M. Alexander Otto

Patients who used cholinesterase inhibitors had a 38% lower risk of heart attacks, based on a study of Swedish Alzheimer’s disease patients published online June 4 in the European Heart Journal.

"This is an observational study, [so] we cannot say that cholinesterase inhibitor use is causing the reduction in risk, only that it is associated with a reduction. It would be of great value if a meta-analysis of previous, randomized controlled trials could be performed, as this might produce answers on which clinical recommendations could be based," lead investigator Dr. Peter Nordstrom, of Umea University in Sweden, said in a statement.

The findings were not adjusted for statin use, which was unknown.

The investigators cross-linked the records of 7,073 patients in the Swedish Dementia Registry to myocardial infarction and death records in national registries. The results were then adjusted for age, gender, weight, height, dementia type, living conditions, home care, cognitive function, cardiovascular disease history, baseline health, and the use of antidepressants, neuroleptics, antihypertensives, and antidiabetics.

Compared with 1,914 Alzheimer’s patients who never took cholinesterase inhibitors, the 5,159 patients who used the drugs during a mean period of 495 days had a 38% lower risk of myocardial infarction (hazard ratio, 0.62; 95% confidence interval, 0.40-0.95), a 34% lower risk of MI or death (HR, 0.66; 95% CI, 0.56-0.78), a 26% lower risk of death from all cardiovascular causes (HR, 0.74; 95% CI, 0.57-0.97), and a 36% lower risk of death from any cause (HR, 0.64; 95% CI, 0.54-0.76). A case-control analysis produced similar results (Eur. Heart J. 2013 June 4 [doi: 10.1093/eurheartj/eht182]).

Patients who, in their last recorded prescription, were taking higher doses of cholinesterase inhibitors – 10 mg of donepezil, 24 mg of galantamine, or more than 6 mg of rivastigmine daily – had the lowest risk of MI (HR, 0.35; 95% CI, 0.19-0.64) and death (HR, 0.54; 95% CI 0.43-0.67). Among those with baseline cardiovascular disease, high doses of cholinesterase inhibitors reduced MI risk by 71% (HR, 0.29; 95% CI, 0.09-0.94).

Memantine, an Alzheimer’s drug with a different mechanism, was not associated with lower rates of death.

"If you translate these reductions in risk into absolute figures, it means that for every 100,000 people with Alzheimer’s disease, there would be 180 fewer heart attacks – 295 as opposed to 475 – and 1,125 fewer deaths from all causes – 2,000 versus 3,125 – every year among those taking cholinesterase inhibitors compared to those not using them," Dr. Nordstrom said in a statement.

If cholinesterase inhibitors really do protect the heart, it might have something to do with their known anti-inflammatory properties or their effects on the vagus nerve, the investigators noted.

The subjects were enrolled in the Swedish Dementia Registry between May 2007 and December 2010 with newly diagnosed Alzheimer’s disease. Their mean age was 79 years at baseline, about 60% were women, and 831 had an MI or died.

The investigators reported no conflicts of interest. The Swedish Research Council, the Swedish Association of Local Authorities and Regions, and other groups paid for the work.

[email protected]

Patients who used cholinesterase inhibitors had a 38% lower risk of heart attacks, based on a study of Swedish Alzheimer’s disease patients published online June 4 in the European Heart Journal.

"This is an observational study, [so] we cannot say that cholinesterase inhibitor use is causing the reduction in risk, only that it is associated with a reduction. It would be of great value if a meta-analysis of previous, randomized controlled trials could be performed, as this might produce answers on which clinical recommendations could be based," lead investigator Dr. Peter Nordstrom, of Umea University in Sweden, said in a statement.

The findings were not adjusted for statin use, which was unknown.

The investigators cross-linked the records of 7,073 patients in the Swedish Dementia Registry to myocardial infarction and death records in national registries. The results were then adjusted for age, gender, weight, height, dementia type, living conditions, home care, cognitive function, cardiovascular disease history, baseline health, and the use of antidepressants, neuroleptics, antihypertensives, and antidiabetics.

Compared with 1,914 Alzheimer’s patients who never took cholinesterase inhibitors, the 5,159 patients who used the drugs during a mean period of 495 days had a 38% lower risk of myocardial infarction (hazard ratio, 0.62; 95% confidence interval, 0.40-0.95), a 34% lower risk of MI or death (HR, 0.66; 95% CI, 0.56-0.78), a 26% lower risk of death from all cardiovascular causes (HR, 0.74; 95% CI, 0.57-0.97), and a 36% lower risk of death from any cause (HR, 0.64; 95% CI, 0.54-0.76). A case-control analysis produced similar results (Eur. Heart J. 2013 June 4 [doi: 10.1093/eurheartj/eht182]).

Patients who, in their last recorded prescription, were taking higher doses of cholinesterase inhibitors – 10 mg of donepezil, 24 mg of galantamine, or more than 6 mg of rivastigmine daily – had the lowest risk of MI (HR, 0.35; 95% CI, 0.19-0.64) and death (HR, 0.54; 95% CI 0.43-0.67). Among those with baseline cardiovascular disease, high doses of cholinesterase inhibitors reduced MI risk by 71% (HR, 0.29; 95% CI, 0.09-0.94).

Memantine, an Alzheimer’s drug with a different mechanism, was not associated with lower rates of death.

"If you translate these reductions in risk into absolute figures, it means that for every 100,000 people with Alzheimer’s disease, there would be 180 fewer heart attacks – 295 as opposed to 475 – and 1,125 fewer deaths from all causes – 2,000 versus 3,125 – every year among those taking cholinesterase inhibitors compared to those not using them," Dr. Nordstrom said in a statement.

If cholinesterase inhibitors really do protect the heart, it might have something to do with their known anti-inflammatory properties or their effects on the vagus nerve, the investigators noted.

The subjects were enrolled in the Swedish Dementia Registry between May 2007 and December 2010 with newly diagnosed Alzheimer’s disease. Their mean age was 79 years at baseline, about 60% were women, and 831 had an MI or died.

The investigators reported no conflicts of interest. The Swedish Research Council, the Swedish Association of Local Authorities and Regions, and other groups paid for the work.

[email protected]

Patients who used cholinesterase inhibitors had a 38% lower risk of heart attacks, based on a study of Swedish Alzheimer’s disease patients published online June 4 in the European Heart Journal.

"This is an observational study, [so] we cannot say that cholinesterase inhibitor use is causing the reduction in risk, only that it is associated with a reduction. It would be of great value if a meta-analysis of previous, randomized controlled trials could be performed, as this might produce answers on which clinical recommendations could be based," lead investigator Dr. Peter Nordstrom, of Umea University in Sweden, said in a statement.

The findings were not adjusted for statin use, which was unknown.

The investigators cross-linked the records of 7,073 patients in the Swedish Dementia Registry to myocardial infarction and death records in national registries. The results were then adjusted for age, gender, weight, height, dementia type, living conditions, home care, cognitive function, cardiovascular disease history, baseline health, and the use of antidepressants, neuroleptics, antihypertensives, and antidiabetics.

Compared with 1,914 Alzheimer’s patients who never took cholinesterase inhibitors, the 5,159 patients who used the drugs during a mean period of 495 days had a 38% lower risk of myocardial infarction (hazard ratio, 0.62; 95% confidence interval, 0.40-0.95), a 34% lower risk of MI or death (HR, 0.66; 95% CI, 0.56-0.78), a 26% lower risk of death from all cardiovascular causes (HR, 0.74; 95% CI, 0.57-0.97), and a 36% lower risk of death from any cause (HR, 0.64; 95% CI, 0.54-0.76). A case-control analysis produced similar results (Eur. Heart J. 2013 June 4 [doi: 10.1093/eurheartj/eht182]).

Patients who, in their last recorded prescription, were taking higher doses of cholinesterase inhibitors – 10 mg of donepezil, 24 mg of galantamine, or more than 6 mg of rivastigmine daily – had the lowest risk of MI (HR, 0.35; 95% CI, 0.19-0.64) and death (HR, 0.54; 95% CI 0.43-0.67). Among those with baseline cardiovascular disease, high doses of cholinesterase inhibitors reduced MI risk by 71% (HR, 0.29; 95% CI, 0.09-0.94).

Memantine, an Alzheimer’s drug with a different mechanism, was not associated with lower rates of death.

"If you translate these reductions in risk into absolute figures, it means that for every 100,000 people with Alzheimer’s disease, there would be 180 fewer heart attacks – 295 as opposed to 475 – and 1,125 fewer deaths from all causes – 2,000 versus 3,125 – every year among those taking cholinesterase inhibitors compared to those not using them," Dr. Nordstrom said in a statement.

