Pulmonary Health Hub

KEYSTONE, COLO. – Parents often fail to acknowledge the earliest signs of a child’s eosinophilic esophagitis, such as vomiting, coughing, choking, or refusing certain foods, because the brevity of such manifestations make them seem relatively unimportant.

Due to the pathologic similarities it shares with gastroesophageal reflux disease (GERD), a more common malady, physicians may be just as likely to miss early signals of eosinophilic esophagitis – often waiting until the child begins to lose weight before making the proper call, warned Dr. F. Dan Atkins, medical director of the pediatric day program at National Jewish Health in Denver.

"Oftentimes we have to get to the point where the child is failing to thrive before we say that there is something really wrong here," he said at a meeting on allergy and respiratory diseases. "We tend to ascribe the majority of their symptoms to the more common GERD that we see."

Eosinophilic esophagitis and GERD are both characterized by abnormal eosinophil counts, and can manifest at the same time. In one scenario, peptic erosion in the esophagus may lead to increased allergen sensitivity and promote the onset of eosinophilic esophagitis. In other cases, stiffening of the esophagus can damage the lower esophageal sphincter and stimulate the onset of GERD in tandem with eosinophilic esophagitis.

"I kind of think about this just like that group we see in asthma," Dr. Atkins said at the meeting, which was sponsored by National Jewish Health. "There are some people who have vocal cord dysfunction and some people who have asthma, and then some who have a combination of both."

The study of eosinophilic esophagitis has accelerated in recent years. It is a T cell–mediated sickness in which eosinophils invade the esophagus, creating rigidity, along with ring structures, ridges, or furrows in the wall of the organ. Symptoms include eating-related pain in children and adults and dysphagia in adults. Due to its frequent misdiagnosis, the condition has often been treated improperly with proton-pump inhibitor (PPI) therapy. Signs of normal pH in the digestive tract and lack of response to PPI therapy are usually sufficient to rule out GERD (Gastroenterology 2007;133:1342-63). The physician can then biopsy multiple sites at the upper and lower esophagus for confirmation of 15 eosinophils per high-power field, indicating the presence of eosinophilic esophagitis, said Dr. Atkins, also of the department of pediatrics at the University of Colorado, Denver.

In a review that included 500 children over the past 4 years, Dr. Atkins and his associates identified 33 eosinophilic esophagitis patients in an attempt to quantify feeding dysfunctions. Over the course of a year’s observation, 88% of this group demonstrated sensitivity to food allergens and 94% exhibited a variety of maladaptive eating behaviors. Failure to thrive was evident in 21%. About 70% of the children ultimately required feeding therapy.

"When we looked at the learned maladaptive behaviors they had, a large number of them had selected out their diet. Usually what they’re doing is avoiding all foods that have significant texture. So they don’t eat meats, they don’t like breads, and they don’t like foods that distend their esophagus," he said.

Children can have signs of eosinophilic esophagitis at any age, including their first year. Evidence of the cytokine eotaxin-3 is especially notable because it is the protein particularly implicated in the recruitment of eosinophils to the esophagus. Physicians and parents should be alert to early vomiting and choking, as well as complaints of epigastric or chest pain, he advised.

The psychology associated with eating disorder therapy doesn’t make the management of eosinophilic esophagitis any easier. Continual shunning of a three-meal-per-day eating pattern changes the child’s attitude toward food in general. Those kids who do not manifest symptoms until several days after eating a favorite food to which they are sensitized will typically protest when told to stay away from it, and psychological feeding dysfunctions often continue even after inflammation has subsided.

Just as in asthma patients, eosinophilic esophagitis carries with it a risk of progression to esophageal fibrosis. "That’s what we’re trying to prevent, particularly in children," Dr. Atkins added. "We’d like to prevent the occurrence of these esophageal strictures over time."

Dr. Atkins is a consultant to Sunovion Pharmaceuticals and an investigator for AstraZeneca.

KEYSTONE, COLO. – Parents often fail to acknowledge the earliest signs of a child’s eosinophilic esophagitis, such as vomiting, coughing, choking, or refusing certain foods, because the brevity of such manifestations make them seem relatively unimportant.

Due to the pathologic similarities it shares with gastroesophageal reflux disease (GERD), a more common malady, physicians may be just as likely to miss early signals of eosinophilic esophagitis – often waiting until the child begins to lose weight before making the proper call, warned Dr. F. Dan Atkins, medical director of the pediatric day program at National Jewish Health in Denver.

"Oftentimes we have to get to the point where the child is failing to thrive before we say that there is something really wrong here," he said at a meeting on allergy and respiratory diseases. "We tend to ascribe the majority of their symptoms to the more common GERD that we see."

Eosinophilic esophagitis and GERD are both characterized by abnormal eosinophil counts, and can manifest at the same time. In one scenario, peptic erosion in the esophagus may lead to increased allergen sensitivity and promote the onset of eosinophilic esophagitis. In other cases, stiffening of the esophagus can damage the lower esophageal sphincter and stimulate the onset of GERD in tandem with eosinophilic esophagitis.

"I kind of think about this just like that group we see in asthma," Dr. Atkins said at the meeting, which was sponsored by National Jewish Health. "There are some people who have vocal cord dysfunction and some people who have asthma, and then some who have a combination of both."

The study of eosinophilic esophagitis has accelerated in recent years. It is a T cell–mediated sickness in which eosinophils invade the esophagus, creating rigidity, along with ring structures, ridges, or furrows in the wall of the organ. Symptoms include eating-related pain in children and adults and dysphagia in adults. Due to its frequent misdiagnosis, the condition has often been treated improperly with proton-pump inhibitor (PPI) therapy. Signs of normal pH in the digestive tract and lack of response to PPI therapy are usually sufficient to rule out GERD (Gastroenterology 2007;133:1342-63). The physician can then biopsy multiple sites at the upper and lower esophagus for confirmation of 15 eosinophils per high-power field, indicating the presence of eosinophilic esophagitis, said Dr. Atkins, also of the department of pediatrics at the University of Colorado, Denver.

In a review that included 500 children over the past 4 years, Dr. Atkins and his associates identified 33 eosinophilic esophagitis patients in an attempt to quantify feeding dysfunctions. Over the course of a year’s observation, 88% of this group demonstrated sensitivity to food allergens and 94% exhibited a variety of maladaptive eating behaviors. Failure to thrive was evident in 21%. About 70% of the children ultimately required feeding therapy.

"When we looked at the learned maladaptive behaviors they had, a large number of them had selected out their diet. Usually what they’re doing is avoiding all foods that have significant texture. So they don’t eat meats, they don’t like breads, and they don’t like foods that distend their esophagus," he said.

Children can have signs of eosinophilic esophagitis at any age, including their first year. Evidence of the cytokine eotaxin-3 is especially notable because it is the protein particularly implicated in the recruitment of eosinophils to the esophagus. Physicians and parents should be alert to early vomiting and choking, as well as complaints of epigastric or chest pain, he advised.

The psychology associated with eating disorder therapy doesn’t make the management of eosinophilic esophagitis any easier. Continual shunning of a three-meal-per-day eating pattern changes the child’s attitude toward food in general. Those kids who do not manifest symptoms until several days after eating a favorite food to which they are sensitized will typically protest when told to stay away from it, and psychological feeding dysfunctions often continue even after inflammation has subsided.

Just as in asthma patients, eosinophilic esophagitis carries with it a risk of progression to esophageal fibrosis. "That’s what we’re trying to prevent, particularly in children," Dr. Atkins added. "We’d like to prevent the occurrence of these esophageal strictures over time."

Dr. Atkins is a consultant to Sunovion Pharmaceuticals and an investigator for AstraZeneca.

KEYSTONE, COLO. – Parents often fail to acknowledge the earliest signs of a child’s eosinophilic esophagitis, such as vomiting, coughing, choking, or refusing certain foods, because the brevity of such manifestations make them seem relatively unimportant.

Due to the pathologic similarities it shares with gastroesophageal reflux disease (GERD), a more common malady, physicians may be just as likely to miss early signals of eosinophilic esophagitis – often waiting until the child begins to lose weight before making the proper call, warned Dr. F. Dan Atkins, medical director of the pediatric day program at National Jewish Health in Denver.

"Oftentimes we have to get to the point where the child is failing to thrive before we say that there is something really wrong here," he said at a meeting on allergy and respiratory diseases. "We tend to ascribe the majority of their symptoms to the more common GERD that we see."

Eosinophilic esophagitis and GERD are both characterized by abnormal eosinophil counts, and can manifest at the same time. In one scenario, peptic erosion in the esophagus may lead to increased allergen sensitivity and promote the onset of eosinophilic esophagitis. In other cases, stiffening of the esophagus can damage the lower esophageal sphincter and stimulate the onset of GERD in tandem with eosinophilic esophagitis.

"I kind of think about this just like that group we see in asthma," Dr. Atkins said at the meeting, which was sponsored by National Jewish Health. "There are some people who have vocal cord dysfunction and some people who have asthma, and then some who have a combination of both."

The study of eosinophilic esophagitis has accelerated in recent years. It is a T cell–mediated sickness in which eosinophils invade the esophagus, creating rigidity, along with ring structures, ridges, or furrows in the wall of the organ. Symptoms include eating-related pain in children and adults and dysphagia in adults. Due to its frequent misdiagnosis, the condition has often been treated improperly with proton-pump inhibitor (PPI) therapy. Signs of normal pH in the digestive tract and lack of response to PPI therapy are usually sufficient to rule out GERD (Gastroenterology 2007;133:1342-63). The physician can then biopsy multiple sites at the upper and lower esophagus for confirmation of 15 eosinophils per high-power field, indicating the presence of eosinophilic esophagitis, said Dr. Atkins, also of the department of pediatrics at the University of Colorado, Denver.

In a review that included 500 children over the past 4 years, Dr. Atkins and his associates identified 33 eosinophilic esophagitis patients in an attempt to quantify feeding dysfunctions. Over the course of a year’s observation, 88% of this group demonstrated sensitivity to food allergens and 94% exhibited a variety of maladaptive eating behaviors. Failure to thrive was evident in 21%. About 70% of the children ultimately required feeding therapy.

"When we looked at the learned maladaptive behaviors they had, a large number of them had selected out their diet. Usually what they’re doing is avoiding all foods that have significant texture. So they don’t eat meats, they don’t like breads, and they don’t like foods that distend their esophagus," he said.

Children can have signs of eosinophilic esophagitis at any age, including their first year. Evidence of the cytokine eotaxin-3 is especially notable because it is the protein particularly implicated in the recruitment of eosinophils to the esophagus. Physicians and parents should be alert to early vomiting and choking, as well as complaints of epigastric or chest pain, he advised.

The psychology associated with eating disorder therapy doesn’t make the management of eosinophilic esophagitis any easier. Continual shunning of a three-meal-per-day eating pattern changes the child’s attitude toward food in general. Those kids who do not manifest symptoms until several days after eating a favorite food to which they are sensitized will typically protest when told to stay away from it, and psychological feeding dysfunctions often continue even after inflammation has subsided.

Just as in asthma patients, eosinophilic esophagitis carries with it a risk of progression to esophageal fibrosis. "That’s what we’re trying to prevent, particularly in children," Dr. Atkins added. "We’d like to prevent the occurrence of these esophageal strictures over time."

Dr. Atkins is a consultant to Sunovion Pharmaceuticals and an investigator for AstraZeneca.

Rescue therapy with beclomethasone combined with albuterol reduced the risk of exacerbations requiring oral corticosteroid treatment, even without daily steroid use, according to a placebo-controlled study of children and adolescents with mild persistent asthma.

“Assessed from a risk-benefit point of view, our data suggest that, in children with mild persistent asthma, use of rescue inhaled corticosteroid could be an effective step-down alternative to discontinuation of such treatment after asthma control is achieved,” Dr. Fernando D. Martinez of the Arizona Respiratory Center and the University of Tucson (Ariz.), and his associates said.

This approach “could also be an alternative, step 2 therapeutic approach for mild persistent asthma in individuals who have not previously received a course of daily corticosteroid treatment,” they added, although they noted that the 44-month randomized, double-blind study was not designed to address this issue.

The TREXA study, funded by the National Heart, Lung, and Blood Institute, appeared online Feb. 15 in the Lancet (doi:10.1016/S0140-6736(10)62145-9).

The study was conducted to determine whether discontinuing treatment with daily inhaled corticosteroids (ICS) in children with well-controlled mild persistent asthma increased the risk of exacerbations, and whether combining beclomethasone and albuterol as rescue therapy, with or without daily beclomethasone, was more protective against asthma exacerbations than was an albuterol-only rescue strategy.

In the study, 288 children and adolescents aged 5-18 years from five U.S. clinical centers, with mild persistent asthma during the previous 2 years, were randomized to one of four treatment groups:

P Beclomethasone twice daily, with beclomethasone plus albuterol as rescue (combined group).

P Beclomethasone twice daily, with placebo plus albuterol as rescue (daily beclomethasone group).

P Placebo twice daily, with beclomethasone plus albuterol as rescue (rescue beclomethasone group).

P Placebo twice daily, with placebo plus albuterol as rescue (placebo group).

Twice-daily beclomethasone treatment was one puff (40 mcg per puff) in the morning and evening; rescue beclomethasone treatment was two puffs of beclomethasone (80 mcg) for every two puffs of albuterol (180 mcg) needed for relief of symptoms. The primary outcome was the time to first exacerbation requiring treatment with oral corticosteroids.

Among those in the placebo group, who received only albuterol as rescue, the exacerbation rate was 49%, compared with 31% in the combined group, 28% in the daily group, and 35% in the rescue group. “Compared with the placebo group, the hazard ratios for asthma exacerbations were significantly lower in the daily beclomethasone group and the combined group, but the difference was not significant in the rescue beclomethasone group,” they found.

