Abstract
Interesting article that some day may translate into the clinical practice at the bedside.
OBJECTIVE: Biomarkers for detection of acute kidney injury and prediction of mortality will be useful to improve the outcomes of critically ill patients. Although several promising acute kidney injury biomarkers have been reported, evaluation in heterogeneous disease-oriented populations is necessary to confirm their reliability before their translation to clinical use. This study was undertaken to evaluate the reliability of new acute kidney injury biomarkers including urinary L-type fatty acid-binding protein with heterogeneous intensive care unit populations.
DESIGN: Prospective observational cohort study.
SETTING: Single-center study, 15-bed medical-surgical mixed intensive care unit at a university hospital. PATIENTS: Three hundred thirty-nine adult critically ill patients who had been admitted to the intensive care unit were studied prospectively.
INTERVENTIONS: None. MEASUREMENTS AND
MAIN RESULTS: Five urinary biomarkers (L-type fatty acid-binding protein, neutrophil gelatinase-associated lipocalin, interleukin-18, N-acetyl-beta-D-glucosaminidase, and albumin) were measured at intensive care unit admission. By the RIFLE (Risk, Injury, Failure, Loss, End-stage kidney disease) criteria, 131 patients (39%) were diagnosed as acute kidney injury. Urinary L-type fatty acid-binding protein detected acute kidney injury better than the other biomarkers did (the area under the receiver operating characteristic curves for L-type fatty acid-binding protein 0.75, neutrophil gelatinase-associated lipocalin 0.70, interleukin-18 0.69, N-acetyl-beta-D-glucosaminidase 0.62, albumin 0.69). Urinary L-type fatty acid-binding protein predicted later-onset acute kidney injury after intensive care unit admission with the highest area under the receiver operating characteristic curve value of 0.70. Furthermore, L-type fatty acid-binding protein, neutrophil gelatinase-associated lipocalin, and interleukin-18 were able to predict 14-day mortality with higher area under the receiver operating characteristic curves than acute kidney injury detection (area under the receiver operating characteristic curve for L-type fatty acid-binding protein 0.90, neutrophil gelatinase-associated lipocalin 0.83, interleukin-18 0.83). The combination of L-type fatty acid-binding protein and neutrophil gelatinase-associated lipocalin improved mortality prediction (area under the receiver operating characteristic curve 0.93).
CONCLUSION: This prospective observational study with a cohort of heterogeneous patients treated in a mixed intensive care unit revealed that new acute kidney injury biomarkers have a significantly and moderately predictive use for acute kidney injury diagnosis and that urinary L-type fatty acid-binding protein and neutrophil gelatinase-associated lipocalin can serve as new biomarkers of mortality prediction in critical care.
Friday, December 30, 2011
Thursday, December 29, 2011
Stop Routinely Anticoagulating Hospital Patients
Medpage Editorial Link
By George Lundberg, MD, Editor-at-Large, MedPage Today, Editor-at-Large, MedPage Today
Published: December 27, 2011
Transcript:
Hello and welcome. I'm Dr. George Lundberg and this is At Large at MedPage Today.
Another medical shibboleth bites the dust.
Again and again, physicians confront bad disease. They use treatments that make intuitive sense without hard data because there aren't any. Then, over time, those procedures become "standard of practice" still without supporting evidence. Then the evidence against the treatment begins to accumulate but, like turning an oil tanker around in the Atlantic, it takes time and a lot of effort.
The current best example is routine use of anticoagulants to prevent venous thromboembolism in hospitalized non-surgical patients.
Lederle and three co-authors from Minnesota published an article entitled "Venous Thromboembolism in Hospitalized Medical Patients and Those with Stroke: A Background Review for an American College of Physicians Clinical Practice Guideline" in the Annals of Internal Medicine in November 2011.
In order "to assess the benefits and harms of anticoagulant prophylaxis in hospitalized adult medical patients and those with acute stroke the authors used MEDLINE and the Cochrane Library from 1950 through April 2011, plus reference lists."
