency program in Durham, N.C., after graduating from New York Medical College in Valhalla, N.Y. He serves as health sciences associate clinical professor of medicine and pediatrics at the University of California at San Diego (UCSD) School of Medicine, and serves as a hospitalist at both UCSD Medical Center and Rady Children’s Hospital, just across town from UCSD.

As pediatric editor, Dr. Chang hopes to help grow the field of pediatric hospital medicine, just as adult HM has grown over the last decade.

“In the past 10 years of HM being in existence, I think adult hospitalists have gone from being a fill-in-type player to really being leaders in their institutions,” he says, “and I think pediatric hospitalists are beginning to fill that role. What I’d like to highlight is how pediatric hospitalists can follow their adult hospitalist brothers and sisters into the role of being leaders … in how to handle challenges that their hospitals face.”

Danielle Scheurer, MD, MSCR, SFHM, The Hospitalist’s physician editor, echoed Dr. Change’s enthusiasm. “We are thrilled to have Weijen Chang as our new pediatric editor,” Dr. Scheurer says. “He is a long-time member of Team Hospitalist, active SHM member, and a respected mentor in the pediatric hospitalist community. He will bring insight and depth to the pediatric HM community. We are lucky to be able to recruit him to this position.”

Dr. Chang says he’s looking forward to his new role and new contacts he will be making. He recently joined SHM’s Pediatrics Committee, and will continue engagement with Team Hospitalist, the magazine’s editorial advisory board.

“I’m really excited to get the chance to contact other pediatric hospitalists around the country to gauge opinions about various issues that we face,” Dr. Chang says. “For me, the most exciting part is having an excuse to call people to see what’s going on in their institutions. As hospitalists, we’re so focused on what happens within our walls that we don’t get to see what’s happening elsewhere.”

Michael O’Neal is a freelance writer in New York.

SHM announced in May the launch of a new interdisciplinary partnership, the Alliance to Advance Patient Nutrition, in conjunction with four other organizations. The alliance’s mission is to improve patient outcomes through nutrition intervention in the hospital.

Representing more than 100,000 dietitians, nurses, hospitalists, and other physicians and clinicians from across the nation, the following organizations have come together with SHM to champion for early nutrition screening, assessment, and intervention in hospitals:

• Academy of Medical-Surgical Nurses (AMSN);
• Academy of Nutrition and Dietetics (AND);
• American Society for Parenteral and Enteral Nutrition (ASPEN); and
• Abbott Nutrition.

Malnutrition increases costs, length of stay, and unfavorable outcomes. Properly addressing hospital malnutrition creates an opportunity to improve quality of care while also reducing healthcare costs. Additional clinical research finds that malnourished patients are two times more likely to develop a pressure ulcer, while patients with malnutrition have three times the rate of infection.

Yet when hospitalized patients are provided intervention via oral nutrition supplements, health economic research finds associated benefits:

Nutrition intervention can reduce hospital length of stay by an average of two days, and nutrition intervention has been shown to reduce patient hospitalization costs by 21.6%, or $4,734 per episode.

Additionally, there was a 6.7% reduction in the probability of 30-day readmission with patients who had at least one known subsequent readmission and were offered oral nutrition supplements during hospitalization.

“There is a growing body of evidence supporting the positive impact nutrition has on improving patient outcomes,” says hospitalist Melissa Parkhurst, MD, FHM, who serves as medical director for the University of Kansas Hospital’s hospitalist section and its nutrition support service. “We are seeing that early intervention can make a significant difference. As physicians, we need to work with the entire clinician team to ensure that nutrition is an integral part of our patients’ treatment plans.”

The alliance launched a website at www.malnutrition.org to provide hospital-based clinicians with the following resources:

• Research and fact sheets about malnutrition and the positive impact nutrition intervention has on patient care and outcomes;
• The Alliance Nutrition Toolkit, which facilitates clinician collaboration and nutrition integration; and
• Information about educational events, such as quick learning modules, continuing medical education (CME) programs.

The Alliance to Advance Patient Nutrition is made possible with support from Abbott’s nutrition business.

SHM announced in May the launch of a new interdisciplinary partnership, the Alliance to Advance Patient Nutrition, in conjunction with four other organizations. The alliance’s mission is to improve patient outcomes through nutrition intervention in the hospital.

Representing more than 100,000 dietitians, nurses, hospitalists, and other physicians and clinicians from across the nation, the following organizations have come together with SHM to champion for early nutrition screening, assessment, and intervention in hospitals:

• Academy of Medical-Surgical Nurses (AMSN);
• Academy of Nutrition and Dietetics (AND);
• American Society for Parenteral and Enteral Nutrition (ASPEN); and
• Abbott Nutrition.

Malnutrition increases costs, length of stay, and unfavorable outcomes. Properly addressing hospital malnutrition creates an opportunity to improve quality of care while also reducing healthcare costs. Additional clinical research finds that malnourished patients are two times more likely to develop a pressure ulcer, while patients with malnutrition have three times the rate of infection.

Yet when hospitalized patients are provided intervention via oral nutrition supplements, health economic research finds associated benefits:

Nutrition intervention can reduce hospital length of stay by an average of two days, and nutrition intervention has been shown to reduce patient hospitalization costs by 21.6%, or $4,734 per episode.

Additionally, there was a 6.7% reduction in the probability of 30-day readmission with patients who had at least one known subsequent readmission and were offered oral nutrition supplements during hospitalization.

“There is a growing body of evidence supporting the positive impact nutrition has on improving patient outcomes,” says hospitalist Melissa Parkhurst, MD, FHM, who serves as medical director for the University of Kansas Hospital’s hospitalist section and its nutrition support service. “We are seeing that early intervention can make a significant difference. As physicians, we need to work with the entire clinician team to ensure that nutrition is an integral part of our patients’ treatment plans.”

The alliance launched a website at www.malnutrition.org to provide hospital-based clinicians with the following resources:

• Research and fact sheets about malnutrition and the positive impact nutrition intervention has on patient care and outcomes;
• The Alliance Nutrition Toolkit, which facilitates clinician collaboration and nutrition integration; and
• Information about educational events, such as quick learning modules, continuing medical education (CME) programs.

The Alliance to Advance Patient Nutrition is made possible with support from Abbott’s nutrition business.

SHM announced in May the launch of a new interdisciplinary partnership, the Alliance to Advance Patient Nutrition, in conjunction with four other organizations. The alliance’s mission is to improve patient outcomes through nutrition intervention in the hospital.

Representing more than 100,000 dietitians, nurses, hospitalists, and other physicians and clinicians from across the nation, the following organizations have come together with SHM to champion for early nutrition screening, assessment, and intervention in hospitals:

• Academy of Medical-Surgical Nurses (AMSN);
• Academy of Nutrition and Dietetics (AND);
• American Society for Parenteral and Enteral Nutrition (ASPEN); and
• Abbott Nutrition.

Malnutrition increases costs, length of stay, and unfavorable outcomes. Properly addressing hospital malnutrition creates an opportunity to improve quality of care while also reducing healthcare costs. Additional clinical research finds that malnourished patients are two times more likely to develop a pressure ulcer, while patients with malnutrition have three times the rate of infection.

Yet when hospitalized patients are provided intervention via oral nutrition supplements, health economic research finds associated benefits:

Nutrition intervention can reduce hospital length of stay by an average of two days, and nutrition intervention has been shown to reduce patient hospitalization costs by 21.6%, or $4,734 per episode.

Additionally, there was a 6.7% reduction in the probability of 30-day readmission with patients who had at least one known subsequent readmission and were offered oral nutrition supplements during hospitalization.

“There is a growing body of evidence supporting the positive impact nutrition has on improving patient outcomes,” says hospitalist Melissa Parkhurst, MD, FHM, who serves as medical director for the University of Kansas Hospital’s hospitalist section and its nutrition support service. “We are seeing that early intervention can make a significant difference. As physicians, we need to work with the entire clinician team to ensure that nutrition is an integral part of our patients’ treatment plans.”

The alliance launched a website at www.malnutrition.org to provide hospital-based clinicians with the following resources:

• Research and fact sheets about malnutrition and the positive impact nutrition intervention has on patient care and outcomes;
• The Alliance Nutrition Toolkit, which facilitates clinician collaboration and nutrition integration; and
• Information about educational events, such as quick learning modules, continuing medical education (CME) programs.

The Alliance to Advance Patient Nutrition is made possible with support from Abbott’s nutrition business.

Clinical question: What is the impact of a peer benchmarking network on resource utilization in acute bronchiolitis?

Background: Acute bronchiolitis is the most common illness requiring hospitalization in children. Despite the publication of national evidence-based guidelines, variation and overuse of common therapies remains. Despite one report of successful implementation of evidence-based guidelines in a collaborative of freestanding children’s hospitals, most children are hospitalized outside of such institutions, and large-scale, lower-resource efforts have not been described.

Study design: Voluntary, quality-improvement (QI), and benchmarking collaborative.

Setting: Seventeen hospitals, including both community and freestanding children’s facilities.

Synopsis: Over a four-year period, data on 11,568 bronchiolitis hospitalizations were collected. The collaborative facilitated sharing of resources (e.g. scoring tools, guidelines), celebrated high performers on an annual basis, and encouraged regular data collection, primarily via conference calls and email. Notably, a common bundle of interventions were not used; groups worked on local improvement cycles, with only a few groups forming a small subcollaborative utilizing a shared pathway. A significant decrease in bronchodilator utilization and chest physiotherapy was seen over the course of the collaborative, although no change in chest radiography, steroid utilization, and RSV testing was noted.

This voluntary and low-resource effort by similarly motivated peers across a variety of inpatient settings demonstrated improvement over time. It is particularly notable as inpatient collaboratives with face-to-face meeting requirements, and annual fees, become more commonplace.

Study limitations include the lack of a conceptual model for studying contextual factors that might have led to improvement in the varied settings and secular changes over this time period. Additionally, EDs were not included in this initiative, which likely accounted for the lack of improvement in chest radiography and RSV testing. Nonetheless, scalable innovations such as this will become increasingly important as hospitalists search for value in health care.

Bottom line: Creating a national community of practice may reduce overutilization in bronchiolitis.

Citation: Ralston S, Garber M, Narang S, et al. Decreasing unnecessary utilization in acute bronchiolitis care: results from the Value in Inpatient Pediatrics Network. J Hosp Med. 2013;8(1):25-30.

Reviewed by Pediatric Editor Mark Shen, MD, SFHM, medical director of hospital medicine at Dell Children's Medical Center, Austin, Texas.

Clinical question: What is the impact of a peer benchmarking network on resource utilization in acute bronchiolitis?

Background: Acute bronchiolitis is the most common illness requiring hospitalization in children. Despite the publication of national evidence-based guidelines, variation and overuse of common therapies remains. Despite one report of successful implementation of evidence-based guidelines in a collaborative of freestanding children’s hospitals, most children are hospitalized outside of such institutions, and large-scale, lower-resource efforts have not been described.

Study design: Voluntary, quality-improvement (QI), and benchmarking collaborative.

Setting: Seventeen hospitals, including both community and freestanding children’s facilities.

Synopsis: Over a four-year period, data on 11,568 bronchiolitis hospitalizations were collected. The collaborative facilitated sharing of resources (e.g. scoring tools, guidelines), celebrated high performers on an annual basis, and encouraged regular data collection, primarily via conference calls and email. Notably, a common bundle of interventions were not used; groups worked on local improvement cycles, with only a few groups forming a small subcollaborative utilizing a shared pathway. A significant decrease in bronchodilator utilization and chest physiotherapy was seen over the course of the collaborative, although no change in chest radiography, steroid utilization, and RSV testing was noted.

This voluntary and low-resource effort by similarly motivated peers across a variety of inpatient settings demonstrated improvement over time. It is particularly notable as inpatient collaboratives with face-to-face meeting requirements, and annual fees, become more commonplace.

Study limitations include the lack of a conceptual model for studying contextual factors that might have led to improvement in the varied settings and secular changes over this time period. Additionally, EDs were not included in this initiative, which likely accounted for the lack of improvement in chest radiography and RSV testing. Nonetheless, scalable innovations such as this will become increasingly important as hospitalists search for value in health care.

Bottom line: Creating a national community of practice may reduce overutilization in bronchiolitis.