The children in the two groups using daily beclomethasone also showed signs of less linear growth, a secondary end point: Children in these two groups grew a mean of 1.1 cm less than did those in the placebo group, a statistically significant difference. But the children in the rescue beclomethasone group (who received less than a quarter of the total daily ICS dose that the children in the combined and daily beclomethasone groups received) grew a mean of 0.3 cm less than did those in the placebo group, which was not a significant difference.

There were two adverse events considered severe in the study: a case of viral meningitis in the daily beclomethasone group and a case of bronchitis in the combined group.

Noting that children with mild persistent asthma should not be treated with rescue albuterol alone and that daily ICS is the most effective treatment to prevent exacerbations in this age group, the authors said that “our data suggest that inhaled corticosteroids used as rescue together with albuterol show benefits over rescue albuterol alone and avoids the growth effects associated with use of daily inhaled corticosteroids.”

They added that to their knowledge, the study was the first to look at the use of ICS with albuterol as rescue therapy in school-aged children.

These results “have potentially important implications for the management of asthma,” Dr. William Checkley wrote in an accompanying editorial (Lancet 2011 Feb. 15 [doi:10.1016/S0140-6736(10)62313-6]).

He noted that the British Thoracic Society and NHLBI National Asthma Education and Prevention Program guidelines recommend daily ICS use as initial and step-up treatment for persistent asthma, and “step-down is possible if asthma symptoms are well controlled for at least 3 months.” The results of this study, however, “suggest that step-down from daily inhaled corticosteroids to such treatment as rescue in combination with rescue short-acting beta agonists could be a reasonable step-down strategy for patients with mild persistent asthma,” wrote Dr. Checkley of the pulmonary and critical care division at Johns Hopkins University, Baltimore. This strategy would reduce the cumulative exposure to ICS “and obviate concerns about compliance with long-term controller treatment,” he added, noting that more studies are needed.

Beclomethasone and the placebo inhalers were provided by Teva Pharmaceutical Industries, the manufacturer of a generic formulation of beclomethasone. Of the 20 coauthors, 12, including lead author Dr. Martinez, reported having been a board member and/or received consulting fees, honoraria, and/or pending grant support from various pharmaceutical companies, including AstraZeneca, GlaxoSmithKline, MedImmune, and Merck. The remaining authors had no disclosures.

Rescue therapy with beclomethasone combined with albuterol reduced the risk of exacerbations requiring oral corticosteroid treatment, even without daily steroid use, according to a placebo-controlled study of children and adolescents with mild persistent asthma.

“Assessed from a risk-benefit point of view, our data suggest that, in children with mild persistent asthma, use of rescue inhaled corticosteroid could be an effective step-down alternative to discontinuation of such treatment after asthma control is achieved,” Dr. Fernando D. Martinez of the Arizona Respiratory Center and the University of Tucson (Ariz.), and his associates said.

This approach “could also be an alternative, step 2 therapeutic approach for mild persistent asthma in individuals who have not previously received a course of daily corticosteroid treatment,” they added, although they noted that the 44-month randomized, double-blind study was not designed to address this issue.

The TREXA study, funded by the National Heart, Lung, and Blood Institute, appeared online Feb. 15 in the Lancet (doi:10.1016/S0140-6736(10)62145-9).

The study was conducted to determine whether discontinuing treatment with daily inhaled corticosteroids (ICS) in children with well-controlled mild persistent asthma increased the risk of exacerbations, and whether combining beclomethasone and albuterol as rescue therapy, with or without daily beclomethasone, was more protective against asthma exacerbations than was an albuterol-only rescue strategy.

In the study, 288 children and adolescents aged 5-18 years from five U.S. clinical centers, with mild persistent asthma during the previous 2 years, were randomized to one of four treatment groups:

P Beclomethasone twice daily, with beclomethasone plus albuterol as rescue (combined group).

P Beclomethasone twice daily, with placebo plus albuterol as rescue (daily beclomethasone group).

P Placebo twice daily, with beclomethasone plus albuterol as rescue (rescue beclomethasone group).

P Placebo twice daily, with placebo plus albuterol as rescue (placebo group).

Twice-daily beclomethasone treatment was one puff (40 mcg per puff) in the morning and evening; rescue beclomethasone treatment was two puffs of beclomethasone (80 mcg) for every two puffs of albuterol (180 mcg) needed for relief of symptoms. The primary outcome was the time to first exacerbation requiring treatment with oral corticosteroids.

Among those in the placebo group, who received only albuterol as rescue, the exacerbation rate was 49%, compared with 31% in the combined group, 28% in the daily group, and 35% in the rescue group. “Compared with the placebo group, the hazard ratios for asthma exacerbations were significantly lower in the daily beclomethasone group and the combined group, but the difference was not significant in the rescue beclomethasone group,” they found.

The children in the two groups using daily beclomethasone also showed signs of less linear growth, a secondary end point: Children in these two groups grew a mean of 1.1 cm less than did those in the placebo group, a statistically significant difference. But the children in the rescue beclomethasone group (who received less than a quarter of the total daily ICS dose that the children in the combined and daily beclomethasone groups received) grew a mean of 0.3 cm less than did those in the placebo group, which was not a significant difference.

There were two adverse events considered severe in the study: a case of viral meningitis in the daily beclomethasone group and a case of bronchitis in the combined group.

Noting that children with mild persistent asthma should not be treated with rescue albuterol alone and that daily ICS is the most effective treatment to prevent exacerbations in this age group, the authors said that “our data suggest that inhaled corticosteroids used as rescue together with albuterol show benefits over rescue albuterol alone and avoids the growth effects associated with use of daily inhaled corticosteroids.”

They added that to their knowledge, the study was the first to look at the use of ICS with albuterol as rescue therapy in school-aged children.

These results “have potentially important implications for the management of asthma,” Dr. William Checkley wrote in an accompanying editorial (Lancet 2011 Feb. 15 [doi:10.1016/S0140-6736(10)62313-6]).

He noted that the British Thoracic Society and NHLBI National Asthma Education and Prevention Program guidelines recommend daily ICS use as initial and step-up treatment for persistent asthma, and “step-down is possible if asthma symptoms are well controlled for at least 3 months.” The results of this study, however, “suggest that step-down from daily inhaled corticosteroids to such treatment as rescue in combination with rescue short-acting beta agonists could be a reasonable step-down strategy for patients with mild persistent asthma,” wrote Dr. Checkley of the pulmonary and critical care division at Johns Hopkins University, Baltimore. This strategy would reduce the cumulative exposure to ICS “and obviate concerns about compliance with long-term controller treatment,” he added, noting that more studies are needed.

Beclomethasone and the placebo inhalers were provided by Teva Pharmaceutical Industries, the manufacturer of a generic formulation of beclomethasone. Of the 20 coauthors, 12, including lead author Dr. Martinez, reported having been a board member and/or received consulting fees, honoraria, and/or pending grant support from various pharmaceutical companies, including AstraZeneca, GlaxoSmithKline, MedImmune, and Merck. The remaining authors had no disclosures.

Rescue therapy with beclomethasone combined with albuterol reduced the risk of exacerbations requiring oral corticosteroid treatment, even without daily steroid use, according to a placebo-controlled study of children and adolescents with mild persistent asthma.

“Assessed from a risk-benefit point of view, our data suggest that, in children with mild persistent asthma, use of rescue inhaled corticosteroid could be an effective step-down alternative to discontinuation of such treatment after asthma control is achieved,” Dr. Fernando D. Martinez of the Arizona Respiratory Center and the University of Tucson (Ariz.), and his associates said.

This approach “could also be an alternative, step 2 therapeutic approach for mild persistent asthma in individuals who have not previously received a course of daily corticosteroid treatment,” they added, although they noted that the 44-month randomized, double-blind study was not designed to address this issue.

The TREXA study, funded by the National Heart, Lung, and Blood Institute, appeared online Feb. 15 in the Lancet (doi:10.1016/S0140-6736(10)62145-9).

The study was conducted to determine whether discontinuing treatment with daily inhaled corticosteroids (ICS) in children with well-controlled mild persistent asthma increased the risk of exacerbations, and whether combining beclomethasone and albuterol as rescue therapy, with or without daily beclomethasone, was more protective against asthma exacerbations than was an albuterol-only rescue strategy.

In the study, 288 children and adolescents aged 5-18 years from five U.S. clinical centers, with mild persistent asthma during the previous 2 years, were randomized to one of four treatment groups:

P Beclomethasone twice daily, with beclomethasone plus albuterol as rescue (combined group).

P Beclomethasone twice daily, with placebo plus albuterol as rescue (daily beclomethasone group).

P Placebo twice daily, with beclomethasone plus albuterol as rescue (rescue beclomethasone group).

P Placebo twice daily, with placebo plus albuterol as rescue (placebo group).

Twice-daily beclomethasone treatment was one puff (40 mcg per puff) in the morning and evening; rescue beclomethasone treatment was two puffs of beclomethasone (80 mcg) for every two puffs of albuterol (180 mcg) needed for relief of symptoms. The primary outcome was the time to first exacerbation requiring treatment with oral corticosteroids.

Among those in the placebo group, who received only albuterol as rescue, the exacerbation rate was 49%, compared with 31% in the combined group, 28% in the daily group, and 35% in the rescue group. “Compared with the placebo group, the hazard ratios for asthma exacerbations were significantly lower in the daily beclomethasone group and the combined group, but the difference was not significant in the rescue beclomethasone group,” they found.

The children in the two groups using daily beclomethasone also showed signs of less linear growth, a secondary end point: Children in these two groups grew a mean of 1.1 cm less than did those in the placebo group, a statistically significant difference. But the children in the rescue beclomethasone group (who received less than a quarter of the total daily ICS dose that the children in the combined and daily beclomethasone groups received) grew a mean of 0.3 cm less than did those in the placebo group, which was not a significant difference.

There were two adverse events considered severe in the study: a case of viral meningitis in the daily beclomethasone group and a case of bronchitis in the combined group.

Noting that children with mild persistent asthma should not be treated with rescue albuterol alone and that daily ICS is the most effective treatment to prevent exacerbations in this age group, the authors said that “our data suggest that inhaled corticosteroids used as rescue together with albuterol show benefits over rescue albuterol alone and avoids the growth effects associated with use of daily inhaled corticosteroids.”

They added that to their knowledge, the study was the first to look at the use of ICS with albuterol as rescue therapy in school-aged children.

These results “have potentially important implications for the management of asthma,” Dr. William Checkley wrote in an accompanying editorial (Lancet 2011 Feb. 15 [doi:10.1016/S0140-6736(10)62313-6]).

He noted that the British Thoracic Society and NHLBI National Asthma Education and Prevention Program guidelines recommend daily ICS use as initial and step-up treatment for persistent asthma, and “step-down is possible if asthma symptoms are well controlled for at least 3 months.” The results of this study, however, “suggest that step-down from daily inhaled corticosteroids to such treatment as rescue in combination with rescue short-acting beta agonists could be a reasonable step-down strategy for patients with mild persistent asthma,” wrote Dr. Checkley of the pulmonary and critical care division at Johns Hopkins University, Baltimore. This strategy would reduce the cumulative exposure to ICS “and obviate concerns about compliance with long-term controller treatment,” he added, noting that more studies are needed.

Beclomethasone and the placebo inhalers were provided by Teva Pharmaceutical Industries, the manufacturer of a generic formulation of beclomethasone. Of the 20 coauthors, 12, including lead author Dr. Martinez, reported having been a board member and/or received consulting fees, honoraria, and/or pending grant support from various pharmaceutical companies, including AstraZeneca, GlaxoSmithKline, MedImmune, and Merck. The remaining authors had no disclosures.

NAPLES, Fla. – Patients who underwent surgical rib fixation for flail chest spent on average 10 fewer days on mechanical ventilation than did those managed traditionally in a single-center analysis of 21 patients with severe blunt chest trauma.

The total number of ventilator days was significantly lower in patients who underwent rib fixation, at a median of 4.5 days (range 0-30 days), compared with a median of 16 days (range 4-40 days) in those managed with pain control and respiratory therapy (P = .04).

Hospital length of stay was a median of 22 days in the nonsurgical group vs. 13 days in the surgical group, and ICU length of stay was a median of 18 days vs. 9 days, but those differences were not statistically significant. There was one postoperative seroma and no deaths in the surgical group.

Surgical rib fixation can be used as a rescue technique when the last resort is prolonged mechanical ventilation, but a large multicenter trial is needed to determine the best approach, Dr. Andrew R. Doben said at the annual meeting of the Eastern Association for the Surgery of Trauma.

"This study provides some of the first data suggesting that surgical fixation may prevent prolonged ventilation in flail chest patients who initially do not require invasive mechanical ventilation," he said in an interview.

Dr. Doben pointed out that major trauma centers see roughly two flail chest injuries per month and that up to 60% of patients do not return to full-time employment. A prospective randomized trial showed benefits with surgical stabilization with Judet struts, compared with internal pneumatic stabilization (J. Trauma 2002;52:727-32), but that trial included only 18 fixation patients and all required invasive mechanical ventilation, he said.

Dr. Doben and his colleagues at the Medical University of South Carolina, Charleston, defined flail chest deformity as three consecutive ribs broken in two or more locations, and they initially focused on patients who failed to wean from the ventilator 5 days post injury, had isolated chest wall trauma, and had good neurologic status. Surgical fixation using a combination of plates and intramedullary nails in three such patients produced positive results similar to those in the literature, but raised the question of whether mechanical ventilation could be avoided in patients who are failing, Dr. Doben said.

"Everybody’s seen these patients – the ‘in-betweeners’ – they’re not really failing, they’re not yet vented, but they’re heading that way," he said.