"English-language randomized trials were selected if they provided clinical outcomes and evaluated therapy with low-dose heparin or related agents or mechanical measures compared with placebo, no treatment, or other active prophylaxis in the target population."
"Two independent investigators extracted data on study characteristics and clinical outcomes up to 120 days after randomization. The primary outcome was total mortality."
"In medical patients, heparin prophylaxis did not reduce total mortality but did result in fewer pulmonary embolisms (PEs) and an increase in all bleeding events. Heparin prophylaxis had no statistically significant effect on any outcome in patients with acute stroke except for an increase in major bleeding events."
"When trials of medical patients and those with stroke were considered together (18 studies, 36,122 patients), heparin prophylaxis reduced the incidence of PE; absolute reduction, three events per 1,000 patients treated but increased the incidence of all bleeding and major bleeding events, with an absolute increase of nine bleeding events per 1,000 patients treated, four of which were major. No statistically significant differences in clinical outcomes were observed in the 14 trials that compared unfractionated heparin with low-molecular-weight heparin."
They concluded that "heparin prophylaxis had no significant effect on mortality," may have reduced non-fatal pulmonary embolism in medical patients and all patients combined, but "led to more bleeding and major bleeding events, thus resulting in little or no net benefit."
The authors did not report on the economic costs of this widespread practice but they are large indeed, and with no real benefit.
Play it again, Sam, 100,000 times, until the doctors hear the data and practice evidence-based medicine.
That's my opinion. I'm Dr. George Lundberg, At Large at MedPage Today.
Drug Trials Not Representative, Researchers Charge
Medpage Link
By Emily P. Walker, Washington Correspondent, MedPage Today
Published: December 27, 2011
Few major randomized, controlled clinical trials examine the effects of a drug in patients who have multiple chronic conditions, even though more than one-quarter of all Americans are living with at least two chronic health conditions, researchers reported.
The proportion is even greater for older individuals, two out of three of whom are likely to have at least two chronic health conditions, according to Alejandro Jadad, MD, and colleagues from the Centre for Health, Wellness and Cancer Survivorship at the University Health Network in Toronto.
That means that most trials on which the FDA bases its approval of new drugs are not generalizable to the U.S. population, they wrote in a research letter published in the Dec. 28 issue of the Journal of the American Medical Association.
Jadad and his colleagues examined all randomized controlled studies that dealt with an intervention for a long-lasting or chronic disease or condition that were published from January-March in 1995, 2000, 2005, and 2010 in five major peer-reviewed medical journals -- BMJ, CMAJ, JAMA, The Lancet, and the New England Journal of Medicine -- as well as six journals that focus on the most prevalent chronic conditions, including Circulation and Annals of General Psychiatry.
Only six of the 284 published trials analyzed (2.1%) explicitly included patients with multiple chronic conditions, and that percentage didn't change much from 1995 to 2010. In 179 of the randomized controlled trials, patients with multiple medical conditions were explicitly excluded from the trial.
Patients with multiple conditions were mentioned often in trial reports, although not actually included in the trial. About 70% of the published trial reports mentioned multiple coexisting diseases; with general medical journals describing them more often than specialized journals (72% versus 69%; P=0.02).
The letter authors concluded that few randomized controlled clinical trials published in the last 15 years have included patients with multiple chronic conditions.
Although the study was small, the authors said the finding "invites reflection about the risk of unintended harm from inappropriate generalization of trial results conducted in populations with a single disease."
"Given the possible drug-to-drug, drug-to-disease, and disease-to-disease interactions that remain unexamined, most of the evidence gathered to date by [randomized controlled clinical trials] is of limited value to guide decisions," they wrote.
The study authors said it may be useful for the FDA to have drug companies include subgroups of patients with the most common combinations of diseases in their drug development process; to observe safety outcomes of adding a new drug to patients who are already medicated for other conditions; and to have post-marketing studies that include the risk stratification to allow for meta-analyses across populations, such as those with multiple conditions.
The study was supported by funds from the Canada Research Chair in eHealth Innovation, the University of Toronto, and the University Health Network.
One of the letter writers, Alejandro Jadad, reported being a consultant to Foresight Links Corporation and that he receives royalties from Wiley for a book on randomized controlled trials.