Citation: Ralston S, Garber M, Narang S, et al. Decreasing unnecessary utilization in acute bronchiolitis care: results from the Value in Inpatient Pediatrics Network. J Hosp Med. 2013;8(1):25-30.

Reviewed by Pediatric Editor Mark Shen, MD, SFHM, medical director of hospital medicine at Dell Children's Medical Center, Austin, Texas.

Clinical question: What is the impact of a peer benchmarking network on resource utilization in acute bronchiolitis?

Background: Acute bronchiolitis is the most common illness requiring hospitalization in children. Despite the publication of national evidence-based guidelines, variation and overuse of common therapies remains. Despite one report of successful implementation of evidence-based guidelines in a collaborative of freestanding children’s hospitals, most children are hospitalized outside of such institutions, and large-scale, lower-resource efforts have not been described.

Study design: Voluntary, quality-improvement (QI), and benchmarking collaborative.

Setting: Seventeen hospitals, including both community and freestanding children’s facilities.

Synopsis: Over a four-year period, data on 11,568 bronchiolitis hospitalizations were collected. The collaborative facilitated sharing of resources (e.g. scoring tools, guidelines), celebrated high performers on an annual basis, and encouraged regular data collection, primarily via conference calls and email. Notably, a common bundle of interventions were not used; groups worked on local improvement cycles, with only a few groups forming a small subcollaborative utilizing a shared pathway. A significant decrease in bronchodilator utilization and chest physiotherapy was seen over the course of the collaborative, although no change in chest radiography, steroid utilization, and RSV testing was noted.

This voluntary and low-resource effort by similarly motivated peers across a variety of inpatient settings demonstrated improvement over time. It is particularly notable as inpatient collaboratives with face-to-face meeting requirements, and annual fees, become more commonplace.

Study limitations include the lack of a conceptual model for studying contextual factors that might have led to improvement in the varied settings and secular changes over this time period. Additionally, EDs were not included in this initiative, which likely accounted for the lack of improvement in chest radiography and RSV testing. Nonetheless, scalable innovations such as this will become increasingly important as hospitalists search for value in health care.

Bottom line: Creating a national community of practice may reduce overutilization in bronchiolitis.

Citation: Ralston S, Garber M, Narang S, et al. Decreasing unnecessary utilization in acute bronchiolitis care: results from the Value in Inpatient Pediatrics Network. J Hosp Med. 2013;8(1):25-30.

Reviewed by Pediatric Editor Mark Shen, MD, SFHM, medical director of hospital medicine at Dell Children's Medical Center, Austin, Texas.

Case

A 25-year-old male with HIV/AIDS and a CD4 count of 65 cells/μL presents to the ED with intractable nausea and vomiting for one week. Laboratory evaluation revealed a white blood cell of 67,000 cells/mm3. An extended chemistry panel reveals creatinine 3.5 mg/dL, potassium 3.0 mmol/L, LDH 250 IU/L, and uric acid 5mg/dL. Calcium and phosphorus were both normal. The patient was admitted for further evaluation and management, and was later diagnosed with Burkitt’s lymphoma.

Overview

Tumor lysis syndrome (TLS) is an acute cell lysis of tumor cells with the release of cell content into circulation either spontaneously or in response to therapy, leading to hyperurecemia, hyperkalemia, hyperphosphatemia, and hypocalcemia.^1-3

TLS is one of the most common oncology emergencies encountered by hospitalists caring for patients with hematologic malignancies. The incidence and severity of TLS depend on the cell burden, cell proliferation rate, potential for cell lysis or chemo sensitivity, baseline clinical characteristics, and preventive measures taken (see Table 1).^2,4

TLS is classified as laboratory or clinical. Laboratory TLS is described as the presence of two or more of the following serum abnormalities at the same time, present within three days before or seven days after the start of therapy.⁵

• Uric acid >8 mg/dL (475.8 micromole/L) or 25% increase;
• Potassium >6 mEq/L (6 mmol/L) or 25% increase;
• Phosphorus >6.5 mg/dL (2.1 mmol/L) for children or >4.5 mg/dl (1.45 mmol/L) for adults or 25% increase; and
• Calcium >7 mg/dL (1.75 mmol/L) or 25% increase.

Clinical TLS is defined as laboratory TLS in association with increased creatinine levels, seizures, cardiac arrhythmias, or death (see Table 2).⁵

Pathogenesis

Tumor cell lysis releases DNA, cytokines, phosphate, and potassium. DNA is metabolized into adenosine and guanosine, which are then converted into xanthines. Xanthines are oxidized by xanthine oxidase into uric acid, which is then excreted through the kidneys.

TLS develops when the accumulation of xanthine, uric acid, potassium, and phosphorus exceeds the kidney’s capacity to excrete them. Cytokines cause hypotension, inflammation, and kidney injury, and worsen the kidney’s excretory capacity. Damage to the kidneys also occurs by renal precipitation of uric acid, xanthine, and calcium phosphate.⁴

Phosphorus concentrations in tumor cells are four times higher than in normal cells. When the calcium phosphorus product exceeds 60 mg2/dL2, there is an increased risk of calcium phosphate precipitation in the kidney tubules, which could lead to kidney failure. Accumulation of calcium phosphate product may also be cardiotoxic and can lead to cardiac arrhythmias. In addition, hyperphosphatemia can cause secondary hypocalcemia, which may lead to parasthesias, tetany, and cardiac arrhythmias.^2,4

TLS is most common in tumors with high proliferative rates and high tumor burden, such as acute lymphoblastic leukemia and Burkitt’s lymphoma, but it can occur with other hematologic malignancies, such as T-cell precursor acute lymphocytic leukemia (ALL), B-cell precursor ALL, acute myeloid leukemia (AML), chronic lymphocytic leukemia (CLL), anaplastic large cell lymphoma, and plasma cell disorders (e.g. multiple myeloma and plasmacytoma).^6,7 TLS has also been reported with the treatment of solid organ nonhematologic tumors (see Table 3).

In hematologic tumors, TLS frequently is associated with cytotoxic chemotherapy, and less frequently with glucocorticoid treatment, monoclonal antibodies (eg, rituximab, bortezomab, imatinib), and radiation therapy.^25-29

Patient factors, such as baseline kidney disease or lack of prophylactic/preventive measures for TLS, also increase the risk.4 TLS, however, can develop in patients classified as low risk (see Table 1.

click for large version

click for large version

TLS Prevention

Intravenous fluids. Every patient at intermediate or high risk of TLS should receive intravenous fluids (IVF) prior to cancer treatment; those at low risk may receive IVF based on the provider’s clinical judgment.³⁰ The purpose of administering IVF is to generate high urine output to reduce the risk of precipitation of uric acid in the renal tubules.³⁰ Both adults and children should receive approximately 2 to 3 L/m2 per day of IVF,30 and urine output should be maintained at 2 ml/kg/hr (or 4 to 6 ml/kg/hr for children <10kg).30 IVF should be cautiously administered in patients with renal insufficiency or heart failure, and diuretics may be used to maintain goal urine output. Recommended initial fluids are D51/4 normal saline, or normal saline for patients who are dehydrated or hyponatremic.³⁰

Allopurinol. Allopurinol is usually also administered to patients at risk for developing TLS.³⁰ Allopurinol inhibits the metabolism of hypoxanthine and xanthine to uric acid, which decreases the accumulation of uric acid in the renal tubules, thus preventing obstructive renal disease from precipitation of uric acid.⁴ The recommended dose of allopurinol is 100 mg/m2 every eight hours, and should not exceed 800 mg per day in adults. It should be started one to two days prior to induction chemotherapy and continued for three to seven days after the treatment and until uric acid levels and other electrolyte levels have returned to normal. The dose is adjusted to 50 mg/m2 every eight hours in patients with kidney failure.³⁰

In some cases, allopurinol can lead to increased levels of xanthine crystals in the renal tubules, leading to acute kidney injury. Also, allopurinol does not have any effect on uric acid that has already been formed, so patients with elevated uric acid levels prior to the initiation of cancer therapy will not have any reduction in the levels of uric acid. Allopurinol reduces the degradation of other purines, so it can cause toxicity in patients on azathioprine and 6-mercaptopurine if the doses of these medications are not adjusted.

Rasburicase. Rasburicase is a recombinant urate oxidase, derived from aspergillus favus, which catalyzes the breakdown of uric acid to allantoin, which is a water-soluble product. Rasburicase is recommended as a first-line treatment for patients at high risk for clinical TLS.³⁰ Rasburicase has an earlier onset than allopurinol and rapidly decreases serum levels of uric acid within four hours of administration.^30,31 The recommended dose is 0.10 to 0.20 mg/kg once a day for five days in adults.³⁰

A Phase III trial compared the efficiency and safety of rasburicase to rasburicase with allopurinol or allopurinol alone.³² A significantly higher normalization of uric acid was found in patients on rasburicase compared to allopurinol alone. The incidence of laboratory TLS was also significantly lower with rasburicase alone compared to allopurinol alone, and was even lower with allopurinol plus rasburicase. The incidence of acute kidney injury was the same with rasburicase alone or allopurinol alone but was higher with rasburicase plus allopurinol.

Serum uric acid, phosphorus, potassium, and calcium need to be monitored every four hours for 24 hours after the completion of chemotherapy in patients on rasburicase.⁴ The sample of blood drawn to check the uric acid levels has to be placed on ice and processed within four hours in order to avoid falsely lower levels of uric acid due to the conversion of uric acid to allantoin. Rasburicase is contraindicated in patients with G6PD deficiency and pregnant women, because one of the byproducts of uric acid breakdown is hydrogen peroxide, which can cause severe hemolysis and the formation of methemoglobin in these patients.³⁰

Rasburicase has been approved for use in both children and adults, but there is more evidence for the use in children. Rasburicase has a black-box label for patients with anaphylaxis, methemoglobinemia, hemolysis, and hemoglobinuria, and there is a recommendation to check G6PD deficiency before use in high-risk patients.³⁰

TLS Treatment

Alkalinization. Alkalinization of urine is controversial in the management of TLS. Urine alkalinization increases uric acid solubility but causes hyperphosphatemia and decreases calcium phosphate solubility, which can then deposit in the kidney once cancer treatment starts. Of note, hyperphosphatemia is much more difficult to correct than high levels of uric acid, and there are no clinical trials proving the superiority of urine alkalinization over normal saline.

Normalization of electrolytes. Electrolyte abnormalities should be corrected to avoid arrhythmias and seizures. Phosphorus levels >6.5 mg/dl (2.1 mmol/L) should be managed by restricting phosphorus intake, and by the use of phosphate binders (calcium acetate, calcium carbonate, sevelamer, lanthanum, or aluminum hydroxide). Aluminum hydroxide should be avoided in patients with renal insufficiency. In severe cases of hyperphosphatemia, dialysis should be considered.

Symptomatic hypocalcemia should be treated with calcium gluconate if changes are present on the electrocardiography (ECG). Hypocalcemia in the presence of hyperphosphatemia should be treated only in patients with tetany or cardiac arrhythmias; otherwise, hypocalcemia should not be treated until hyperphosphatemia has been corrected.

In cases of hyperkalemia, patients should be placed on a cardiac monitor and stabilized with calcium gluconate; kayexalate should be administered to reduce total body potassium. Other interventions, such as intravenous insulin given with dextrose, sodium bicarbonate, and albuterol, have a temporary effect on hyperkalemia and can be used as adjunct treatments in patients with severe hyperkalemia (>7). Hemodialysis should be strongly considered in severe cases of hyperkalemia, particularly in patients with persistently elevated potassium levels despite other treatments.

Back to the Case

Our patient was started on IVFs with close monitoring of his urine output. He was considered intermediate risk for developing TLS. Allopurinol, renally dosed, was administered for two days prior to initiating treatment with rituximab plus chemotherapy. His chemistry panel was monitored daily and he did not develop any form of TLS.

Bottom Line

TLS is a common oncology emergency in patients with hematologic malignancies. Preventative measures include starting IVF prior to cancer treatment, and administering allopurinol and/or rasburicase to patients at risk of developing TLS. Treatment should include normalizing electrolytes to avoid arrhythmias and seizures.

Dr. Akwe is assistant professor of medicine at the Emory University School of Medicine and a clinical instructor of medicine at the Morehouse School of Medicine, both in Atlanta. Dr. Smith is an assistant director for education in the division of hospital medicine at Emory. Both work as hospitalists at the Atlanta VA Medical Center.

