User login
Herbal medicine can reduce pain, fatigue in SCD patients
Convention Center, site of
the 2016 ASH Annual Meeting
SAN DIEGO—Results of a phase 1 study suggest that SCD-101, a botanical extract based on an herbal medicine used in Nigeria to treat sickle cell disease (SCD), can reduce pain and fatigue in people with SCD.
The anti-sickling drug also improves the shape of red blood cells but doesn’t produce a change in hemoglobin, according to researchers.
Peter Gillette, MD, of SUNY Downstate in Brooklyn, New York, reported these results at the 2016 ASH Annual Meeting (abstract 121*).
A 6-month phase 2b study conducted previously in Nigeria showed that the herbal medicine Niprisan reduced pain crises and school absenteeism and raised hemoglobin levels compared to placebo.
Based on this study and positive preclinical activity, Dr Gillette and his colleagues undertook a phase 1 study to determine the safety of escalating doses of SCD-101.
Dr Gillette pointed out that Niprisan had been produced commercially in Nigeria but was later removed by the government from the commercial market because of production problems.
The researchers evaluated 23 patients with homozygous SCD or S/beta0 thalassemia.
Patients were aged 18 to 55 years with hemoglobin F of 15% or less and hemoglobin levels between 6.0 and 9.5 g/dL.
Patients could not have had hydroxyurea treatment within 6 months of enrollment, red blood cell transfusion within 3 months, or hospitalization within 4 weeks.
Patients received SCD-101 orally for 28 days administered 2 times daily (BID) or 3 times daily (TID). Doses were 550 mg BID, 1100 mg BID, 2200 mg BID, 4400 mg BID, and 2750 mg TID.
Dr Gillette explained that by distributing the highest dose 3 times over the course of a day, the researchers were able to decrease the side effects of bloating and flatulence on the highest dose.
“Interestingly, with the dose-distributed TID, we found that the hemoglobin had increased by 10%,” he said. “In other words, it appears that the effects are very short-acting, and that by going from a Q12 to a Q8 dosage, the hemoglobin suddenly looks like it might be significant, although this is not a significant change.”
Laboratory outcomes included hemoglobin and hemolysis (LDH, bilirubin, and reticulocyte measurements). Patient-reported outcomes included pain and fatigue.
The most common adverse events (AEs) were pain, flatulence, bloating, diarrhea, constipation, nausea, and headache.
Seven patients in the 2200 mg BID and 4400 mg BID cohorts had dose-related bloating, gas, flatulence or diarrhea, which subsided in a few days.
Patients in the 2750 mg TID cohort did not experience gas side effects.
The gastrointestinal symptoms were most likely dose-related from an excipient of SCD-101, Dr Gillette said.
He and his colleagues found no significant side effects after 28 days of dosing, and there were no dose reductions or interruptions due to drug-related AEs.
There were also no laboratory or electrocardiogram abnormalities.
“Almost all pain AEs stopped by day 13 in 22 of 23 patients,” Dr Gillette said.
“And unexpectedly, patients began to report that they slept better and had improved energy and cognition,” he noted.
Six patients in the 2200 and 4400 mg BID cohorts reported reduced fatigue as measured by the PROMIS fatigue questionnaire.
And 2 patients with ankle ulcers in the 2 highest dose cohorts reported improved healing.
Two weeks after treatment stopped, patients were almost back to baseline in terms of their chronic pain and fatigue levels, Dr Gillette said.
A parallel design, double-blind, placebo-controlled pilot study of the 2750 mg TID dose is ongoing.
Future studies include a crossover-design, exploratory study of the 2750 mg TID dose and a phase 2 parallel design study of the 2200 mg BID and 2750 mg TID doses.
While the researchers are uncertain about the mechanism of action of SCD-101, they hypothesize that its effects could be due to increased vascular flow, increased oxygen delivery, or a reduction in inflammation.
“This is a promising drug potentially for low-income countries or middle-income countries elsewhere in the world where gene therapy and transplant are really not that feasible,” Dr Gillette said.
Research for this study was supported in part by the National Heart, Lung, and Blood Institute and National Center for Complementary and Integrative Health of the National Institutes of Health.
*Information presented at the meeting differs from the abstract.
Convention Center, site of
the 2016 ASH Annual Meeting
SAN DIEGO—Results of a phase 1 study suggest that SCD-101, a botanical extract based on an herbal medicine used in Nigeria to treat sickle cell disease (SCD), can reduce pain and fatigue in people with SCD.
The anti-sickling drug also improves the shape of red blood cells but doesn’t produce a change in hemoglobin, according to researchers.
Peter Gillette, MD, of SUNY Downstate in Brooklyn, New York, reported these results at the 2016 ASH Annual Meeting (abstract 121*).
A 6-month phase 2b study conducted previously in Nigeria showed that the herbal medicine Niprisan reduced pain crises and school absenteeism and raised hemoglobin levels compared to placebo.
Based on this study and positive preclinical activity, Dr Gillette and his colleagues undertook a phase 1 study to determine the safety of escalating doses of SCD-101.
Dr Gillette pointed out that Niprisan had been produced commercially in Nigeria but was later removed by the government from the commercial market because of production problems.
The researchers evaluated 23 patients with homozygous SCD or S/beta0 thalassemia.
Patients were aged 18 to 55 years with hemoglobin F of 15% or less and hemoglobin levels between 6.0 and 9.5 g/dL.
Patients could not have had hydroxyurea treatment within 6 months of enrollment, red blood cell transfusion within 3 months, or hospitalization within 4 weeks.
Patients received SCD-101 orally for 28 days administered 2 times daily (BID) or 3 times daily (TID). Doses were 550 mg BID, 1100 mg BID, 2200 mg BID, 4400 mg BID, and 2750 mg TID.
Dr Gillette explained that by distributing the highest dose 3 times over the course of a day, the researchers were able to decrease the side effects of bloating and flatulence on the highest dose.
“Interestingly, with the dose-distributed TID, we found that the hemoglobin had increased by 10%,” he said. “In other words, it appears that the effects are very short-acting, and that by going from a Q12 to a Q8 dosage, the hemoglobin suddenly looks like it might be significant, although this is not a significant change.”
Laboratory outcomes included hemoglobin and hemolysis (LDH, bilirubin, and reticulocyte measurements). Patient-reported outcomes included pain and fatigue.
The most common adverse events (AEs) were pain, flatulence, bloating, diarrhea, constipation, nausea, and headache.
Seven patients in the 2200 mg BID and 4400 mg BID cohorts had dose-related bloating, gas, flatulence or diarrhea, which subsided in a few days.
Patients in the 2750 mg TID cohort did not experience gas side effects.
The gastrointestinal symptoms were most likely dose-related from an excipient of SCD-101, Dr Gillette said.
He and his colleagues found no significant side effects after 28 days of dosing, and there were no dose reductions or interruptions due to drug-related AEs.
There were also no laboratory or electrocardiogram abnormalities.
“Almost all pain AEs stopped by day 13 in 22 of 23 patients,” Dr Gillette said.
“And unexpectedly, patients began to report that they slept better and had improved energy and cognition,” he noted.
Six patients in the 2200 and 4400 mg BID cohorts reported reduced fatigue as measured by the PROMIS fatigue questionnaire.