None of others reported having any financial disclosures.
Primary source: Journal of the American Medical Association
Source reference:
Jahad A, et al "Consideration of multiple chronic diseases in randomized controlled trial" JAMA 2011; 306(24): 2670-2674.
Wednesday, December 28, 2011
2-Stage Plan for Managing Gout May Keep Joints Clean
Original Medscape Article
Janis C. Kelly
Author
December 26, 2011 — Maintaining serum urate levels at less than 6 mg/dL is necessary for clearing tophi and dissolving monosodium urate monohydrate crystals in gout, but once it has been achieved, keeping serum urate just below the threshold for saturation (6.0 - 6.9 mg/dL) is likely to be enough to prevent gout recurrence, according to data reported in the December issue of Arthritis & Rheumatism.
Fernando Perez-Ruiz, MD, PhD, from Hospital Universitario Cruces in Vizcaya, Spain, and colleagues analyzed recurrence and serum urate data in a prospective cohort of 211 patients with gout. For patients who did not have tophi at baseline, urate-lowering therapy was withdrawn after 5 years. For those with tophi at baseline, urate-lowering therapy was withdrawn 5 years after the resolution of the last tophus.
Serum urate levels were measured at least twice during the first year, after withdrawal of urate-lowering therapy, and then at least yearly. Recurrence was defined as a clinical event suggesting gout flare, and was confirmed by a finding of monosodium urate monohydrate crystals.
The analysis included 211 patients, 52 of whom had tophi at baseline. Mean duration of urate-lowering treatment was 66 months, and mean follow-up after withdrawal of urate-lowering therapy was 33.1 months.
Estimated median time to recurrence was 47 months after the end of therapy, and the cumulative recurrence rate was 6.6% at 1 year, 11.4% at 2 years, 20.4% at 3 years, and 29.4% at 4 years. The authors report, "None of the patients who had average serum levels of <7 mg/dl after urate-lowering therapy withdrawal developed a crystal-proven recurrence of gout."
Dr. Perez-Ruiz told Medscape Medical News, "You may need full doses for the first stage (low serum urate target), and lower doses for lifelong maintenance therapy."
A post hoc analysis found that weight loss and use of drugs such as losartan or fenofibrate were associated with maintaining serum urate levels below 7 mg/dL during follow-up after urate-lowering therapy withdrawal, and that use of diuretics was associated with failure to keep serum urate levels below 7 mg/dL.
According to Dr. Perez-Ruiz, this suggests that once crystals are cleared, lower doses of urate-lowering drugs will be sufficient for preventing recurrence. The "therapeutic target" for clearing crystals remains 5 years of serum urate less than 6 mg/dL, but once this has been achieved, the "preventive target" should be 6.00 to 6.99 mg/dL. This approach is being validated in ongoing studies.
Gout expert Eliseo Pascual, MD, who reviewed the article for Medscape Medical News, said, "The point of Dr. Fernando Perez-Ruiz's study is that (1) the rate of crystal dissolution is faster when lower serum urate levels are reached, according to his own work showing faster reduction of tophi size in patients in whom lower serum uric acid were reached, and (2) the real problem in gout patients is that urate crystal formation occurs in some tissues due to local conditions."
He continued, "So, if after fully dissolving the urate crystals by lowering serum uric acid to low levels, serum urate levels are allowed to rise above normal...urate crystals will form again, quite likely on the same tissues, and a new gout flare will occur. To avoid [recurrence]...serum uric acid should be kept within normal values, even if they are high-normal." Dr. Pascual heads the rheumatology section at Universidad Miguel Hernández in Alicante, Spain.
Dr. Perez-Ruiz describes this strategy as the "clean dish" approach: "[T]he initial effort to clean the disease (serum urate therapeutic target) would depend on how dirty it is (urate deposition burden), and, once it is clean, light daily wiping may be enough (serum preventive target) from then on to avoid dust (new urate crystal) accumulation and keep it clean (no recurrence)."