References

1. Abu-Alfa AK, Younes A. Tumor lysis syndrome and acute kidney injury: evaluation, prevention, and management. Am J Kidney Dis. 2010;55:Suppl 3:S1-S13.
2. Cairo MS, Coiffier B, Reiter A, Younes A. Recommendations for the evaluation of risk and prophylaxis of tumour lysis syndrome (TLS) in adults and children with malignant diseases: an expert TLS panel consensus. Br J Haematol. 2010;149:578-586.
3. Gertz MA. Managing tumor lysis syndrome in 2010. Leuk Lymphoma. 2010;51:179-180.
4. Howard SC, Jones DP, Pui CH. The tumor lysis syndrome. N Engl J Med. 2011;364:1844.
5. Cairo MS, Bishop M. Tumour lysis syndrome: new therapeutic strategies and classification. Br J Haematol. 2004;127:3.
6. Wössmann W, Schrappe M, Meyer U, et al. Incidence of tumor lysis syndrome in children with advanced stage Burkitt’s lymphoma/leukemia before and after introduction of prophylactic use of urate oxidase. Ann Hematol. 2003;82:160.
7. Hussain K, Mazza JJ, Clouse LH. Tumor lysis syndrome (TLS) following fludarabine therapy Gemici C. Tumor lysis syndrome in solid tumors. J Clin Oncol. 2009;27:2738-2739
8. Rostom AY, El-Hussainy G, Kandil A, Allam A. Tumor lysis syndrome following hemi-body irradiation for metastatic breast cancer. Ann Oncol. 2000;11:1349.
9. Drakos P, Bar-Ziv J, Catane R. Tumor lysis syndrome in nonhematologic malignancies. Report of a case and review of the literature. Am J Clin Oncol. 1994;17:502.
10. Baeksgaard L, Sørensen JB. Acute tumor lysis syndrome in solid tumors—a case report and review of the literature. Cancer Chemother Pharmacol. 2003;51:187.
11. Kalemkerian GP, Darwish B, Varterasian ML. Tumor lysis syndrome in small cell carcinoma and other solid tumors. Am J Med. 1997;103:363.
12. Noh GY, Choe DH, Kim CH, Lee JC. Fatal tumor lysis syndrome during radiotherapy for non-small-cell lung cancer. J Clin Oncol. 2008;26:6005-6006.
13. Pentheroudakis G, O’Neill VJ, Vasey P, Kaye SB. Spontaneous acute tumour lysis syndrome in patients with metastatic germ cell tumours. Report of two cases. Support Care Cancer. 2001;9:554.
14. Joshita S, Yoshizawa K, Sano K, et al., A patient with advanced hepatocellular carcinoma treated with sorafenib tosylate showed massive tumor lysis with avoidance of tumor lysis syndrome. Intern Med. 2010;49:991-994.
15. Huang WS, Yang CH. Sorafenib-induced tumor lysis syndrome in an advanced hepatocellular carcinoma patient. World J Gastroenterol. 2009;15:4464-4466.
16. Bilgrami SF, Fallon BG. Tumor lysis syndrome after combination chemotherapy for ovarian cancer. Med Pediatr Oncol. 1993;21:521.
17. Chan JK, Lin SS, McMeekin DS, Berman ML. Patients with malignancy requiring urgent therapy: CASE 3. Tumor lysis syndrome associated with chemotherapy in ovarian cancer. J Clin Oncol. 2005;23:6794.
18. Godoy H, Kesterson JP, Lele S. Tumor lysis syndrome associated with carboplatin and paclitaxel in a woman with recurrent endometrial cancer. Int J Gynaecol Obstet. 2010;109:254.
19. Shamseddine AI, Khalil AM, Wehbeh MH. Acute tumor lysis syndrome with squamous cell carcinoma of the vulva. Gynecol Oncol 1993;51:258
20. Pinder EM, Atwal GS, Ayantunde AA, et al. Tumour lysis syndrome occurring in a patient with metastatic gastrointestinal stromal tumour treated with Glivec (imatinib mesylate, Gleevec, STI571). Sarcoma. 2007;2007:82012.
21. Krishnan G, D’Silva K, Al-Janadi A. Cetuximab-related tumor lysis syndrome in metastatic colon carcinoma. J Clin Oncol. 2008;26:2406-2408.
22. Oztop I, Demirkan B, Yaren A, et al. Rapid tumor lysis syndrome in a patient with metastatic colon cancer as a complication of treatment with 5-fluorouracil/leucoverin and irinotecan. Tumori. 2004;90:514.
23. Lin CJ, Lim KH, Cheng YC, et al. Tumor lysis syndrome after treatment with gemcitabine for metastatic transitional cell carcinoma. Med Oncol. 2007;24:455.
24. Malik IA, Abubakar S, Alam F, Khan A. Dexamethasone-induced tumor lysis syndrome in high-grade non-Hodgkin’s lymphoma. South Med J. 1994;87:409.
25. Jabr FI. Acute tumor lysis syndrome induced by rituximab in diffuse large B-cell lymphoma. Int J Hematol. 2005;82:312.
26. Sezer O, Vesole DH, Singhal S, et al. Bortezomib-induced tumor lysis syndrome in multiple myeloma. Clin Lymphoma Myeloma. 2006;7:233.
27. Jensen M, Winkler U, Manzke O, et al. Rapid tumor lysis in a patient with B-cell chronic lymphocytic leukemia and lymphocytosis treated with an anti-CD20 monoclonal antibody (IDEC-C2B8, rituximab). Ann Hematol. 1998;77:89.
28. Linck D, Basara N, Tran V, et al. Peracute onset of severe tumor lysis syndrome immediately after 4 Gy fractionated TBI as part of reduced intensity preparative regimen in a patient with T-ALL with high tumor burden. Bone Marrow Transplant. 2003;31:935.
29. Coiffier B, Altman A, Pui CH, Younes A, Cairo MS. Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review. J Clin Oncol. 2008;26(16):2767-2778. [Erratum, J Clin Oncol. 2010;28:708.]
30. Cheuk DK, Chiang AK, Chan GC, Ha SY. Urate oxidase for the prevention and treatment of tumor lysis syndrome in children with cancer. Cochrane Database Syst Rev. 2010;(6):CD006945.
31. Cortes J, Moore JO, Maziarz RT, et al. Control of plasma uric acid in adults at risk for tumor Lysis syndrome: efficacy and safety of rasburicase alone and rasburicase followed by allopurinol compared with allopurinol alone—results of a multicenter phase III study. J Clin Oncol. 2010;28:4207.

Case

A 25-year-old male with HIV/AIDS and a CD4 count of 65 cells/μL presents to the ED with intractable nausea and vomiting for one week. Laboratory evaluation revealed a white blood cell of 67,000 cells/mm3. An extended chemistry panel reveals creatinine 3.5 mg/dL, potassium 3.0 mmol/L, LDH 250 IU/L, and uric acid 5mg/dL. Calcium and phosphorus were both normal. The patient was admitted for further evaluation and management, and was later diagnosed with Burkitt’s lymphoma.

Overview

Tumor lysis syndrome (TLS) is an acute cell lysis of tumor cells with the release of cell content into circulation either spontaneously or in response to therapy, leading to hyperurecemia, hyperkalemia, hyperphosphatemia, and hypocalcemia.^1-3

TLS is one of the most common oncology emergencies encountered by hospitalists caring for patients with hematologic malignancies. The incidence and severity of TLS depend on the cell burden, cell proliferation rate, potential for cell lysis or chemo sensitivity, baseline clinical characteristics, and preventive measures taken (see Table 1).^2,4

TLS is classified as laboratory or clinical. Laboratory TLS is described as the presence of two or more of the following serum abnormalities at the same time, present within three days before or seven days after the start of therapy.⁵

• Uric acid >8 mg/dL (475.8 micromole/L) or 25% increase;
• Potassium >6 mEq/L (6 mmol/L) or 25% increase;
• Phosphorus >6.5 mg/dL (2.1 mmol/L) for children or >4.5 mg/dl (1.45 mmol/L) for adults or 25% increase; and
• Calcium >7 mg/dL (1.75 mmol/L) or 25% increase.

Clinical TLS is defined as laboratory TLS in association with increased creatinine levels, seizures, cardiac arrhythmias, or death (see Table 2).⁵

Pathogenesis

Tumor cell lysis releases DNA, cytokines, phosphate, and potassium. DNA is metabolized into adenosine and guanosine, which are then converted into xanthines. Xanthines are oxidized by xanthine oxidase into uric acid, which is then excreted through the kidneys.

TLS develops when the accumulation of xanthine, uric acid, potassium, and phosphorus exceeds the kidney’s capacity to excrete them. Cytokines cause hypotension, inflammation, and kidney injury, and worsen the kidney’s excretory capacity. Damage to the kidneys also occurs by renal precipitation of uric acid, xanthine, and calcium phosphate.⁴

Phosphorus concentrations in tumor cells are four times higher than in normal cells. When the calcium phosphorus product exceeds 60 mg2/dL2, there is an increased risk of calcium phosphate precipitation in the kidney tubules, which could lead to kidney failure. Accumulation of calcium phosphate product may also be cardiotoxic and can lead to cardiac arrhythmias. In addition, hyperphosphatemia can cause secondary hypocalcemia, which may lead to parasthesias, tetany, and cardiac arrhythmias.^2,4

TLS is most common in tumors with high proliferative rates and high tumor burden, such as acute lymphoblastic leukemia and Burkitt’s lymphoma, but it can occur with other hematologic malignancies, such as T-cell precursor acute lymphocytic leukemia (ALL), B-cell precursor ALL, acute myeloid leukemia (AML), chronic lymphocytic leukemia (CLL), anaplastic large cell lymphoma, and plasma cell disorders (e.g. multiple myeloma and plasmacytoma).^6,7 TLS has also been reported with the treatment of solid organ nonhematologic tumors (see Table 3).

In hematologic tumors, TLS frequently is associated with cytotoxic chemotherapy, and less frequently with glucocorticoid treatment, monoclonal antibodies (eg, rituximab, bortezomab, imatinib), and radiation therapy.^25-29

Patient factors, such as baseline kidney disease or lack of prophylactic/preventive measures for TLS, also increase the risk.4 TLS, however, can develop in patients classified as low risk (see Table 1.

click for large version

click for large version

TLS Prevention

Intravenous fluids. Every patient at intermediate or high risk of TLS should receive intravenous fluids (IVF) prior to cancer treatment; those at low risk may receive IVF based on the provider’s clinical judgment.³⁰ The purpose of administering IVF is to generate high urine output to reduce the risk of precipitation of uric acid in the renal tubules.³⁰ Both adults and children should receive approximately 2 to 3 L/m2 per day of IVF,30 and urine output should be maintained at 2 ml/kg/hr (or 4 to 6 ml/kg/hr for children <10kg).30 IVF should be cautiously administered in patients with renal insufficiency or heart failure, and diuretics may be used to maintain goal urine output. Recommended initial fluids are D51/4 normal saline, or normal saline for patients who are dehydrated or hyponatremic.³⁰

Allopurinol. Allopurinol is usually also administered to patients at risk for developing TLS.³⁰ Allopurinol inhibits the metabolism of hypoxanthine and xanthine to uric acid, which decreases the accumulation of uric acid in the renal tubules, thus preventing obstructive renal disease from precipitation of uric acid.⁴ The recommended dose of allopurinol is 100 mg/m2 every eight hours, and should not exceed 800 mg per day in adults. It should be started one to two days prior to induction chemotherapy and continued for three to seven days after the treatment and until uric acid levels and other electrolyte levels have returned to normal. The dose is adjusted to 50 mg/m2 every eight hours in patients with kidney failure.³⁰

In some cases, allopurinol can lead to increased levels of xanthine crystals in the renal tubules, leading to acute kidney injury. Also, allopurinol does not have any effect on uric acid that has already been formed, so patients with elevated uric acid levels prior to the initiation of cancer therapy will not have any reduction in the levels of uric acid. Allopurinol reduces the degradation of other purines, so it can cause toxicity in patients on azathioprine and 6-mercaptopurine if the doses of these medications are not adjusted.