If cholinesterase inhibitors really do protect the heart, it might have something to do with their known anti-inflammatory properties or their effects on the vagus nerve, the investigators noted.

The subjects were enrolled in the Swedish Dementia Registry between May 2007 and December 2010 with newly diagnosed Alzheimer’s disease. Their mean age was 79 years at baseline, about 60% were women, and 831 had an MI or died.

The investigators reported no conflicts of interest. The Swedish Research Council, the Swedish Association of Local Authorities and Regions, and other groups paid for the work.

[email protected]

Blood glucose levels should be targeted to 140-200 mg/dL in surgical or medical ICU patients on insulin therapy, according to advice the American College of Physicians published online May 24 in the American Journal of Medical Quality.

Also, "clinicians should avoid targets less than ... 140 mg/dL because harms are likely to increase with lower blood glucose targets," the group said (Am. J. Med. Qual. 2013 [doi: 10.1177/1062860613489339]).

The advice isn’t new, but instead a restatement of ACP’s 2011 inpatient glycemic control guidelines reissued as part of its "Best Practice Advice" campaign, said Paul G. Shekelle, Ph.D., senior author of both the advice paper and guidelines (Ann. Intern. Med. 2011;154:260-7).

"This is based on the prior guidelines, so there’s nothing new here in that sense. The Best Practice Advice series sometimes runs in parallel to the guidelines, sometimes it is something completely different than any ACP guidelines, and sometimes, like this case, it runs asynchronous to the guidelines. Ideally, these will be more synchronous in the future," Dr. Shekelle, director of the RAND Corporation’s Southern California Evidence-Based Practice Center, said in an interview.

ACP’s advice is largely in keeping with glucose control recommendations from other groups, which have tended toward liberalization in recent years amid evidence that aggressive, euglycemic control in hospitalized patients, even if they have diabetes, doesn’t improve outcomes and carries too high a risk of hypoglycemia and its attendant problems.

"Nobody is advocating tight glycemic control anymore in the hospital. It isn’t necessary and may be harmful," said Dr. Etie S. Moghissi, the lead author on a 2009 inpatient glycemic control consensus statement issued by the American Association of Clinical Endocrinologists and American Diabetes Association (Diabetes Care 2009;32:1119-31).

The consensus statement recommended an upper limit of 180 mg/dL based on the pivotal NICE-SUGAR study, instead of 200 mg/dL, which Dr. Shekelle said ACP chose because it was the upper target limit in several of the additional studies upon which the group based its 2011 guidelines (N. Engl. .J Med. 2009;360:1283-97).

But Dr. Moghissi, who is with the department of medicine at the University of California, Los Angeles, said she’s concerned that 200 mg/dL might be too high.

"We know that when we set targets, people do not achieve them. So when we set a higher target, most of the time people go above that. The concern" is that a target of 200 mg/dL "may be perceived [as meaning that] a little bit over 200 mg/dL is okay," but "above 200 mg/dL, usually there are issues with increased risk of infection, poor wound healing, volume depletion," and other problems, she said in an interview.

Dr. Shekelle and Dr. Moghissi said they have no relevant disclosures.

[email protected]

Blood glucose levels should be targeted to 140-200 mg/dL in surgical or medical ICU patients on insulin therapy, according to advice the American College of Physicians published online May 24 in the American Journal of Medical Quality.

Also, "clinicians should avoid targets less than ... 140 mg/dL because harms are likely to increase with lower blood glucose targets," the group said (Am. J. Med. Qual. 2013 [doi: 10.1177/1062860613489339]).

The advice isn’t new, but instead a restatement of ACP’s 2011 inpatient glycemic control guidelines reissued as part of its "Best Practice Advice" campaign, said Paul G. Shekelle, Ph.D., senior author of both the advice paper and guidelines (Ann. Intern. Med. 2011;154:260-7).

"This is based on the prior guidelines, so there’s nothing new here in that sense. The Best Practice Advice series sometimes runs in parallel to the guidelines, sometimes it is something completely different than any ACP guidelines, and sometimes, like this case, it runs asynchronous to the guidelines. Ideally, these will be more synchronous in the future," Dr. Shekelle, director of the RAND Corporation’s Southern California Evidence-Based Practice Center, said in an interview.

ACP’s advice is largely in keeping with glucose control recommendations from other groups, which have tended toward liberalization in recent years amid evidence that aggressive, euglycemic control in hospitalized patients, even if they have diabetes, doesn’t improve outcomes and carries too high a risk of hypoglycemia and its attendant problems.

"Nobody is advocating tight glycemic control anymore in the hospital. It isn’t necessary and may be harmful," said Dr. Etie S. Moghissi, the lead author on a 2009 inpatient glycemic control consensus statement issued by the American Association of Clinical Endocrinologists and American Diabetes Association (Diabetes Care 2009;32:1119-31).

The consensus statement recommended an upper limit of 180 mg/dL based on the pivotal NICE-SUGAR study, instead of 200 mg/dL, which Dr. Shekelle said ACP chose because it was the upper target limit in several of the additional studies upon which the group based its 2011 guidelines (N. Engl. .J Med. 2009;360:1283-97).

But Dr. Moghissi, who is with the department of medicine at the University of California, Los Angeles, said she’s concerned that 200 mg/dL might be too high.

"We know that when we set targets, people do not achieve them. So when we set a higher target, most of the time people go above that. The concern" is that a target of 200 mg/dL "may be perceived [as meaning that] a little bit over 200 mg/dL is okay," but "above 200 mg/dL, usually there are issues with increased risk of infection, poor wound healing, volume depletion," and other problems, she said in an interview.

Dr. Shekelle and Dr. Moghissi said they have no relevant disclosures.

[email protected]

Blood glucose levels should be targeted to 140-200 mg/dL in surgical or medical ICU patients on insulin therapy, according to advice the American College of Physicians published online May 24 in the American Journal of Medical Quality.

Also, "clinicians should avoid targets less than ... 140 mg/dL because harms are likely to increase with lower blood glucose targets," the group said (Am. J. Med. Qual. 2013 [doi: 10.1177/1062860613489339]).

The advice isn’t new, but instead a restatement of ACP’s 2011 inpatient glycemic control guidelines reissued as part of its "Best Practice Advice" campaign, said Paul G. Shekelle, Ph.D., senior author of both the advice paper and guidelines (Ann. Intern. Med. 2011;154:260-7).

"This is based on the prior guidelines, so there’s nothing new here in that sense. The Best Practice Advice series sometimes runs in parallel to the guidelines, sometimes it is something completely different than any ACP guidelines, and sometimes, like this case, it runs asynchronous to the guidelines. Ideally, these will be more synchronous in the future," Dr. Shekelle, director of the RAND Corporation’s Southern California Evidence-Based Practice Center, said in an interview.

ACP’s advice is largely in keeping with glucose control recommendations from other groups, which have tended toward liberalization in recent years amid evidence that aggressive, euglycemic control in hospitalized patients, even if they have diabetes, doesn’t improve outcomes and carries too high a risk of hypoglycemia and its attendant problems.

"Nobody is advocating tight glycemic control anymore in the hospital. It isn’t necessary and may be harmful," said Dr. Etie S. Moghissi, the lead author on a 2009 inpatient glycemic control consensus statement issued by the American Association of Clinical Endocrinologists and American Diabetes Association (Diabetes Care 2009;32:1119-31).

The consensus statement recommended an upper limit of 180 mg/dL based on the pivotal NICE-SUGAR study, instead of 200 mg/dL, which Dr. Shekelle said ACP chose because it was the upper target limit in several of the additional studies upon which the group based its 2011 guidelines (N. Engl. .J Med. 2009;360:1283-97).

But Dr. Moghissi, who is with the department of medicine at the University of California, Los Angeles, said she’s concerned that 200 mg/dL might be too high.

"We know that when we set targets, people do not achieve them. So when we set a higher target, most of the time people go above that. The concern" is that a target of 200 mg/dL "may be perceived [as meaning that] a little bit over 200 mg/dL is okay," but "above 200 mg/dL, usually there are issues with increased risk of infection, poor wound healing, volume depletion," and other problems, she said in an interview.

Dr. Shekelle and Dr. Moghissi said they have no relevant disclosures.

[email protected]

PORTLAND, ORE. – Fecal transplants are proving useful for pediatric ulcerative colitis, and enteral feedings are already well established in Europe to help kids with Crohn’s disease; together, the findings suggest that gut flora is more important to pediatric gastrointestinal health than previously thought, according to Dr. Linda Muir.

In both cases, "they think a lot of [the effect] has to do with modification of bowel flora. I think we are all starting to realize that the bacteria we carry around in our bodies drive and determine a lot of our health and illness. A lot of autoimmune disorders may be related to [imbalances in our] gut microbiome," said Dr. Muir, chief of pediatric gastroenterology at the Oregon Health and Science University in Portland.