Dr. Perez-Ruiz has received consulting fees and/or speaking fees from Menarini, Ardea, and Novartis. Dr. Pascual has disclosed no relevant financial relationships.
Arthritis Rheum. 2011:63:4002-4006. Abstract
Janis C. Kelly
Author
December 26, 2011 — Maintaining serum urate levels at less than 6 mg/dL is necessary for clearing tophi and dissolving monosodium urate monohydrate crystals in gout, but once it has been achieved, keeping serum urate just below the threshold for saturation (6.0 - 6.9 mg/dL) is likely to be enough to prevent gout recurrence, according to data reported in the December issue of Arthritis & Rheumatism.
Fernando Perez-Ruiz, MD, PhD, from Hospital Universitario Cruces in Vizcaya, Spain, and colleagues analyzed recurrence and serum urate data in a prospective cohort of 211 patients with gout. For patients who did not have tophi at baseline, urate-lowering therapy was withdrawn after 5 years. For those with tophi at baseline, urate-lowering therapy was withdrawn 5 years after the resolution of the last tophus.
Serum urate levels were measured at least twice during the first year, after withdrawal of urate-lowering therapy, and then at least yearly. Recurrence was defined as a clinical event suggesting gout flare, and was confirmed by a finding of monosodium urate monohydrate crystals.
The analysis included 211 patients, 52 of whom had tophi at baseline. Mean duration of urate-lowering treatment was 66 months, and mean follow-up after withdrawal of urate-lowering therapy was 33.1 months.
Estimated median time to recurrence was 47 months after the end of therapy, and the cumulative recurrence rate was 6.6% at 1 year, 11.4% at 2 years, 20.4% at 3 years, and 29.4% at 4 years. The authors report, "None of the patients who had average serum levels of <7 mg/dl after urate-lowering therapy withdrawal developed a crystal-proven recurrence of gout."
Dr. Perez-Ruiz told Medscape Medical News, "You may need full doses for the first stage (low serum urate target), and lower doses for lifelong maintenance therapy."
A post hoc analysis found that weight loss and use of drugs such as losartan or fenofibrate were associated with maintaining serum urate levels below 7 mg/dL during follow-up after urate-lowering therapy withdrawal, and that use of diuretics was associated with failure to keep serum urate levels below 7 mg/dL.
According to Dr. Perez-Ruiz, this suggests that once crystals are cleared, lower doses of urate-lowering drugs will be sufficient for preventing recurrence. The "therapeutic target" for clearing crystals remains 5 years of serum urate less than 6 mg/dL, but once this has been achieved, the "preventive target" should be 6.00 to 6.99 mg/dL. This approach is being validated in ongoing studies.
Gout expert Eliseo Pascual, MD, who reviewed the article for Medscape Medical News, said, "The point of Dr. Fernando Perez-Ruiz's study is that (1) the rate of crystal dissolution is faster when lower serum urate levels are reached, according to his own work showing faster reduction of tophi size in patients in whom lower serum uric acid were reached, and (2) the real problem in gout patients is that urate crystal formation occurs in some tissues due to local conditions."
He continued, "So, if after fully dissolving the urate crystals by lowering serum uric acid to low levels, serum urate levels are allowed to rise above normal...urate crystals will form again, quite likely on the same tissues, and a new gout flare will occur. To avoid [recurrence]...serum uric acid should be kept within normal values, even if they are high-normal." Dr. Pascual heads the rheumatology section at Universidad Miguel Hernández in Alicante, Spain.
Dr. Perez-Ruiz describes this strategy as the "clean dish" approach: "[T]he initial effort to clean the disease (serum urate therapeutic target) would depend on how dirty it is (urate deposition burden), and, once it is clean, light daily wiping may be enough (serum preventive target) from then on to avoid dust (new urate crystal) accumulation and keep it clean (no recurrence)."
Dr. Perez-Ruiz has received consulting fees and/or speaking fees from Menarini, Ardea, and Novartis. Dr. Pascual has disclosed no relevant financial relationships.