Dr. Doben highlighted the case of a 60-year-old man with seven total rib fractures including five segmental fractures and paradoxical chest wall motion, who had an epidural in place, was on oxycodone, NSAIDs, acetaminophen, and gabapentin, and was experiencing progressive pulmonary decline on bilevel positive airway pressure therapy for 3 days in the ICU. The patient underwent surgical rib fixation on hospital day 6, was mechanically ventilated overnight, and was extubated the following morning. He was discharged to home on hospital day 11, with no long-acting narcotics needed for pain, he said.

The retrospective chart review included the first 10 patients treated with surgical fixation from September 2008 to May 2010, matched with a previous group of 11 patients managed with standard therapy. Patients were required to have a Chest Abbreviated Injury Scale score of more than 3, a diagnosis of flail chest, and an ICU length of stay greater than 5 days. There were no surgical complications, and the average time on a ventilator after surgery was 1.5 days, said Dr. Doben, now with Baystate Medical Center in Springfield, Mass.

Invited discussant Dr. John C. Mayberry said no strong conclusions supporting flail chest repair can be drawn because of the small study size, but commended the authors for providing new data on its use in patients who do not require ventilation, but clinically worsen.

Dr. Mayberry, with Oregon Health and Science University in Portland, asked whether the study protocol evolved over time, and whether the 10 fixation patients represent the authors’ first experience with the technique. This line of questioning was continued by an audience member who asked what kind of course work prepared the authors to perform rib fixation.

Dr. Doben responded that he had limited experience with chest repairs as a general surgery resident in Maine, but that these were indeed the first 10 rib fixation patients in Charleston. The surgeries in both Maine and Charleston were performed in conjunction with cardiothoracic and orthopedic surgeons who had expertise in hardware insertion, he noted.

With respect to the study protocol, Dr. Doben said initially the authors were very strict and only treated patients on mechanical ventilation, as suggested in the literature, but expanded the scope to include those on nonmechanical ventilation. The analysis excluded patients with a Glasgow Coma Scale score of 8 or less for 5 days, all in-hospital deaths in the control group, and two 80-year-olds with "do not intubate" orders who declined surgery.

Finally, audience members asked why ICU times were not lower in the surgical group and how the authors addressed pulmonary contusions, since previous reports suggest either no benefit or worsened morbidity in patients with a significant underlying pulmonary contusion who undergo fixation for flail chest.

Dr. Doben said length of stay was likely not lower because they delayed surgery in a number of patients until their chest became their primary medical issue. He called for studies to address the issue of flail chest and contusions, but said that he and his colleagues have performed fixation in these patients reasonably early on, at 2 or 3 days into the course of their contusion, when their PaO2/FiO2 (P/F) ratio was markedly improved.

"Really, what kept them on the vent was more their mechanics and not their P/F ratios, and I think that’s a pretty definable time period," he said.

Dr. Doben and his coauthors reported having no conflicts of interest. Dr. Mayberry has grant/research support from, serves as a consultant to, and is on the speakers bureau for, Acute Innovations, a maker of thoracic surgery devices.

NAPLES, Fla. – Patients who underwent surgical rib fixation for flail chest spent on average 10 fewer days on mechanical ventilation than did those managed traditionally in a single-center analysis of 21 patients with severe blunt chest trauma.

The total number of ventilator days was significantly lower in patients who underwent rib fixation, at a median of 4.5 days (range 0-30 days), compared with a median of 16 days (range 4-40 days) in those managed with pain control and respiratory therapy (P = .04).

Hospital length of stay was a median of 22 days in the nonsurgical group vs. 13 days in the surgical group, and ICU length of stay was a median of 18 days vs. 9 days, but those differences were not statistically significant. There was one postoperative seroma and no deaths in the surgical group.

Surgical rib fixation can be used as a rescue technique when the last resort is prolonged mechanical ventilation, but a large multicenter trial is needed to determine the best approach, Dr. Andrew R. Doben said at the annual meeting of the Eastern Association for the Surgery of Trauma.

"This study provides some of the first data suggesting that surgical fixation may prevent prolonged ventilation in flail chest patients who initially do not require invasive mechanical ventilation," he said in an interview.

Dr. Doben pointed out that major trauma centers see roughly two flail chest injuries per month and that up to 60% of patients do not return to full-time employment. A prospective randomized trial showed benefits with surgical stabilization with Judet struts, compared with internal pneumatic stabilization (J. Trauma 2002;52:727-32), but that trial included only 18 fixation patients and all required invasive mechanical ventilation, he said.

Dr. Doben and his colleagues at the Medical University of South Carolina, Charleston, defined flail chest deformity as three consecutive ribs broken in two or more locations, and they initially focused on patients who failed to wean from the ventilator 5 days post injury, had isolated chest wall trauma, and had good neurologic status. Surgical fixation using a combination of plates and intramedullary nails in three such patients produced positive results similar to those in the literature, but raised the question of whether mechanical ventilation could be avoided in patients who are failing, Dr. Doben said.

"Everybody’s seen these patients – the ‘in-betweeners’ – they’re not really failing, they’re not yet vented, but they’re heading that way," he said.

Dr. Doben highlighted the case of a 60-year-old man with seven total rib fractures including five segmental fractures and paradoxical chest wall motion, who had an epidural in place, was on oxycodone, NSAIDs, acetaminophen, and gabapentin, and was experiencing progressive pulmonary decline on bilevel positive airway pressure therapy for 3 days in the ICU. The patient underwent surgical rib fixation on hospital day 6, was mechanically ventilated overnight, and was extubated the following morning. He was discharged to home on hospital day 11, with no long-acting narcotics needed for pain, he said.

The retrospective chart review included the first 10 patients treated with surgical fixation from September 2008 to May 2010, matched with a previous group of 11 patients managed with standard therapy. Patients were required to have a Chest Abbreviated Injury Scale score of more than 3, a diagnosis of flail chest, and an ICU length of stay greater than 5 days. There were no surgical complications, and the average time on a ventilator after surgery was 1.5 days, said Dr. Doben, now with Baystate Medical Center in Springfield, Mass.

Invited discussant Dr. John C. Mayberry said no strong conclusions supporting flail chest repair can be drawn because of the small study size, but commended the authors for providing new data on its use in patients who do not require ventilation, but clinically worsen.

Dr. Mayberry, with Oregon Health and Science University in Portland, asked whether the study protocol evolved over time, and whether the 10 fixation patients represent the authors’ first experience with the technique. This line of questioning was continued by an audience member who asked what kind of course work prepared the authors to perform rib fixation.

Dr. Doben responded that he had limited experience with chest repairs as a general surgery resident in Maine, but that these were indeed the first 10 rib fixation patients in Charleston. The surgeries in both Maine and Charleston were performed in conjunction with cardiothoracic and orthopedic surgeons who had expertise in hardware insertion, he noted.

With respect to the study protocol, Dr. Doben said initially the authors were very strict and only treated patients on mechanical ventilation, as suggested in the literature, but expanded the scope to include those on nonmechanical ventilation. The analysis excluded patients with a Glasgow Coma Scale score of 8 or less for 5 days, all in-hospital deaths in the control group, and two 80-year-olds with "do not intubate" orders who declined surgery.

Finally, audience members asked why ICU times were not lower in the surgical group and how the authors addressed pulmonary contusions, since previous reports suggest either no benefit or worsened morbidity in patients with a significant underlying pulmonary contusion who undergo fixation for flail chest.

Dr. Doben said length of stay was likely not lower because they delayed surgery in a number of patients until their chest became their primary medical issue. He called for studies to address the issue of flail chest and contusions, but said that he and his colleagues have performed fixation in these patients reasonably early on, at 2 or 3 days into the course of their contusion, when their PaO2/FiO2 (P/F) ratio was markedly improved.

"Really, what kept them on the vent was more their mechanics and not their P/F ratios, and I think that’s a pretty definable time period," he said.

Dr. Doben and his coauthors reported having no conflicts of interest. Dr. Mayberry has grant/research support from, serves as a consultant to, and is on the speakers bureau for, Acute Innovations, a maker of thoracic surgery devices.

NAPLES, Fla. – Patients who underwent surgical rib fixation for flail chest spent on average 10 fewer days on mechanical ventilation than did those managed traditionally in a single-center analysis of 21 patients with severe blunt chest trauma.

The total number of ventilator days was significantly lower in patients who underwent rib fixation, at a median of 4.5 days (range 0-30 days), compared with a median of 16 days (range 4-40 days) in those managed with pain control and respiratory therapy (P = .04).

Hospital length of stay was a median of 22 days in the nonsurgical group vs. 13 days in the surgical group, and ICU length of stay was a median of 18 days vs. 9 days, but those differences were not statistically significant. There was one postoperative seroma and no deaths in the surgical group.

Surgical rib fixation can be used as a rescue technique when the last resort is prolonged mechanical ventilation, but a large multicenter trial is needed to determine the best approach, Dr. Andrew R. Doben said at the annual meeting of the Eastern Association for the Surgery of Trauma.

"This study provides some of the first data suggesting that surgical fixation may prevent prolonged ventilation in flail chest patients who initially do not require invasive mechanical ventilation," he said in an interview.

Dr. Doben pointed out that major trauma centers see roughly two flail chest injuries per month and that up to 60% of patients do not return to full-time employment. A prospective randomized trial showed benefits with surgical stabilization with Judet struts, compared with internal pneumatic stabilization (J. Trauma 2002;52:727-32), but that trial included only 18 fixation patients and all required invasive mechanical ventilation, he said.

Dr. Doben and his colleagues at the Medical University of South Carolina, Charleston, defined flail chest deformity as three consecutive ribs broken in two or more locations, and they initially focused on patients who failed to wean from the ventilator 5 days post injury, had isolated chest wall trauma, and had good neurologic status. Surgical fixation using a combination of plates and intramedullary nails in three such patients produced positive results similar to those in the literature, but raised the question of whether mechanical ventilation could be avoided in patients who are failing, Dr. Doben said.

"Everybody’s seen these patients – the ‘in-betweeners’ – they’re not really failing, they’re not yet vented, but they’re heading that way," he said.

Dr. Doben highlighted the case of a 60-year-old man with seven total rib fractures including five segmental fractures and paradoxical chest wall motion, who had an epidural in place, was on oxycodone, NSAIDs, acetaminophen, and gabapentin, and was experiencing progressive pulmonary decline on bilevel positive airway pressure therapy for 3 days in the ICU. The patient underwent surgical rib fixation on hospital day 6, was mechanically ventilated overnight, and was extubated the following morning. He was discharged to home on hospital day 11, with no long-acting narcotics needed for pain, he said.

The retrospective chart review included the first 10 patients treated with surgical fixation from September 2008 to May 2010, matched with a previous group of 11 patients managed with standard therapy. Patients were required to have a Chest Abbreviated Injury Scale score of more than 3, a diagnosis of flail chest, and an ICU length of stay greater than 5 days. There were no surgical complications, and the average time on a ventilator after surgery was 1.5 days, said Dr. Doben, now with Baystate Medical Center in Springfield, Mass.

Invited discussant Dr. John C. Mayberry said no strong conclusions supporting flail chest repair can be drawn because of the small study size, but commended the authors for providing new data on its use in patients who do not require ventilation, but clinically worsen.

Dr. Mayberry, with Oregon Health and Science University in Portland, asked whether the study protocol evolved over time, and whether the 10 fixation patients represent the authors’ first experience with the technique. This line of questioning was continued by an audience member who asked what kind of course work prepared the authors to perform rib fixation.

Dr. Doben responded that he had limited experience with chest repairs as a general surgery resident in Maine, but that these were indeed the first 10 rib fixation patients in Charleston. The surgeries in both Maine and Charleston were performed in conjunction with cardiothoracic and orthopedic surgeons who had expertise in hardware insertion, he noted.

With respect to the study protocol, Dr. Doben said initially the authors were very strict and only treated patients on mechanical ventilation, as suggested in the literature, but expanded the scope to include those on nonmechanical ventilation. The analysis excluded patients with a Glasgow Coma Scale score of 8 or less for 5 days, all in-hospital deaths in the control group, and two 80-year-olds with "do not intubate" orders who declined surgery.

Finally, audience members asked why ICU times were not lower in the surgical group and how the authors addressed pulmonary contusions, since previous reports suggest either no benefit or worsened morbidity in patients with a significant underlying pulmonary contusion who undergo fixation for flail chest.

Dr. Doben said length of stay was likely not lower because they delayed surgery in a number of patients until their chest became their primary medical issue. He called for studies to address the issue of flail chest and contusions, but said that he and his colleagues have performed fixation in these patients reasonably early on, at 2 or 3 days into the course of their contusion, when their PaO2/FiO2 (P/F) ratio was markedly improved.

"Really, what kept them on the vent was more their mechanics and not their P/F ratios, and I think that’s a pretty definable time period," he said.

Dr. Doben and his coauthors reported having no conflicts of interest. Dr. Mayberry has grant/research support from, serves as a consultant to, and is on the speakers bureau for, Acute Innovations, a maker of thoracic surgery devices.

The choice of treatment for the management of adult pulmonary fungal infections should be based on diagnostic findings and individual risk factors, according to a new policy statement issued by the American Thoracic Society. "In most cases, treatment of fungal infections must be based on the causative fungus, the severity of disease, and the clinical features of each patient," the authors wrote.

The policy statement provides organism- and infection-site specific guidelines for therapy, including dosing recommendations, and incorporates the range of novel antifungal medications, such as the extended-spectrum triazoles and echinocandins, that have been introduced since the previous guidelines were published in 1988, according to Dr. Andrew Limper of the Mayo Clinic in Rochester, Minn., and his colleagues on the American Thoracic Society (ATS) Fungal Infections Working Group.