Although it’s unclear at the moment if donor stool is best delivered by nasogastric tube, colonoscope, or enema, it’s easy to understand how fecal transplants might correct such an imbalance. They’ve proven remarkably effective for Clostridium difficile infections, and now "good studies are being published for [their] application in [inflammatory bowel disease]. They’re very promising" for pediatric ulcerative colitis (UC), she said at a conference sponsored by the North Pacific Pediatric Society.

In one study from Michigan State and Emory universities, 10 children (aged 7-21 years) with mild to moderate UC received fecal enemas, 165 mL on average, for 5 days. Seven of nine (78%) – the 10th couldn’t retain the enema – showed a significant clinical response within a week, including three remissions. Six (67%) maintained their response at 1 month. There were no serious adverse events (J. Pediatr. Gastroenterol. Nutr. 2013;56:597-601).

If other studies have results like that, "I think [fecal transplants] may become more common in our practice. [Perhaps] we can turn around kids who are not responding to medication," Dr. Muir said.

It’s less clear how enteral feedings might rebalance the gut flora in Crohn’s kids. Typically, a child gets 100% of his or her nutrition for a period of time from milk-based products such as Ensure, Boost, or Nutren delivered by nasogastric tube at home; older children often learn to place the tube themselves. Dr. Muir favors products that pack the most calories in the least volume so kids don’t have to get up in the middle of the night to urinate; she uses enteral therapy as a supplement to the more usual Crohn’s approaches.

"Why does this make them better? We don’t know. Is it because of the nutrients? Are you removing food protein antigens? It may tie together with what we are seeing with fecal transplant, somehow modifying the fecal flora to allow mucosal healing. [Kids] obviously have much improved growth and they actually get true mucosal healing" on enteral feeding, unlike with steroids, Dr. Muir said.

Whatever the reason, pediatric gastroenterologists in Europe have been using the technique for years and touting its benefits. "They don’t use nearly the steroids U.S. physicians use," she said. In 2012, the North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition noted that enteral feeding offers "an alternative to corticosteroids to induce remission in pediatric CD [Crohn’s disease] and should be supported as a first-line induction therapy in pediatric CD" (J. Pediatr. Gastroenterol. Nutr. 2012;54:298-305). And it just might be the case that CD kids don’t need to get all their calories through a tube. Researchers at the Children’s Hospital of Philadelphia recently reviewed the charts of 23 kids who got 80%-90% of their calories by enteral feedings and found that 20 (87%) had a clinical response, and 15 (65%) went into remission after a mean of 2 months (Inflamm. Bowel Dis. 2013;19:1374-8).

Even though they were on the tube at home, they could pull it out in the morning and have lunch with their friends at school just like any other kid, Dr. Muir said.

She said she had no relevant financial disclosures.

[email protected]

PORTLAND, ORE. – Fecal transplants are proving useful for pediatric ulcerative colitis, and enteral feedings are already well established in Europe to help kids with Crohn’s disease; together, the findings suggest that gut flora is more important to pediatric gastrointestinal health than previously thought, according to Dr. Linda Muir.

In both cases, "they think a lot of [the effect] has to do with modification of bowel flora. I think we are all starting to realize that the bacteria we carry around in our bodies drive and determine a lot of our health and illness. A lot of autoimmune disorders may be related to [imbalances in our] gut microbiome," said Dr. Muir, chief of pediatric gastroenterology at the Oregon Health and Science University in Portland.

Although it’s unclear at the moment if donor stool is best delivered by nasogastric tube, colonoscope, or enema, it’s easy to understand how fecal transplants might correct such an imbalance. They’ve proven remarkably effective for Clostridium difficile infections, and now "good studies are being published for [their] application in [inflammatory bowel disease]. They’re very promising" for pediatric ulcerative colitis (UC), she said at a conference sponsored by the North Pacific Pediatric Society.

In one study from Michigan State and Emory universities, 10 children (aged 7-21 years) with mild to moderate UC received fecal enemas, 165 mL on average, for 5 days. Seven of nine (78%) – the 10th couldn’t retain the enema – showed a significant clinical response within a week, including three remissions. Six (67%) maintained their response at 1 month. There were no serious adverse events (J. Pediatr. Gastroenterol. Nutr. 2013;56:597-601).

If other studies have results like that, "I think [fecal transplants] may become more common in our practice. [Perhaps] we can turn around kids who are not responding to medication," Dr. Muir said.

It’s less clear how enteral feedings might rebalance the gut flora in Crohn’s kids. Typically, a child gets 100% of his or her nutrition for a period of time from milk-based products such as Ensure, Boost, or Nutren delivered by nasogastric tube at home; older children often learn to place the tube themselves. Dr. Muir favors products that pack the most calories in the least volume so kids don’t have to get up in the middle of the night to urinate; she uses enteral therapy as a supplement to the more usual Crohn’s approaches.

"Why does this make them better? We don’t know. Is it because of the nutrients? Are you removing food protein antigens? It may tie together with what we are seeing with fecal transplant, somehow modifying the fecal flora to allow mucosal healing. [Kids] obviously have much improved growth and they actually get true mucosal healing" on enteral feeding, unlike with steroids, Dr. Muir said.

Whatever the reason, pediatric gastroenterologists in Europe have been using the technique for years and touting its benefits. "They don’t use nearly the steroids U.S. physicians use," she said. In 2012, the North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition noted that enteral feeding offers "an alternative to corticosteroids to induce remission in pediatric CD [Crohn’s disease] and should be supported as a first-line induction therapy in pediatric CD" (J. Pediatr. Gastroenterol. Nutr. 2012;54:298-305). And it just might be the case that CD kids don’t need to get all their calories through a tube. Researchers at the Children’s Hospital of Philadelphia recently reviewed the charts of 23 kids who got 80%-90% of their calories by enteral feedings and found that 20 (87%) had a clinical response, and 15 (65%) went into remission after a mean of 2 months (Inflamm. Bowel Dis. 2013;19:1374-8).

Even though they were on the tube at home, they could pull it out in the morning and have lunch with their friends at school just like any other kid, Dr. Muir said.

She said she had no relevant financial disclosures.

[email protected]

PORTLAND, ORE. – Fecal transplants are proving useful for pediatric ulcerative colitis, and enteral feedings are already well established in Europe to help kids with Crohn’s disease; together, the findings suggest that gut flora is more important to pediatric gastrointestinal health than previously thought, according to Dr. Linda Muir.

In both cases, "they think a lot of [the effect] has to do with modification of bowel flora. I think we are all starting to realize that the bacteria we carry around in our bodies drive and determine a lot of our health and illness. A lot of autoimmune disorders may be related to [imbalances in our] gut microbiome," said Dr. Muir, chief of pediatric gastroenterology at the Oregon Health and Science University in Portland.

Although it’s unclear at the moment if donor stool is best delivered by nasogastric tube, colonoscope, or enema, it’s easy to understand how fecal transplants might correct such an imbalance. They’ve proven remarkably effective for Clostridium difficile infections, and now "good studies are being published for [their] application in [inflammatory bowel disease]. They’re very promising" for pediatric ulcerative colitis (UC), she said at a conference sponsored by the North Pacific Pediatric Society.

In one study from Michigan State and Emory universities, 10 children (aged 7-21 years) with mild to moderate UC received fecal enemas, 165 mL on average, for 5 days. Seven of nine (78%) – the 10th couldn’t retain the enema – showed a significant clinical response within a week, including three remissions. Six (67%) maintained their response at 1 month. There were no serious adverse events (J. Pediatr. Gastroenterol. Nutr. 2013;56:597-601).

If other studies have results like that, "I think [fecal transplants] may become more common in our practice. [Perhaps] we can turn around kids who are not responding to medication," Dr. Muir said.

It’s less clear how enteral feedings might rebalance the gut flora in Crohn’s kids. Typically, a child gets 100% of his or her nutrition for a period of time from milk-based products such as Ensure, Boost, or Nutren delivered by nasogastric tube at home; older children often learn to place the tube themselves. Dr. Muir favors products that pack the most calories in the least volume so kids don’t have to get up in the middle of the night to urinate; she uses enteral therapy as a supplement to the more usual Crohn’s approaches.

"Why does this make them better? We don’t know. Is it because of the nutrients? Are you removing food protein antigens? It may tie together with what we are seeing with fecal transplant, somehow modifying the fecal flora to allow mucosal healing. [Kids] obviously have much improved growth and they actually get true mucosal healing" on enteral feeding, unlike with steroids, Dr. Muir said.