Rasburicase. Rasburicase is a recombinant urate oxidase, derived from aspergillus favus, which catalyzes the breakdown of uric acid to allantoin, which is a water-soluble product. Rasburicase is recommended as a first-line treatment for patients at high risk for clinical TLS.³⁰ Rasburicase has an earlier onset than allopurinol and rapidly decreases serum levels of uric acid within four hours of administration.^30,31 The recommended dose is 0.10 to 0.20 mg/kg once a day for five days in adults.³⁰

A Phase III trial compared the efficiency and safety of rasburicase to rasburicase with allopurinol or allopurinol alone.³² A significantly higher normalization of uric acid was found in patients on rasburicase compared to allopurinol alone. The incidence of laboratory TLS was also significantly lower with rasburicase alone compared to allopurinol alone, and was even lower with allopurinol plus rasburicase. The incidence of acute kidney injury was the same with rasburicase alone or allopurinol alone but was higher with rasburicase plus allopurinol.

Serum uric acid, phosphorus, potassium, and calcium need to be monitored every four hours for 24 hours after the completion of chemotherapy in patients on rasburicase.⁴ The sample of blood drawn to check the uric acid levels has to be placed on ice and processed within four hours in order to avoid falsely lower levels of uric acid due to the conversion of uric acid to allantoin. Rasburicase is contraindicated in patients with G6PD deficiency and pregnant women, because one of the byproducts of uric acid breakdown is hydrogen peroxide, which can cause severe hemolysis and the formation of methemoglobin in these patients.³⁰

Rasburicase has been approved for use in both children and adults, but there is more evidence for the use in children. Rasburicase has a black-box label for patients with anaphylaxis, methemoglobinemia, hemolysis, and hemoglobinuria, and there is a recommendation to check G6PD deficiency before use in high-risk patients.³⁰

TLS Treatment

Alkalinization. Alkalinization of urine is controversial in the management of TLS. Urine alkalinization increases uric acid solubility but causes hyperphosphatemia and decreases calcium phosphate solubility, which can then deposit in the kidney once cancer treatment starts. Of note, hyperphosphatemia is much more difficult to correct than high levels of uric acid, and there are no clinical trials proving the superiority of urine alkalinization over normal saline.

Normalization of electrolytes. Electrolyte abnormalities should be corrected to avoid arrhythmias and seizures. Phosphorus levels >6.5 mg/dl (2.1 mmol/L) should be managed by restricting phosphorus intake, and by the use of phosphate binders (calcium acetate, calcium carbonate, sevelamer, lanthanum, or aluminum hydroxide). Aluminum hydroxide should be avoided in patients with renal insufficiency. In severe cases of hyperphosphatemia, dialysis should be considered.

Symptomatic hypocalcemia should be treated with calcium gluconate if changes are present on the electrocardiography (ECG). Hypocalcemia in the presence of hyperphosphatemia should be treated only in patients with tetany or cardiac arrhythmias; otherwise, hypocalcemia should not be treated until hyperphosphatemia has been corrected.

In cases of hyperkalemia, patients should be placed on a cardiac monitor and stabilized with calcium gluconate; kayexalate should be administered to reduce total body potassium. Other interventions, such as intravenous insulin given with dextrose, sodium bicarbonate, and albuterol, have a temporary effect on hyperkalemia and can be used as adjunct treatments in patients with severe hyperkalemia (>7). Hemodialysis should be strongly considered in severe cases of hyperkalemia, particularly in patients with persistently elevated potassium levels despite other treatments.

Back to the Case

Our patient was started on IVFs with close monitoring of his urine output. He was considered intermediate risk for developing TLS. Allopurinol, renally dosed, was administered for two days prior to initiating treatment with rituximab plus chemotherapy. His chemistry panel was monitored daily and he did not develop any form of TLS.

Bottom Line

TLS is a common oncology emergency in patients with hematologic malignancies. Preventative measures include starting IVF prior to cancer treatment, and administering allopurinol and/or rasburicase to patients at risk of developing TLS. Treatment should include normalizing electrolytes to avoid arrhythmias and seizures.

Dr. Akwe is assistant professor of medicine at the Emory University School of Medicine and a clinical instructor of medicine at the Morehouse School of Medicine, both in Atlanta. Dr. Smith is an assistant director for education in the division of hospital medicine at Emory. Both work as hospitalists at the Atlanta VA Medical Center.

References

1. Abu-Alfa AK, Younes A. Tumor lysis syndrome and acute kidney injury: evaluation, prevention, and management. Am J Kidney Dis. 2010;55:Suppl 3:S1-S13.
2. Cairo MS, Coiffier B, Reiter A, Younes A. Recommendations for the evaluation of risk and prophylaxis of tumour lysis syndrome (TLS) in adults and children with malignant diseases: an expert TLS panel consensus. Br J Haematol. 2010;149:578-586.
3. Gertz MA. Managing tumor lysis syndrome in 2010. Leuk Lymphoma. 2010;51:179-180.
4. Howard SC, Jones DP, Pui CH. The tumor lysis syndrome. N Engl J Med. 2011;364:1844.
5. Cairo MS, Bishop M. Tumour lysis syndrome: new therapeutic strategies and classification. Br J Haematol. 2004;127:3.
6. Wössmann W, Schrappe M, Meyer U, et al. Incidence of tumor lysis syndrome in children with advanced stage Burkitt’s lymphoma/leukemia before and after introduction of prophylactic use of urate oxidase. Ann Hematol. 2003;82:160.
7. Hussain K, Mazza JJ, Clouse LH. Tumor lysis syndrome (TLS) following fludarabine therapy Gemici C. Tumor lysis syndrome in solid tumors. J Clin Oncol. 2009;27:2738-2739
8. Rostom AY, El-Hussainy G, Kandil A, Allam A. Tumor lysis syndrome following hemi-body irradiation for metastatic breast cancer. Ann Oncol. 2000;11:1349.
9. Drakos P, Bar-Ziv J, Catane R. Tumor lysis syndrome in nonhematologic malignancies. Report of a case and review of the literature. Am J Clin Oncol. 1994;17:502.
10. Baeksgaard L, Sørensen JB. Acute tumor lysis syndrome in solid tumors—a case report and review of the literature. Cancer Chemother Pharmacol. 2003;51:187.
11. Kalemkerian GP, Darwish B, Varterasian ML. Tumor lysis syndrome in small cell carcinoma and other solid tumors. Am J Med. 1997;103:363.
12. Noh GY, Choe DH, Kim CH, Lee JC. Fatal tumor lysis syndrome during radiotherapy for non-small-cell lung cancer. J Clin Oncol. 2008;26:6005-6006.
13. Pentheroudakis G, O’Neill VJ, Vasey P, Kaye SB. Spontaneous acute tumour lysis syndrome in patients with metastatic germ cell tumours. Report of two cases. Support Care Cancer. 2001;9:554.
14. Joshita S, Yoshizawa K, Sano K, et al., A patient with advanced hepatocellular carcinoma treated with sorafenib tosylate showed massive tumor lysis with avoidance of tumor lysis syndrome. Intern Med. 2010;49:991-994.
15. Huang WS, Yang CH. Sorafenib-induced tumor lysis syndrome in an advanced hepatocellular carcinoma patient. World J Gastroenterol. 2009;15:4464-4466.
16. Bilgrami SF, Fallon BG. Tumor lysis syndrome after combination chemotherapy for ovarian cancer. Med Pediatr Oncol. 1993;21:521.
17. Chan JK, Lin SS, McMeekin DS, Berman ML. Patients with malignancy requiring urgent therapy: CASE 3. Tumor lysis syndrome associated with chemotherapy in ovarian cancer. J Clin Oncol. 2005;23:6794.
18. Godoy H, Kesterson JP, Lele S. Tumor lysis syndrome associated with carboplatin and paclitaxel in a woman with recurrent endometrial cancer. Int J Gynaecol Obstet. 2010;109:254.
19. Shamseddine AI, Khalil AM, Wehbeh MH. Acute tumor lysis syndrome with squamous cell carcinoma of the vulva. Gynecol Oncol 1993;51:258
20. Pinder EM, Atwal GS, Ayantunde AA, et al. Tumour lysis syndrome occurring in a patient with metastatic gastrointestinal stromal tumour treated with Glivec (imatinib mesylate, Gleevec, STI571). Sarcoma. 2007;2007:82012.
21. Krishnan G, D’Silva K, Al-Janadi A. Cetuximab-related tumor lysis syndrome in metastatic colon carcinoma. J Clin Oncol. 2008;26:2406-2408.
22. Oztop I, Demirkan B, Yaren A, et al. Rapid tumor lysis syndrome in a patient with metastatic colon cancer as a complication of treatment with 5-fluorouracil/leucoverin and irinotecan. Tumori. 2004;90:514.
23. Lin CJ, Lim KH, Cheng YC, et al. Tumor lysis syndrome after treatment with gemcitabine for metastatic transitional cell carcinoma. Med Oncol. 2007;24:455.
24. Malik IA, Abubakar S, Alam F, Khan A. Dexamethasone-induced tumor lysis syndrome in high-grade non-Hodgkin’s lymphoma. South Med J. 1994;87:409.
25. Jabr FI. Acute tumor lysis syndrome induced by rituximab in diffuse large B-cell lymphoma. Int J Hematol. 2005;82:312.
26. Sezer O, Vesole DH, Singhal S, et al. Bortezomib-induced tumor lysis syndrome in multiple myeloma. Clin Lymphoma Myeloma. 2006;7:233.
27. Jensen M, Winkler U, Manzke O, et al. Rapid tumor lysis in a patient with B-cell chronic lymphocytic leukemia and lymphocytosis treated with an anti-CD20 monoclonal antibody (IDEC-C2B8, rituximab). Ann Hematol. 1998;77:89.
28. Linck D, Basara N, Tran V, et al. Peracute onset of severe tumor lysis syndrome immediately after 4 Gy fractionated TBI as part of reduced intensity preparative regimen in a patient with T-ALL with high tumor burden. Bone Marrow Transplant. 2003;31:935.
29. Coiffier B, Altman A, Pui CH, Younes A, Cairo MS. Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review. J Clin Oncol. 2008;26(16):2767-2778. [Erratum, J Clin Oncol. 2010;28:708.]
30. Cheuk DK, Chiang AK, Chan GC, Ha SY. Urate oxidase for the prevention and treatment of tumor lysis syndrome in children with cancer. Cochrane Database Syst Rev. 2010;(6):CD006945.
31. Cortes J, Moore JO, Maziarz RT, et al. Control of plasma uric acid in adults at risk for tumor Lysis syndrome: efficacy and safety of rasburicase alone and rasburicase followed by allopurinol compared with allopurinol alone—results of a multicenter phase III study. J Clin Oncol. 2010;28:4207.

Case

A 25-year-old male with HIV/AIDS and a CD4 count of 65 cells/μL presents to the ED with intractable nausea and vomiting for one week. Laboratory evaluation revealed a white blood cell of 67,000 cells/mm3. An extended chemistry panel reveals creatinine 3.5 mg/dL, potassium 3.0 mmol/L, LDH 250 IU/L, and uric acid 5mg/dL. Calcium and phosphorus were both normal. The patient was admitted for further evaluation and management, and was later diagnosed with Burkitt’s lymphoma.

Overview

Tumor lysis syndrome (TLS) is an acute cell lysis of tumor cells with the release of cell content into circulation either spontaneously or in response to therapy, leading to hyperurecemia, hyperkalemia, hyperphosphatemia, and hypocalcemia.^1-3

TLS is one of the most common oncology emergencies encountered by hospitalists caring for patients with hematologic malignancies. The incidence and severity of TLS depend on the cell burden, cell proliferation rate, potential for cell lysis or chemo sensitivity, baseline clinical characteristics, and preventive measures taken (see Table 1).^2,4

TLS is classified as laboratory or clinical. Laboratory TLS is described as the presence of two or more of the following serum abnormalities at the same time, present within three days before or seven days after the start of therapy.⁵

• Uric acid >8 mg/dL (475.8 micromole/L) or 25% increase;
• Potassium >6 mEq/L (6 mmol/L) or 25% increase;
• Phosphorus >6.5 mg/dL (2.1 mmol/L) for children or >4.5 mg/dl (1.45 mmol/L) for adults or 25% increase; and
• Calcium >7 mg/dL (1.75 mmol/L) or 25% increase.

Clinical TLS is defined as laboratory TLS in association with increased creatinine levels, seizures, cardiac arrhythmias, or death (see Table 2).⁵

Pathogenesis

Tumor cell lysis releases DNA, cytokines, phosphate, and potassium. DNA is metabolized into adenosine and guanosine, which are then converted into xanthines. Xanthines are oxidized by xanthine oxidase into uric acid, which is then excreted through the kidneys.