And 2 patients with ankle ulcers in the 2 highest dose cohorts reported improved healing.
Two weeks after treatment stopped, patients were almost back to baseline in terms of their chronic pain and fatigue levels, Dr Gillette said.
A parallel design, double-blind, placebo-controlled pilot study of the 2750 mg TID dose is ongoing.
Future studies include a crossover-design, exploratory study of the 2750 mg TID dose and a phase 2 parallel design study of the 2200 mg BID and 2750 mg TID doses.
While the researchers are uncertain about the mechanism of action of SCD-101, they hypothesize that its effects could be due to increased vascular flow, increased oxygen delivery, or a reduction in inflammation.
“This is a promising drug potentially for low-income countries or middle-income countries elsewhere in the world where gene therapy and transplant are really not that feasible,” Dr Gillette said.
Research for this study was supported in part by the National Heart, Lung, and Blood Institute and National Center for Complementary and Integrative Health of the National Institutes of Health.
*Information presented at the meeting differs from the abstract.
Convention Center, site of
the 2016 ASH Annual Meeting
SAN DIEGO—Results of a phase 1 study suggest that SCD-101, a botanical extract based on an herbal medicine used in Nigeria to treat sickle cell disease (SCD), can reduce pain and fatigue in people with SCD.
The anti-sickling drug also improves the shape of red blood cells but doesn’t produce a change in hemoglobin, according to researchers.
Peter Gillette, MD, of SUNY Downstate in Brooklyn, New York, reported these results at the 2016 ASH Annual Meeting (abstract 121*).
A 6-month phase 2b study conducted previously in Nigeria showed that the herbal medicine Niprisan reduced pain crises and school absenteeism and raised hemoglobin levels compared to placebo.
Based on this study and positive preclinical activity, Dr Gillette and his colleagues undertook a phase 1 study to determine the safety of escalating doses of SCD-101.
Dr Gillette pointed out that Niprisan had been produced commercially in Nigeria but was later removed by the government from the commercial market because of production problems.
The researchers evaluated 23 patients with homozygous SCD or S/beta0 thalassemia.
Patients were aged 18 to 55 years with hemoglobin F of 15% or less and hemoglobin levels between 6.0 and 9.5 g/dL.
Patients could not have had hydroxyurea treatment within 6 months of enrollment, red blood cell transfusion within 3 months, or hospitalization within 4 weeks.
Patients received SCD-101 orally for 28 days administered 2 times daily (BID) or 3 times daily (TID). Doses were 550 mg BID, 1100 mg BID, 2200 mg BID, 4400 mg BID, and 2750 mg TID.
Dr Gillette explained that by distributing the highest dose 3 times over the course of a day, the researchers were able to decrease the side effects of bloating and flatulence on the highest dose.
“Interestingly, with the dose-distributed TID, we found that the hemoglobin had increased by 10%,” he said. “In other words, it appears that the effects are very short-acting, and that by going from a Q12 to a Q8 dosage, the hemoglobin suddenly looks like it might be significant, although this is not a significant change.”
Laboratory outcomes included hemoglobin and hemolysis (LDH, bilirubin, and reticulocyte measurements). Patient-reported outcomes included pain and fatigue.
The most common adverse events (AEs) were pain, flatulence, bloating, diarrhea, constipation, nausea, and headache.
Seven patients in the 2200 mg BID and 4400 mg BID cohorts had dose-related bloating, gas, flatulence or diarrhea, which subsided in a few days.
Patients in the 2750 mg TID cohort did not experience gas side effects.
The gastrointestinal symptoms were most likely dose-related from an excipient of SCD-101, Dr Gillette said.
He and his colleagues found no significant side effects after 28 days of dosing, and there were no dose reductions or interruptions due to drug-related AEs.
There were also no laboratory or electrocardiogram abnormalities.
“Almost all pain AEs stopped by day 13 in 22 of 23 patients,” Dr Gillette said.
“And unexpectedly, patients began to report that they slept better and had improved energy and cognition,” he noted.
Six patients in the 2200 and 4400 mg BID cohorts reported reduced fatigue as measured by the PROMIS fatigue questionnaire.
And 2 patients with ankle ulcers in the 2 highest dose cohorts reported improved healing.
Two weeks after treatment stopped, patients were almost back to baseline in terms of their chronic pain and fatigue levels, Dr Gillette said.
A parallel design, double-blind, placebo-controlled pilot study of the 2750 mg TID dose is ongoing.
Future studies include a crossover-design, exploratory study of the 2750 mg TID dose and a phase 2 parallel design study of the 2200 mg BID and 2750 mg TID doses.
While the researchers are uncertain about the mechanism of action of SCD-101, they hypothesize that its effects could be due to increased vascular flow, increased oxygen delivery, or a reduction in inflammation.
“This is a promising drug potentially for low-income countries or middle-income countries elsewhere in the world where gene therapy and transplant are really not that feasible,” Dr Gillette said.
Research for this study was supported in part by the National Heart, Lung, and Blood Institute and National Center for Complementary and Integrative Health of the National Institutes of Health.
*Information presented at the meeting differs from the abstract.
Observational hospital stays for HF linked to worse outcomes
NEW ORLEANS – The Centers for Medicare & Medicaid Services policy providing financial incentives for hospitals to readmit patients for heart failure for an observational stay rather than as an inpatient is antithetical to the patients’ best interests, according to data presented at the American Heart Association scientific sessions.
“We showed that if you get admitted under observation, the risk of you coming back is much higher than if you’re under an inpatient stay,” said Ahmad Masri, MBBS, of the University of Pittsburgh.
“Since CMS instituted this rule in 2013, there has been a surge in utilization of observational status versus inpatient status,” Dr. Masri noted.
That might make sense if the patients selected for in-hospital observation were less ill at the time than the heart failure patients admitted as inpatients, but that wasn’t the case in his large, retrospective study.
Dr. Masri reported on 21,339 patients with a total of 52,493 admissions for a primary diagnosis of heart failure during 2008-2015 in an 18-hospital health care system. After excluding admissions which involved cardiac surgery or in-hospital mortality, the total was 50,654 admissions.
Of these admissions, 5% were for in-hospital observation; 17% were inpatient admissions with discharge in less than 2 days. The two groups were similar in terms of age, comorbid conditions, and use of guideline-directed medications, although 36% of patients admitted under observation had a left ventricular ejection fraction below 40%, compared with 30% of those with an inpatient admission for less than 2 days.
The majority of patients in both groups were readmitted for heart failure within 1 year; however, the readmission rate was 23% lower in the group with an inpatient stay of less than 2 days, in an analysis adjusted for age, sex, ejection fraction, hypertension, diabetes, pneumonia, chronic obstructive pulmonary disease, liver disease, and renal failure.
Similarly, the group with an inpatient stay of less than 2 days’ duration was 24% less likely to have a cardiac readmission within 1 year than the group admitted for a penalty-free observational stay. The short inpatient stay group’s 1-year all-cause readmission rate was also 24% lower. All of these differences were statistically significant and clinically meaningful.
Yet 1-year all-cause mortality in the two groups was no different.
“This suggests that the difference between these two groups is more of an administrative distinction than a reflection of patient status at time of admission. It looks like it’s just random,” according to Dr. Masri. “There is a real need for a patient-centered, streamlined approach in evaluating and treating patients with heart failure, with a revised treatment-based algorithm and admission rules that guide physicians and shape health care policy.”