Whatever the reason, pediatric gastroenterologists in Europe have been using the technique for years and touting its benefits. "They don’t use nearly the steroids U.S. physicians use," she said. In 2012, the North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition noted that enteral feeding offers "an alternative to corticosteroids to induce remission in pediatric CD [Crohn’s disease] and should be supported as a first-line induction therapy in pediatric CD" (J. Pediatr. Gastroenterol. Nutr. 2012;54:298-305). And it just might be the case that CD kids don’t need to get all their calories through a tube. Researchers at the Children’s Hospital of Philadelphia recently reviewed the charts of 23 kids who got 80%-90% of their calories by enteral feedings and found that 20 (87%) had a clinical response, and 15 (65%) went into remission after a mean of 2 months (Inflamm. Bowel Dis. 2013;19:1374-8).

Even though they were on the tube at home, they could pull it out in the morning and have lunch with their friends at school just like any other kid, Dr. Muir said.

She said she had no relevant financial disclosures.

[email protected]

LAS VEGAS – Vancomycin is as safe on the kidneys of critically ill patients as linezolid, so long as trough levels don’t exceed the recommended upper limit of 20 mcg/mL, according to researchers from the University of Virginia in Charlottesville.

"When correct dosing is performed, the use of alternative agents to treat Gram-positive infections – specifically to avoid [vancomycin] nephrotoxicity – is unnecessary. Vancomycin use in critically ill patients is no different than linezolid use regarding nephrotoxicity or new-onset need for hemodialysis," said lead investigator Stephen Davies, a resident in the department of surgery, said at the annual meeting of the Surgical Infection Society.

The kidney safety of vancomycin has been in doubt, with mixed results from prior studies. To shed light on the issue, Dr. Davies and his team compared renal outcomes in 298 critically ill patients treated with vancomycin for 571 Gram-positive infections with outcomes in 247 patients treated with linezolid for 475 Gram-positive infections.

Infection sites included the lungs, peritoneum, blood stream, and urinary tract, among others, and isolates included Staphylococcus aureus (77 methicillin-resistant S. aureus), Enterococcus faecium (67 vancomycin-resistant Enterococcus), E. faecalis, and Streptococcus species. Vancomycin patients were dosed at 15-20 mg/kg, with serial trough monitoring, and treated for a mean of 16.2 days, vs. 14.3 days for linezolid. Patients were on no other nephrotoxic agents.

In the end, "there were no [statistically significant] differences between the two groups regarding maximum creatinine during treatment, final creatinine after treatment, change in creatinine maximum and initial values, and final and initial creatinine values." There were also no differences "in new-onset hemodialysis or death," Dr. Davies said.

APACHE II (Acute Physiology and Chronic Health Evaluation II) scores above 30 and initial creatinine levels above 1.2 mg/dL both predicted the need for new-onset hemodialysis, but antibiotic choice did not.

Those same two variables also predicted an increase in creatinine of more than 1.0 mg/dl during treatment; vancomycin use did, as well (relative risk, vancomycin 0.49; 95% confidence interval: 0.25-0.94). Concerned, the team looked into the issue. "What we found was that a rise in creatinine was typically not encountered until trough levels greater than 20 mg/dL were reached. As long as you stay within the recommended doses, you should be safe," Dr. Davies said.

There were no statistically significant baseline differences between the two groups in renal function, hemodialysis, creatinine levels, or APACHE II scores.

Despite the results, Dr. Philip Barie, who helped moderate Dr. Davies’ talk, said in an interview that he’s still concerned about vancomycin kidney safety.

"We are having to use higher doses to treat tougher bugs, and whereas nephrotoxicity pretty much went away with vancomycin after they purified the drug [decades ago], now we are having to use higher doses more, and nephrotoxicity is beginning to creep back into the picture. You have to dose really carefully, and if you have an organism that is among the more resistant to vancomycin, the safest thing to do with vancomycin is to use linezolid," said Dr. Barie, a professor of surgery and public heath at Cornell University, New York.

Dr. Davies and Dr. Barie reported no relevant disclosures.

[email protected]

LAS VEGAS – Vancomycin is as safe on the kidneys of critically ill patients as linezolid, so long as trough levels don’t exceed the recommended upper limit of 20 mcg/mL, according to researchers from the University of Virginia in Charlottesville.

"When correct dosing is performed, the use of alternative agents to treat Gram-positive infections – specifically to avoid [vancomycin] nephrotoxicity – is unnecessary. Vancomycin use in critically ill patients is no different than linezolid use regarding nephrotoxicity or new-onset need for hemodialysis," said lead investigator Stephen Davies, a resident in the department of surgery, said at the annual meeting of the Surgical Infection Society.

The kidney safety of vancomycin has been in doubt, with mixed results from prior studies. To shed light on the issue, Dr. Davies and his team compared renal outcomes in 298 critically ill patients treated with vancomycin for 571 Gram-positive infections with outcomes in 247 patients treated with linezolid for 475 Gram-positive infections.

Infection sites included the lungs, peritoneum, blood stream, and urinary tract, among others, and isolates included Staphylococcus aureus (77 methicillin-resistant S. aureus), Enterococcus faecium (67 vancomycin-resistant Enterococcus), E. faecalis, and Streptococcus species. Vancomycin patients were dosed at 15-20 mg/kg, with serial trough monitoring, and treated for a mean of 16.2 days, vs. 14.3 days for linezolid. Patients were on no other nephrotoxic agents.

In the end, "there were no [statistically significant] differences between the two groups regarding maximum creatinine during treatment, final creatinine after treatment, change in creatinine maximum and initial values, and final and initial creatinine values." There were also no differences "in new-onset hemodialysis or death," Dr. Davies said.

APACHE II (Acute Physiology and Chronic Health Evaluation II) scores above 30 and initial creatinine levels above 1.2 mg/dL both predicted the need for new-onset hemodialysis, but antibiotic choice did not.

Those same two variables also predicted an increase in creatinine of more than 1.0 mg/dl during treatment; vancomycin use did, as well (relative risk, vancomycin 0.49; 95% confidence interval: 0.25-0.94). Concerned, the team looked into the issue. "What we found was that a rise in creatinine was typically not encountered until trough levels greater than 20 mg/dL were reached. As long as you stay within the recommended doses, you should be safe," Dr. Davies said.

There were no statistically significant baseline differences between the two groups in renal function, hemodialysis, creatinine levels, or APACHE II scores.

Despite the results, Dr. Philip Barie, who helped moderate Dr. Davies’ talk, said in an interview that he’s still concerned about vancomycin kidney safety.

"We are having to use higher doses to treat tougher bugs, and whereas nephrotoxicity pretty much went away with vancomycin after they purified the drug [decades ago], now we are having to use higher doses more, and nephrotoxicity is beginning to creep back into the picture. You have to dose really carefully, and if you have an organism that is among the more resistant to vancomycin, the safest thing to do with vancomycin is to use linezolid," said Dr. Barie, a professor of surgery and public heath at Cornell University, New York.

Dr. Davies and Dr. Barie reported no relevant disclosures.

[email protected]

LAS VEGAS – Vancomycin is as safe on the kidneys of critically ill patients as linezolid, so long as trough levels don’t exceed the recommended upper limit of 20 mcg/mL, according to researchers from the University of Virginia in Charlottesville.

"When correct dosing is performed, the use of alternative agents to treat Gram-positive infections – specifically to avoid [vancomycin] nephrotoxicity – is unnecessary. Vancomycin use in critically ill patients is no different than linezolid use regarding nephrotoxicity or new-onset need for hemodialysis," said lead investigator Stephen Davies, a resident in the department of surgery, said at the annual meeting of the Surgical Infection Society.

The kidney safety of vancomycin has been in doubt, with mixed results from prior studies. To shed light on the issue, Dr. Davies and his team compared renal outcomes in 298 critically ill patients treated with vancomycin for 571 Gram-positive infections with outcomes in 247 patients treated with linezolid for 475 Gram-positive infections.

Infection sites included the lungs, peritoneum, blood stream, and urinary tract, among others, and isolates included Staphylococcus aureus (77 methicillin-resistant S. aureus), Enterococcus faecium (67 vancomycin-resistant Enterococcus), E. faecalis, and Streptococcus species. Vancomycin patients were dosed at 15-20 mg/kg, with serial trough monitoring, and treated for a mean of 16.2 days, vs. 14.3 days for linezolid. Patients were on no other nephrotoxic agents.

In the end, "there were no [statistically significant] differences between the two groups regarding maximum creatinine during treatment, final creatinine after treatment, change in creatinine maximum and initial values, and final and initial creatinine values." There were also no differences "in new-onset hemodialysis or death," Dr. Davies said.

APACHE II (Acute Physiology and Chronic Health Evaluation II) scores above 30 and initial creatinine levels above 1.2 mg/dL both predicted the need for new-onset hemodialysis, but antibiotic choice did not.