TLS develops when the accumulation of xanthine, uric acid, potassium, and phosphorus exceeds the kidney’s capacity to excrete them. Cytokines cause hypotension, inflammation, and kidney injury, and worsen the kidney’s excretory capacity. Damage to the kidneys also occurs by renal precipitation of uric acid, xanthine, and calcium phosphate.⁴

Phosphorus concentrations in tumor cells are four times higher than in normal cells. When the calcium phosphorus product exceeds 60 mg2/dL2, there is an increased risk of calcium phosphate precipitation in the kidney tubules, which could lead to kidney failure. Accumulation of calcium phosphate product may also be cardiotoxic and can lead to cardiac arrhythmias. In addition, hyperphosphatemia can cause secondary hypocalcemia, which may lead to parasthesias, tetany, and cardiac arrhythmias.^2,4

TLS is most common in tumors with high proliferative rates and high tumor burden, such as acute lymphoblastic leukemia and Burkitt’s lymphoma, but it can occur with other hematologic malignancies, such as T-cell precursor acute lymphocytic leukemia (ALL), B-cell precursor ALL, acute myeloid leukemia (AML), chronic lymphocytic leukemia (CLL), anaplastic large cell lymphoma, and plasma cell disorders (e.g. multiple myeloma and plasmacytoma).^6,7 TLS has also been reported with the treatment of solid organ nonhematologic tumors (see Table 3).

In hematologic tumors, TLS frequently is associated with cytotoxic chemotherapy, and less frequently with glucocorticoid treatment, monoclonal antibodies (eg, rituximab, bortezomab, imatinib), and radiation therapy.^25-29

Patient factors, such as baseline kidney disease or lack of prophylactic/preventive measures for TLS, also increase the risk.4 TLS, however, can develop in patients classified as low risk (see Table 1.

click for large version

click for large version

TLS Prevention

Intravenous fluids. Every patient at intermediate or high risk of TLS should receive intravenous fluids (IVF) prior to cancer treatment; those at low risk may receive IVF based on the provider’s clinical judgment.³⁰ The purpose of administering IVF is to generate high urine output to reduce the risk of precipitation of uric acid in the renal tubules.³⁰ Both adults and children should receive approximately 2 to 3 L/m2 per day of IVF,30 and urine output should be maintained at 2 ml/kg/hr (or 4 to 6 ml/kg/hr for children <10kg).30 IVF should be cautiously administered in patients with renal insufficiency or heart failure, and diuretics may be used to maintain goal urine output. Recommended initial fluids are D51/4 normal saline, or normal saline for patients who are dehydrated or hyponatremic.³⁰

Allopurinol. Allopurinol is usually also administered to patients at risk for developing TLS.³⁰ Allopurinol inhibits the metabolism of hypoxanthine and xanthine to uric acid, which decreases the accumulation of uric acid in the renal tubules, thus preventing obstructive renal disease from precipitation of uric acid.⁴ The recommended dose of allopurinol is 100 mg/m2 every eight hours, and should not exceed 800 mg per day in adults. It should be started one to two days prior to induction chemotherapy and continued for three to seven days after the treatment and until uric acid levels and other electrolyte levels have returned to normal. The dose is adjusted to 50 mg/m2 every eight hours in patients with kidney failure.³⁰

In some cases, allopurinol can lead to increased levels of xanthine crystals in the renal tubules, leading to acute kidney injury. Also, allopurinol does not have any effect on uric acid that has already been formed, so patients with elevated uric acid levels prior to the initiation of cancer therapy will not have any reduction in the levels of uric acid. Allopurinol reduces the degradation of other purines, so it can cause toxicity in patients on azathioprine and 6-mercaptopurine if the doses of these medications are not adjusted.

Rasburicase. Rasburicase is a recombinant urate oxidase, derived from aspergillus favus, which catalyzes the breakdown of uric acid to allantoin, which is a water-soluble product. Rasburicase is recommended as a first-line treatment for patients at high risk for clinical TLS.³⁰ Rasburicase has an earlier onset than allopurinol and rapidly decreases serum levels of uric acid within four hours of administration.^30,31 The recommended dose is 0.10 to 0.20 mg/kg once a day for five days in adults.³⁰

A Phase III trial compared the efficiency and safety of rasburicase to rasburicase with allopurinol or allopurinol alone.³² A significantly higher normalization of uric acid was found in patients on rasburicase compared to allopurinol alone. The incidence of laboratory TLS was also significantly lower with rasburicase alone compared to allopurinol alone, and was even lower with allopurinol plus rasburicase. The incidence of acute kidney injury was the same with rasburicase alone or allopurinol alone but was higher with rasburicase plus allopurinol.

Serum uric acid, phosphorus, potassium, and calcium need to be monitored every four hours for 24 hours after the completion of chemotherapy in patients on rasburicase.⁴ The sample of blood drawn to check the uric acid levels has to be placed on ice and processed within four hours in order to avoid falsely lower levels of uric acid due to the conversion of uric acid to allantoin. Rasburicase is contraindicated in patients with G6PD deficiency and pregnant women, because one of the byproducts of uric acid breakdown is hydrogen peroxide, which can cause severe hemolysis and the formation of methemoglobin in these patients.³⁰

Rasburicase has been approved for use in both children and adults, but there is more evidence for the use in children. Rasburicase has a black-box label for patients with anaphylaxis, methemoglobinemia, hemolysis, and hemoglobinuria, and there is a recommendation to check G6PD deficiency before use in high-risk patients.³⁰

TLS Treatment

Alkalinization. Alkalinization of urine is controversial in the management of TLS. Urine alkalinization increases uric acid solubility but causes hyperphosphatemia and decreases calcium phosphate solubility, which can then deposit in the kidney once cancer treatment starts. Of note, hyperphosphatemia is much more difficult to correct than high levels of uric acid, and there are no clinical trials proving the superiority of urine alkalinization over normal saline.

Normalization of electrolytes. Electrolyte abnormalities should be corrected to avoid arrhythmias and seizures. Phosphorus levels >6.5 mg/dl (2.1 mmol/L) should be managed by restricting phosphorus intake, and by the use of phosphate binders (calcium acetate, calcium carbonate, sevelamer, lanthanum, or aluminum hydroxide). Aluminum hydroxide should be avoided in patients with renal insufficiency. In severe cases of hyperphosphatemia, dialysis should be considered.

Symptomatic hypocalcemia should be treated with calcium gluconate if changes are present on the electrocardiography (ECG). Hypocalcemia in the presence of hyperphosphatemia should be treated only in patients with tetany or cardiac arrhythmias; otherwise, hypocalcemia should not be treated until hyperphosphatemia has been corrected.

In cases of hyperkalemia, patients should be placed on a cardiac monitor and stabilized with calcium gluconate; kayexalate should be administered to reduce total body potassium. Other interventions, such as intravenous insulin given with dextrose, sodium bicarbonate, and albuterol, have a temporary effect on hyperkalemia and can be used as adjunct treatments in patients with severe hyperkalemia (>7). Hemodialysis should be strongly considered in severe cases of hyperkalemia, particularly in patients with persistently elevated potassium levels despite other treatments.

Back to the Case

Our patient was started on IVFs with close monitoring of his urine output. He was considered intermediate risk for developing TLS. Allopurinol, renally dosed, was administered for two days prior to initiating treatment with rituximab plus chemotherapy. His chemistry panel was monitored daily and he did not develop any form of TLS.

Bottom Line

TLS is a common oncology emergency in patients with hematologic malignancies. Preventative measures include starting IVF prior to cancer treatment, and administering allopurinol and/or rasburicase to patients at risk of developing TLS. Treatment should include normalizing electrolytes to avoid arrhythmias and seizures.

Dr. Akwe is assistant professor of medicine at the Emory University School of Medicine and a clinical instructor of medicine at the Morehouse School of Medicine, both in Atlanta. Dr. Smith is an assistant director for education in the division of hospital medicine at Emory. Both work as hospitalists at the Atlanta VA Medical Center.

References

1. Abu-Alfa AK, Younes A. Tumor lysis syndrome and acute kidney injury: evaluation, prevention, and management. Am J Kidney Dis. 2010;55:Suppl 3:S1-S13.
2. Cairo MS, Coiffier B, Reiter A, Younes A. Recommendations for the evaluation of risk and prophylaxis of tumour lysis syndrome (TLS) in adults and children with malignant diseases: an expert TLS panel consensus. Br J Haematol. 2010;149:578-586.
3. Gertz MA. Managing tumor lysis syndrome in 2010. Leuk Lymphoma. 2010;51:179-180.
4. Howard SC, Jones DP, Pui CH. The tumor lysis syndrome. N Engl J Med. 2011;364:1844.
5. Cairo MS, Bishop M. Tumour lysis syndrome: new therapeutic strategies and classification. Br J Haematol. 2004;127:3.
6. Wössmann W, Schrappe M, Meyer U, et al. Incidence of tumor lysis syndrome in children with advanced stage Burkitt’s lymphoma/leukemia before and after introduction of prophylactic use of urate oxidase. Ann Hematol. 2003;82:160.
7. Hussain K, Mazza JJ, Clouse LH. Tumor lysis syndrome (TLS) following fludarabine therapy Gemici C. Tumor lysis syndrome in solid tumors. J Clin Oncol. 2009;27:2738-2739
8. Rostom AY, El-Hussainy G, Kandil A, Allam A. Tumor lysis syndrome following hemi-body irradiation for metastatic breast cancer. Ann Oncol. 2000;11:1349.
9. Drakos P, Bar-Ziv J, Catane R. Tumor lysis syndrome in nonhematologic malignancies. Report of a case and review of the literature. Am J Clin Oncol. 1994;17:502.
10. Baeksgaard L, Sørensen JB. Acute tumor lysis syndrome in solid tumors—a case report and review of the literature. Cancer Chemother Pharmacol. 2003;51:187.
11. Kalemkerian GP, Darwish B, Varterasian ML. Tumor lysis syndrome in small cell carcinoma and other solid tumors. Am J Med. 1997;103:363.
12. Noh GY, Choe DH, Kim CH, Lee JC. Fatal tumor lysis syndrome during radiotherapy for non-small-cell lung cancer. J Clin Oncol. 2008;26:6005-6006.
13. Pentheroudakis G, O’Neill VJ, Vasey P, Kaye SB. Spontaneous acute tumour lysis syndrome in patients with metastatic germ cell tumours. Report of two cases. Support Care Cancer. 2001;9:554.
14. Joshita S, Yoshizawa K, Sano K, et al., A patient with advanced hepatocellular carcinoma treated with sorafenib tosylate showed massive tumor lysis with avoidance of tumor lysis syndrome. Intern Med. 2010;49:991-994.
15. Huang WS, Yang CH. Sorafenib-induced tumor lysis syndrome in an advanced hepatocellular carcinoma patient. World J Gastroenterol. 2009;15:4464-4466.
16. Bilgrami SF, Fallon BG. Tumor lysis syndrome after combination chemotherapy for ovarian cancer. Med Pediatr Oncol. 1993;21:521.
17. Chan JK, Lin SS, McMeekin DS, Berman ML. Patients with malignancy requiring urgent therapy: CASE 3. Tumor lysis syndrome associated with chemotherapy in ovarian cancer. J Clin Oncol. 2005;23:6794.
18. Godoy H, Kesterson JP, Lele S. Tumor lysis syndrome associated with carboplatin and paclitaxel in a woman with recurrent endometrial cancer. Int J Gynaecol Obstet. 2010;109:254.
19. Shamseddine AI, Khalil AM, Wehbeh MH. Acute tumor lysis syndrome with squamous cell carcinoma of the vulva. Gynecol Oncol 1993;51:258
20. Pinder EM, Atwal GS, Ayantunde AA, et al. Tumour lysis syndrome occurring in a patient with metastatic gastrointestinal stromal tumour treated with Glivec (imatinib mesylate, Gleevec, STI571). Sarcoma. 2007;2007:82012.
21. Krishnan G, D’Silva K, Al-Janadi A. Cetuximab-related tumor lysis syndrome in metastatic colon carcinoma. J Clin Oncol. 2008;26:2406-2408.
22. Oztop I, Demirkan B, Yaren A, et al. Rapid tumor lysis syndrome in a patient with metastatic colon cancer as a complication of treatment with 5-fluorouracil/leucoverin and irinotecan. Tumori. 2004;90:514.
23. Lin CJ, Lim KH, Cheng YC, et al. Tumor lysis syndrome after treatment with gemcitabine for metastatic transitional cell carcinoma. Med Oncol. 2007;24:455.
24. Malik IA, Abubakar S, Alam F, Khan A. Dexamethasone-induced tumor lysis syndrome in high-grade non-Hodgkin’s lymphoma. South Med J. 1994;87:409.
25. Jabr FI. Acute tumor lysis syndrome induced by rituximab in diffuse large B-cell lymphoma. Int J Hematol. 2005;82:312.
26. Sezer O, Vesole DH, Singhal S, et al. Bortezomib-induced tumor lysis syndrome in multiple myeloma. Clin Lymphoma Myeloma. 2006;7:233.
27. Jensen M, Winkler U, Manzke O, et al. Rapid tumor lysis in a patient with B-cell chronic lymphocytic leukemia and lymphocytosis treated with an anti-CD20 monoclonal antibody (IDEC-C2B8, rituximab). Ann Hematol. 1998;77:89.
28. Linck D, Basara N, Tran V, et al. Peracute onset of severe tumor lysis syndrome immediately after 4 Gy fractionated TBI as part of reduced intensity preparative regimen in a patient with T-ALL with high tumor burden. Bone Marrow Transplant. 2003;31:935.
29. Coiffier B, Altman A, Pui CH, Younes A, Cairo MS. Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review. J Clin Oncol. 2008;26(16):2767-2778. [Erratum, J Clin Oncol. 2010;28:708.]
30. Cheuk DK, Chiang AK, Chan GC, Ha SY. Urate oxidase for the prevention and treatment of tumor lysis syndrome in children with cancer. Cochrane Database Syst Rev. 2010;(6):CD006945.
31. Cortes J, Moore JO, Maziarz RT, et al. Control of plasma uric acid in adults at risk for tumor Lysis syndrome: efficacy and safety of rasburicase alone and rasburicase followed by allopurinol compared with allopurinol alone—results of a multicenter phase III study. J Clin Oncol. 2010;28:4207.