He reported having no financial conflicts of interest regarding this study.
NEW ORLEANS – The Centers for Medicare & Medicaid Services policy providing financial incentives for hospitals to readmit patients for heart failure for an observational stay rather than as an inpatient is antithetical to the patients’ best interests, according to data presented at the American Heart Association scientific sessions.
“We showed that if you get admitted under observation, the risk of you coming back is much higher than if you’re under an inpatient stay,” said Ahmad Masri, MBBS, of the University of Pittsburgh.
“Since CMS instituted this rule in 2013, there has been a surge in utilization of observational status versus inpatient status,” Dr. Masri noted.
That might make sense if the patients selected for in-hospital observation were less ill at the time than the heart failure patients admitted as inpatients, but that wasn’t the case in his large, retrospective study.
Dr. Masri reported on 21,339 patients with a total of 52,493 admissions for a primary diagnosis of heart failure during 2008-2015 in an 18-hospital health care system. After excluding admissions which involved cardiac surgery or in-hospital mortality, the total was 50,654 admissions.
Of these admissions, 5% were for in-hospital observation; 17% were inpatient admissions with discharge in less than 2 days. The two groups were similar in terms of age, comorbid conditions, and use of guideline-directed medications, although 36% of patients admitted under observation had a left ventricular ejection fraction below 40%, compared with 30% of those with an inpatient admission for less than 2 days.
The majority of patients in both groups were readmitted for heart failure within 1 year; however, the readmission rate was 23% lower in the group with an inpatient stay of less than 2 days, in an analysis adjusted for age, sex, ejection fraction, hypertension, diabetes, pneumonia, chronic obstructive pulmonary disease, liver disease, and renal failure.
Similarly, the group with an inpatient stay of less than 2 days’ duration was 24% less likely to have a cardiac readmission within 1 year than the group admitted for a penalty-free observational stay. The short inpatient stay group’s 1-year all-cause readmission rate was also 24% lower. All of these differences were statistically significant and clinically meaningful.
Yet 1-year all-cause mortality in the two groups was no different.
“This suggests that the difference between these two groups is more of an administrative distinction than a reflection of patient status at time of admission. It looks like it’s just random,” according to Dr. Masri. “There is a real need for a patient-centered, streamlined approach in evaluating and treating patients with heart failure, with a revised treatment-based algorithm and admission rules that guide physicians and shape health care policy.”
He reported having no financial conflicts of interest regarding this study.
NEW ORLEANS – The Centers for Medicare & Medicaid Services policy providing financial incentives for hospitals to readmit patients for heart failure for an observational stay rather than as an inpatient is antithetical to the patients’ best interests, according to data presented at the American Heart Association scientific sessions.
“We showed that if you get admitted under observation, the risk of you coming back is much higher than if you’re under an inpatient stay,” said Ahmad Masri, MBBS, of the University of Pittsburgh.
“Since CMS instituted this rule in 2013, there has been a surge in utilization of observational status versus inpatient status,” Dr. Masri noted.
That might make sense if the patients selected for in-hospital observation were less ill at the time than the heart failure patients admitted as inpatients, but that wasn’t the case in his large, retrospective study.
Dr. Masri reported on 21,339 patients with a total of 52,493 admissions for a primary diagnosis of heart failure during 2008-2015 in an 18-hospital health care system. After excluding admissions which involved cardiac surgery or in-hospital mortality, the total was 50,654 admissions.
Of these admissions, 5% were for in-hospital observation; 17% were inpatient admissions with discharge in less than 2 days. The two groups were similar in terms of age, comorbid conditions, and use of guideline-directed medications, although 36% of patients admitted under observation had a left ventricular ejection fraction below 40%, compared with 30% of those with an inpatient admission for less than 2 days.
The majority of patients in both groups were readmitted for heart failure within 1 year; however, the readmission rate was 23% lower in the group with an inpatient stay of less than 2 days, in an analysis adjusted for age, sex, ejection fraction, hypertension, diabetes, pneumonia, chronic obstructive pulmonary disease, liver disease, and renal failure.
Similarly, the group with an inpatient stay of less than 2 days’ duration was 24% less likely to have a cardiac readmission within 1 year than the group admitted for a penalty-free observational stay. The short inpatient stay group’s 1-year all-cause readmission rate was also 24% lower. All of these differences were statistically significant and clinically meaningful.
Yet 1-year all-cause mortality in the two groups was no different.
“This suggests that the difference between these two groups is more of an administrative distinction than a reflection of patient status at time of admission. It looks like it’s just random,” according to Dr. Masri. “There is a real need for a patient-centered, streamlined approach in evaluating and treating patients with heart failure, with a revised treatment-based algorithm and admission rules that guide physicians and shape health care policy.”
He reported having no financial conflicts of interest regarding this study.
AT THE AHA SCIENTIFIC SESSIONS
Key clinical point:
Major finding: The 1-year rates of readmission for heart failure, cardiac readmission, and all-cause readmission were each 23%-24% lower in heart failure patients admitted for an inpatient stay of less than 2 days’ duration than if they were designated as being admitted under observation.
Data source: A retrospective analysis of more than 50,000 hospital admissions with a primary diagnosis of heart failure in 21,339 patients during 2008-2015.
Disclosures: The presenter reported having no financial conflicts of interest regarding the study.
Halogenated anesthetic linked to less chronic postop mastectomy pain
The use of halogenated agents for anesthetic during a mastectomy operation may be associated with a lower incidence of long-term chronic postmastectomy pain (CPMP), according to a paper published in the the Journal of Clinical Anesthesia.
The retrospective cross-sectional survey of 128 women who underwent mastectomy with axillary lymph node dissection set out to determine whether the anesthetic or analgesic regimen used perioperatively had any impact on the risk of long-term chronic postoperative pain.
Overall, 43.8% of the women reported chronic pain, and nearly half of these showed neuropathic characteristics with an ID Pain score greater than or equal to 2 (J Clin Anesthesia. 2016;33:20-25. doi: 10.1016/j.jclinane.2015.07.010).
Those who were given a halogenated agent for anesthesia during the operation – 64% of patients in the survey - had a significant 19% lower incidence of chronic long-term postoperative mastectomy pain (95% CI, 0.70-0.95; P = .012).
Arnaud Steyaert, MD, and colleagues at the Catholic University of Louvain (Belgium) described this result as surprising, noting that sevoflurane use was recently found to be a risk factor for chronic pain after breast cancer surgery.
“An explanation for this discrepancy could be that the influence of sevoflurane on the development of CPMP depends on the other components of the anesthetic regimen,” the authors wrote, pointing out that the aforementioned study included the use of remifentanil in all patients, which can trigger acute opioid-induced hyperalgesia and chronic pain after surgery.
Apart from this effect, the authors said they did not see any impact from other analgesics – which included sufentanil, ketamine, clonidine, NSAIDs, and/or magnesium sulfate – on the risk of long-term chronic pain. However, patients treated with piritramide in the recovery room did have a significant 30% greater risk of chronic postoperative pain.