Arthritis Rheum. 2011:63:4002-4006. Abstract
More People Diagnosed With Kidney Cancer in the United States
Original Medscape Article
By Will Boggs, MD
NEW YORK (Reuters Health) Dec 23 - The incidence of kidney cancer has increased significantly over the past three decades in the United States, according to a report in the November 16 online issue of The Journal of Urology.
"As imaging tests are ordered for a variety of reasons, incidental renal cancers are being increasingly found," Dr. Seth A. Strope from Washington University School of Medicine in St. Louis, Missouri, told Reuters Health by email.
"Since most of these tumors are now found in an asymptomatic state, internists should be vigilant for these findings on their scans."
Dr. Strope and colleagues used National Cancer Institute SEER cancer registry data for 1975 to 2006 to determine the kidney cancer incidence by age.
During this interval, the overall age-adjusted kidney cancer incidence increased 238%, from 7/100,000 to 17.6/100,000 adults. The annual rise was higher between 1976 and 1990 (3.6% annually) than between 1991 and 2006 (2.9% annually).
Renal tumors diagnosed after 1991 were more likely to be smaller and localized to the kidney than tumors diagnosed earlier.
All age groups showed an increase in renal cancer diagnoses during the more contemporary periods, with the most rapid increases appearing in the younger age groups during the second half of the study.
The fastest increase in renal cancer incidence was in the 20- to 39-year-old group, followed by the 60-to-69- and 70-to-79-year-old groups.
"The trend toward increased exposure to risk factors for kidney cancer at earlier ages combined with imaging may help explain why the youngest age group had the fastest increase in renal cancer relative to the other age groups," the researchers note.
"Rising incidence of kidney cancer points to the need to appropriately tailor therapy to individual patients," Dr. Strope said. "Younger patients would most benefit from kidney preservation through removal of only the tumor, while older patients may benefit from surveillance of small renal masses."
"Further research into the rising incidence of kidney cancer will need to focus on new risk factors," Dr. Strope added. "Exploration of large cohort studies with focus on risk factors in past versus more current years will be needed to determine these risk factors."
SOURCE: http://bit.ly/s3edud
J Urol 2011;187:32-38.
By Will Boggs, MD
NEW YORK (Reuters Health) Dec 23 - The incidence of kidney cancer has increased significantly over the past three decades in the United States, according to a report in the November 16 online issue of The Journal of Urology.
"As imaging tests are ordered for a variety of reasons, incidental renal cancers are being increasingly found," Dr. Seth A. Strope from Washington University School of Medicine in St. Louis, Missouri, told Reuters Health by email.
"Since most of these tumors are now found in an asymptomatic state, internists should be vigilant for these findings on their scans."
Dr. Strope and colleagues used National Cancer Institute SEER cancer registry data for 1975 to 2006 to determine the kidney cancer incidence by age.
During this interval, the overall age-adjusted kidney cancer incidence increased 238%, from 7/100,000 to 17.6/100,000 adults. The annual rise was higher between 1976 and 1990 (3.6% annually) than between 1991 and 2006 (2.9% annually).
Renal tumors diagnosed after 1991 were more likely to be smaller and localized to the kidney than tumors diagnosed earlier.
All age groups showed an increase in renal cancer diagnoses during the more contemporary periods, with the most rapid increases appearing in the younger age groups during the second half of the study.
The fastest increase in renal cancer incidence was in the 20- to 39-year-old group, followed by the 60-to-69- and 70-to-79-year-old groups.
"The trend toward increased exposure to risk factors for kidney cancer at earlier ages combined with imaging may help explain why the youngest age group had the fastest increase in renal cancer relative to the other age groups," the researchers note.
"Rising incidence of kidney cancer points to the need to appropriately tailor therapy to individual patients," Dr. Strope said. "Younger patients would most benefit from kidney preservation through removal of only the tumor, while older patients may benefit from surveillance of small renal masses."
"Further research into the rising incidence of kidney cancer will need to focus on new risk factors," Dr. Strope added. "Exploration of large cohort studies with focus on risk factors in past versus more current years will be needed to determine these risk factors."
SOURCE: http://bit.ly/s3edud
J Urol 2011;187:32-38.