Those same two variables also predicted an increase in creatinine of more than 1.0 mg/dl during treatment; vancomycin use did, as well (relative risk, vancomycin 0.49; 95% confidence interval: 0.25-0.94). Concerned, the team looked into the issue. "What we found was that a rise in creatinine was typically not encountered until trough levels greater than 20 mg/dL were reached. As long as you stay within the recommended doses, you should be safe," Dr. Davies said.

There were no statistically significant baseline differences between the two groups in renal function, hemodialysis, creatinine levels, or APACHE II scores.

Despite the results, Dr. Philip Barie, who helped moderate Dr. Davies’ talk, said in an interview that he’s still concerned about vancomycin kidney safety.

"We are having to use higher doses to treat tougher bugs, and whereas nephrotoxicity pretty much went away with vancomycin after they purified the drug [decades ago], now we are having to use higher doses more, and nephrotoxicity is beginning to creep back into the picture. You have to dose really carefully, and if you have an organism that is among the more resistant to vancomycin, the safest thing to do with vancomycin is to use linezolid," said Dr. Barie, a professor of surgery and public heath at Cornell University, New York.

Dr. Davies and Dr. Barie reported no relevant disclosures.

[email protected]

LAS VEGAS – Although inpatient glucose levels in critically ill adults are generally kept between 140 and 180 mg/dL, Toronto investigators have found that it might be best to keep pediatric burn patients between 130 and 140 mg/dL.

Morbidity and mortality outcomes were better in that range when 760 children – the majority boys under 10 years old burned over half their bodies, usually by flame – were followed for 2 months after ICU admission.

"We used about 300,000 glucose measurements" during the study "to determine the ideal glucose target. For burn patients, the range of 130-140 mg/dL should be targeted. You avoid hyperglycemia as well as hypoglycemia. [Also,] a major factor to be considered" in burns "is that protein glycosylation starts at around 150 mg/dL; we burn surgeons try to be below that," said lead researcher Dr. Marc Jeschke, director of the burn center at Toronto’s Sunnybrook Health Sciences Centre.

Dr. Jeschke’s study isn’t the first to suggest that range for critically ill children. "There seems to be a signal [across] studies that this is the range we should target in order to see the benefits of glucose control," he said (e.g., J. Pediatr. 2009;155:734-9).

It’s been known that burns cause a hyperglycemic response, especially those in excess of 40% of the body. When not reined in, "you lose more grafts, you have more infections, and you [are more likely to] die," Dr. Jeschke said at the annual meeting of the Surgical Infection Society.

In its investigation, however, his team also found that, as in critically ill adults, hypoglycemia must also be avoided in pediatric burn patients.

Eighty-five patients had one hypoglycemia episode in the study, defined as blood glucose below 60?mg/dL, and 107 had two or more. The remaining 568 children had no episodes.

Twenty-one percent of patients who had hypoglycemic episodes – versus 6.5% of those who did not – developed sepsis; 47.9%, versus 10%, developed multiple organ failure, and a quarter died. Mortality was 3.3% in the nonhypoglycemic group. The differences were statistically significant.

"We [also] found that hypoglycemic patients are more inflammatory and hypermetabolic," Dr. Jeschke said.

Hypoglycemia was associated with larger burns and more inhalation injuries, so the team did a propensity analysis comparing 166 children who had hypoglycemic episodes to 166 with similar injury severities who did not.

Among those matched patients, children were 2.67 more likely to die (95% confidence interval 1.15-6.20) if they had one hypoglycemic episode, 5.58 more likely to die if they had two (95% CI 2.26-13.81), and 9.25 times more likely if they had three (95% CI 4.30-19.88).

Hypoglycemia during sepsis or at time of death was excluded in the analysis. Even so, "we don’t know" if hypoglycemia was the cause of death or a marker for another fatal process, Dr. Jeschke noted.

Whatever the case, the results indicate that just as in sick adults, "glycemic control in [pediatric] burns is an integral part of good clinical outcomes," he said.

Dr. Jeschke said he has no conflicts of interest.

[email protected]

LAS VEGAS – Although inpatient glucose levels in critically ill adults are generally kept between 140 and 180 mg/dL, Toronto investigators have found that it might be best to keep pediatric burn patients between 130 and 140 mg/dL.

Morbidity and mortality outcomes were better in that range when 760 children – the majority boys under 10 years old burned over half their bodies, usually by flame – were followed for 2 months after ICU admission.

"We used about 300,000 glucose measurements" during the study "to determine the ideal glucose target. For burn patients, the range of 130-140 mg/dL should be targeted. You avoid hyperglycemia as well as hypoglycemia. [Also,] a major factor to be considered" in burns "is that protein glycosylation starts at around 150 mg/dL; we burn surgeons try to be below that," said lead researcher Dr. Marc Jeschke, director of the burn center at Toronto’s Sunnybrook Health Sciences Centre.

Dr. Jeschke’s study isn’t the first to suggest that range for critically ill children. "There seems to be a signal [across] studies that this is the range we should target in order to see the benefits of glucose control," he said (e.g., J. Pediatr. 2009;155:734-9).

It’s been known that burns cause a hyperglycemic response, especially those in excess of 40% of the body. When not reined in, "you lose more grafts, you have more infections, and you [are more likely to] die," Dr. Jeschke said at the annual meeting of the Surgical Infection Society.

In its investigation, however, his team also found that, as in critically ill adults, hypoglycemia must also be avoided in pediatric burn patients.

Eighty-five patients had one hypoglycemia episode in the study, defined as blood glucose below 60?mg/dL, and 107 had two or more. The remaining 568 children had no episodes.

Twenty-one percent of patients who had hypoglycemic episodes – versus 6.5% of those who did not – developed sepsis; 47.9%, versus 10%, developed multiple organ failure, and a quarter died. Mortality was 3.3% in the nonhypoglycemic group. The differences were statistically significant.

"We [also] found that hypoglycemic patients are more inflammatory and hypermetabolic," Dr. Jeschke said.

Hypoglycemia was associated with larger burns and more inhalation injuries, so the team did a propensity analysis comparing 166 children who had hypoglycemic episodes to 166 with similar injury severities who did not.

Among those matched patients, children were 2.67 more likely to die (95% confidence interval 1.15-6.20) if they had one hypoglycemic episode, 5.58 more likely to die if they had two (95% CI 2.26-13.81), and 9.25 times more likely if they had three (95% CI 4.30-19.88).

Hypoglycemia during sepsis or at time of death was excluded in the analysis. Even so, "we don’t know" if hypoglycemia was the cause of death or a marker for another fatal process, Dr. Jeschke noted.

Whatever the case, the results indicate that just as in sick adults, "glycemic control in [pediatric] burns is an integral part of good clinical outcomes," he said.

Dr. Jeschke said he has no conflicts of interest.

[email protected]

LAS VEGAS – Although inpatient glucose levels in critically ill adults are generally kept between 140 and 180 mg/dL, Toronto investigators have found that it might be best to keep pediatric burn patients between 130 and 140 mg/dL.

Morbidity and mortality outcomes were better in that range when 760 children – the majority boys under 10 years old burned over half their bodies, usually by flame – were followed for 2 months after ICU admission.

"We used about 300,000 glucose measurements" during the study "to determine the ideal glucose target. For burn patients, the range of 130-140 mg/dL should be targeted. You avoid hyperglycemia as well as hypoglycemia. [Also,] a major factor to be considered" in burns "is that protein glycosylation starts at around 150 mg/dL; we burn surgeons try to be below that," said lead researcher Dr. Marc Jeschke, director of the burn center at Toronto’s Sunnybrook Health Sciences Centre.

Dr. Jeschke’s study isn’t the first to suggest that range for critically ill children. "There seems to be a signal [across] studies that this is the range we should target in order to see the benefits of glucose control," he said (e.g., J. Pediatr. 2009;155:734-9).

It’s been known that burns cause a hyperglycemic response, especially those in excess of 40% of the body. When not reined in, "you lose more grafts, you have more infections, and you [are more likely to] die," Dr. Jeschke said at the annual meeting of the Surgical Infection Society.

In its investigation, however, his team also found that, as in critically ill adults, hypoglycemia must also be avoided in pediatric burn patients.

Eighty-five patients had one hypoglycemia episode in the study, defined as blood glucose below 60?mg/dL, and 107 had two or more. The remaining 568 children had no episodes.

Twenty-one percent of patients who had hypoglycemic episodes – versus 6.5% of those who did not – developed sepsis; 47.9%, versus 10%, developed multiple organ failure, and a quarter died. Mortality was 3.3% in the nonhypoglycemic group. The differences were statistically significant.

"We [also] found that hypoglycemic patients are more inflammatory and hypermetabolic," Dr. Jeschke said.