The study also found that patients who needed strong opioids in the postanesthesia care unit had a 30% higher risk of chronic long-term pain (95% CI, 1.11-1.53). “This was expected, as more intense acute postoperative pain is a known risk factor for developing chronic postsurgical pain, including CPMP,” the authors wrote.
Patients who had received adjuvant chemotherapy had a 32% higher incidence of chronic long-term pain, but there was no increase in risk associated with adjuvant radiotherapy. Both are known to cause neurotoxicity and therefore neuropathic pain, the authors commented.
No conflicts of interest were declared.
The use of halogenated agents for anesthetic during a mastectomy operation may be associated with a lower incidence of long-term chronic postmastectomy pain (CPMP), according to a paper published in the the Journal of Clinical Anesthesia.
The retrospective cross-sectional survey of 128 women who underwent mastectomy with axillary lymph node dissection set out to determine whether the anesthetic or analgesic regimen used perioperatively had any impact on the risk of long-term chronic postoperative pain.
Overall, 43.8% of the women reported chronic pain, and nearly half of these showed neuropathic characteristics with an ID Pain score greater than or equal to 2 (J Clin Anesthesia. 2016;33:20-25. doi: 10.1016/j.jclinane.2015.07.010).
Those who were given a halogenated agent for anesthesia during the operation – 64% of patients in the survey - had a significant 19% lower incidence of chronic long-term postoperative mastectomy pain (95% CI, 0.70-0.95; P = .012).
Arnaud Steyaert, MD, and colleagues at the Catholic University of Louvain (Belgium) described this result as surprising, noting that sevoflurane use was recently found to be a risk factor for chronic pain after breast cancer surgery.
“An explanation for this discrepancy could be that the influence of sevoflurane on the development of CPMP depends on the other components of the anesthetic regimen,” the authors wrote, pointing out that the aforementioned study included the use of remifentanil in all patients, which can trigger acute opioid-induced hyperalgesia and chronic pain after surgery.
Apart from this effect, the authors said they did not see any impact from other analgesics – which included sufentanil, ketamine, clonidine, NSAIDs, and/or magnesium sulfate – on the risk of long-term chronic pain. However, patients treated with piritramide in the recovery room did have a significant 30% greater risk of chronic postoperative pain.
The study also found that patients who needed strong opioids in the postanesthesia care unit had a 30% higher risk of chronic long-term pain (95% CI, 1.11-1.53). “This was expected, as more intense acute postoperative pain is a known risk factor for developing chronic postsurgical pain, including CPMP,” the authors wrote.
Patients who had received adjuvant chemotherapy had a 32% higher incidence of chronic long-term pain, but there was no increase in risk associated with adjuvant radiotherapy. Both are known to cause neurotoxicity and therefore neuropathic pain, the authors commented.
No conflicts of interest were declared.
The use of halogenated agents for anesthetic during a mastectomy operation may be associated with a lower incidence of long-term chronic postmastectomy pain (CPMP), according to a paper published in the the Journal of Clinical Anesthesia.
The retrospective cross-sectional survey of 128 women who underwent mastectomy with axillary lymph node dissection set out to determine whether the anesthetic or analgesic regimen used perioperatively had any impact on the risk of long-term chronic postoperative pain.
Overall, 43.8% of the women reported chronic pain, and nearly half of these showed neuropathic characteristics with an ID Pain score greater than or equal to 2 (J Clin Anesthesia. 2016;33:20-25. doi: 10.1016/j.jclinane.2015.07.010).
Those who were given a halogenated agent for anesthesia during the operation – 64% of patients in the survey - had a significant 19% lower incidence of chronic long-term postoperative mastectomy pain (95% CI, 0.70-0.95; P = .012).
Arnaud Steyaert, MD, and colleagues at the Catholic University of Louvain (Belgium) described this result as surprising, noting that sevoflurane use was recently found to be a risk factor for chronic pain after breast cancer surgery.
“An explanation for this discrepancy could be that the influence of sevoflurane on the development of CPMP depends on the other components of the anesthetic regimen,” the authors wrote, pointing out that the aforementioned study included the use of remifentanil in all patients, which can trigger acute opioid-induced hyperalgesia and chronic pain after surgery.
Apart from this effect, the authors said they did not see any impact from other analgesics – which included sufentanil, ketamine, clonidine, NSAIDs, and/or magnesium sulfate – on the risk of long-term chronic pain. However, patients treated with piritramide in the recovery room did have a significant 30% greater risk of chronic postoperative pain.
The study also found that patients who needed strong opioids in the postanesthesia care unit had a 30% higher risk of chronic long-term pain (95% CI, 1.11-1.53). “This was expected, as more intense acute postoperative pain is a known risk factor for developing chronic postsurgical pain, including CPMP,” the authors wrote.
Patients who had received adjuvant chemotherapy had a 32% higher incidence of chronic long-term pain, but there was no increase in risk associated with adjuvant radiotherapy. Both are known to cause neurotoxicity and therefore neuropathic pain, the authors commented.
No conflicts of interest were declared.
FROM THE JOURNAL OF CLINICAL ANESTHESIA
Key clinical point: The use of halogenated agents for anesthetic during a mastectomy operation may be associated with a lower incidence of long-term chronic postmastectomy pain.
Major finding: Patients given a halogenated agent for anesthesia during a mastectomy had a significant 19% lower incidence of chronic long-term postoperative mastectomy pain.
Data source: A retrospective cross-sectional survey.
Disclosures: No conflicts of interest were declared.
Wrist-worn system detected convulsive seizures in home setting
HOUSTON – A wrist-worn device and smartphone-based alert system worn by a patient outside of the epilepsy monitoring unit for 3 months effectively detected convulsive seizure events and minimized false alarms, results from a long-term study found.
The automated device, known as Embrace, relies on an accelerometer and electrodermal activity to detect convulsive seizures. It pairs a wrist-worn device with a smartphone-based application that provides an alert to designated caregivers when an unusual event is detected. Embrace, which is being developed by Empatica Inc., received clearance by the European Union as a medical device for convulsive seizure detection but is still under consideration by the Food and Drug Administration. Previous reports evaluating the automated detector used by Embrace have always relied on data from epilepsy monitoring units (EMUs), where it achieved sensitivity scores ranging from 92% to 100% and 0.15-2.02 false alarms per day in detecting convulsive seizures.
To find out, Dr. Picard, chief scientist at Empatica, and her associates conducted a case study of a 14-year-old patient with Dravet syndrome who was enrolled in a trial of Embrace in the outpatient setting. No data from this patient were used in training the system. The patient’s caregiver was asked to annotate the occurrence of each convulsive seizure and any activity that generated an alert. The number of false alerts was obtained by subtracting the number of correctly recognized convulsive seizures from the total alerts fired by the device. Sensitivity was the percentage of convulsive seizures that automatically triggered an alert.
“Embrace can work for patients outside the EMU, detecting events and issuing alerts through a paired smartphone to a designated caregiver. Also, for clinicians who understand machine learning, we should be clear that we used the strongest test possible: none of the patient’s data were used to train the algorithm that was used, nor was it tuned in any way special for this patient. Had we done so, the results could have possibly appeared even better. However, we chose to use this test of generalization to better get a sense of how it might work on new patients, whose data had never been seen before.”