Gastroparesis Less Common Than Thought in Diabetics
Original Medscape Article
By Anne Harding
NEW YORK (Reuters Health) Dec 23 - Gastroparesis may not be as common among people with diabetes as had previously been thought, new findings show.
Over a 10-year follow-up period, just 5% of people with type 1 diabetes developed gastroparesis, while 1% of type 2 diabetics did, Dr. G. Richard Locke III of the Mayo Clinic in Rochester, Minnesota and his colleagues found.
"Our sense is there's a perception out there that as soon as someone with diabetes has a stomach problem, it gets called gastroparesis," Dr. Locke told Reuters Health. "While it's true that people with bad, long-standing diabetes get gastroparesis, most people don't."
Studies have shown that many people with gastroparesis have diabetes mellitus (DM), and cross-sectional studies have also found a high prevalence of abnormally slow stomach emptying among people with long-standing type 1 or type 2 DM.
Still, it hasn't been clear how common gastroparesis is among the general population of diabetic patients, Dr. Locke and his team explain in their report, published online November 15 in the American Journal of Gastroenterology.
To investigate, the researchers gathered data on 227 patients with type 1 DM and 360 with type 2 DM as of January 1995, and 639 non-diabetic controls.
Over the following 10 years, 10 of the patients with type 1 DM and four of those with type 2 DM developed gastroparesis, compared to just one of the controls. Cumulative risk of gastroparesis was 5.2% for patients with type 1 DM, 1% for patients with type 2 DM, and 0.2% for the controls. The adjusted hazard ratio for gastroparesis was 33 for type 1 DM and 7.5 for type 2, although the latter finding was not statistically significant.
Heartburn was the only gastrointestinal symptom independently associated with gastroparesis risk at baseline among type 1 diabetics; these patients were 6.6 times more likely to develop gastroparesis during follow-up.
The finding of a greater risk of gastroparesis in type 1 diabetes patients is "consistent with poorer diabetic control and high rates of autonomic neuropathy that occur in patients with type 1 DM," Dr. Locke and colleagues write. "A remarkable finding of the current study is that the incidence of clinically evident gastroparesis among those with diabetes is still rare."
The prevalence of the condition among diabetics may have been overestimated, the researchers suggest, because many studies have used surveys asking patients about symptoms rather than relying on medical tests and diagnosis.
"One needs to be aware that there are other causes of nausea, vomiting and stomach discomfort in people with diabetes," Dr. Locke said. When gastroparesis is suspected, he added, patients will typically undergo endoscopy and possibly abdominal imaging with CT scanning or ultrasound. Patients may also complete a gastric emptying study. According to Dr. Locke, while many centers still do two-hour gastric emptying studies, a full four-hour study is preferred.
While doctors and patients may prefer the clearer diagnosis of gastroparesis, he added, most patients are likely to have normal gastric emptying, which points to a diagnosis of functional dyspepsia.
"We think it's more accurate to think of these people as having functional dyspepsia, with a few having gastroparesis," Dr. Locke said. "We think it's important to find out, to do the testing and see."
SOURCE: http://bit.ly/tBaIcG
Am J Gastroenterol 2011.
By Anne Harding
NEW YORK (Reuters Health) Dec 23 - Gastroparesis may not be as common among people with diabetes as had previously been thought, new findings show.
Over a 10-year follow-up period, just 5% of people with type 1 diabetes developed gastroparesis, while 1% of type 2 diabetics did, Dr. G. Richard Locke III of the Mayo Clinic in Rochester, Minnesota and his colleagues found.
"Our sense is there's a perception out there that as soon as someone with diabetes has a stomach problem, it gets called gastroparesis," Dr. Locke told Reuters Health. "While it's true that people with bad, long-standing diabetes get gastroparesis, most people don't."
Studies have shown that many people with gastroparesis have diabetes mellitus (DM), and cross-sectional studies have also found a high prevalence of abnormally slow stomach emptying among people with long-standing type 1 or type 2 DM.
Still, it hasn't been clear how common gastroparesis is among the general population of diabetic patients, Dr. Locke and his team explain in their report, published online November 15 in the American Journal of Gastroenterology.