In particular, the recommendations outline the management of endemic mycoses, including histoplasmosis, sporotrichosis, blastomycosis, and coccidioidomycosis; fungal infections with increased prevalence in immune-compromised and critically ill patients, including cryptococcosis, aspergillosis, candidiasis, and Pneumocystis pneumonia; and rare and emerging fungal infections, such as zygomycoses, hyalohyphomycoses, the phaeohyphomycoses, and infections related to Trichosporon species (Am. J. Respir. Crit. Care. Med. 2011;183:96-128).

Endemic Mycoses. The guidelines recommend treatment with itraconazole for mild to moderate histoplasmosis, sporotrichosis, and blastomycosis, and treatment with amphotericin B for severe disease (followed by itraconazole in patients with sporotrichosis). Patients with severe histoplasmosis with diffuse pulmonary infiltrates and critically ill patients with severe pulmonary blastomycosis may require systemic steroid therapy, as well. Further, for patients with pulmonary blastomycosis and concomitant CNS involvement, combination therapy with liposomal amphotericin B (vs. amphotericin B deoxycholate) and fluconazole "should be considered due to theoretic better CNS penetration," the authors wrote.

Antifungal therapy is not recommended for primary pulmonary coccidioidomycosis in immunocompetent patients who have no risk factors for dissemination, while patients with disseminated infection should be treated with an extended-spectrum triazole, according to the guidelines, which also specify that critically ill patients with disseminated paracoccidioidomycosis should be treated initially with amphotericin B, followed by ketoconazole, itraconazole, or sulfadiazine.

Immunocompromised Patients. The treatment options for fungal infections in patients with compromised immune systems, including transplant patients, those being treated for autoimmune inflammatory conditions, and HIV-infected patients, include oral trimethoprim and sulfamethoxazole, oral primaquine plus clindamycin, or oral atovaquone for mild to moderate Pneumocystis pneumonia. Patients with moderate to severe disease should be given trimethoprim, sulfamethoxazole, and possibly prednisone, the guidelines recommend.

Emerging Fungal Infections. "The management of emerging or rare fungi is supported by limited evidence-based studies with no randomized, blinded comparative studies," the authors wrote, noting that treatment recommendations are thus based on clinical experience and in vitro susceptibility testing. Because the majority of affected patients are immunocompromised, "a primary strategy for management of these infections with underlying diseases is to maximally reduce immunosuppressive drugs, provide immunostimulants, and/or rapidly control the underlying diseases or conditions, such as HIV infection, diabetes, and/or chemotherapy-induced neutropenia," they stated.

Secondarily, particularly in the angioinvasive zygomycoses, necrotic tissues, cysts, or true abscesses should be debulked or debrided, they emphasized.

The third management strategy includes specific antifungal recommendations, such as amphotericin B for zygomycosis; voriconazole, posaconazole, or lipid formulations of amphotericin B for fusariosis; voriconazole or posaconazole for scedosporiosis; itraconazole, voriconazole, or posaconazole for phaeohyphomycoses; and, possibly, voriconazole, posaconazole, or itraconazole for trichosporonis and Paecilomyces infections.

"The exact dosing and duration of treatment for these emerging, rare infections are not precise, and consultation with an expert in infectious disease regarding these clinical decisions should be considered," the authors stressed.

The policy statement also includes recommendations for the treatment of Candida and Aspergillus infections, which are becoming increasingly common in the intensive care unit, the authors stated. For candidemia, the guidelines recommend that all existing central venous catheters should be removed, if possible, or a new placement site should be obtained and initial antifungal treatment should be with fluconazole, an amphotericin B formulation, an echinocandin, or a combination of fluconazole and amphotericin. With respect to Aspergillus infections, the guidelines recommend intravenous voriconazole or liposomal amphotericin B for invasive pulmonary aspergillosis; voriconazole or itraconazole for mild to moderate chronic necrotizing aspergillosis; and liposomal amphotericin B or intravenous voriconazole for severe chronic necrotizing aspergillosis.

The authors reported financial relationships with AlphaMed Pharmaceuticals, Pfizer, Ortho-McNeil, MiraBella Technologies, AstraZeneca, GlaxoSmithKline, Bayer, Novartis, Aradigm, Astellas, Enzon, Merck, and Schering-Plough.

The choice of treatment for the management of adult pulmonary fungal infections should be based on diagnostic findings and individual risk factors, according to a new policy statement issued by the American Thoracic Society. "In most cases, treatment of fungal infections must be based on the causative fungus, the severity of disease, and the clinical features of each patient," the authors wrote.

The policy statement provides organism- and infection-site specific guidelines for therapy, including dosing recommendations, and incorporates the range of novel antifungal medications, such as the extended-spectrum triazoles and echinocandins, that have been introduced since the previous guidelines were published in 1988, according to Dr. Andrew Limper of the Mayo Clinic in Rochester, Minn., and his colleagues on the American Thoracic Society (ATS) Fungal Infections Working Group.

In particular, the recommendations outline the management of endemic mycoses, including histoplasmosis, sporotrichosis, blastomycosis, and coccidioidomycosis; fungal infections with increased prevalence in immune-compromised and critically ill patients, including cryptococcosis, aspergillosis, candidiasis, and Pneumocystis pneumonia; and rare and emerging fungal infections, such as zygomycoses, hyalohyphomycoses, the phaeohyphomycoses, and infections related to Trichosporon species (Am. J. Respir. Crit. Care. Med. 2011;183:96-128).

Endemic Mycoses. The guidelines recommend treatment with itraconazole for mild to moderate histoplasmosis, sporotrichosis, and blastomycosis, and treatment with amphotericin B for severe disease (followed by itraconazole in patients with sporotrichosis). Patients with severe histoplasmosis with diffuse pulmonary infiltrates and critically ill patients with severe pulmonary blastomycosis may require systemic steroid therapy, as well. Further, for patients with pulmonary blastomycosis and concomitant CNS involvement, combination therapy with liposomal amphotericin B (vs. amphotericin B deoxycholate) and fluconazole "should be considered due to theoretic better CNS penetration," the authors wrote.

Antifungal therapy is not recommended for primary pulmonary coccidioidomycosis in immunocompetent patients who have no risk factors for dissemination, while patients with disseminated infection should be treated with an extended-spectrum triazole, according to the guidelines, which also specify that critically ill patients with disseminated paracoccidioidomycosis should be treated initially with amphotericin B, followed by ketoconazole, itraconazole, or sulfadiazine.

Immunocompromised Patients. The treatment options for fungal infections in patients with compromised immune systems, including transplant patients, those being treated for autoimmune inflammatory conditions, and HIV-infected patients, include oral trimethoprim and sulfamethoxazole, oral primaquine plus clindamycin, or oral atovaquone for mild to moderate Pneumocystis pneumonia. Patients with moderate to severe disease should be given trimethoprim, sulfamethoxazole, and possibly prednisone, the guidelines recommend.

Emerging Fungal Infections. "The management of emerging or rare fungi is supported by limited evidence-based studies with no randomized, blinded comparative studies," the authors wrote, noting that treatment recommendations are thus based on clinical experience and in vitro susceptibility testing. Because the majority of affected patients are immunocompromised, "a primary strategy for management of these infections with underlying diseases is to maximally reduce immunosuppressive drugs, provide immunostimulants, and/or rapidly control the underlying diseases or conditions, such as HIV infection, diabetes, and/or chemotherapy-induced neutropenia," they stated.

Secondarily, particularly in the angioinvasive zygomycoses, necrotic tissues, cysts, or true abscesses should be debulked or debrided, they emphasized.

The third management strategy includes specific antifungal recommendations, such as amphotericin B for zygomycosis; voriconazole, posaconazole, or lipid formulations of amphotericin B for fusariosis; voriconazole or posaconazole for scedosporiosis; itraconazole, voriconazole, or posaconazole for phaeohyphomycoses; and, possibly, voriconazole, posaconazole, or itraconazole for trichosporonis and Paecilomyces infections.

"The exact dosing and duration of treatment for these emerging, rare infections are not precise, and consultation with an expert in infectious disease regarding these clinical decisions should be considered," the authors stressed.

The policy statement also includes recommendations for the treatment of Candida and Aspergillus infections, which are becoming increasingly common in the intensive care unit, the authors stated. For candidemia, the guidelines recommend that all existing central venous catheters should be removed, if possible, or a new placement site should be obtained and initial antifungal treatment should be with fluconazole, an amphotericin B formulation, an echinocandin, or a combination of fluconazole and amphotericin. With respect to Aspergillus infections, the guidelines recommend intravenous voriconazole or liposomal amphotericin B for invasive pulmonary aspergillosis; voriconazole or itraconazole for mild to moderate chronic necrotizing aspergillosis; and liposomal amphotericin B or intravenous voriconazole for severe chronic necrotizing aspergillosis.

The authors reported financial relationships with AlphaMed Pharmaceuticals, Pfizer, Ortho-McNeil, MiraBella Technologies, AstraZeneca, GlaxoSmithKline, Bayer, Novartis, Aradigm, Astellas, Enzon, Merck, and Schering-Plough.

The choice of treatment for the management of adult pulmonary fungal infections should be based on diagnostic findings and individual risk factors, according to a new policy statement issued by the American Thoracic Society. "In most cases, treatment of fungal infections must be based on the causative fungus, the severity of disease, and the clinical features of each patient," the authors wrote.

The policy statement provides organism- and infection-site specific guidelines for therapy, including dosing recommendations, and incorporates the range of novel antifungal medications, such as the extended-spectrum triazoles and echinocandins, that have been introduced since the previous guidelines were published in 1988, according to Dr. Andrew Limper of the Mayo Clinic in Rochester, Minn., and his colleagues on the American Thoracic Society (ATS) Fungal Infections Working Group.

In particular, the recommendations outline the management of endemic mycoses, including histoplasmosis, sporotrichosis, blastomycosis, and coccidioidomycosis; fungal infections with increased prevalence in immune-compromised and critically ill patients, including cryptococcosis, aspergillosis, candidiasis, and Pneumocystis pneumonia; and rare and emerging fungal infections, such as zygomycoses, hyalohyphomycoses, the phaeohyphomycoses, and infections related to Trichosporon species (Am. J. Respir. Crit. Care. Med. 2011;183:96-128).

Endemic Mycoses. The guidelines recommend treatment with itraconazole for mild to moderate histoplasmosis, sporotrichosis, and blastomycosis, and treatment with amphotericin B for severe disease (followed by itraconazole in patients with sporotrichosis). Patients with severe histoplasmosis with diffuse pulmonary infiltrates and critically ill patients with severe pulmonary blastomycosis may require systemic steroid therapy, as well. Further, for patients with pulmonary blastomycosis and concomitant CNS involvement, combination therapy with liposomal amphotericin B (vs. amphotericin B deoxycholate) and fluconazole "should be considered due to theoretic better CNS penetration," the authors wrote.

Antifungal therapy is not recommended for primary pulmonary coccidioidomycosis in immunocompetent patients who have no risk factors for dissemination, while patients with disseminated infection should be treated with an extended-spectrum triazole, according to the guidelines, which also specify that critically ill patients with disseminated paracoccidioidomycosis should be treated initially with amphotericin B, followed by ketoconazole, itraconazole, or sulfadiazine.

Immunocompromised Patients. The treatment options for fungal infections in patients with compromised immune systems, including transplant patients, those being treated for autoimmune inflammatory conditions, and HIV-infected patients, include oral trimethoprim and sulfamethoxazole, oral primaquine plus clindamycin, or oral atovaquone for mild to moderate Pneumocystis pneumonia. Patients with moderate to severe disease should be given trimethoprim, sulfamethoxazole, and possibly prednisone, the guidelines recommend.

Emerging Fungal Infections. "The management of emerging or rare fungi is supported by limited evidence-based studies with no randomized, blinded comparative studies," the authors wrote, noting that treatment recommendations are thus based on clinical experience and in vitro susceptibility testing. Because the majority of affected patients are immunocompromised, "a primary strategy for management of these infections with underlying diseases is to maximally reduce immunosuppressive drugs, provide immunostimulants, and/or rapidly control the underlying diseases or conditions, such as HIV infection, diabetes, and/or chemotherapy-induced neutropenia," they stated.

Secondarily, particularly in the angioinvasive zygomycoses, necrotic tissues, cysts, or true abscesses should be debulked or debrided, they emphasized.

The third management strategy includes specific antifungal recommendations, such as amphotericin B for zygomycosis; voriconazole, posaconazole, or lipid formulations of amphotericin B for fusariosis; voriconazole or posaconazole for scedosporiosis; itraconazole, voriconazole, or posaconazole for phaeohyphomycoses; and, possibly, voriconazole, posaconazole, or itraconazole for trichosporonis and Paecilomyces infections.

"The exact dosing and duration of treatment for these emerging, rare infections are not precise, and consultation with an expert in infectious disease regarding these clinical decisions should be considered," the authors stressed.

The policy statement also includes recommendations for the treatment of Candida and Aspergillus infections, which are becoming increasingly common in the intensive care unit, the authors stated. For candidemia, the guidelines recommend that all existing central venous catheters should be removed, if possible, or a new placement site should be obtained and initial antifungal treatment should be with fluconazole, an amphotericin B formulation, an echinocandin, or a combination of fluconazole and amphotericin. With respect to Aspergillus infections, the guidelines recommend intravenous voriconazole or liposomal amphotericin B for invasive pulmonary aspergillosis; voriconazole or itraconazole for mild to moderate chronic necrotizing aspergillosis; and liposomal amphotericin B or intravenous voriconazole for severe chronic necrotizing aspergillosis.

The authors reported financial relationships with AlphaMed Pharmaceuticals, Pfizer, Ortho-McNeil, MiraBella Technologies, AstraZeneca, GlaxoSmithKline, Bayer, Novartis, Aradigm, Astellas, Enzon, Merck, and Schering-Plough.