Dr. Picard acknowledged certain limitations of the study, including the fact that it was a single case and that the patient had Dravet syndrome. She disclosed that she is a cofounder of Empatica and owns shares in the company.
HOUSTON – A wrist-worn device and smartphone-based alert system worn by a patient outside of the epilepsy monitoring unit for 3 months effectively detected convulsive seizure events and minimized false alarms, results from a long-term study found.
The automated device, known as Embrace, relies on an accelerometer and electrodermal activity to detect convulsive seizures. It pairs a wrist-worn device with a smartphone-based application that provides an alert to designated caregivers when an unusual event is detected. Embrace, which is being developed by Empatica Inc., received clearance by the European Union as a medical device for convulsive seizure detection but is still under consideration by the Food and Drug Administration. Previous reports evaluating the automated detector used by Embrace have always relied on data from epilepsy monitoring units (EMUs), where it achieved sensitivity scores ranging from 92% to 100% and 0.15-2.02 false alarms per day in detecting convulsive seizures.
To find out, Dr. Picard, chief scientist at Empatica, and her associates conducted a case study of a 14-year-old patient with Dravet syndrome who was enrolled in a trial of Embrace in the outpatient setting. No data from this patient were used in training the system. The patient’s caregiver was asked to annotate the occurrence of each convulsive seizure and any activity that generated an alert. The number of false alerts was obtained by subtracting the number of correctly recognized convulsive seizures from the total alerts fired by the device. Sensitivity was the percentage of convulsive seizures that automatically triggered an alert.
“Embrace can work for patients outside the EMU, detecting events and issuing alerts through a paired smartphone to a designated caregiver. Also, for clinicians who understand machine learning, we should be clear that we used the strongest test possible: none of the patient’s data were used to train the algorithm that was used, nor was it tuned in any way special for this patient. Had we done so, the results could have possibly appeared even better. However, we chose to use this test of generalization to better get a sense of how it might work on new patients, whose data had never been seen before.”
Dr. Picard acknowledged certain limitations of the study, including the fact that it was a single case and that the patient had Dravet syndrome. She disclosed that she is a cofounder of Empatica and owns shares in the company.
HOUSTON – A wrist-worn device and smartphone-based alert system worn by a patient outside of the epilepsy monitoring unit for 3 months effectively detected convulsive seizure events and minimized false alarms, results from a long-term study found.
The automated device, known as Embrace, relies on an accelerometer and electrodermal activity to detect convulsive seizures. It pairs a wrist-worn device with a smartphone-based application that provides an alert to designated caregivers when an unusual event is detected. Embrace, which is being developed by Empatica Inc., received clearance by the European Union as a medical device for convulsive seizure detection but is still under consideration by the Food and Drug Administration. Previous reports evaluating the automated detector used by Embrace have always relied on data from epilepsy monitoring units (EMUs), where it achieved sensitivity scores ranging from 92% to 100% and 0.15-2.02 false alarms per day in detecting convulsive seizures.
To find out, Dr. Picard, chief scientist at Empatica, and her associates conducted a case study of a 14-year-old patient with Dravet syndrome who was enrolled in a trial of Embrace in the outpatient setting. No data from this patient were used in training the system. The patient’s caregiver was asked to annotate the occurrence of each convulsive seizure and any activity that generated an alert. The number of false alerts was obtained by subtracting the number of correctly recognized convulsive seizures from the total alerts fired by the device. Sensitivity was the percentage of convulsive seizures that automatically triggered an alert.
“Embrace can work for patients outside the EMU, detecting events and issuing alerts through a paired smartphone to a designated caregiver. Also, for clinicians who understand machine learning, we should be clear that we used the strongest test possible: none of the patient’s data were used to train the algorithm that was used, nor was it tuned in any way special for this patient. Had we done so, the results could have possibly appeared even better. However, we chose to use this test of generalization to better get a sense of how it might work on new patients, whose data had never been seen before.”
Dr. Picard acknowledged certain limitations of the study, including the fact that it was a single case and that the patient had Dravet syndrome. She disclosed that she is a cofounder of Empatica and owns shares in the company.
AT AES 2016
Key clinical point:
Major finding: A device known as Embrace detected 22 of the patient’s 24 convulsive seizure events, for a sensitivity of 92% and a false-alarm rate of 0.35 false alarms per day worn.
Data source: Case study of a 14-year-old patient with Dravet syndrome who was enrolled in a trial of Embrace in the outpatient setting and used the device for 113 days.
Disclosures: Dr. Picard is a cofounder of Empatica. She also owns shares in the company.
EMTALA – statutory law
This is the first of a two-part series.
Question: Which of the following statements regarding the Emergency Medical Treatment & Labor Act (EMTALA) is correct?
A. Deals with the standard of care in emergency medicine.
B. Provides safeguards for uninsured and nonpaying patients with an emergency medical condition.
C. Mandates uniform screening and treatment stabilization prior to transfer, irrespective of the hospital’s capability.
D. Is mostly directed at hospitals and emergency department staff doctors, but excludes on-call physicians.
E. Violations can result in fines, loss of Medicare provider participation, or even imprisonment.
Answer: B. In 1985, the CBS investigative news show “60 Minutes” ran an exposé on abuses in the emergency departments of U.S. hospitals, featuring the case of Eugene Barnes, a 32-year-old man brought to the Brookside Hospital emergency department (ED) in San Pablo, Calif., with a penetrating stab wound.
In another case, William Jenness, injured in an auto accident, died after a delayed transfer to a county hospital, because the original hospital required a $1,000 deposit in advance before initiating treatment.
In response to the widespread perception that uninsured patients were being denied treatment in the nation’s emergency departments, Congress enacted the Emergency Medical Treatment & Labor Act.1
Originally referred to as the “antidumping law,” EMTALA was designed to prevent hospitals from transferring financially undesirable patients to public hospitals without providing a medical screening examination and stabilizing treatment prior to transfer.
The purpose and intent of the law is to ensure that all patients who come to the ED have access to emergency services, although the statute itself is silent on payment ability.
EMTALA is not meant to replace or override state tort law, and does not deal with quality of care issues that may arise in the emergency department. Over the 30-year period since its enactment, EMTALA has received mixed reviews, with one scholar complaining that the statute is sloppily drafted and the premise of the statute, silly at best.2
EMTALA defines an emergency medical condition as:
1. A medical condition manifesting itself by acute symptoms of sufficient severity (including severe pain, psychiatric disturbances, and/or symptoms of substance abuse) such that the absence of immediate medical attention could reasonably be expected to result in placing the health of the individual (or, with respect to a pregnant woman, the health of the woman or her unborn child) in serious jeopardy, cause serious impairment to bodily functions, or result in serious dysfunction of any bodily organ or part.
2. With respect to a pregnant woman who is having contractions, there is inadequate time to effect a safe transfer to another hospital before delivery, or that transfer may pose a threat to the health or safety of the woman or the unborn child.3
Whether an emergency medical condition exists is determined by a medical screening exam (MSE). EMTALA is about a process directed at the well-being and safety of all patients with a medical emergency who come to the ED, defined as being licensed by the state or held out to the public as a place that provides care for emergency medical conditions. Hospital-based outpatient clinics that handle less than one-third of emergency visits and physician offices are exempt.