New CDC research published in the June issue of Infection Control and Hospital Epidemiology estimates that as many as 200,000 central-line-associated bloodstream infections (CLABSIs) in ICUs nationally have been prevented since 1990.³ The report indicates much of the success is due to U.S. hospitals adopting successful prevention strategies, namely the dissemination of guideline-supported central-line insertion and maintenance best practices, infection-control treatment bundles, and widespread availability of alcohol-based hand rubs.

Between 462,000 and 636,000 CLABSIs occurred in non-neonatal ICU patients from 1990-2010, CDC estimates, about 104,000 to 198,000 less CLABSIs than would have occurred if rates had remained the same as they were in 1990.

“These findings suggest that technical innovations and dissemination of evidence-based CLABSI prevention practices have likely been effective on a national scale,” Matthew Wise, PhD, lead author of the study, said in a statement.

At the same time, a CLABSI-reduction intervention in a hospital in Hawaii found that while the costs of care were much higher for patients who developed a CLABSI, reimbursement and the hospital’s margin also were higher (margin of $54,906 vs. $6,506).⁴ The authors conclude that current reimbursement practices offer a perverse incentive for hospitals to have more line infections, “while an optimal reimbursement system would reward them for prevention rather than treating illness.”

Lead author Eugene Hsu, MD, MBA, of Johns Hopkins University School of Medicine said in an email that the study demonstrates how a quality initiative led by providers and funded by a major commercial insurer can save both lives and money. “Hospitalists, like all healthcare providers, must be aware of the distorted financial incentives that may affect how they provide care to patients,” Dr. Hsu said.

Larry Beresford is a freelance writer in Oakland, Calif.

References

1. Stobbe, M. Germ-zapping “robots”: Hospitals combat superbugs. Associated Press website. Available at: http://bigstory.ap.org/article/hospitals-see-surge-superbug-fighting-products. Accessed June 7, 2013.
2. Centers for Disease Control and Prevention. Vital Signs: Carbapenem-Resistant Enterobacteriaceae. Centers for Disease Control and Prevention website. Available at: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6209a3.htm?s_cid=mm6209a3_w. Accessed June 7, 2013.
3. Wise ME, Scott RD, Baggs JM, et al. National estimates of central line-associated bloodstream infections in critical care patients. Infect Control Hosp Epidemiol, 2013;34(6):547-554.
4. Hsu E, Lin D, Evans SJ, et al. Doing well by doing good: assessing the cost savings of an intervention to reduce central line-associated bloodstream infections in a Hawaii hospital. Am J Med Qual, 2013 May 7 [Epub ahead of print].
5. Association of American Medical Colleges. Medical school enrollment on pace to reach 30 percent increase by 2017. Association of American Medical Colleges website. Available at: https://www.aamc.org/newsroom/newsreleases/ 335244/050213.html. Accessed June 7, 2013.

New CDC research published in the June issue of Infection Control and Hospital Epidemiology estimates that as many as 200,000 central-line-associated bloodstream infections (CLABSIs) in ICUs nationally have been prevented since 1990.³ The report indicates much of the success is due to U.S. hospitals adopting successful prevention strategies, namely the dissemination of guideline-supported central-line insertion and maintenance best practices, infection-control treatment bundles, and widespread availability of alcohol-based hand rubs.

Between 462,000 and 636,000 CLABSIs occurred in non-neonatal ICU patients from 1990-2010, CDC estimates, about 104,000 to 198,000 less CLABSIs than would have occurred if rates had remained the same as they were in 1990.

“These findings suggest that technical innovations and dissemination of evidence-based CLABSI prevention practices have likely been effective on a national scale,” Matthew Wise, PhD, lead author of the study, said in a statement.

At the same time, a CLABSI-reduction intervention in a hospital in Hawaii found that while the costs of care were much higher for patients who developed a CLABSI, reimbursement and the hospital’s margin also were higher (margin of $54,906 vs. $6,506).⁴ The authors conclude that current reimbursement practices offer a perverse incentive for hospitals to have more line infections, “while an optimal reimbursement system would reward them for prevention rather than treating illness.”

Lead author Eugene Hsu, MD, MBA, of Johns Hopkins University School of Medicine said in an email that the study demonstrates how a quality initiative led by providers and funded by a major commercial insurer can save both lives and money. “Hospitalists, like all healthcare providers, must be aware of the distorted financial incentives that may affect how they provide care to patients,” Dr. Hsu said.

Larry Beresford is a freelance writer in Oakland, Calif.

References

1. Stobbe, M. Germ-zapping “robots”: Hospitals combat superbugs. Associated Press website. Available at: http://bigstory.ap.org/article/hospitals-see-surge-superbug-fighting-products. Accessed June 7, 2013.
2. Centers for Disease Control and Prevention. Vital Signs: Carbapenem-Resistant Enterobacteriaceae. Centers for Disease Control and Prevention website. Available at: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6209a3.htm?s_cid=mm6209a3_w. Accessed June 7, 2013.
3. Wise ME, Scott RD, Baggs JM, et al. National estimates of central line-associated bloodstream infections in critical care patients. Infect Control Hosp Epidemiol, 2013;34(6):547-554.
4. Hsu E, Lin D, Evans SJ, et al. Doing well by doing good: assessing the cost savings of an intervention to reduce central line-associated bloodstream infections in a Hawaii hospital. Am J Med Qual, 2013 May 7 [Epub ahead of print].
5. Association of American Medical Colleges. Medical school enrollment on pace to reach 30 percent increase by 2017. Association of American Medical Colleges website. Available at: https://www.aamc.org/newsroom/newsreleases/ 335244/050213.html. Accessed June 7, 2013.

New CDC research published in the June issue of Infection Control and Hospital Epidemiology estimates that as many as 200,000 central-line-associated bloodstream infections (CLABSIs) in ICUs nationally have been prevented since 1990.³ The report indicates much of the success is due to U.S. hospitals adopting successful prevention strategies, namely the dissemination of guideline-supported central-line insertion and maintenance best practices, infection-control treatment bundles, and widespread availability of alcohol-based hand rubs.

Between 462,000 and 636,000 CLABSIs occurred in non-neonatal ICU patients from 1990-2010, CDC estimates, about 104,000 to 198,000 less CLABSIs than would have occurred if rates had remained the same as they were in 1990.

“These findings suggest that technical innovations and dissemination of evidence-based CLABSI prevention practices have likely been effective on a national scale,” Matthew Wise, PhD, lead author of the study, said in a statement.

At the same time, a CLABSI-reduction intervention in a hospital in Hawaii found that while the costs of care were much higher for patients who developed a CLABSI, reimbursement and the hospital’s margin also were higher (margin of $54,906 vs. $6,506).⁴ The authors conclude that current reimbursement practices offer a perverse incentive for hospitals to have more line infections, “while an optimal reimbursement system would reward them for prevention rather than treating illness.”

Lead author Eugene Hsu, MD, MBA, of Johns Hopkins University School of Medicine said in an email that the study demonstrates how a quality initiative led by providers and funded by a major commercial insurer can save both lives and money. “Hospitalists, like all healthcare providers, must be aware of the distorted financial incentives that may affect how they provide care to patients,” Dr. Hsu said.

Larry Beresford is a freelance writer in Oakland, Calif.

References

1. Stobbe, M. Germ-zapping “robots”: Hospitals combat superbugs. Associated Press website. Available at: http://bigstory.ap.org/article/hospitals-see-surge-superbug-fighting-products. Accessed June 7, 2013.
2. Centers for Disease Control and Prevention. Vital Signs: Carbapenem-Resistant Enterobacteriaceae. Centers for Disease Control and Prevention website. Available at: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6209a3.htm?s_cid=mm6209a3_w. Accessed June 7, 2013.
3. Wise ME, Scott RD, Baggs JM, et al. National estimates of central line-associated bloodstream infections in critical care patients. Infect Control Hosp Epidemiol, 2013;34(6):547-554.
4. Hsu E, Lin D, Evans SJ, et al. Doing well by doing good: assessing the cost savings of an intervention to reduce central line-associated bloodstream infections in a Hawaii hospital. Am J Med Qual, 2013 May 7 [Epub ahead of print].
5. Association of American Medical Colleges. Medical school enrollment on pace to reach 30 percent increase by 2017. Association of American Medical Colleges website. Available at: https://www.aamc.org/newsroom/newsreleases/ 335244/050213.html. Accessed June 7, 2013.

One in 20 hospitalized patients picks up an infection in the hospital, and a recent article by the Associated Press describes the emergence of new technologies to fight antibiotic-resistant superbugs: “They sweep. They swab. They sterilize. And still the germs persist.”¹

Hospitals across the country are testing new approaches to stop the spread of superbugs, which are tied to an estimated 100,000 deaths per year, according to the CDC. New approaches include robotlike machines that emit ultraviolet light or hydrogen-peroxide vapors, germ-resistant copper bed rails and call buttons, antimicrobial linens and wall paint, and hydrogel post-surgical dressings infused with silver ions that have antimicrobial properties.

Research firm Frost & Sullivan estimates that the market for bug-killing products and technologies will grow to $80 million from $30 million in the next three years. And yet evidence of positive outcomes from them continues to be debated.

“In short, escalating antimicrobial-resistance issues have us facing the prospect of untreatable bacterial pathogens, particularly involving gram-negative organisms,” James Pile, MD, FACP, SFHM, a hospital medicine and infectious diseases physician at Cleveland Clinic, wrote in an email. “In fact, many of our hospitals already deal with a limited number of infections caused by bacteria we have no clearly effective antibiotics against; the issue is only going to get worse.”

As an example, the CDC recently issued a warning about carbapenum-resistant Enterobacteriaceae (CRE), which has a 40% mortality rate and last year was reported in 4.6% of U.S. hospitals.² CDC recommends that hospitals use more of the existing prevention measures against CRE, including active-case detection and segregation of patients and the staff who care for them. Dr. Pile says health facilities need to do a better job of preventing infections involving multi-drug-resistant pathogens, but in the meantime, “proven technologies such as proper hand hygiene and antimicrobial stewardship are more important than ever.”

Larry Beresford is a freelance writer in Oakland, Calif.