San Antonio – Psychiatric comorbidities are present in two-thirds of children with restless legs syndrome, according to a study.

Moreover, multiple psychiatric diagnoses were extremely common in this retrospective study of 376 children aged 2–18 years who met National Institutes of Health consensus criteria for definite or probable restless legs syndrome (RLS). Indeed, boys with RLS were actually more likely to have two or more psychiatric diagnoses than a single one. Multiple psychiatric comorbidities also were quite common in girls with RLS, reported Dr. Samuel J. Pullen of the Mayo Clinic, Rochester, Minn.

Attention-deficit/hyperactivity disorder (ADHD) has been shown in other studies to be common in children with RLS. That was the case in this large series as well, with 1 in 4 of the youths carrying a diagnosis of ADHD.

However, other psychiatric comorbidities were common in these patients, too. This observation constitutes a novel contribution to the field, as previously there has been uncertainty surrounding the rates of psychiatric disorders other than ADHD in children with RLS, according to Dr. Pullen.

Mood disorders were present in 21% of the youths with RLS, anxiety disorders in 12.8%, and disruptive behavior disorder in 10.6%.

ADHD and disruptive behavior disorder were more than twice as frequent in boys as in girls with RLS. Mood disorders were more common in girls.

Two psychiatric diagnoses were present in 27.8% of boys and 19.9% of girls. Three or more psychiatric diagnoses were carried by 15.6% of boys and 7.1% of girls.

Many of the children received multiple trials of psychotropic medications during the course of their treatment. This is concerning, as other studies have linked these drugs to worsening RLS symptoms, Dr. Pullen noted.

The mean serum ferritin level in the study population was 27.8 ng/mL.

Twelve of 15 study participants who underwent psychogenomic profiling displayed genetic derangement at one of three cytochrome P-450 alleles known to be associated with ultrarapid metabolism of psychotropic drugs. This may be associated with increased susceptibility to drug side effects–such as worsening of RLS symptoms. Dr. Pullen indicated that he and his coinvestigators plan further studies of this phenomenon.

The chief take-away point from this 376-patient study, he added, is that sleep specialists should inquire about psychiatric comorbidities in their patients with childhood RLS, while child psychiatrists should ask their patients about symptoms of RLS, a treatable comorbidity.

Dr. Pullen reported having no relevant financial disclosures.

San Antonio – Psychiatric comorbidities are present in two-thirds of children with restless legs syndrome, according to a study.

Moreover, multiple psychiatric diagnoses were extremely common in this retrospective study of 376 children aged 2–18 years who met National Institutes of Health consensus criteria for definite or probable restless legs syndrome (RLS). Indeed, boys with RLS were actually more likely to have two or more psychiatric diagnoses than a single one. Multiple psychiatric comorbidities also were quite common in girls with RLS, reported Dr. Samuel J. Pullen of the Mayo Clinic, Rochester, Minn.

Attention-deficit/hyperactivity disorder (ADHD) has been shown in other studies to be common in children with RLS. That was the case in this large series as well, with 1 in 4 of the youths carrying a diagnosis of ADHD.

However, other psychiatric comorbidities were common in these patients, too. This observation constitutes a novel contribution to the field, as previously there has been uncertainty surrounding the rates of psychiatric disorders other than ADHD in children with RLS, according to Dr. Pullen.

Mood disorders were present in 21% of the youths with RLS, anxiety disorders in 12.8%, and disruptive behavior disorder in 10.6%.

ADHD and disruptive behavior disorder were more than twice as frequent in boys as in girls with RLS. Mood disorders were more common in girls.

Two psychiatric diagnoses were present in 27.8% of boys and 19.9% of girls. Three or more psychiatric diagnoses were carried by 15.6% of boys and 7.1% of girls.

Many of the children received multiple trials of psychotropic medications during the course of their treatment. This is concerning, as other studies have linked these drugs to worsening RLS symptoms, Dr. Pullen noted.

The mean serum ferritin level in the study population was 27.8 ng/mL.

Twelve of 15 study participants who underwent psychogenomic profiling displayed genetic derangement at one of three cytochrome P-450 alleles known to be associated with ultrarapid metabolism of psychotropic drugs. This may be associated with increased susceptibility to drug side effects–such as worsening of RLS symptoms. Dr. Pullen indicated that he and his coinvestigators plan further studies of this phenomenon.

The chief take-away point from this 376-patient study, he added, is that sleep specialists should inquire about psychiatric comorbidities in their patients with childhood RLS, while child psychiatrists should ask their patients about symptoms of RLS, a treatable comorbidity.

Dr. Pullen reported having no relevant financial disclosures.

San Antonio – Psychiatric comorbidities are present in two-thirds of children with restless legs syndrome, according to a study.

Moreover, multiple psychiatric diagnoses were extremely common in this retrospective study of 376 children aged 2–18 years who met National Institutes of Health consensus criteria for definite or probable restless legs syndrome (RLS). Indeed, boys with RLS were actually more likely to have two or more psychiatric diagnoses than a single one. Multiple psychiatric comorbidities also were quite common in girls with RLS, reported Dr. Samuel J. Pullen of the Mayo Clinic, Rochester, Minn.

Attention-deficit/hyperactivity disorder (ADHD) has been shown in other studies to be common in children with RLS. That was the case in this large series as well, with 1 in 4 of the youths carrying a diagnosis of ADHD.

However, other psychiatric comorbidities were common in these patients, too. This observation constitutes a novel contribution to the field, as previously there has been uncertainty surrounding the rates of psychiatric disorders other than ADHD in children with RLS, according to Dr. Pullen.

Mood disorders were present in 21% of the youths with RLS, anxiety disorders in 12.8%, and disruptive behavior disorder in 10.6%.

ADHD and disruptive behavior disorder were more than twice as frequent in boys as in girls with RLS. Mood disorders were more common in girls.

Two psychiatric diagnoses were present in 27.8% of boys and 19.9% of girls. Three or more psychiatric diagnoses were carried by 15.6% of boys and 7.1% of girls.

Many of the children received multiple trials of psychotropic medications during the course of their treatment. This is concerning, as other studies have linked these drugs to worsening RLS symptoms, Dr. Pullen noted.

The mean serum ferritin level in the study population was 27.8 ng/mL.

Twelve of 15 study participants who underwent psychogenomic profiling displayed genetic derangement at one of three cytochrome P-450 alleles known to be associated with ultrarapid metabolism of psychotropic drugs. This may be associated with increased susceptibility to drug side effects–such as worsening of RLS symptoms. Dr. Pullen indicated that he and his coinvestigators plan further studies of this phenomenon.

The chief take-away point from this 376-patient study, he added, is that sleep specialists should inquire about psychiatric comorbidities in their patients with childhood RLS, while child psychiatrists should ask their patients about symptoms of RLS, a treatable comorbidity.

Dr. Pullen reported having no relevant financial disclosures.

Contrary to previous studies, only 1 in 100 patients with pulmonary embolism die in emergency departments, but more standardized treatment, including earlier use of anticoagulants, is needed, according to the initial report of the EMPEROR study in the Feb. 8, 2011, issue of the Journal of the American College of Cardiology.

Of the 20 patients in this study whose death was due to PE, only 3 received anticoagulant treatment before a diagnosis was confirmed, even though previous studies have shown that delays in starting anticoagulants can be fatal. Only another 3 of the 20 patients received fibrinolytic therapy in the emergency department, the Emergency Medicine Pulmonary Embolism in the Real World Registry (EMPEROR) researchers found.

Dr. Charles V. Pollack of Pennsylvania Hospital, Philadelphia, and colleagues created the national, prospective, multicenter, observational registry to establish more definitive signs and symptoms of PE, compare treatment strategies, and measure use of risk stratification methods, frequency of empiric anticoagulation use, and rates of major hemorrhage and death. Earlier registries of patients with PE have not provided specific data about race or ethnicity, risk stratification methods, or the frequency of anticoagulant use in the emergency department.

Between Jan. 1, 2005, and Dec. 29, 2008, the researchers enrolled 2,408 patients from 22 emergency departments, 1,880 of whom had confirmed PE (J. Am. Coll. Cardiol. 2011;57:700-6).

Systemic non–vitamin K–dependent anticoagulation was initiated in the ED in 1,593 (84%) patients, but only 173 (9%) received heparin of any type before the results of diagnostic imaging were available and 33 (1.7%) received a fibrinolytic agent.

While other registries show a mortality of 10%-15%, only 20 of the 1,880 patients (1%) in this study died as a direct result of the embolism, with 0.2% mortality from hemorrhage. At 30 days, patients whose acute PE was diagnosed in emergency departments had an all-cause mortality of 5.4%. The lower mortality in this report may reflect the fact that the registry included only outpatients who experienced PE and that this population was younger and less ill than those in other registries, the researchers said.

Of the 1,880 patients with confirmed PE, 1,654 (88%) were diagnosed based on CT pulmonary angiogram, 91 (5%) on formal pulmonary angiography, 82 (4%) on ventilation-perfusion scan, 51 (3%) on deep vein thrombosis with appropriate PE symptoms, and 2 (0.1%) on pulmonary MRI.

The mean age was 57 years, with one-third past age 65; 53% of the patients were women, and 68% were white. The racial and ethnic distribution of patients with PE closely parallels that of all patients who present to emergency departments.

The most common presenting signs and symptoms of PE were dyspnea at rest (50%), pleuritic chest pain (39%), dyspnea with exertion (27%), extremity swelling suggestive of deep vein thrombosis (24%), and syncope (5%).

The most common comorbidities that could represent potential risk factors for PE were hypertension (46%), obesity (27%), recent hospitalization (24%), and active malignancy (22%). Based on the absence of any predefined risk factors for PE, 312 (16.6%) of the 1,880 patients were considered to have idiopathic PE.

Most patients (79%) diagnosed with PE in the ED lived independently, while 11.6% reported generalized immobility.

The low rate of early treatment found by the study "suggested that empiric anticoagulation in patients with suspected PE should be instituted more often in the ED and that timely, therapeutic anticoagulation should be administered after the diagnosis is confirmed," the researchers wrote. "Future treatment studies of PE conducted in U.S. EDs should focus on accelerating the time frame of administration of systemic anticoagulation and fibrinolysis to patients with evidence of severe PE."

Several coauthors disclosed consulting relationships with and/or funding from a wide range of pharmaceutical companies that make anticoagulant agents.

Contrary to previous studies, only 1 in 100 patients with pulmonary embolism die in emergency departments, but more standardized treatment, including earlier use of anticoagulants, is needed, according to the initial report of the EMPEROR study in the Feb. 8, 2011, issue of the Journal of the American College of Cardiology.

Of the 20 patients in this study whose death was due to PE, only 3 received anticoagulant treatment before a diagnosis was confirmed, even though previous studies have shown that delays in starting anticoagulants can be fatal. Only another 3 of the 20 patients received fibrinolytic therapy in the emergency department, the Emergency Medicine Pulmonary Embolism in the Real World Registry (EMPEROR) researchers found.

Dr. Charles V. Pollack of Pennsylvania Hospital, Philadelphia, and colleagues created the national, prospective, multicenter, observational registry to establish more definitive signs and symptoms of PE, compare treatment strategies, and measure use of risk stratification methods, frequency of empiric anticoagulation use, and rates of major hemorrhage and death. Earlier registries of patients with PE have not provided specific data about race or ethnicity, risk stratification methods, or the frequency of anticoagulant use in the emergency department.

Between Jan. 1, 2005, and Dec. 29, 2008, the researchers enrolled 2,408 patients from 22 emergency departments, 1,880 of whom had confirmed PE (J. Am. Coll. Cardiol. 2011;57:700-6).

Systemic non–vitamin K–dependent anticoagulation was initiated in the ED in 1,593 (84%) patients, but only 173 (9%) received heparin of any type before the results of diagnostic imaging were available and 33 (1.7%) received a fibrinolytic agent.

While other registries show a mortality of 10%-15%, only 20 of the 1,880 patients (1%) in this study died as a direct result of the embolism, with 0.2% mortality from hemorrhage. At 30 days, patients whose acute PE was diagnosed in emergency departments had an all-cause mortality of 5.4%. The lower mortality in this report may reflect the fact that the registry included only outpatients who experienced PE and that this population was younger and less ill than those in other registries, the researchers said.

Of the 1,880 patients with confirmed PE, 1,654 (88%) were diagnosed based on CT pulmonary angiogram, 91 (5%) on formal pulmonary angiography, 82 (4%) on ventilation-perfusion scan, 51 (3%) on deep vein thrombosis with appropriate PE symptoms, and 2 (0.1%) on pulmonary MRI.

The mean age was 57 years, with one-third past age 65; 53% of the patients were women, and 68% were white. The racial and ethnic distribution of patients with PE closely parallels that of all patients who present to emergency departments.

The most common presenting signs and symptoms of PE were dyspnea at rest (50%), pleuritic chest pain (39%), dyspnea with exertion (27%), extremity swelling suggestive of deep vein thrombosis (24%), and syncope (5%).

The most common comorbidities that could represent potential risk factors for PE were hypertension (46%), obesity (27%), recent hospitalization (24%), and active malignancy (22%). Based on the absence of any predefined risk factors for PE, 312 (16.6%) of the 1,880 patients were considered to have idiopathic PE.

Most patients (79%) diagnosed with PE in the ED lived independently, while 11.6% reported generalized immobility.

The low rate of early treatment found by the study "suggested that empiric anticoagulation in patients with suspected PE should be instituted more often in the ED and that timely, therapeutic anticoagulation should be administered after the diagnosis is confirmed," the researchers wrote. "Future treatment studies of PE conducted in U.S. EDs should focus on accelerating the time frame of administration of systemic anticoagulation and fibrinolysis to patients with evidence of severe PE."