To investigate, the researchers gathered data on 227 patients with type 1 DM and 360 with type 2 DM as of January 1995, and 639 non-diabetic controls.
Over the following 10 years, 10 of the patients with type 1 DM and four of those with type 2 DM developed gastroparesis, compared to just one of the controls. Cumulative risk of gastroparesis was 5.2% for patients with type 1 DM, 1% for patients with type 2 DM, and 0.2% for the controls. The adjusted hazard ratio for gastroparesis was 33 for type 1 DM and 7.5 for type 2, although the latter finding was not statistically significant.
Heartburn was the only gastrointestinal symptom independently associated with gastroparesis risk at baseline among type 1 diabetics; these patients were 6.6 times more likely to develop gastroparesis during follow-up.
The finding of a greater risk of gastroparesis in type 1 diabetes patients is "consistent with poorer diabetic control and high rates of autonomic neuropathy that occur in patients with type 1 DM," Dr. Locke and colleagues write. "A remarkable finding of the current study is that the incidence of clinically evident gastroparesis among those with diabetes is still rare."
The prevalence of the condition among diabetics may have been overestimated, the researchers suggest, because many studies have used surveys asking patients about symptoms rather than relying on medical tests and diagnosis.
"One needs to be aware that there are other causes of nausea, vomiting and stomach discomfort in people with diabetes," Dr. Locke said. When gastroparesis is suspected, he added, patients will typically undergo endoscopy and possibly abdominal imaging with CT scanning or ultrasound. Patients may also complete a gastric emptying study. According to Dr. Locke, while many centers still do two-hour gastric emptying studies, a full four-hour study is preferred.
While doctors and patients may prefer the clearer diagnosis of gastroparesis, he added, most patients are likely to have normal gastric emptying, which points to a diagnosis of functional dyspepsia.
"We think it's more accurate to think of these people as having functional dyspepsia, with a few having gastroparesis," Dr. Locke said. "We think it's important to find out, to do the testing and see."
SOURCE: http://bit.ly/tBaIcG
Am J Gastroenterol 2011.
One Fourth of ICU Clinicians Report Inappropriate Care
Original Medscape Article
December 27, 2011 — A survey of intensive care unit (ICU) physicians
and nurses in Europe and Israel reveals that these clinicians often
perceive that they are providing inappropriate care, most often "too
much care," to patients admitted to ICUs, according to a report
published in the December 28 issue of JAMA.
According to the report, this perception of providing inappropriate care can lead to moral distress among clinicians, who may eventually decide to leave their jobs, further jeopardizing care of future patients. More than half of the respondents in this survey "were not confident that these situations would be resolved in the near future."
Researchers led by Ruth D. Piers, MD, from Ghent University Hospital in Belgium, conducted surveys at 82 ICUs. Of the 1651 survey respondents, 439 (27%) reported perceived inappropriate care for at least 1 patient during a 24-hour period, for a total 445 inappropriate care incidents. In 89% of those incidents, clinicians attributed "too much care" as the reason, and insufficient care in 11%. In other cases, they cited "distributive injustice," meaning other patients could have been better served under the specific circumstances.
The respondents defined inappropriate care as care that clinicians view as contradictory to their own personal beliefs and professional knowledge.
"Although the report by Piers et al provides a hazy lens through which to view appropriateness of care, it yields more clarity than prior studies," writes Scott D. Halpern, MD, PhD, from the University of Pennsylvania School of Medicine in Philadelphia, in an accompanying editorial. The report may turn out to be "the clarion call needed to spur more rigorous study of what happens to clinicians and the care they provide," he writes.
The researchers conducted the surveys in Europe on May 11 to 12, 2010, and in Israel on May 25, 2010. They used 3 types of questionnaires: 1 collecting characteristics of each ICU, such as mortality rate and number of clinicians; 1 collecting personal characteristics of clinicians, such as age, role, and job strain; and 1 collecting details about perceived inappropriateness of care.