All patients who present to the ED seeking treatment are entitled to an MSE, and EDs are required to post such notification on their premises. A triage nurse may not be qualified to conduct the MSE unless he or she possesses special competencies, and has approval from the medical staff and the hospital’s governing body.
It is important that the MSE be documented soon after the patient’s arrival to determine if the medical condition warrants immediate treatment. It is definitely not acceptable to delay performing an MSE while awaiting information on insurance coverage, and one cannot “hold” the patient and delay stabilizing treatment because of the carrier’s insistence on using only certain approved facilities.
EMTALA requires that the screening exam be “appropriate,” but the statute does not define the term except to note that it is to be “within the capability of the hospital’s emergency department.” However, it is generally recognized that triage alone is insufficient, and the screening exam should be based on the patient’s symptoms and performed by a qualified person.
The important point is that it is uniformly applied, without discrimination, to all who seek treatment in the ED. The hospital itself is expected to have in place policies addressing the broad aspects of the screening process in a nondisparate manner.
The second key issue under the EMTALA statute concerns treatment and transfer.4 If an emergency medical condition exists, treatment must be provided until the emergency is resolved or stabilized.
Under the law, a patient is considered stable for transfer (or discharge) if the treating physician determines that no material deterioration is reasonably likely to occur during or as a result of the transfer between facilities. A receiving hospital is obligated to report any individual who has been transferred in an unstable condition in violation of EMTALA.
However, in the event the hospital does not have the capability to stabilize the emergency medical condition, EMTALA mandates an appropriate transfer, under prescribed conditions, to another hospital whose specialized capabilities obligate it to cooperate. The ED physician in the sending hospital will directly request acceptance of such a transfer. If the patient is unstable, the physician must certify that the medical benefits expected from the transfer outweigh the risks, unless the patient insists on a transfer in writing after being informed of the hospital’s obligations under EMTALA and the risks of transfer.
Furthermore, the transferring hospital must: 1. provide ongoing care within its capability until transfer to minimize transfer risks, 2. provide copies of medical records, 3. confirm that the receiving facility has space and qualified personnel to treat the condition and has agreed to accept the transfer, and 4. ensure that the transfer is made with qualified personnel and appropriate medical equipment.
On-call physicians at both transferring and accepting facilities are also subject to EMTALA. The U.S. Department of Health & Human Services’ Office of Inspector General (OIG) has promulgated rules regarding on-call physicians, even touching on reimbursement.
The American College of Emergency Physicians subscribes to the view that hospitals, medical staff, and payers share an ethical responsibility for the provision of emergency care, acknowledging that EDs require a reliable on-call system that provides for the availability of medical staff members for consultation and participation in the evaluation and treatment of emergency patients.5
Penalties for EMTALA violations include fines up to $50,000 per violation, and/or nullification of Medicare provider agreements. There is a 2-year statute of limitations for civil enforcement of any violation,6 carried out by the OIG and the Centers for Medicare & Medicaid Services (CMS).
A receiving facility, having suffered financial loss as a result of another hospital’s violation of EMTALA, can bring suit to recover damages, and patients may bring private lawsuits against hospitals, though not against physicians. EMTALA, being a civil rather than a criminal statute, does not impose any prison terms.
Investigations and citations by the OIG/CMS are common, with about half of all hospitals subjected to EMTALA investigations and a quarter receiving a violation citation over a recent 10-year period.
However, a recently published study covering 2002-2015 found that, despite 40% of investigations ending up with EMTALA violations, only 3% of investigations triggered fines – and none resulted in suspension of Medicare provider participation.7
There were a total of 192 settlements, or an average of 14 per year for the 4,000 hospitals in the United States. Most were for failing to provide screening (75%) and stabilization (42%). The vast majority of violations affected hospitals, and only eight physicians were involved.
Fines against hospitals and physicians totaled $6,357,000 (averages, $33,435 and $25,625, respectively). Patient dumping attributable to insurance or financial discrimination accounted for 15.6% of settlements.
References
1. 42 USC §1395dd et seq.
2. Chest. 2015 Jun;147(6):1691-6.
3. 42 USC §1395dd(a).
4. 42 USC §1395dd(b)(c).
5. “EMTALA and On-call Responsibility for Emergency Department Patients,” American College of Emergency Physicians.
6. 42 USC §1395dd(d).
7. West J Emerg Med. 2016 May;17(3):245-51.
Dr. Tan is emeritus professor of medicine and former adjunct professor of law at the University of Hawaii, and currently directs the St. Francis International Center for Healthcare Ethics in Honolulu. This article is meant to be educational and does not constitute medical, ethical, or legal advice. Some of the articles in this series are adapted from the author’s 2006 book, “Medical Malpractice: Understanding the Law, Managing the Risk,” and his 2012 Halsbury treatise, “Medical Negligence and Professional Misconduct.” For additional information, readers may contact the author at [email protected].
This is the first of a two-part series.
Question: Which of the following statements regarding the Emergency Medical Treatment & Labor Act (EMTALA) is correct?
A. Deals with the standard of care in emergency medicine.
B. Provides safeguards for uninsured and nonpaying patients with an emergency medical condition.
C. Mandates uniform screening and treatment stabilization prior to transfer, irrespective of the hospital’s capability.
D. Is mostly directed at hospitals and emergency department staff doctors, but excludes on-call physicians.
E. Violations can result in fines, loss of Medicare provider participation, or even imprisonment.
Answer: B. In 1985, the CBS investigative news show “60 Minutes” ran an exposé on abuses in the emergency departments of U.S. hospitals, featuring the case of Eugene Barnes, a 32-year-old man brought to the Brookside Hospital emergency department (ED) in San Pablo, Calif., with a penetrating stab wound.
In another case, William Jenness, injured in an auto accident, died after a delayed transfer to a county hospital, because the original hospital required a $1,000 deposit in advance before initiating treatment.
In response to the widespread perception that uninsured patients were being denied treatment in the nation’s emergency departments, Congress enacted the Emergency Medical Treatment & Labor Act.1
Originally referred to as the “antidumping law,” EMTALA was designed to prevent hospitals from transferring financially undesirable patients to public hospitals without providing a medical screening examination and stabilizing treatment prior to transfer.
The purpose and intent of the law is to ensure that all patients who come to the ED have access to emergency services, although the statute itself is silent on payment ability.
EMTALA is not meant to replace or override state tort law, and does not deal with quality of care issues that may arise in the emergency department. Over the 30-year period since its enactment, EMTALA has received mixed reviews, with one scholar complaining that the statute is sloppily drafted and the premise of the statute, silly at best.2
EMTALA defines an emergency medical condition as:
1. A medical condition manifesting itself by acute symptoms of sufficient severity (including severe pain, psychiatric disturbances, and/or symptoms of substance abuse) such that the absence of immediate medical attention could reasonably be expected to result in placing the health of the individual (or, with respect to a pregnant woman, the health of the woman or her unborn child) in serious jeopardy, cause serious impairment to bodily functions, or result in serious dysfunction of any bodily organ or part.
2. With respect to a pregnant woman who is having contractions, there is inadequate time to effect a safe transfer to another hospital before delivery, or that transfer may pose a threat to the health or safety of the woman or the unborn child.3
Whether an emergency medical condition exists is determined by a medical screening exam (MSE). EMTALA is about a process directed at the well-being and safety of all patients with a medical emergency who come to the ED, defined as being licensed by the state or held out to the public as a place that provides care for emergency medical conditions. Hospital-based outpatient clinics that handle less than one-third of emergency visits and physician offices are exempt.