Several coauthors disclosed consulting relationships with and/or funding from a wide range of pharmaceutical companies that make anticoagulant agents.

Contrary to previous studies, only 1 in 100 patients with pulmonary embolism die in emergency departments, but more standardized treatment, including earlier use of anticoagulants, is needed, according to the initial report of the EMPEROR study in the Feb. 8, 2011, issue of the Journal of the American College of Cardiology.

Of the 20 patients in this study whose death was due to PE, only 3 received anticoagulant treatment before a diagnosis was confirmed, even though previous studies have shown that delays in starting anticoagulants can be fatal. Only another 3 of the 20 patients received fibrinolytic therapy in the emergency department, the Emergency Medicine Pulmonary Embolism in the Real World Registry (EMPEROR) researchers found.

Dr. Charles V. Pollack of Pennsylvania Hospital, Philadelphia, and colleagues created the national, prospective, multicenter, observational registry to establish more definitive signs and symptoms of PE, compare treatment strategies, and measure use of risk stratification methods, frequency of empiric anticoagulation use, and rates of major hemorrhage and death. Earlier registries of patients with PE have not provided specific data about race or ethnicity, risk stratification methods, or the frequency of anticoagulant use in the emergency department.

Between Jan. 1, 2005, and Dec. 29, 2008, the researchers enrolled 2,408 patients from 22 emergency departments, 1,880 of whom had confirmed PE (J. Am. Coll. Cardiol. 2011;57:700-6).

Systemic non–vitamin K–dependent anticoagulation was initiated in the ED in 1,593 (84%) patients, but only 173 (9%) received heparin of any type before the results of diagnostic imaging were available and 33 (1.7%) received a fibrinolytic agent.

While other registries show a mortality of 10%-15%, only 20 of the 1,880 patients (1%) in this study died as a direct result of the embolism, with 0.2% mortality from hemorrhage. At 30 days, patients whose acute PE was diagnosed in emergency departments had an all-cause mortality of 5.4%. The lower mortality in this report may reflect the fact that the registry included only outpatients who experienced PE and that this population was younger and less ill than those in other registries, the researchers said.

Of the 1,880 patients with confirmed PE, 1,654 (88%) were diagnosed based on CT pulmonary angiogram, 91 (5%) on formal pulmonary angiography, 82 (4%) on ventilation-perfusion scan, 51 (3%) on deep vein thrombosis with appropriate PE symptoms, and 2 (0.1%) on pulmonary MRI.

The mean age was 57 years, with one-third past age 65; 53% of the patients were women, and 68% were white. The racial and ethnic distribution of patients with PE closely parallels that of all patients who present to emergency departments.

The most common presenting signs and symptoms of PE were dyspnea at rest (50%), pleuritic chest pain (39%), dyspnea with exertion (27%), extremity swelling suggestive of deep vein thrombosis (24%), and syncope (5%).

The most common comorbidities that could represent potential risk factors for PE were hypertension (46%), obesity (27%), recent hospitalization (24%), and active malignancy (22%). Based on the absence of any predefined risk factors for PE, 312 (16.6%) of the 1,880 patients were considered to have idiopathic PE.

Most patients (79%) diagnosed with PE in the ED lived independently, while 11.6% reported generalized immobility.

The low rate of early treatment found by the study "suggested that empiric anticoagulation in patients with suspected PE should be instituted more often in the ED and that timely, therapeutic anticoagulation should be administered after the diagnosis is confirmed," the researchers wrote. "Future treatment studies of PE conducted in U.S. EDs should focus on accelerating the time frame of administration of systemic anticoagulation and fibrinolysis to patients with evidence of severe PE."

Several coauthors disclosed consulting relationships with and/or funding from a wide range of pharmaceutical companies that make anticoagulant agents.

CHICAGO - Chronic obstructive pulmonary disease is a powerful risk factor for in-hospital mortality or cardiogenic shock in patients presenting with ST-elevation MI, according to a large retrospective study.

The clinical inference is that the reduced cardiopulmonary reserve imposed by COPD – a disease often marked by pulmonary hypertension and right ventricular dysfunction – renders the circulatory system less capable of coping with the effects of an MI, Dr. Kohei Wakabayashi said at the annual scientific sessions of the American Heart Association.

In a series of 3,249 patients who underwent emergent percutaneous coronary intervention for STEMI at Washington (D.C.) Hospital Center, 365 were known to have COPD. Their rate of in-hospital mortality or cardiogenic shock (24%) was substantially greater than in patients with no COPD (14%).

Patients with COPD were significantly older, were more often smokers and women, and had a higher prevalence of chronic renal insufficiency, hypertension, and diabetes. In a multivariate logistic regression analysis adjusted for these factors, COPD emerged as the single strongest independent predictor of in-hospital mortality or cardiogenic shock in patients undergoing PCI for STEMI, with an associated 83% increased risk.

The other independent predictors of in-hospital mortality or cardiogenic shock in STEMI patients were the number of diseased vessels, maximum creatine kinase value, and age, according to Dr. Wakabayashi of the center.

He declared having no relevant financial interests.

CHICAGO - Chronic obstructive pulmonary disease is a powerful risk factor for in-hospital mortality or cardiogenic shock in patients presenting with ST-elevation MI, according to a large retrospective study.

The clinical inference is that the reduced cardiopulmonary reserve imposed by COPD – a disease often marked by pulmonary hypertension and right ventricular dysfunction – renders the circulatory system less capable of coping with the effects of an MI, Dr. Kohei Wakabayashi said at the annual scientific sessions of the American Heart Association.

In a series of 3,249 patients who underwent emergent percutaneous coronary intervention for STEMI at Washington (D.C.) Hospital Center, 365 were known to have COPD. Their rate of in-hospital mortality or cardiogenic shock (24%) was substantially greater than in patients with no COPD (14%).

Patients with COPD were significantly older, were more often smokers and women, and had a higher prevalence of chronic renal insufficiency, hypertension, and diabetes. In a multivariate logistic regression analysis adjusted for these factors, COPD emerged as the single strongest independent predictor of in-hospital mortality or cardiogenic shock in patients undergoing PCI for STEMI, with an associated 83% increased risk.

The other independent predictors of in-hospital mortality or cardiogenic shock in STEMI patients were the number of diseased vessels, maximum creatine kinase value, and age, according to Dr. Wakabayashi of the center.

He declared having no relevant financial interests.

CHICAGO - Chronic obstructive pulmonary disease is a powerful risk factor for in-hospital mortality or cardiogenic shock in patients presenting with ST-elevation MI, according to a large retrospective study.

The clinical inference is that the reduced cardiopulmonary reserve imposed by COPD – a disease often marked by pulmonary hypertension and right ventricular dysfunction – renders the circulatory system less capable of coping with the effects of an MI, Dr. Kohei Wakabayashi said at the annual scientific sessions of the American Heart Association.

In a series of 3,249 patients who underwent emergent percutaneous coronary intervention for STEMI at Washington (D.C.) Hospital Center, 365 were known to have COPD. Their rate of in-hospital mortality or cardiogenic shock (24%) was substantially greater than in patients with no COPD (14%).

Patients with COPD were significantly older, were more often smokers and women, and had a higher prevalence of chronic renal insufficiency, hypertension, and diabetes. In a multivariate logistic regression analysis adjusted for these factors, COPD emerged as the single strongest independent predictor of in-hospital mortality or cardiogenic shock in patients undergoing PCI for STEMI, with an associated 83% increased risk.

The other independent predictors of in-hospital mortality or cardiogenic shock in STEMI patients were the number of diseased vessels, maximum creatine kinase value, and age, according to Dr. Wakabayashi of the center.

He declared having no relevant financial interests.

VANCOUVER, B.C. – Contemporary management of pulmonary sarcoidosis is moving away from hard clinical targets and toward patients’ self-reported well-being and goals, according to Dr. Daniel A. Culver, a pulmonologist at the Cleveland Clinic.

Physicians may treat sarcoidosis for a variety of reasons, and research is helping to sort out which of them are valid, he said at the annual meeting of the American College of Chest Physicians.

One reason might be to improve radiographic or physiologic parameters. In particular, the Scadding stage of a patient’s chest x-ray at presentation has been used for about 50 years to estimate prognosis and the need for treatment.

"But in fact there are a number of pieces of data coming out now that suggest that the chest x-ray may not be the most ideal way to measure how things are going to go for patients," he commented.

In one study, for example, half of patients with pulmonary sarcoidosis were rated as having a better chest x-ray during an exacerbation as compared with before, despite their worsening symptoms and spirometry (Respirology 2008;13:97-102).

Another reason for undertaking treatment might be to improve patients’ symptoms, according to Dr. Culver.

In this regard, a recent review has described a so-called sarcoidosis penumbra, a collection of disease-related issues that affect patients’ well-being but are often not well captured by tests physicians rely on (Semin. Respir. Crit. Care Med. 2010;31:501-18). For instance, two in every three patients have depression, and one in six has sleep apnea.

"This took us a long time as sarcoidologists to recognize, that it’s not the x-ray and vital capacity that the patients care about," but rather their daily ability to function and enjoy life, he commented.

"To optimally treat sarcoidosis, one of the new things we are discovering is that we need to ask the patients the questions that get to these sorts of issues and target our treatment to these sorts of issues," Dr. Culver said. "Going forward ... for both immunosuppressive therapy and the treatment of sarcoidosis in general, we are going to see it more focused on patient-centered outcomes and quality of life rather than things that we’d all like to measure, like the vital capacity."

Another reason that physicians may treat sarcoidosis is to alter the natural history of the disease and prevent fibrosis.

But "most sarcoidosis will resolve within the first 5 years, at least radiologically," Dr. Culver noted, and current evidence suggests treatment does little to alter this trajectory.

In one study, 39% of patients with stage 2 or 3 disease on chest x-ray had neither progression nor improvement during a 6-month period. When these stable patients were assigned either to immediate treatment with a fairly aggressive regimen of prednisolone or to as-needed treatment only if spirometry showed deterioration, just 19% of the latter group required treatment during the next 5 years (Thorax 1996;51:238-47).

"If you can hold off on treating, you may be able to prevent side effects from medicines ... and still have a patient who has their disease spontaneously resolve," he commented.

That said, the as-needed treatment group had a smaller improvement in forced vital capacity (FVC), and there were some other potentially important differences in outcomes between groups.

"Suffice it to say that right now, we don’t think that steroid therapy given preemptively has a tremendous impact on the natural history of the disease," Dr. Culver commented. "This is probably the best study that addresses this question, but this doesn’t necessarily resolve the issue."

Finally, physicians may initiate treatment for sarcoidosis because they feel compelled to do something, according to Dr. Culver.

"It makes us feel better when we go home at night: We have done something for the patient who came to see us," he commented. "But the evidence for this [practice] really is not very strong, despite the fact that steroids have been used for about 60 years now."

A recently proposed algorithm for treating pulmonary sarcoidosis draws on all of these accumulated data and recommends symptom assessment as a first step (Semin. Respir. Crit. Care Med. 2010;31:501-18).

"If the symptoms are relatively mild or modest – and this requires a discussion with the patient – then I think observation is completely reasonable," Dr. Culver said.

In more severe cases, the algorithm proposes short-course, moderate-dose therapy with prednisone 20-30 mg daily for 3-4 weeks, as supported by several studies, including a recent one among patients with acute exacerbations (Am. J. Med. Sci. 2010;339:1-4).

In other words, "be less aggressive with your steroid dosing," he recommended. "You can really get away with shorter courses, with lower doses than we have been using in the past."

For patients who have a good response, the goal is to taper to 10 mg daily or less, a practice endorsed by a Delphi consensus study of sarcoidosis management (Respir. Med. 2010;104:717-23).

"That’s evolving as an important target for long-term management of sarcoidosis patients," he noted, and it also helps minimize steroid adverse effects.

When patients have an inadequate response to prednisone or are unable to reduce the dosage to 10 mg daily, the algorithm suggests adding an immune modulator (methotrexate, azathioprine, leflunomide, or mycophenolate) to therapy.

"The choice of immune modulators ... is really dealer’s choice," Dr. Culver commented. "Suffice it to say that it’s most important that you become comfortable with something and you are used to how to use it, more so than necessarily exactly which one to use."

There have been few head-to-head comparisons of these agents, although methotrexate is by far the agent preferred by U.S. physicians treating sarcoidosis, partly because it has been the best studied.

"That’s the drug that we use as our second-line agent," he noted. "The reason that we like methotrexate is it seems to work pretty well, it’s pretty inexpensive and pretty reliable, and it’s not hard to get through the insurance company."

Data from his institution show that leflunomide also works well. A review of 40 patients with pulmonary sarcoidosis found they had an improvement in FVC within 6 months of starting this drug (P = .01), as well as a reduction in the average prednisone dose to 5 mg daily. "So we have really moved leflunomide to the next agent in our algorithm after methotrexate," he said.

Infliximab is the only agent that has been shown to be efficacious in a double-blind, randomized controlled trial of patients with sarcoidosis, according to Dr. Culver.

In unselected patients, infliximab is associated with just a 2.5% improvement in percent predicted FVC (Clin. Chest Med. 2008;29:533-48, ix-x) – or about that seen with steroids. But among the subset having more severe lung disease, with an FVC of less than 69%, there is a roughly 3.25% improvement. The improvement was 6% in the randomized trial (Sarcoidosis Vasc. Diffuse Lung Dis. 2006;23:201-8).

"So, in fact, we think for patients failing cytotoxic agents that infliximab is a nice option," Dr. Culver commented.

And studies are helping to identify which patients are most likely to benefit from infliximab: those who have had disease for more than 2 years, have worse dyspnea (a Medical Research Council dyspnea score of at least 2), lower FVC, poorer quality of life (assessed with the St. George’s Respiratory Questionnaire), reticulonodular changes on their chest x-ray, or an elevated C-reactive protein level.