Hypoglycemia was associated with larger burns and more inhalation injuries, so the team did a propensity analysis comparing 166 children who had hypoglycemic episodes to 166 with similar injury severities who did not.

Among those matched patients, children were 2.67 more likely to die (95% confidence interval 1.15-6.20) if they had one hypoglycemic episode, 5.58 more likely to die if they had two (95% CI 2.26-13.81), and 9.25 times more likely if they had three (95% CI 4.30-19.88).

Hypoglycemia during sepsis or at time of death was excluded in the analysis. Even so, "we don’t know" if hypoglycemia was the cause of death or a marker for another fatal process, Dr. Jeschke noted.

Whatever the case, the results indicate that just as in sick adults, "glycemic control in [pediatric] burns is an integral part of good clinical outcomes," he said.

Dr. Jeschke said he has no conflicts of interest.

[email protected]

LAS VEGAS – It’s a good idea to swab both the throat and nose when looking for Staphylococcus aureus colonization; doing so picks up cases missed by swabbing the nares alone, according to researchers from the Baylor College of Medicine in Houston.

That holds true whether testing is by culture or PCR [polymerase chain reaction], said the lead investigator, Dr. Meredith Knofsky, a surgery resident there.

The team swabbed both areas preoperatively and on the day of surgery in patients undergoing operations involving hardware implants, such as new knees or hips. The 109 samples they obtained were then tested for methicillin-sensitive (MSSA) and methicillin-resistant (MRSA) S. aureus by both MRSA select media culture and the GeneXpert PCR system.

By culture, 7 throat swabs and 18 nares swabs were positive for MRSA; 20 throat and 40 nares swabs were positive for MSSA.

Courtesy Janice Haney Carr/CDC

By PCR, 7 throat and 21 nares samples were MRSA positive; 33 throat and 51 nares swabs were positive for MSSA.

The detection rate differences weren’t surprising; PCR is known to be more accurate and the results confirm its greater sensitivity, Dr. Knofsky said at the annual meeting of the Surgical Infection Society.

The bigger finding is that "throat screening identifies additional patients missed by screening the nares alone," she said.

Adding PCR throat testing to PCR nasal screening picked up one additional MRSA and 14 additional MSSA carriers. Similarly, the addition of throat cultures to nares cultures picked up an additional MRSA and eight additional MSSA carriers.

Not infrequently, patients were positive in one location, such as the throat, but not in the other. Although "nasal carrier status of Staphylococcus aureus is an important risk factor for surgical site infections," it’s not known at the moment if that’s also true for carriage limited to the throat, Dr. Knofsky said.

"We have plans to go back and evaluate which of these patients colonized only in the oropharynx actually developed a surgical site infection. It’s important that we invest in evaluating pharyngeal carriage," she said.

In the meantime, session moderator and surgeon Dr. E. Patchen Dellinger of the University of Washington in Seattle, noted that MSSA in the study "was two to three times more common than MRSA; an MSSA infection of implanted hardware is just as devastating to the patient as an MRSA infection. I would like to urge that we not focus on MRSA alone, but consider at least in selected surgical populations seeking and suppressing any Staph that colonizes our surgical patients."

PCR could help with that because it "has the advantage of very rapid answers. The logistics of getting [colonization] information in time to do something [before an operation] is very difficult for us. PCR could make that better, [but it] isn’t standard of care mostly because it costs a lot more" than does culture, he said.

Dr. Knofsky and Dr. Dellinger said they have no relevant disclosures.

[email protected]

LAS VEGAS – It’s a good idea to swab both the throat and nose when looking for Staphylococcus aureus colonization; doing so picks up cases missed by swabbing the nares alone, according to researchers from the Baylor College of Medicine in Houston.

That holds true whether testing is by culture or PCR [polymerase chain reaction], said the lead investigator, Dr. Meredith Knofsky, a surgery resident there.

The team swabbed both areas preoperatively and on the day of surgery in patients undergoing operations involving hardware implants, such as new knees or hips. The 109 samples they obtained were then tested for methicillin-sensitive (MSSA) and methicillin-resistant (MRSA) S. aureus by both MRSA select media culture and the GeneXpert PCR system.

By culture, 7 throat swabs and 18 nares swabs were positive for MRSA; 20 throat and 40 nares swabs were positive for MSSA.

Courtesy Janice Haney Carr/CDC

By PCR, 7 throat and 21 nares samples were MRSA positive; 33 throat and 51 nares swabs were positive for MSSA.

The detection rate differences weren’t surprising; PCR is known to be more accurate and the results confirm its greater sensitivity, Dr. Knofsky said at the annual meeting of the Surgical Infection Society.

The bigger finding is that "throat screening identifies additional patients missed by screening the nares alone," she said.

Adding PCR throat testing to PCR nasal screening picked up one additional MRSA and 14 additional MSSA carriers. Similarly, the addition of throat cultures to nares cultures picked up an additional MRSA and eight additional MSSA carriers.

Not infrequently, patients were positive in one location, such as the throat, but not in the other. Although "nasal carrier status of Staphylococcus aureus is an important risk factor for surgical site infections," it’s not known at the moment if that’s also true for carriage limited to the throat, Dr. Knofsky said.

"We have plans to go back and evaluate which of these patients colonized only in the oropharynx actually developed a surgical site infection. It’s important that we invest in evaluating pharyngeal carriage," she said.

In the meantime, session moderator and surgeon Dr. E. Patchen Dellinger of the University of Washington in Seattle, noted that MSSA in the study "was two to three times more common than MRSA; an MSSA infection of implanted hardware is just as devastating to the patient as an MRSA infection. I would like to urge that we not focus on MRSA alone, but consider at least in selected surgical populations seeking and suppressing any Staph that colonizes our surgical patients."

PCR could help with that because it "has the advantage of very rapid answers. The logistics of getting [colonization] information in time to do something [before an operation] is very difficult for us. PCR could make that better, [but it] isn’t standard of care mostly because it costs a lot more" than does culture, he said.

Dr. Knofsky and Dr. Dellinger said they have no relevant disclosures.

[email protected]

LAS VEGAS – It’s a good idea to swab both the throat and nose when looking for Staphylococcus aureus colonization; doing so picks up cases missed by swabbing the nares alone, according to researchers from the Baylor College of Medicine in Houston.

That holds true whether testing is by culture or PCR [polymerase chain reaction], said the lead investigator, Dr. Meredith Knofsky, a surgery resident there.

The team swabbed both areas preoperatively and on the day of surgery in patients undergoing operations involving hardware implants, such as new knees or hips. The 109 samples they obtained were then tested for methicillin-sensitive (MSSA) and methicillin-resistant (MRSA) S. aureus by both MRSA select media culture and the GeneXpert PCR system.

By culture, 7 throat swabs and 18 nares swabs were positive for MRSA; 20 throat and 40 nares swabs were positive for MSSA.

Courtesy Janice Haney Carr/CDC

By PCR, 7 throat and 21 nares samples were MRSA positive; 33 throat and 51 nares swabs were positive for MSSA.

The detection rate differences weren’t surprising; PCR is known to be more accurate and the results confirm its greater sensitivity, Dr. Knofsky said at the annual meeting of the Surgical Infection Society.

The bigger finding is that "throat screening identifies additional patients missed by screening the nares alone," she said.

Adding PCR throat testing to PCR nasal screening picked up one additional MRSA and 14 additional MSSA carriers. Similarly, the addition of throat cultures to nares cultures picked up an additional MRSA and eight additional MSSA carriers.

Not infrequently, patients were positive in one location, such as the throat, but not in the other. Although "nasal carrier status of Staphylococcus aureus is an important risk factor for surgical site infections," it’s not known at the moment if that’s also true for carriage limited to the throat, Dr. Knofsky said.

"We have plans to go back and evaluate which of these patients colonized only in the oropharynx actually developed a surgical site infection. It’s important that we invest in evaluating pharyngeal carriage," she said.

In the meantime, session moderator and surgeon Dr. E. Patchen Dellinger of the University of Washington in Seattle, noted that MSSA in the study "was two to three times more common than MRSA; an MSSA infection of implanted hardware is just as devastating to the patient as an MRSA infection. I would like to urge that we not focus on MRSA alone, but consider at least in selected surgical populations seeking and suppressing any Staph that colonizes our surgical patients."

PCR could help with that because it "has the advantage of very rapid answers. The logistics of getting [colonization] information in time to do something [before an operation] is very difficult for us. PCR could make that better, [but it] isn’t standard of care mostly because it costs a lot more" than does culture, he said.

Dr. Knofsky and Dr. Dellinger said they have no relevant disclosures.

[email protected]

PORTLAND, ORE. – Joint pain isn’t usually part of the clinical picture when children have juvenile idiopathic arthritis, according to pediatric rheumatologist Victoria Cartwright.