All patients who present to the ED seeking treatment are entitled to an MSE, and EDs are required to post such notification on their premises. A triage nurse may not be qualified to conduct the MSE unless he or she possesses special competencies, and has approval from the medical staff and the hospital’s governing body.
It is important that the MSE be documented soon after the patient’s arrival to determine if the medical condition warrants immediate treatment. It is definitely not acceptable to delay performing an MSE while awaiting information on insurance coverage, and one cannot “hold” the patient and delay stabilizing treatment because of the carrier’s insistence on using only certain approved facilities.
EMTALA requires that the screening exam be “appropriate,” but the statute does not define the term except to note that it is to be “within the capability of the hospital’s emergency department.” However, it is generally recognized that triage alone is insufficient, and the screening exam should be based on the patient’s symptoms and performed by a qualified person.
The important point is that it is uniformly applied, without discrimination, to all who seek treatment in the ED. The hospital itself is expected to have in place policies addressing the broad aspects of the screening process in a nondisparate manner.
The second key issue under the EMTALA statute concerns treatment and transfer.4 If an emergency medical condition exists, treatment must be provided until the emergency is resolved or stabilized.
Under the law, a patient is considered stable for transfer (or discharge) if the treating physician determines that no material deterioration is reasonably likely to occur during or as a result of the transfer between facilities. A receiving hospital is obligated to report any individual who has been transferred in an unstable condition in violation of EMTALA.
However, in the event the hospital does not have the capability to stabilize the emergency medical condition, EMTALA mandates an appropriate transfer, under prescribed conditions, to another hospital whose specialized capabilities obligate it to cooperate. The ED physician in the sending hospital will directly request acceptance of such a transfer. If the patient is unstable, the physician must certify that the medical benefits expected from the transfer outweigh the risks, unless the patient insists on a transfer in writing after being informed of the hospital’s obligations under EMTALA and the risks of transfer.
Furthermore, the transferring hospital must: 1. provide ongoing care within its capability until transfer to minimize transfer risks, 2. provide copies of medical records, 3. confirm that the receiving facility has space and qualified personnel to treat the condition and has agreed to accept the transfer, and 4. ensure that the transfer is made with qualified personnel and appropriate medical equipment.
On-call physicians at both transferring and accepting facilities are also subject to EMTALA. The U.S. Department of Health & Human Services’ Office of Inspector General (OIG) has promulgated rules regarding on-call physicians, even touching on reimbursement.
The American College of Emergency Physicians subscribes to the view that hospitals, medical staff, and payers share an ethical responsibility for the provision of emergency care, acknowledging that EDs require a reliable on-call system that provides for the availability of medical staff members for consultation and participation in the evaluation and treatment of emergency patients.5
Penalties for EMTALA violations include fines up to $50,000 per violation, and/or nullification of Medicare provider agreements. There is a 2-year statute of limitations for civil enforcement of any violation,6 carried out by the OIG and the Centers for Medicare & Medicaid Services (CMS).
A receiving facility, having suffered financial loss as a result of another hospital’s violation of EMTALA, can bring suit to recover damages, and patients may bring private lawsuits against hospitals, though not against physicians. EMTALA, being a civil rather than a criminal statute, does not impose any prison terms.
Investigations and citations by the OIG/CMS are common, with about half of all hospitals subjected to EMTALA investigations and a quarter receiving a violation citation over a recent 10-year period.
However, a recently published study covering 2002-2015 found that, despite 40% of investigations ending up with EMTALA violations, only 3% of investigations triggered fines – and none resulted in suspension of Medicare provider participation.7
There were a total of 192 settlements, or an average of 14 per year for the 4,000 hospitals in the United States. Most were for failing to provide screening (75%) and stabilization (42%). The vast majority of violations affected hospitals, and only eight physicians were involved.
Fines against hospitals and physicians totaled $6,357,000 (averages, $33,435 and $25,625, respectively). Patient dumping attributable to insurance or financial discrimination accounted for 15.6% of settlements.
References
1. 42 USC §1395dd et seq.
2. Chest. 2015 Jun;147(6):1691-6.
3. 42 USC §1395dd(a).
4. 42 USC §1395dd(b)(c).
5. “EMTALA and On-call Responsibility for Emergency Department Patients,” American College of Emergency Physicians.
6. 42 USC §1395dd(d).
7. West J Emerg Med. 2016 May;17(3):245-51.
Dr. Tan is emeritus professor of medicine and former adjunct professor of law at the University of Hawaii, and currently directs the St. Francis International Center for Healthcare Ethics in Honolulu. This article is meant to be educational and does not constitute medical, ethical, or legal advice. Some of the articles in this series are adapted from the author’s 2006 book, “Medical Malpractice: Understanding the Law, Managing the Risk,” and his 2012 Halsbury treatise, “Medical Negligence and Professional Misconduct.” For additional information, readers may contact the author at [email protected].
This is the first of a two-part series.
Question: Which of the following statements regarding the Emergency Medical Treatment & Labor Act (EMTALA) is correct?
A. Deals with the standard of care in emergency medicine.
B. Provides safeguards for uninsured and nonpaying patients with an emergency medical condition.
C. Mandates uniform screening and treatment stabilization prior to transfer, irrespective of the hospital’s capability.
D. Is mostly directed at hospitals and emergency department staff doctors, but excludes on-call physicians.
E. Violations can result in fines, loss of Medicare provider participation, or even imprisonment.
Answer: B. In 1985, the CBS investigative news show “60 Minutes” ran an exposé on abuses in the emergency departments of U.S. hospitals, featuring the case of Eugene Barnes, a 32-year-old man brought to the Brookside Hospital emergency department (ED) in San Pablo, Calif., with a penetrating stab wound.
In another case, William Jenness, injured in an auto accident, died after a delayed transfer to a county hospital, because the original hospital required a $1,000 deposit in advance before initiating treatment.
In response to the widespread perception that uninsured patients were being denied treatment in the nation’s emergency departments, Congress enacted the Emergency Medical Treatment & Labor Act.1
Originally referred to as the “antidumping law,” EMTALA was designed to prevent hospitals from transferring financially undesirable patients to public hospitals without providing a medical screening examination and stabilizing treatment prior to transfer.
The purpose and intent of the law is to ensure that all patients who come to the ED have access to emergency services, although the statute itself is silent on payment ability.
EMTALA is not meant to replace or override state tort law, and does not deal with quality of care issues that may arise in the emergency department. Over the 30-year period since its enactment, EMTALA has received mixed reviews, with one scholar complaining that the statute is sloppily drafted and the premise of the statute, silly at best.2
EMTALA defines an emergency medical condition as:
1. A medical condition manifesting itself by acute symptoms of sufficient severity (including severe pain, psychiatric disturbances, and/or symptoms of substance abuse) such that the absence of immediate medical attention could reasonably be expected to result in placing the health of the individual (or, with respect to a pregnant woman, the health of the woman or her unborn child) in serious jeopardy, cause serious impairment to bodily functions, or result in serious dysfunction of any bodily organ or part.