"In fact, these are some of the same entry criteria that are being used for the current trial of biologics in sarcoidosis, trying to target that more severe patient population," he noted.

In concluding, Dr. Culver advised physicians to establish and keep in mind the goals of treatment, and to remember the chronic nature of sarcoidosis.

"If I can leave you with one thing, the message is ... you have to sit and talk to your patient and find out what’s important to them, what do they want to accomplish," he said. "That’s the best thing that you can do as you think about treating your patient longitudinally, because remember, you are not treating this as if it’s an infection, you are treating this as if it’s hypertension that needs to be controlled in the long term."

Dr. Culver reported having affiliations with the biotechnology and pharmaceutical companies Centocor (manufacturer of infliximab), Takeda, and Actelion.

VANCOUVER, B.C. – Contemporary management of pulmonary sarcoidosis is moving away from hard clinical targets and toward patients’ self-reported well-being and goals, according to Dr. Daniel A. Culver, a pulmonologist at the Cleveland Clinic.

Physicians may treat sarcoidosis for a variety of reasons, and research is helping to sort out which of them are valid, he said at the annual meeting of the American College of Chest Physicians.

One reason might be to improve radiographic or physiologic parameters. In particular, the Scadding stage of a patient’s chest x-ray at presentation has been used for about 50 years to estimate prognosis and the need for treatment.

"But in fact there are a number of pieces of data coming out now that suggest that the chest x-ray may not be the most ideal way to measure how things are going to go for patients," he commented.

In one study, for example, half of patients with pulmonary sarcoidosis were rated as having a better chest x-ray during an exacerbation as compared with before, despite their worsening symptoms and spirometry (Respirology 2008;13:97-102).

Another reason for undertaking treatment might be to improve patients’ symptoms, according to Dr. Culver.

In this regard, a recent review has described a so-called sarcoidosis penumbra, a collection of disease-related issues that affect patients’ well-being but are often not well captured by tests physicians rely on (Semin. Respir. Crit. Care Med. 2010;31:501-18). For instance, two in every three patients have depression, and one in six has sleep apnea.

"This took us a long time as sarcoidologists to recognize, that it’s not the x-ray and vital capacity that the patients care about," but rather their daily ability to function and enjoy life, he commented.

"To optimally treat sarcoidosis, one of the new things we are discovering is that we need to ask the patients the questions that get to these sorts of issues and target our treatment to these sorts of issues," Dr. Culver said. "Going forward ... for both immunosuppressive therapy and the treatment of sarcoidosis in general, we are going to see it more focused on patient-centered outcomes and quality of life rather than things that we’d all like to measure, like the vital capacity."

Another reason that physicians may treat sarcoidosis is to alter the natural history of the disease and prevent fibrosis.

But "most sarcoidosis will resolve within the first 5 years, at least radiologically," Dr. Culver noted, and current evidence suggests treatment does little to alter this trajectory.

In one study, 39% of patients with stage 2 or 3 disease on chest x-ray had neither progression nor improvement during a 6-month period. When these stable patients were assigned either to immediate treatment with a fairly aggressive regimen of prednisolone or to as-needed treatment only if spirometry showed deterioration, just 19% of the latter group required treatment during the next 5 years (Thorax 1996;51:238-47).

"If you can hold off on treating, you may be able to prevent side effects from medicines ... and still have a patient who has their disease spontaneously resolve," he commented.

That said, the as-needed treatment group had a smaller improvement in forced vital capacity (FVC), and there were some other potentially important differences in outcomes between groups.

"Suffice it to say that right now, we don’t think that steroid therapy given preemptively has a tremendous impact on the natural history of the disease," Dr. Culver commented. "This is probably the best study that addresses this question, but this doesn’t necessarily resolve the issue."

Finally, physicians may initiate treatment for sarcoidosis because they feel compelled to do something, according to Dr. Culver.

"It makes us feel better when we go home at night: We have done something for the patient who came to see us," he commented. "But the evidence for this [practice] really is not very strong, despite the fact that steroids have been used for about 60 years now."

A recently proposed algorithm for treating pulmonary sarcoidosis draws on all of these accumulated data and recommends symptom assessment as a first step (Semin. Respir. Crit. Care Med. 2010;31:501-18).

"If the symptoms are relatively mild or modest – and this requires a discussion with the patient – then I think observation is completely reasonable," Dr. Culver said.

In more severe cases, the algorithm proposes short-course, moderate-dose therapy with prednisone 20-30 mg daily for 3-4 weeks, as supported by several studies, including a recent one among patients with acute exacerbations (Am. J. Med. Sci. 2010;339:1-4).

In other words, "be less aggressive with your steroid dosing," he recommended. "You can really get away with shorter courses, with lower doses than we have been using in the past."

For patients who have a good response, the goal is to taper to 10 mg daily or less, a practice endorsed by a Delphi consensus study of sarcoidosis management (Respir. Med. 2010;104:717-23).

"That’s evolving as an important target for long-term management of sarcoidosis patients," he noted, and it also helps minimize steroid adverse effects.

When patients have an inadequate response to prednisone or are unable to reduce the dosage to 10 mg daily, the algorithm suggests adding an immune modulator (methotrexate, azathioprine, leflunomide, or mycophenolate) to therapy.

"The choice of immune modulators ... is really dealer’s choice," Dr. Culver commented. "Suffice it to say that it’s most important that you become comfortable with something and you are used to how to use it, more so than necessarily exactly which one to use."

There have been few head-to-head comparisons of these agents, although methotrexate is by far the agent preferred by U.S. physicians treating sarcoidosis, partly because it has been the best studied.

"That’s the drug that we use as our second-line agent," he noted. "The reason that we like methotrexate is it seems to work pretty well, it’s pretty inexpensive and pretty reliable, and it’s not hard to get through the insurance company."

Data from his institution show that leflunomide also works well. A review of 40 patients with pulmonary sarcoidosis found they had an improvement in FVC within 6 months of starting this drug (P = .01), as well as a reduction in the average prednisone dose to 5 mg daily. "So we have really moved leflunomide to the next agent in our algorithm after methotrexate," he said.

Infliximab is the only agent that has been shown to be efficacious in a double-blind, randomized controlled trial of patients with sarcoidosis, according to Dr. Culver.

In unselected patients, infliximab is associated with just a 2.5% improvement in percent predicted FVC (Clin. Chest Med. 2008;29:533-48, ix-x) – or about that seen with steroids. But among the subset having more severe lung disease, with an FVC of less than 69%, there is a roughly 3.25% improvement. The improvement was 6% in the randomized trial (Sarcoidosis Vasc. Diffuse Lung Dis. 2006;23:201-8).

"So, in fact, we think for patients failing cytotoxic agents that infliximab is a nice option," Dr. Culver commented.

And studies are helping to identify which patients are most likely to benefit from infliximab: those who have had disease for more than 2 years, have worse dyspnea (a Medical Research Council dyspnea score of at least 2), lower FVC, poorer quality of life (assessed with the St. George’s Respiratory Questionnaire), reticulonodular changes on their chest x-ray, or an elevated C-reactive protein level.

"In fact, these are some of the same entry criteria that are being used for the current trial of biologics in sarcoidosis, trying to target that more severe patient population," he noted.

In concluding, Dr. Culver advised physicians to establish and keep in mind the goals of treatment, and to remember the chronic nature of sarcoidosis.

"If I can leave you with one thing, the message is ... you have to sit and talk to your patient and find out what’s important to them, what do they want to accomplish," he said. "That’s the best thing that you can do as you think about treating your patient longitudinally, because remember, you are not treating this as if it’s an infection, you are treating this as if it’s hypertension that needs to be controlled in the long term."

Dr. Culver reported having affiliations with the biotechnology and pharmaceutical companies Centocor (manufacturer of infliximab), Takeda, and Actelion.

VANCOUVER, B.C. – Contemporary management of pulmonary sarcoidosis is moving away from hard clinical targets and toward patients’ self-reported well-being and goals, according to Dr. Daniel A. Culver, a pulmonologist at the Cleveland Clinic.

Physicians may treat sarcoidosis for a variety of reasons, and research is helping to sort out which of them are valid, he said at the annual meeting of the American College of Chest Physicians.

One reason might be to improve radiographic or physiologic parameters. In particular, the Scadding stage of a patient’s chest x-ray at presentation has been used for about 50 years to estimate prognosis and the need for treatment.

"But in fact there are a number of pieces of data coming out now that suggest that the chest x-ray may not be the most ideal way to measure how things are going to go for patients," he commented.

In one study, for example, half of patients with pulmonary sarcoidosis were rated as having a better chest x-ray during an exacerbation as compared with before, despite their worsening symptoms and spirometry (Respirology 2008;13:97-102).

Another reason for undertaking treatment might be to improve patients’ symptoms, according to Dr. Culver.

In this regard, a recent review has described a so-called sarcoidosis penumbra, a collection of disease-related issues that affect patients’ well-being but are often not well captured by tests physicians rely on (Semin. Respir. Crit. Care Med. 2010;31:501-18). For instance, two in every three patients have depression, and one in six has sleep apnea.

"This took us a long time as sarcoidologists to recognize, that it’s not the x-ray and vital capacity that the patients care about," but rather their daily ability to function and enjoy life, he commented.

"To optimally treat sarcoidosis, one of the new things we are discovering is that we need to ask the patients the questions that get to these sorts of issues and target our treatment to these sorts of issues," Dr. Culver said. "Going forward ... for both immunosuppressive therapy and the treatment of sarcoidosis in general, we are going to see it more focused on patient-centered outcomes and quality of life rather than things that we’d all like to measure, like the vital capacity."

Another reason that physicians may treat sarcoidosis is to alter the natural history of the disease and prevent fibrosis.

But "most sarcoidosis will resolve within the first 5 years, at least radiologically," Dr. Culver noted, and current evidence suggests treatment does little to alter this trajectory.

In one study, 39% of patients with stage 2 or 3 disease on chest x-ray had neither progression nor improvement during a 6-month period. When these stable patients were assigned either to immediate treatment with a fairly aggressive regimen of prednisolone or to as-needed treatment only if spirometry showed deterioration, just 19% of the latter group required treatment during the next 5 years (Thorax 1996;51:238-47).

"If you can hold off on treating, you may be able to prevent side effects from medicines ... and still have a patient who has their disease spontaneously resolve," he commented.

That said, the as-needed treatment group had a smaller improvement in forced vital capacity (FVC), and there were some other potentially important differences in outcomes between groups.

"Suffice it to say that right now, we don’t think that steroid therapy given preemptively has a tremendous impact on the natural history of the disease," Dr. Culver commented. "This is probably the best study that addresses this question, but this doesn’t necessarily resolve the issue."

Finally, physicians may initiate treatment for sarcoidosis because they feel compelled to do something, according to Dr. Culver.

"It makes us feel better when we go home at night: We have done something for the patient who came to see us," he commented. "But the evidence for this [practice] really is not very strong, despite the fact that steroids have been used for about 60 years now."

A recently proposed algorithm for treating pulmonary sarcoidosis draws on all of these accumulated data and recommends symptom assessment as a first step (Semin. Respir. Crit. Care Med. 2010;31:501-18).

"If the symptoms are relatively mild or modest – and this requires a discussion with the patient – then I think observation is completely reasonable," Dr. Culver said.

In more severe cases, the algorithm proposes short-course, moderate-dose therapy with prednisone 20-30 mg daily for 3-4 weeks, as supported by several studies, including a recent one among patients with acute exacerbations (Am. J. Med. Sci. 2010;339:1-4).

In other words, "be less aggressive with your steroid dosing," he recommended. "You can really get away with shorter courses, with lower doses than we have been using in the past."

For patients who have a good response, the goal is to taper to 10 mg daily or less, a practice endorsed by a Delphi consensus study of sarcoidosis management (Respir. Med. 2010;104:717-23).

"That’s evolving as an important target for long-term management of sarcoidosis patients," he noted, and it also helps minimize steroid adverse effects.

When patients have an inadequate response to prednisone or are unable to reduce the dosage to 10 mg daily, the algorithm suggests adding an immune modulator (methotrexate, azathioprine, leflunomide, or mycophenolate) to therapy.

"The choice of immune modulators ... is really dealer’s choice," Dr. Culver commented. "Suffice it to say that it’s most important that you become comfortable with something and you are used to how to use it, more so than necessarily exactly which one to use."

There have been few head-to-head comparisons of these agents, although methotrexate is by far the agent preferred by U.S. physicians treating sarcoidosis, partly because it has been the best studied.

"That’s the drug that we use as our second-line agent," he noted. "The reason that we like methotrexate is it seems to work pretty well, it’s pretty inexpensive and pretty reliable, and it’s not hard to get through the insurance company."

Data from his institution show that leflunomide also works well. A review of 40 patients with pulmonary sarcoidosis found they had an improvement in FVC within 6 months of starting this drug (P = .01), as well as a reduction in the average prednisone dose to 5 mg daily. "So we have really moved leflunomide to the next agent in our algorithm after methotrexate," he said.

Infliximab is the only agent that has been shown to be efficacious in a double-blind, randomized controlled trial of patients with sarcoidosis, according to Dr. Culver.

In unselected patients, infliximab is associated with just a 2.5% improvement in percent predicted FVC (Clin. Chest Med. 2008;29:533-48, ix-x) – or about that seen with steroids. But among the subset having more severe lung disease, with an FVC of less than 69%, there is a roughly 3.25% improvement. The improvement was 6% in the randomized trial (Sarcoidosis Vasc. Diffuse Lung Dis. 2006;23:201-8).

"So, in fact, we think for patients failing cytotoxic agents that infliximab is a nice option," Dr. Culver commented.