"In fact, it helps you discount that juvenile arthritis is going on," she said at a conference sponsored by the North Pacific Pediatric Society.

Pain as an isolated complaint has a negative predictive value for pediatric rheumatic disease of 0.99 and, as one of several reasons for a rheumatology referral, a negative predictive value of 0.91 (Pediatrics 2002;110:354-9).

"That’s better than any lab test or x-ray [and] about as good as MRI. [So] if you’re calling me saying that Johnny has knee pain, I’m not as worried about JIA [juvenile idiopathic arthritis]. I may be worried about [Henoch-Schönlein purpura (HSP)] or a mechanical issue or something else ... but [not] JIA," said Dr. Cartwright of Randall Children’s Hospital at Legacy Emanuel in Portland, Ore.

On the other hand, "labs really don’t help one way or the other to make the diagnosis of arthritis. Rheumatoid factor doesn’t help. [Erythrocyte sedimentation rate] is helpful if it’s abnormal, but only kind of. I can have a kid who has 20 inflamed joints and their sed rate is 2; I can have another kid with one swollen knee, and their sed rate is 30. [However,] if the sed rate is over 100, I worry about other stuff," such as systemic disease, lupus, HSP, vasculitis, or malignancy, she said.

If those problems have been ruled out, Dr. Cartwright said she usually waits until kids have been on NSAIDs – she favors weight-dosed ibuprofen or naproxen – for a month before getting a complete blood count, a liver enzyme panel, and an antinuclear antibody (ANA) test. "I’m not a big fan of labs up front" for JIA "because we end up chasing the lab illness a little bit," she said. JIA kids also need a referral to an ophthalmologist to check for iritis. If this condition is present, ANA testing helps tell how aggressive it is.

As for assessment, Dr. Cartwright noted that obesity makes it tough to check the ankle for swelling; extra pounds obscure the Achilles tendon and the divots to either side. "It’s one of the joints I image a lot with MRI because I [often] can’t see it very well," she said.

Swelling can be hard to detect in kids with polyarticular disease because it can be more or less even on either side of the body, and, thus, less noticeable. One trick, especially helpful with the hands, is to compare the skin folds and wrinkles around corresponding joints. If they aren’t symmetrical, it could be due to swelling.

Check for jaw arthritis, too, Dr. Cartwright said. A lot of children don’t even know there’s a problem because it’s painless, but left unchecked, jaw arthritis can cause growth abnormalities – associated asymmetries are most obvious when the head’s tilted back – and make it difficult to fully open the mouth.

Patients should be able to insert their three middle fingers vertically into their mouth. When they can’t, "we do some dynamic stretching. We’ll stack tongue blades" to reach the appropriate thickness and have patients place them in their mouth to "stretch the muscles out, kind of like doing [physical therapy]," Dr. Cartwright said.

She said she has no relevant financial disclosures.

[email protected]

PORTLAND, ORE. – Joint pain isn’t usually part of the clinical picture when children have juvenile idiopathic arthritis, according to pediatric rheumatologist Victoria Cartwright.

"In fact, it helps you discount that juvenile arthritis is going on," she said at a conference sponsored by the North Pacific Pediatric Society.

Pain as an isolated complaint has a negative predictive value for pediatric rheumatic disease of 0.99 and, as one of several reasons for a rheumatology referral, a negative predictive value of 0.91 (Pediatrics 2002;110:354-9).

"That’s better than any lab test or x-ray [and] about as good as MRI. [So] if you’re calling me saying that Johnny has knee pain, I’m not as worried about JIA [juvenile idiopathic arthritis]. I may be worried about [Henoch-Schönlein purpura (HSP)] or a mechanical issue or something else ... but [not] JIA," said Dr. Cartwright of Randall Children’s Hospital at Legacy Emanuel in Portland, Ore.

On the other hand, "labs really don’t help one way or the other to make the diagnosis of arthritis. Rheumatoid factor doesn’t help. [Erythrocyte sedimentation rate] is helpful if it’s abnormal, but only kind of. I can have a kid who has 20 inflamed joints and their sed rate is 2; I can have another kid with one swollen knee, and their sed rate is 30. [However,] if the sed rate is over 100, I worry about other stuff," such as systemic disease, lupus, HSP, vasculitis, or malignancy, she said.

If those problems have been ruled out, Dr. Cartwright said she usually waits until kids have been on NSAIDs – she favors weight-dosed ibuprofen or naproxen – for a month before getting a complete blood count, a liver enzyme panel, and an antinuclear antibody (ANA) test. "I’m not a big fan of labs up front" for JIA "because we end up chasing the lab illness a little bit," she said. JIA kids also need a referral to an ophthalmologist to check for iritis. If this condition is present, ANA testing helps tell how aggressive it is.

As for assessment, Dr. Cartwright noted that obesity makes it tough to check the ankle for swelling; extra pounds obscure the Achilles tendon and the divots to either side. "It’s one of the joints I image a lot with MRI because I [often] can’t see it very well," she said.

Swelling can be hard to detect in kids with polyarticular disease because it can be more or less even on either side of the body, and, thus, less noticeable. One trick, especially helpful with the hands, is to compare the skin folds and wrinkles around corresponding joints. If they aren’t symmetrical, it could be due to swelling.

Check for jaw arthritis, too, Dr. Cartwright said. A lot of children don’t even know there’s a problem because it’s painless, but left unchecked, jaw arthritis can cause growth abnormalities – associated asymmetries are most obvious when the head’s tilted back – and make it difficult to fully open the mouth.

Patients should be able to insert their three middle fingers vertically into their mouth. When they can’t, "we do some dynamic stretching. We’ll stack tongue blades" to reach the appropriate thickness and have patients place them in their mouth to "stretch the muscles out, kind of like doing [physical therapy]," Dr. Cartwright said.

She said she has no relevant financial disclosures.

[email protected]

PORTLAND, ORE. – Joint pain isn’t usually part of the clinical picture when children have juvenile idiopathic arthritis, according to pediatric rheumatologist Victoria Cartwright.

"In fact, it helps you discount that juvenile arthritis is going on," she said at a conference sponsored by the North Pacific Pediatric Society.

Pain as an isolated complaint has a negative predictive value for pediatric rheumatic disease of 0.99 and, as one of several reasons for a rheumatology referral, a negative predictive value of 0.91 (Pediatrics 2002;110:354-9).

"That’s better than any lab test or x-ray [and] about as good as MRI. [So] if you’re calling me saying that Johnny has knee pain, I’m not as worried about JIA [juvenile idiopathic arthritis]. I may be worried about [Henoch-Schönlein purpura (HSP)] or a mechanical issue or something else ... but [not] JIA," said Dr. Cartwright of Randall Children’s Hospital at Legacy Emanuel in Portland, Ore.

On the other hand, "labs really don’t help one way or the other to make the diagnosis of arthritis. Rheumatoid factor doesn’t help. [Erythrocyte sedimentation rate] is helpful if it’s abnormal, but only kind of. I can have a kid who has 20 inflamed joints and their sed rate is 2; I can have another kid with one swollen knee, and their sed rate is 30. [However,] if the sed rate is over 100, I worry about other stuff," such as systemic disease, lupus, HSP, vasculitis, or malignancy, she said.

If those problems have been ruled out, Dr. Cartwright said she usually waits until kids have been on NSAIDs – she favors weight-dosed ibuprofen or naproxen – for a month before getting a complete blood count, a liver enzyme panel, and an antinuclear antibody (ANA) test. "I’m not a big fan of labs up front" for JIA "because we end up chasing the lab illness a little bit," she said. JIA kids also need a referral to an ophthalmologist to check for iritis. If this condition is present, ANA testing helps tell how aggressive it is.

As for assessment, Dr. Cartwright noted that obesity makes it tough to check the ankle for swelling; extra pounds obscure the Achilles tendon and the divots to either side. "It’s one of the joints I image a lot with MRI because I [often] can’t see it very well," she said.

Swelling can be hard to detect in kids with polyarticular disease because it can be more or less even on either side of the body, and, thus, less noticeable. One trick, especially helpful with the hands, is to compare the skin folds and wrinkles around corresponding joints. If they aren’t symmetrical, it could be due to swelling.

Check for jaw arthritis, too, Dr. Cartwright said. A lot of children don’t even know there’s a problem because it’s painless, but left unchecked, jaw arthritis can cause growth abnormalities – associated asymmetries are most obvious when the head’s tilted back – and make it difficult to fully open the mouth.

Patients should be able to insert their three middle fingers vertically into their mouth. When they can’t, "we do some dynamic stretching. We’ll stack tongue blades" to reach the appropriate thickness and have patients place them in their mouth to "stretch the muscles out, kind of like doing [physical therapy]," Dr. Cartwright said.