References

1. Stobbe, M. Germ-zapping “robots”: Hospitals combat superbugs. Associated Press website. Available at: http://bigstory.ap.org/article/hospitals-see-surge-superbug-fighting-products. Accessed June 7, 2013.
2. Centers for Disease Control and Prevention. Vital Signs: Carbapenem-Resistant Enterobacteriaceae. Centers for Disease Control and Prevention website. Available at: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6209a3.htm?s_cid=mm6209a3_w. Accessed June 7, 2013.
3. Wise ME, Scott RD, Baggs JM, et al. National estimates of central line-associated bloodstream infections in critical care patients. Infect Control Hosp Epidemiol, 2013;34(6):547-554.
4. Hsu E, Lin D, Evans SJ, et al. Doing well by doing good: assessing the cost savings of an intervention to reduce central line-associated bloodstream infections in a Hawaii hospital. Am J Med Qual, 2013 May 7 [Epub ahead of print].
5. Association of American Medical Colleges. Medical school enrollment on pace to reach 30 percent increase by 2017. Association of American Medical Colleges website. Available at: https://www.aamc.org/newsroom/newsreleases/ 335244/050213.html. Accessed June 7, 2013.

One in 20 hospitalized patients picks up an infection in the hospital, and a recent article by the Associated Press describes the emergence of new technologies to fight antibiotic-resistant superbugs: “They sweep. They swab. They sterilize. And still the germs persist.”¹

Hospitals across the country are testing new approaches to stop the spread of superbugs, which are tied to an estimated 100,000 deaths per year, according to the CDC. New approaches include robotlike machines that emit ultraviolet light or hydrogen-peroxide vapors, germ-resistant copper bed rails and call buttons, antimicrobial linens and wall paint, and hydrogel post-surgical dressings infused with silver ions that have antimicrobial properties.

Research firm Frost & Sullivan estimates that the market for bug-killing products and technologies will grow to $80 million from $30 million in the next three years. And yet evidence of positive outcomes from them continues to be debated.

“In short, escalating antimicrobial-resistance issues have us facing the prospect of untreatable bacterial pathogens, particularly involving gram-negative organisms,” James Pile, MD, FACP, SFHM, a hospital medicine and infectious diseases physician at Cleveland Clinic, wrote in an email. “In fact, many of our hospitals already deal with a limited number of infections caused by bacteria we have no clearly effective antibiotics against; the issue is only going to get worse.”

As an example, the CDC recently issued a warning about carbapenum-resistant Enterobacteriaceae (CRE), which has a 40% mortality rate and last year was reported in 4.6% of U.S. hospitals.² CDC recommends that hospitals use more of the existing prevention measures against CRE, including active-case detection and segregation of patients and the staff who care for them. Dr. Pile says health facilities need to do a better job of preventing infections involving multi-drug-resistant pathogens, but in the meantime, “proven technologies such as proper hand hygiene and antimicrobial stewardship are more important than ever.”

Larry Beresford is a freelance writer in Oakland, Calif.

References

1. Stobbe, M. Germ-zapping “robots”: Hospitals combat superbugs. Associated Press website. Available at: http://bigstory.ap.org/article/hospitals-see-surge-superbug-fighting-products. Accessed June 7, 2013.
2. Centers for Disease Control and Prevention. Vital Signs: Carbapenem-Resistant Enterobacteriaceae. Centers for Disease Control and Prevention website. Available at: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6209a3.htm?s_cid=mm6209a3_w. Accessed June 7, 2013.
3. Wise ME, Scott RD, Baggs JM, et al. National estimates of central line-associated bloodstream infections in critical care patients. Infect Control Hosp Epidemiol, 2013;34(6):547-554.
4. Hsu E, Lin D, Evans SJ, et al. Doing well by doing good: assessing the cost savings of an intervention to reduce central line-associated bloodstream infections in a Hawaii hospital. Am J Med Qual, 2013 May 7 [Epub ahead of print].
5. Association of American Medical Colleges. Medical school enrollment on pace to reach 30 percent increase by 2017. Association of American Medical Colleges website. Available at: https://www.aamc.org/newsroom/newsreleases/ 335244/050213.html. Accessed June 7, 2013.

One in 20 hospitalized patients picks up an infection in the hospital, and a recent article by the Associated Press describes the emergence of new technologies to fight antibiotic-resistant superbugs: “They sweep. They swab. They sterilize. And still the germs persist.”¹

Hospitals across the country are testing new approaches to stop the spread of superbugs, which are tied to an estimated 100,000 deaths per year, according to the CDC. New approaches include robotlike machines that emit ultraviolet light or hydrogen-peroxide vapors, germ-resistant copper bed rails and call buttons, antimicrobial linens and wall paint, and hydrogel post-surgical dressings infused with silver ions that have antimicrobial properties.

Research firm Frost & Sullivan estimates that the market for bug-killing products and technologies will grow to $80 million from $30 million in the next three years. And yet evidence of positive outcomes from them continues to be debated.

“In short, escalating antimicrobial-resistance issues have us facing the prospect of untreatable bacterial pathogens, particularly involving gram-negative organisms,” James Pile, MD, FACP, SFHM, a hospital medicine and infectious diseases physician at Cleveland Clinic, wrote in an email. “In fact, many of our hospitals already deal with a limited number of infections caused by bacteria we have no clearly effective antibiotics against; the issue is only going to get worse.”

As an example, the CDC recently issued a warning about carbapenum-resistant Enterobacteriaceae (CRE), which has a 40% mortality rate and last year was reported in 4.6% of U.S. hospitals.² CDC recommends that hospitals use more of the existing prevention measures against CRE, including active-case detection and segregation of patients and the staff who care for them. Dr. Pile says health facilities need to do a better job of preventing infections involving multi-drug-resistant pathogens, but in the meantime, “proven technologies such as proper hand hygiene and antimicrobial stewardship are more important than ever.”

Larry Beresford is a freelance writer in Oakland, Calif.

References

1. Stobbe, M. Germ-zapping “robots”: Hospitals combat superbugs. Associated Press website. Available at: http://bigstory.ap.org/article/hospitals-see-surge-superbug-fighting-products. Accessed June 7, 2013.
2. Centers for Disease Control and Prevention. Vital Signs: Carbapenem-Resistant Enterobacteriaceae. Centers for Disease Control and Prevention website. Available at: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6209a3.htm?s_cid=mm6209a3_w. Accessed June 7, 2013.
3. Wise ME, Scott RD, Baggs JM, et al. National estimates of central line-associated bloodstream infections in critical care patients. Infect Control Hosp Epidemiol, 2013;34(6):547-554.
4. Hsu E, Lin D, Evans SJ, et al. Doing well by doing good: assessing the cost savings of an intervention to reduce central line-associated bloodstream infections in a Hawaii hospital. Am J Med Qual, 2013 May 7 [Epub ahead of print].
5. Association of American Medical Colleges. Medical school enrollment on pace to reach 30 percent increase by 2017. Association of American Medical Colleges website. Available at: https://www.aamc.org/newsroom/newsreleases/ 335244/050213.html. Accessed June 7, 2013.

Job One during your first months as a working hospitalist is to acclimate to your hospital and HM group’s procedures. Increasingly, hospitalist teams include nurse practitioners (NPs) and physician assistants (PAs); for some new hospitalists, this will require another level of learning on the job. The 2012 State of Hospital Medicine report (www.hospitalmedicine.org/survey) noted that approximately half of HM groups serving adults and children utilized NPs and/or PAs. Although the report also acknowledged that identifying trends is difficult, the converging factors of aging U.S. demographics and the growing physician shortage indicate that NPs and PAs will become more prevalent in hospital medicine.

Physicians who have not worked alongside NPs or PAs often are unsure of how to approach the working relationship, says Jeanette Kalupa, DNP, ACNP-BC, SFHM, vice president of clinical operations at Hospitalists of Northern Michigan and a member of SHM’s Nurse Practitioner/Physician Assistant (NP/PA) Committee.

Roles and Scope of Practice

NPs and PAs perform myriad clinical and management responsibilities as hospitalists:

• Coordination of admissions and discharge planning;
• Patient histories, physical examinations, and diagnostic and therapeutic procedures (placing central lines, doing lumbar punctures, etc.);
• Medication orders; and
• Hospital committee work to improve processes of care.

Licensing requirements, physician oversight requirements, and scope of practice vary state to state and hospital to hospital. “If you’ve seen one hospital medicine group, you’ve seen one hospital medicine group”— coined by Mitchell Wilson, MD, SFHM, CMO at Atlanta-based Eagle Hospital Physicians—also applies to the way in which HM groups structure their use of NPs and PAs, says Tracy E. Cardin, ACNP-BC, of the University of Chicago Hospital and chair of the NP/PA Committee. SHM’s website offers information about the scope of practice and best ways to incorporate NPs and PAs into hospitalist practice.

Cardin

To hospitalists who express anxiety about an NP or PA overstepping bounds and putting the physician’s license at risk, Kalupa reminds them that she, too, has a license that is at risk. When roles are clearly delineated for tasks that NPs and PAs will perform, jeopardizing a license will not be an issue.

Literature supports equivalent outcomes in both primary care and inpatient settings when PAs and NPs are implemented to handle responsibilities within their scope of practice.^1,2 Using a PA or NP to handle uncomplicated pneumonia cases, to conduct a stress test, or assemble data for patient rounding, for example, can have a physician multiplier effect, says committee member David A. Friar, MD, SFHM, also a member of the NP/PA Committee. Dr. Friar, based in Traverse City, Mich., works daily with nurse practitioners and physician assistants as part of HNM.

“I think of the healthcare team as a toolbox with which we need to provide care for our patients,” he says. “A screwdriver is not half of a hammer, but it can be the best tool for a certain job. In addition, physicians are often seen as Swiss army knives—that we can do anything. We can make photocopies, but it doesn’t make sense for us to do that. So for cases of simple pneumonia or urinary tract infections, or for following people waiting for discharge, management by an NP or PA makes a lot of sense from an economic standpoint.”

Dr. Friar

Position Parity

Hospital leadership should set the tone for building a strong multidisciplinary team, Cardin says. Individual physicians can make a difference with the right approach to the working relationship. “If you are going to have successful collaborations with NPs and PAs,” she says, “you have to treat them like a doctor.” This does not mean that the pay structure will be the same, but in areas such as continuing medical education and group socializing, every member of the team should be treated as an equal. That approach makes sense to Dr. Friar, who makes it a point to call every person on the HM team a hospitalist.

He and Kalupa also point out that NPs and PAs can successfully fill team leadership roles. “Physicians need to be willing to accept that the personality traits that made them great clinicians are often not those that one would desire in a team leader,” Dr. Friar says. Using a football analogy, he notes that an important part of being a good team member is to play to other members’ strengths and protect them from their weaknesses. “You don’t have the linebacker run the ball, or the quarterback kick the field goal attempt; you use people’s strengths where they will be most effective for the care of your patients.”

When Conflicts Arise

Successful working relationships between physicians and NP/PAs hinge on clear expectations and the willingness to have difficult conversations, Cardin says. She has practiced as a hospitalist for seven years and prior to that worked in the acute-care setting. As a result, she says, she is quite comfortable seeing patients independently.

Hospitalists new to the group or those who have not worked with NPs before may bristle at that idea, she notes. If a problem arises, such as a perceived encroachment on one’s scope of practice, be willing to address it openly. All relationships are constantly evolving, and it’s important not to overreact.

It’s “just like driving a car,” she says. “If you overcorrect when a wheel comes off the road, you will wreck the car. Sometimes all that’s needed is a small adjustment to manage the problem.”

Gretchen Henkel is a freelance writer in California.

What’s in a Name?

Dr. Kalupa

When Jeanette Kalupa, DNP, ACNP-BC, SFHM, vice president of clinical operations for Hospitalists of Northern Michigan, first joined SHM’s Nurse Practitioner/Physician Assistant Committee in 2003, it was called the “NP/PA Task Force.” The name was changed to the Nonphysician Provider (NPP) Committee to accommodate other allied professionals, such as pharmacists and case managers. She and her NP colleagues object to the NPP moniker “because it designates us as what we are not.”

The term “midlevel provider,” another common designation, is also problematic, she says, because it heightens awareness of a hierarchy. Just this past year, the committee name was changed to NP/PA Committee. “We’ve evolved over time,” Kalupa says. “I think rather than labeling someone as a ‘midlevel provider,’ it’s better to just call them what they are.”