And studies are helping to identify which patients are most likely to benefit from infliximab: those who have had disease for more than 2 years, have worse dyspnea (a Medical Research Council dyspnea score of at least 2), lower FVC, poorer quality of life (assessed with the St. George’s Respiratory Questionnaire), reticulonodular changes on their chest x-ray, or an elevated C-reactive protein level.

"In fact, these are some of the same entry criteria that are being used for the current trial of biologics in sarcoidosis, trying to target that more severe patient population," he noted.

In concluding, Dr. Culver advised physicians to establish and keep in mind the goals of treatment, and to remember the chronic nature of sarcoidosis.

"If I can leave you with one thing, the message is ... you have to sit and talk to your patient and find out what’s important to them, what do they want to accomplish," he said. "That’s the best thing that you can do as you think about treating your patient longitudinally, because remember, you are not treating this as if it’s an infection, you are treating this as if it’s hypertension that needs to be controlled in the long term."

Dr. Culver reported having affiliations with the biotechnology and pharmaceutical companies Centocor (manufacturer of infliximab), Takeda, and Actelion.

DENVER – The Ayurvedic medical practice known as shirodhara showed promise as a nonpharmacologic treatment for insomnia in a small pilot study.

Shirodhara is a relaxing procedure that entails dripping warm herbalized oil from a special pot onto the forehead of a supine patient. In Hindu culture, the forehead is the site of the third eye. The term shirodhara comes from the Sanscrit words shir (head) and dhara (flow).

The pilot study involved nine patients who underwent shirodhara for insomnia for 40 minutes daily on 5 consecutive days. Brahmi oil, which is sesame oil processed with waterhyssop (Bacopa monnieri) and other herbs, was used in the study, Dr. S. Prasad Vinjamury explained at the annual meeting of the American Public Health Association.

Mean symptomatic improvement as reflected in Insomnia Severity Index scores was 31% on day 5 compared with baseline. Three patients showed a modest 4%-8% improvement, while the other six experienced more substantial 26%-70% reductions in Insomnia Severity Index scores, said Dr. Vinjamury of the Southern California University of Health Sciences, an institution for complementary and alternative medicine located in Whittier, Calif.

One week following the fifth and final shirodhara treatment session, three patients showed further improvement. The rest either maintained the gains seen at the end of therapy or reverted to baseline.

Patients reported no treatment side effects. That’s a big plus for shirodhara as a potential therapy for insomnia, given that it has been estimated that 1.6 million Americans resort to complementary and alternative medicine for insomnia because they wish to avoid medication side effects, tolerance, and dependence, he observed.

In India, shirodhara is a popular therapy for a wide variety of medical ailments, including insomnia. In the United States, some health spas offer it as part of a relaxing massage package. This pilot study in insomnia was intended as proof of concept, paving the way for properly designed randomized, controlled trials in U.S. patients, according to Dr. Vinjamury.

He declared having no relevant financial interests.

DENVER – The Ayurvedic medical practice known as shirodhara showed promise as a nonpharmacologic treatment for insomnia in a small pilot study.

Shirodhara is a relaxing procedure that entails dripping warm herbalized oil from a special pot onto the forehead of a supine patient. In Hindu culture, the forehead is the site of the third eye. The term shirodhara comes from the Sanscrit words shir (head) and dhara (flow).

The pilot study involved nine patients who underwent shirodhara for insomnia for 40 minutes daily on 5 consecutive days. Brahmi oil, which is sesame oil processed with waterhyssop (Bacopa monnieri) and other herbs, was used in the study, Dr. S. Prasad Vinjamury explained at the annual meeting of the American Public Health Association.

Mean symptomatic improvement as reflected in Insomnia Severity Index scores was 31% on day 5 compared with baseline. Three patients showed a modest 4%-8% improvement, while the other six experienced more substantial 26%-70% reductions in Insomnia Severity Index scores, said Dr. Vinjamury of the Southern California University of Health Sciences, an institution for complementary and alternative medicine located in Whittier, Calif.

One week following the fifth and final shirodhara treatment session, three patients showed further improvement. The rest either maintained the gains seen at the end of therapy or reverted to baseline.

Patients reported no treatment side effects. That’s a big plus for shirodhara as a potential therapy for insomnia, given that it has been estimated that 1.6 million Americans resort to complementary and alternative medicine for insomnia because they wish to avoid medication side effects, tolerance, and dependence, he observed.

In India, shirodhara is a popular therapy for a wide variety of medical ailments, including insomnia. In the United States, some health spas offer it as part of a relaxing massage package. This pilot study in insomnia was intended as proof of concept, paving the way for properly designed randomized, controlled trials in U.S. patients, according to Dr. Vinjamury.

He declared having no relevant financial interests.

DENVER – The Ayurvedic medical practice known as shirodhara showed promise as a nonpharmacologic treatment for insomnia in a small pilot study.

Shirodhara is a relaxing procedure that entails dripping warm herbalized oil from a special pot onto the forehead of a supine patient. In Hindu culture, the forehead is the site of the third eye. The term shirodhara comes from the Sanscrit words shir (head) and dhara (flow).

The pilot study involved nine patients who underwent shirodhara for insomnia for 40 minutes daily on 5 consecutive days. Brahmi oil, which is sesame oil processed with waterhyssop (Bacopa monnieri) and other herbs, was used in the study, Dr. S. Prasad Vinjamury explained at the annual meeting of the American Public Health Association.

Mean symptomatic improvement as reflected in Insomnia Severity Index scores was 31% on day 5 compared with baseline. Three patients showed a modest 4%-8% improvement, while the other six experienced more substantial 26%-70% reductions in Insomnia Severity Index scores, said Dr. Vinjamury of the Southern California University of Health Sciences, an institution for complementary and alternative medicine located in Whittier, Calif.

One week following the fifth and final shirodhara treatment session, three patients showed further improvement. The rest either maintained the gains seen at the end of therapy or reverted to baseline.

Patients reported no treatment side effects. That’s a big plus for shirodhara as a potential therapy for insomnia, given that it has been estimated that 1.6 million Americans resort to complementary and alternative medicine for insomnia because they wish to avoid medication side effects, tolerance, and dependence, he observed.

In India, shirodhara is a popular therapy for a wide variety of medical ailments, including insomnia. In the United States, some health spas offer it as part of a relaxing massage package. This pilot study in insomnia was intended as proof of concept, paving the way for properly designed randomized, controlled trials in U.S. patients, according to Dr. Vinjamury.

He declared having no relevant financial interests.

VANCOUVER, B.C. – Age was independently associated with mortality in patients admitted to the ICU with pneumonia.

Overall mortality was 17% at 30 days and 32% at 1 year in a prospective, population-based cohort study involving 351 ICU patients. After adjustment for pneumonia severity, comorbid disease, sex, smoking status, alcohol use, and other potential confounders, each 10-year increase in age was associated with a 24% increase in 30-day mortality and a 39% increase in 1-year mortality, Dr. Wendy I. Sligl said at the annual meeting of the Infectious Diseases Society of America.

"This is a very high mortality rate, with almost one-third of patients dead at 1 year," said Dr. Sligl of the University of Alberta, Edmonton. Long-term mortality in these patients may rival or exceed that seen in patients with heart failure or end-stage renal disease.

"We tend to think of community-acquired pneumonia as a reversible problem. Patients come in, they get treated for their pneumonia, they come off the ventilator, they go home, and they’re fixed. And that really is not what we’re seeing with this data," she said.

Dr. Sligl and her fellow researchers enrolled all adults aged 17 years and older who were hospitalized with pneumonia in one of the six hospitals and five ICUs in Edmonton. The study excluded patients who were pregnant or lactating, had been previously hospitalized within 30 days, or were immunosuppressed. Of 3,415 patients admitted with pneumonia between 2000 and 2002, 351 were admitted to the ICU within 24 hours of their presentation at the emergency department.

The mean age of the 351 ICU patients was 61 years, with 43% younger than 60, 18% between 60 and 69, 23% between 70 and 79, and 15% aged 80 years and older (percentages do not total to 100% due to rounding). Most (59%) were male.

After adjustment for functional impairment, number of comorbidities, and illness severity in their multivariate analysis, the researchers found several independent predictors of mortality besides age. Patients with a living will had a threefold increase in 30-day mortality and a twofold increase in 1-year mortality. Every 10 points on the modified Pneumonia Severity Index increased the risk of 30-day mortality by 11% and the risk of 1-year mortality by 12%.

Dr. Sligl advanced several possible explanations for the independent relationship between age and mortality. Elderly patients may be frailer or have decreased reserve, she said. "This is very difficult to measure objectively and to include in multivariable modeling. There are many physiologic changes associated with aging that can predispose [a person to] the development of pneumonia and the severity of disease including decreased lung compliance, decreased respiratory muscle strength, retained secretions, ... and dysfunctional and impaired immunity."

Dr. Sligl said that she and her colleagues had no relevant financial disclosures.

VANCOUVER, B.C. – Age was independently associated with mortality in patients admitted to the ICU with pneumonia.

Overall mortality was 17% at 30 days and 32% at 1 year in a prospective, population-based cohort study involving 351 ICU patients. After adjustment for pneumonia severity, comorbid disease, sex, smoking status, alcohol use, and other potential confounders, each 10-year increase in age was associated with a 24% increase in 30-day mortality and a 39% increase in 1-year mortality, Dr. Wendy I. Sligl said at the annual meeting of the Infectious Diseases Society of America.

"This is a very high mortality rate, with almost one-third of patients dead at 1 year," said Dr. Sligl of the University of Alberta, Edmonton. Long-term mortality in these patients may rival or exceed that seen in patients with heart failure or end-stage renal disease.

"We tend to think of community-acquired pneumonia as a reversible problem. Patients come in, they get treated for their pneumonia, they come off the ventilator, they go home, and they’re fixed. And that really is not what we’re seeing with this data," she said.

Dr. Sligl and her fellow researchers enrolled all adults aged 17 years and older who were hospitalized with pneumonia in one of the six hospitals and five ICUs in Edmonton. The study excluded patients who were pregnant or lactating, had been previously hospitalized within 30 days, or were immunosuppressed. Of 3,415 patients admitted with pneumonia between 2000 and 2002, 351 were admitted to the ICU within 24 hours of their presentation at the emergency department.

The mean age of the 351 ICU patients was 61 years, with 43% younger than 60, 18% between 60 and 69, 23% between 70 and 79, and 15% aged 80 years and older (percentages do not total to 100% due to rounding). Most (59%) were male.

After adjustment for functional impairment, number of comorbidities, and illness severity in their multivariate analysis, the researchers found several independent predictors of mortality besides age. Patients with a living will had a threefold increase in 30-day mortality and a twofold increase in 1-year mortality. Every 10 points on the modified Pneumonia Severity Index increased the risk of 30-day mortality by 11% and the risk of 1-year mortality by 12%.

Dr. Sligl advanced several possible explanations for the independent relationship between age and mortality. Elderly patients may be frailer or have decreased reserve, she said. "This is very difficult to measure objectively and to include in multivariable modeling. There are many physiologic changes associated with aging that can predispose [a person to] the development of pneumonia and the severity of disease including decreased lung compliance, decreased respiratory muscle strength, retained secretions, ... and dysfunctional and impaired immunity."

Dr. Sligl said that she and her colleagues had no relevant financial disclosures.

VANCOUVER, B.C. – Age was independently associated with mortality in patients admitted to the ICU with pneumonia.

Overall mortality was 17% at 30 days and 32% at 1 year in a prospective, population-based cohort study involving 351 ICU patients. After adjustment for pneumonia severity, comorbid disease, sex, smoking status, alcohol use, and other potential confounders, each 10-year increase in age was associated with a 24% increase in 30-day mortality and a 39% increase in 1-year mortality, Dr. Wendy I. Sligl said at the annual meeting of the Infectious Diseases Society of America.

"This is a very high mortality rate, with almost one-third of patients dead at 1 year," said Dr. Sligl of the University of Alberta, Edmonton. Long-term mortality in these patients may rival or exceed that seen in patients with heart failure or end-stage renal disease.

"We tend to think of community-acquired pneumonia as a reversible problem. Patients come in, they get treated for their pneumonia, they come off the ventilator, they go home, and they’re fixed. And that really is not what we’re seeing with this data," she said.

Dr. Sligl and her fellow researchers enrolled all adults aged 17 years and older who were hospitalized with pneumonia in one of the six hospitals and five ICUs in Edmonton. The study excluded patients who were pregnant or lactating, had been previously hospitalized within 30 days, or were immunosuppressed. Of 3,415 patients admitted with pneumonia between 2000 and 2002, 351 were admitted to the ICU within 24 hours of their presentation at the emergency department.

The mean age of the 351 ICU patients was 61 years, with 43% younger than 60, 18% between 60 and 69, 23% between 70 and 79, and 15% aged 80 years and older (percentages do not total to 100% due to rounding). Most (59%) were male.

After adjustment for functional impairment, number of comorbidities, and illness severity in their multivariate analysis, the researchers found several independent predictors of mortality besides age. Patients with a living will had a threefold increase in 30-day mortality and a twofold increase in 1-year mortality. Every 10 points on the modified Pneumonia Severity Index increased the risk of 30-day mortality by 11% and the risk of 1-year mortality by 12%.

Dr. Sligl advanced several possible explanations for the independent relationship between age and mortality. Elderly patients may be frailer or have decreased reserve, she said. "This is very difficult to measure objectively and to include in multivariable modeling. There are many physiologic changes associated with aging that can predispose [a person to] the development of pneumonia and the severity of disease including decreased lung compliance, decreased respiratory muscle strength, retained secretions, ... and dysfunctional and impaired immunity."

Dr. Sligl said that she and her colleagues had no relevant financial disclosures.