The researchers suggest that interventions to improve communication and collaboration, relieve work overloads, and give clinicians more autonomy in decision-making could improve the overall picture. "[P]erceived inappropriateness of care was less common in ICUs in which physicians and nurses had a degree of job autonomy, an acceptable workload, and a high level of interdisciplinary collaboration and decision making," they add.
The survey gave clinicians 7 possible reasons to choose for inappropriate care:
Dr. Piers and colleagues report receipt of a grant from the European Society of Intensive Care Medicine/European Critical Care Research Network. One coauthor reports board membership, consultancy, grants received or pending, and speakers bureau participation with Gilead, Pfizer, and Merck, Sharp, & Dohme. Another coauthor reports receipt of meeting expenses from the European Society of Clinical Microbiology and Infectious Diseases, as well as other research grants from Astra-Zeneca, Bayer, Pfizer, General Electric, and Merck, Sharp, & Dohme. One coauthor reports receipt of consultancy fees from Abbott Laboratories, and one coauthor reports receipt of a grant or a pending grant from Pfizer. The remaining authors have disclosed no relevant financial relationships.
JAMA. 2011;306:2694-2703, 2725-2726.
Larry Hand
According to the report, this perception of providing inappropriate care can lead to moral distress among clinicians, who may eventually decide to leave their jobs, further jeopardizing care of future patients. More than half of the respondents in this survey "were not confident that these situations would be resolved in the near future."
Researchers led by Ruth D. Piers, MD, from Ghent University Hospital in Belgium, conducted surveys at 82 ICUs. Of the 1651 survey respondents, 439 (27%) reported perceived inappropriate care for at least 1 patient during a 24-hour period, for a total 445 inappropriate care incidents. In 89% of those incidents, clinicians attributed "too much care" as the reason, and insufficient care in 11%. In other cases, they cited "distributive injustice," meaning other patients could have been better served under the specific circumstances.
The respondents defined inappropriate care as care that clinicians view as contradictory to their own personal beliefs and professional knowledge.
"Although the report by Piers et al provides a hazy lens through which to view appropriateness of care, it yields more clarity than prior studies," writes Scott D. Halpern, MD, PhD, from the University of Pennsylvania School of Medicine in Philadelphia, in an accompanying editorial. The report may turn out to be "the clarion call needed to spur more rigorous study of what happens to clinicians and the care they provide," he writes.
The researchers conducted the surveys in Europe on May 11 to 12, 2010, and in Israel on May 25, 2010. They used 3 types of questionnaires: 1 collecting characteristics of each ICU, such as mortality rate and number of clinicians; 1 collecting personal characteristics of clinicians, such as age, role, and job strain; and 1 collecting details about perceived inappropriateness of care.
The researchers suggest that interventions to improve communication and collaboration, relieve work overloads, and give clinicians more autonomy in decision-making could improve the overall picture. "[P]erceived inappropriateness of care was less common in ICUs in which physicians and nurses had a degree of job autonomy, an acceptable workload, and a high level of interdisciplinary collaboration and decision making," they add.
The survey gave clinicians 7 possible reasons to choose for inappropriate care:
- disproportion between amount of care and expected outcome,
- persistent nonadherence of the patient,
- other patients would benefit more from ICU care,
- inaccurate information was given to patient or family,
- patient's wishes concerning treatment were known but not respected,
- 1 party involved did not participate in treatment decision, and
- patient was not getting good-quality care.
Dr. Piers and colleagues report receipt of a grant from the European Society of Intensive Care Medicine/European Critical Care Research Network. One coauthor reports board membership, consultancy, grants received or pending, and speakers bureau participation with Gilead, Pfizer, and Merck, Sharp, & Dohme. Another coauthor reports receipt of meeting expenses from the European Society of Clinical Microbiology and Infectious Diseases, as well as other research grants from Astra-Zeneca, Bayer, Pfizer, General Electric, and Merck, Sharp, & Dohme. One coauthor reports receipt of consultancy fees from Abbott Laboratories, and one coauthor reports receipt of a grant or a pending grant from Pfizer. The remaining authors have disclosed no relevant financial relationships.
JAMA. 2011;306:2694-2703, 2725-2726.
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