—Gretchen Henkel

References

1. Iglesias B, Ramos F, Serrano B, et al. A randomized controlled trial of nurses vs. doctors in the resolution of acute disease of low complexity in primary care. J Adv Nurs. 2013 March 21. doi: 10.1111/jan.12120 [Epub ahead of print].
2. Hoffman LA, Tasota FJ, Zullo TG, et al. Outcomes of care managed by an acute care nurse practitioner/attending physician team in a subacute medical intensive care unit. Am J Crit Care. 2005;14(2):121-130; quiz 131-132.

Job One during your first months as a working hospitalist is to acclimate to your hospital and HM group’s procedures. Increasingly, hospitalist teams include nurse practitioners (NPs) and physician assistants (PAs); for some new hospitalists, this will require another level of learning on the job. The 2012 State of Hospital Medicine report (www.hospitalmedicine.org/survey) noted that approximately half of HM groups serving adults and children utilized NPs and/or PAs. Although the report also acknowledged that identifying trends is difficult, the converging factors of aging U.S. demographics and the growing physician shortage indicate that NPs and PAs will become more prevalent in hospital medicine.

Physicians who have not worked alongside NPs or PAs often are unsure of how to approach the working relationship, says Jeanette Kalupa, DNP, ACNP-BC, SFHM, vice president of clinical operations at Hospitalists of Northern Michigan and a member of SHM’s Nurse Practitioner/Physician Assistant (NP/PA) Committee.

Roles and Scope of Practice

NPs and PAs perform myriad clinical and management responsibilities as hospitalists:

• Coordination of admissions and discharge planning;
• Patient histories, physical examinations, and diagnostic and therapeutic procedures (placing central lines, doing lumbar punctures, etc.);
• Medication orders; and
• Hospital committee work to improve processes of care.

Licensing requirements, physician oversight requirements, and scope of practice vary state to state and hospital to hospital. “If you’ve seen one hospital medicine group, you’ve seen one hospital medicine group”— coined by Mitchell Wilson, MD, SFHM, CMO at Atlanta-based Eagle Hospital Physicians—also applies to the way in which HM groups structure their use of NPs and PAs, says Tracy E. Cardin, ACNP-BC, of the University of Chicago Hospital and chair of the NP/PA Committee. SHM’s website offers information about the scope of practice and best ways to incorporate NPs and PAs into hospitalist practice.

Cardin

To hospitalists who express anxiety about an NP or PA overstepping bounds and putting the physician’s license at risk, Kalupa reminds them that she, too, has a license that is at risk. When roles are clearly delineated for tasks that NPs and PAs will perform, jeopardizing a license will not be an issue.

Literature supports equivalent outcomes in both primary care and inpatient settings when PAs and NPs are implemented to handle responsibilities within their scope of practice.^1,2 Using a PA or NP to handle uncomplicated pneumonia cases, to conduct a stress test, or assemble data for patient rounding, for example, can have a physician multiplier effect, says committee member David A. Friar, MD, SFHM, also a member of the NP/PA Committee. Dr. Friar, based in Traverse City, Mich., works daily with nurse practitioners and physician assistants as part of HNM.

“I think of the healthcare team as a toolbox with which we need to provide care for our patients,” he says. “A screwdriver is not half of a hammer, but it can be the best tool for a certain job. In addition, physicians are often seen as Swiss army knives—that we can do anything. We can make photocopies, but it doesn’t make sense for us to do that. So for cases of simple pneumonia or urinary tract infections, or for following people waiting for discharge, management by an NP or PA makes a lot of sense from an economic standpoint.”

Dr. Friar

Position Parity

Hospital leadership should set the tone for building a strong multidisciplinary team, Cardin says. Individual physicians can make a difference with the right approach to the working relationship. “If you are going to have successful collaborations with NPs and PAs,” she says, “you have to treat them like a doctor.” This does not mean that the pay structure will be the same, but in areas such as continuing medical education and group socializing, every member of the team should be treated as an equal. That approach makes sense to Dr. Friar, who makes it a point to call every person on the HM team a hospitalist.

He and Kalupa also point out that NPs and PAs can successfully fill team leadership roles. “Physicians need to be willing to accept that the personality traits that made them great clinicians are often not those that one would desire in a team leader,” Dr. Friar says. Using a football analogy, he notes that an important part of being a good team member is to play to other members’ strengths and protect them from their weaknesses. “You don’t have the linebacker run the ball, or the quarterback kick the field goal attempt; you use people’s strengths where they will be most effective for the care of your patients.”

When Conflicts Arise

Successful working relationships between physicians and NP/PAs hinge on clear expectations and the willingness to have difficult conversations, Cardin says. She has practiced as a hospitalist for seven years and prior to that worked in the acute-care setting. As a result, she says, she is quite comfortable seeing patients independently.

Hospitalists new to the group or those who have not worked with NPs before may bristle at that idea, she notes. If a problem arises, such as a perceived encroachment on one’s scope of practice, be willing to address it openly. All relationships are constantly evolving, and it’s important not to overreact.

It’s “just like driving a car,” she says. “If you overcorrect when a wheel comes off the road, you will wreck the car. Sometimes all that’s needed is a small adjustment to manage the problem.”

Gretchen Henkel is a freelance writer in California.

What’s in a Name?

Dr. Kalupa

When Jeanette Kalupa, DNP, ACNP-BC, SFHM, vice president of clinical operations for Hospitalists of Northern Michigan, first joined SHM’s Nurse Practitioner/Physician Assistant Committee in 2003, it was called the “NP/PA Task Force.” The name was changed to the Nonphysician Provider (NPP) Committee to accommodate other allied professionals, such as pharmacists and case managers. She and her NP colleagues object to the NPP moniker “because it designates us as what we are not.”

The term “midlevel provider,” another common designation, is also problematic, she says, because it heightens awareness of a hierarchy. Just this past year, the committee name was changed to NP/PA Committee. “We’ve evolved over time,” Kalupa says. “I think rather than labeling someone as a ‘midlevel provider,’ it’s better to just call them what they are.”

—Gretchen Henkel

References

1. Iglesias B, Ramos F, Serrano B, et al. A randomized controlled trial of nurses vs. doctors in the resolution of acute disease of low complexity in primary care. J Adv Nurs. 2013 March 21. doi: 10.1111/jan.12120 [Epub ahead of print].
2. Hoffman LA, Tasota FJ, Zullo TG, et al. Outcomes of care managed by an acute care nurse practitioner/attending physician team in a subacute medical intensive care unit. Am J Crit Care. 2005;14(2):121-130; quiz 131-132.

Job One during your first months as a working hospitalist is to acclimate to your hospital and HM group’s procedures. Increasingly, hospitalist teams include nurse practitioners (NPs) and physician assistants (PAs); for some new hospitalists, this will require another level of learning on the job. The 2012 State of Hospital Medicine report (www.hospitalmedicine.org/survey) noted that approximately half of HM groups serving adults and children utilized NPs and/or PAs. Although the report also acknowledged that identifying trends is difficult, the converging factors of aging U.S. demographics and the growing physician shortage indicate that NPs and PAs will become more prevalent in hospital medicine.

Physicians who have not worked alongside NPs or PAs often are unsure of how to approach the working relationship, says Jeanette Kalupa, DNP, ACNP-BC, SFHM, vice president of clinical operations at Hospitalists of Northern Michigan and a member of SHM’s Nurse Practitioner/Physician Assistant (NP/PA) Committee.

Roles and Scope of Practice

NPs and PAs perform myriad clinical and management responsibilities as hospitalists:

• Coordination of admissions and discharge planning;
• Patient histories, physical examinations, and diagnostic and therapeutic procedures (placing central lines, doing lumbar punctures, etc.);
• Medication orders; and
• Hospital committee work to improve processes of care.

Licensing requirements, physician oversight requirements, and scope of practice vary state to state and hospital to hospital. “If you’ve seen one hospital medicine group, you’ve seen one hospital medicine group”— coined by Mitchell Wilson, MD, SFHM, CMO at Atlanta-based Eagle Hospital Physicians—also applies to the way in which HM groups structure their use of NPs and PAs, says Tracy E. Cardin, ACNP-BC, of the University of Chicago Hospital and chair of the NP/PA Committee. SHM’s website offers information about the scope of practice and best ways to incorporate NPs and PAs into hospitalist practice.

Cardin

To hospitalists who express anxiety about an NP or PA overstepping bounds and putting the physician’s license at risk, Kalupa reminds them that she, too, has a license that is at risk. When roles are clearly delineated for tasks that NPs and PAs will perform, jeopardizing a license will not be an issue.

Literature supports equivalent outcomes in both primary care and inpatient settings when PAs and NPs are implemented to handle responsibilities within their scope of practice.^1,2 Using a PA or NP to handle uncomplicated pneumonia cases, to conduct a stress test, or assemble data for patient rounding, for example, can have a physician multiplier effect, says committee member David A. Friar, MD, SFHM, also a member of the NP/PA Committee. Dr. Friar, based in Traverse City, Mich., works daily with nurse practitioners and physician assistants as part of HNM.

“I think of the healthcare team as a toolbox with which we need to provide care for our patients,” he says. “A screwdriver is not half of a hammer, but it can be the best tool for a certain job. In addition, physicians are often seen as Swiss army knives—that we can do anything. We can make photocopies, but it doesn’t make sense for us to do that. So for cases of simple pneumonia or urinary tract infections, or for following people waiting for discharge, management by an NP or PA makes a lot of sense from an economic standpoint.”

Dr. Friar

Position Parity

Hospital leadership should set the tone for building a strong multidisciplinary team, Cardin says. Individual physicians can make a difference with the right approach to the working relationship. “If you are going to have successful collaborations with NPs and PAs,” she says, “you have to treat them like a doctor.” This does not mean that the pay structure will be the same, but in areas such as continuing medical education and group socializing, every member of the team should be treated as an equal. That approach makes sense to Dr. Friar, who makes it a point to call every person on the HM team a hospitalist.

He and Kalupa also point out that NPs and PAs can successfully fill team leadership roles. “Physicians need to be willing to accept that the personality traits that made them great clinicians are often not those that one would desire in a team leader,” Dr. Friar says. Using a football analogy, he notes that an important part of being a good team member is to play to other members’ strengths and protect them from their weaknesses. “You don’t have the linebacker run the ball, or the quarterback kick the field goal attempt; you use people’s strengths where they will be most effective for the care of your patients.”

When Conflicts Arise

Successful working relationships between physicians and NP/PAs hinge on clear expectations and the willingness to have difficult conversations, Cardin says. She has practiced as a hospitalist for seven years and prior to that worked in the acute-care setting. As a result, she says, she is quite comfortable seeing patients independently.

Hospitalists new to the group or those who have not worked with NPs before may bristle at that idea, she notes. If a problem arises, such as a perceived encroachment on one’s scope of practice, be willing to address it openly. All relationships are constantly evolving, and it’s important not to overreact.

It’s “just like driving a car,” she says. “If you overcorrect when a wheel comes off the road, you will wreck the car. Sometimes all that’s needed is a small adjustment to manage the problem.”

Gretchen Henkel is a freelance writer in California.

What’s in a Name?

Dr. Kalupa

When Jeanette Kalupa, DNP, ACNP-BC, SFHM, vice president of clinical operations for Hospitalists of Northern Michigan, first joined SHM’s Nurse Practitioner/Physician Assistant Committee in 2003, it was called the “NP/PA Task Force.” The name was changed to the Nonphysician Provider (NPP) Committee to accommodate other allied professionals, such as pharmacists and case managers. She and her NP colleagues object to the NPP moniker “because it designates us as what we are not.”

The term “midlevel provider,” another common designation, is also problematic, she says, because it heightens awareness of a hierarchy. Just this past year, the committee name was changed to NP/PA Committee. “We’ve evolved over time,” Kalupa says. “I think rather than labeling someone as a ‘midlevel provider,’ it’s better to just call them what they are.”

—Gretchen Henkel

References

1. Iglesias B, Ramos F, Serrano B, et al. A randomized controlled trial of nurses vs. doctors in the resolution of acute disease of low complexity in primary care. J Adv Nurs. 2013 March 21. doi: 10.1111/jan.12120 [Epub ahead of print].
2. Hoffman LA, Tasota FJ, Zullo TG, et al. Outcomes of care managed by an acute care nurse practitioner/attending physician team in a subacute medical intensive care unit. Am J Crit Care. 2005;14(2):121-130; quiz 131-132.