She said she has no relevant financial disclosures.

[email protected]

PORTLAND, ORE. – When time-outs don’t work, it’s often because they aren’t being done right, according to Dr. Barbara J. Howard.

Time-outs are "the best evidence-based consequence to change unwanted behavior," effective from as early as 9 months old – when some children are already hitting – and most effective between ages 2-6 years, said Dr. Howard, an assistant professor of pediatrics at Johns Hopkins University in Baltimore.

But parents first need to be taught how to do time-outs right, and practice them; that’s best done before they’re ever needed.

They should know that time-outs should be reserved for just a few serious offenses, such as hitting, kicking, or swearing, and that they are not a substitute for good parenting. If "the kid’s in time-out more than once a day, they are probably not getting enough positive attention for positive behaviors," Dr. Howard said at a conference sponsored by the North Pacific Pediatric Society.

Time-outs for aggressive behavior shouldn’t come with a warning beforehand. Instead, the child should get a brief statement of the offense – for instance, " ‘No hitting, hitting hurts, you’re in time-out.’ Then put [the child] in an uninteresting, but not-scary place." There should be no interaction while the sentence is served. Restraints are an option if the child squirms out of the chair, as is restarting the clock if they act up, said the pediatric developmental and behavioral specialist.

The general rule is 1 minute for each year of age, but if a child with attention-deficit/hyperactivity disorder (ADHD) is unable to sit for a few minutes, even 15 seconds can work. "Have the parent sort of watch them out of the corner of their eye. As soon as the child gives in to the fact that they are sitting there" – lets out a sigh, for example – "that’s the time to [let] them out," she said.

There shouldn’t be a discussion or lecture about what they did wrong when the time’s up. "They are so delicate when they come out of being given a consequence that they fall apart very easily, so it’s better not to talk about it at that moment because they can’t [hear] the lesson." A discussion is just likely to rekindle the situation, Dr. Howard said.

Instead, "return to the scene of the crime and distract them onto some new activity that they can be praised for. Find something positive about their behavior to talk about, or at least give them neutral attention," she said.

And "don’t ask them to apologize. First of all, are they sorry? No. So, if you force them to apologize, you are telling them to lie. That’s not good. [However,] it is appropriate for the adult to apologize to the victim" by saying something like "Oh, I’m sorry you got hurt. That must hurt a lot." The offender just might incorporate the example into their own behavior, she said.

It’s time to revisit the offense later on, after the storm’s passed. The child can be asked what they could have done differently, and given some different options. Role-playing helps.

Parents also need to know that "it’s quite common" for children to go back and do the exact same thing that got them into trouble in the first place, "but that doesn’t mean that the time-out didn’t work; the same thing is true if they get [spanked]. So you can reassure parents they aren’t crazy if they see [that time-outs are] not immediately effective. Tell them to hang in there, and expect change over time," Dr. Howard said.

Dr. Howard is the creator of CHADIS and president of Total Child Health, the management company that licenses its use.

[email protected]

PORTLAND, ORE. – When time-outs don’t work, it’s often because they aren’t being done right, according to Dr. Barbara J. Howard.

Time-outs are "the best evidence-based consequence to change unwanted behavior," effective from as early as 9 months old – when some children are already hitting – and most effective between ages 2-6 years, said Dr. Howard, an assistant professor of pediatrics at Johns Hopkins University in Baltimore.

But parents first need to be taught how to do time-outs right, and practice them; that’s best done before they’re ever needed.

They should know that time-outs should be reserved for just a few serious offenses, such as hitting, kicking, or swearing, and that they are not a substitute for good parenting. If "the kid’s in time-out more than once a day, they are probably not getting enough positive attention for positive behaviors," Dr. Howard said at a conference sponsored by the North Pacific Pediatric Society.

Time-outs for aggressive behavior shouldn’t come with a warning beforehand. Instead, the child should get a brief statement of the offense – for instance, " ‘No hitting, hitting hurts, you’re in time-out.’ Then put [the child] in an uninteresting, but not-scary place." There should be no interaction while the sentence is served. Restraints are an option if the child squirms out of the chair, as is restarting the clock if they act up, said the pediatric developmental and behavioral specialist.

The general rule is 1 minute for each year of age, but if a child with attention-deficit/hyperactivity disorder (ADHD) is unable to sit for a few minutes, even 15 seconds can work. "Have the parent sort of watch them out of the corner of their eye. As soon as the child gives in to the fact that they are sitting there" – lets out a sigh, for example – "that’s the time to [let] them out," she said.

There shouldn’t be a discussion or lecture about what they did wrong when the time’s up. "They are so delicate when they come out of being given a consequence that they fall apart very easily, so it’s better not to talk about it at that moment because they can’t [hear] the lesson." A discussion is just likely to rekindle the situation, Dr. Howard said.

Instead, "return to the scene of the crime and distract them onto some new activity that they can be praised for. Find something positive about their behavior to talk about, or at least give them neutral attention," she said.

And "don’t ask them to apologize. First of all, are they sorry? No. So, if you force them to apologize, you are telling them to lie. That’s not good. [However,] it is appropriate for the adult to apologize to the victim" by saying something like "Oh, I’m sorry you got hurt. That must hurt a lot." The offender just might incorporate the example into their own behavior, she said.

It’s time to revisit the offense later on, after the storm’s passed. The child can be asked what they could have done differently, and given some different options. Role-playing helps.

Parents also need to know that "it’s quite common" for children to go back and do the exact same thing that got them into trouble in the first place, "but that doesn’t mean that the time-out didn’t work; the same thing is true if they get [spanked]. So you can reassure parents they aren’t crazy if they see [that time-outs are] not immediately effective. Tell them to hang in there, and expect change over time," Dr. Howard said.

Dr. Howard is the creator of CHADIS and president of Total Child Health, the management company that licenses its use.

[email protected]

PORTLAND, ORE. – When time-outs don’t work, it’s often because they aren’t being done right, according to Dr. Barbara J. Howard.

Time-outs are "the best evidence-based consequence to change unwanted behavior," effective from as early as 9 months old – when some children are already hitting – and most effective between ages 2-6 years, said Dr. Howard, an assistant professor of pediatrics at Johns Hopkins University in Baltimore.

But parents first need to be taught how to do time-outs right, and practice them; that’s best done before they’re ever needed.

They should know that time-outs should be reserved for just a few serious offenses, such as hitting, kicking, or swearing, and that they are not a substitute for good parenting. If "the kid’s in time-out more than once a day, they are probably not getting enough positive attention for positive behaviors," Dr. Howard said at a conference sponsored by the North Pacific Pediatric Society.

Time-outs for aggressive behavior shouldn’t come with a warning beforehand. Instead, the child should get a brief statement of the offense – for instance, " ‘No hitting, hitting hurts, you’re in time-out.’ Then put [the child] in an uninteresting, but not-scary place." There should be no interaction while the sentence is served. Restraints are an option if the child squirms out of the chair, as is restarting the clock if they act up, said the pediatric developmental and behavioral specialist.

The general rule is 1 minute for each year of age, but if a child with attention-deficit/hyperactivity disorder (ADHD) is unable to sit for a few minutes, even 15 seconds can work. "Have the parent sort of watch them out of the corner of their eye. As soon as the child gives in to the fact that they are sitting there" – lets out a sigh, for example – "that’s the time to [let] them out," she said.

There shouldn’t be a discussion or lecture about what they did wrong when the time’s up. "They are so delicate when they come out of being given a consequence that they fall apart very easily, so it’s better not to talk about it at that moment because they can’t [hear] the lesson." A discussion is just likely to rekindle the situation, Dr. Howard said.

Instead, "return to the scene of the crime and distract them onto some new activity that they can be praised for. Find something positive about their behavior to talk about, or at least give them neutral attention," she said.

And "don’t ask them to apologize. First of all, are they sorry? No. So, if you force them to apologize, you are telling them to lie. That’s not good. [However,] it is appropriate for the adult to apologize to the victim" by saying something like "Oh, I’m sorry you got hurt. That must hurt a lot." The offender just might incorporate the example into their own behavior, she said.

It’s time to revisit the offense later on, after the storm’s passed. The child can be asked what they could have done differently, and given some different options. Role-playing helps.

Parents also need to know that "it’s quite common" for children to go back and do the exact same thing that got them into trouble in the first place, "but that doesn’t mean that the time-out didn’t work; the same thing is true if they get [spanked]. So you can reassure parents they aren’t crazy if they see [that time-outs are] not immediately effective. Tell them to hang in there, and expect change over time," Dr. Howard said.

Dr. Howard is the creator of CHADIS and president of Total Child Health, the management company that licenses its use.

[email protected]