2. With respect to a pregnant woman who is having contractions, there is inadequate time to effect a safe transfer to another hospital before delivery, or that transfer may pose a threat to the health or safety of the woman or the unborn child.3
Whether an emergency medical condition exists is determined by a medical screening exam (MSE). EMTALA is about a process directed at the well-being and safety of all patients with a medical emergency who come to the ED, defined as being licensed by the state or held out to the public as a place that provides care for emergency medical conditions. Hospital-based outpatient clinics that handle less than one-third of emergency visits and physician offices are exempt.
All patients who present to the ED seeking treatment are entitled to an MSE, and EDs are required to post such notification on their premises. A triage nurse may not be qualified to conduct the MSE unless he or she possesses special competencies, and has approval from the medical staff and the hospital’s governing body.
It is important that the MSE be documented soon after the patient’s arrival to determine if the medical condition warrants immediate treatment. It is definitely not acceptable to delay performing an MSE while awaiting information on insurance coverage, and one cannot “hold” the patient and delay stabilizing treatment because of the carrier’s insistence on using only certain approved facilities.
EMTALA requires that the screening exam be “appropriate,” but the statute does not define the term except to note that it is to be “within the capability of the hospital’s emergency department.” However, it is generally recognized that triage alone is insufficient, and the screening exam should be based on the patient’s symptoms and performed by a qualified person.
The important point is that it is uniformly applied, without discrimination, to all who seek treatment in the ED. The hospital itself is expected to have in place policies addressing the broad aspects of the screening process in a nondisparate manner.
The second key issue under the EMTALA statute concerns treatment and transfer.4 If an emergency medical condition exists, treatment must be provided until the emergency is resolved or stabilized.
Under the law, a patient is considered stable for transfer (or discharge) if the treating physician determines that no material deterioration is reasonably likely to occur during or as a result of the transfer between facilities. A receiving hospital is obligated to report any individual who has been transferred in an unstable condition in violation of EMTALA.
However, in the event the hospital does not have the capability to stabilize the emergency medical condition, EMTALA mandates an appropriate transfer, under prescribed conditions, to another hospital whose specialized capabilities obligate it to cooperate. The ED physician in the sending hospital will directly request acceptance of such a transfer. If the patient is unstable, the physician must certify that the medical benefits expected from the transfer outweigh the risks, unless the patient insists on a transfer in writing after being informed of the hospital’s obligations under EMTALA and the risks of transfer.
Furthermore, the transferring hospital must: 1. provide ongoing care within its capability until transfer to minimize transfer risks, 2. provide copies of medical records, 3. confirm that the receiving facility has space and qualified personnel to treat the condition and has agreed to accept the transfer, and 4. ensure that the transfer is made with qualified personnel and appropriate medical equipment.
On-call physicians at both transferring and accepting facilities are also subject to EMTALA. The U.S. Department of Health & Human Services’ Office of Inspector General (OIG) has promulgated rules regarding on-call physicians, even touching on reimbursement.
The American College of Emergency Physicians subscribes to the view that hospitals, medical staff, and payers share an ethical responsibility for the provision of emergency care, acknowledging that EDs require a reliable on-call system that provides for the availability of medical staff members for consultation and participation in the evaluation and treatment of emergency patients.5
Penalties for EMTALA violations include fines up to $50,000 per violation, and/or nullification of Medicare provider agreements. There is a 2-year statute of limitations for civil enforcement of any violation,6 carried out by the OIG and the Centers for Medicare & Medicaid Services (CMS).
A receiving facility, having suffered financial loss as a result of another hospital’s violation of EMTALA, can bring suit to recover damages, and patients may bring private lawsuits against hospitals, though not against physicians. EMTALA, being a civil rather than a criminal statute, does not impose any prison terms.
Investigations and citations by the OIG/CMS are common, with about half of all hospitals subjected to EMTALA investigations and a quarter receiving a violation citation over a recent 10-year period.
However, a recently published study covering 2002-2015 found that, despite 40% of investigations ending up with EMTALA violations, only 3% of investigations triggered fines – and none resulted in suspension of Medicare provider participation.7
There were a total of 192 settlements, or an average of 14 per year for the 4,000 hospitals in the United States. Most were for failing to provide screening (75%) and stabilization (42%). The vast majority of violations affected hospitals, and only eight physicians were involved.
Fines against hospitals and physicians totaled $6,357,000 (averages, $33,435 and $25,625, respectively). Patient dumping attributable to insurance or financial discrimination accounted for 15.6% of settlements.
References
1. 42 USC §1395dd et seq.
2. Chest. 2015 Jun;147(6):1691-6.
3. 42 USC §1395dd(a).
4. 42 USC §1395dd(b)(c).
5. “EMTALA and On-call Responsibility for Emergency Department Patients,” American College of Emergency Physicians.
6. 42 USC §1395dd(d).
7. West J Emerg Med. 2016 May;17(3):245-51.
Dr. Tan is emeritus professor of medicine and former adjunct professor of law at the University of Hawaii, and currently directs the St. Francis International Center for Healthcare Ethics in Honolulu. This article is meant to be educational and does not constitute medical, ethical, or legal advice. Some of the articles in this series are adapted from the author’s 2006 book, “Medical Malpractice: Understanding the Law, Managing the Risk,” and his 2012 Halsbury treatise, “Medical Negligence and Professional Misconduct.” For additional information, readers may contact the author at [email protected].
Pharyngeal reservoir drives gonorrhea epidemic in gay men
VIENNA – , Colm O’Mahony, MD, said at the annual congress of the European Academy of Dermatology and Venereology.
“We think pharyngeal gonorrhea is now the most important factor in this continuing epidemic,” according to Dr. O’Mahony, professor of medicine and a venereologist at the University of Chester (England).
Recent studies have shown that men can carry Neisseria gonorrhoeae in their throats for weeks or months without symptoms and can readily spread the infection through unprotected oral sex.
Also, surveys of men who have sex with men (MSM) indicate that saliva is commonly used as a lubricant for anal sex. Australian investigators have estimated that about half of rectal gonorrhea in MSM would be eliminated if they stopped using their partner’s saliva for this purpose (Sex Trans Infect. 2016 Mar 3. pii:sextrans-2015-052502. doi: 10.1136/sextrans-2015-052502).
And then there is French kissing.
“Men don’t go out to a nightclub and have indiscriminate anal sex anymore. It’s not like that,” according to Dr. O’Mahony. “But they do kiss quite a lot of other men over the course of an evening, and it’s deep kissing. They may French kiss 15-20 other young men. And we think there’s actually a significant risk of transmission of gonorrhea from this simple deep kissing.”
Indeed, Australian investigators are now conducting a study examining whether having young gay men take a bottle of mouthwash with them when they go clubbing so they can take a good swish in between kissing will protect against N. gonorrhoeae infection.
“Apparently gonorrhea is quite sensitive to mouthwashes like Listerine. So we await those study results with interest,” he continued.
Dr. O’Mahony warned that the problem of multidrug-resistant gonorrhea is further along than most noninfectious disease experts realize. That’s a frightening prospect, given that an estimated 800,000 cases of gonorrhea occur annually in the United States alone. Because of well-documented treatment failures with cefixime and other oral cephalosporins, the Centers for Disease Control and Prevention now recommends only one regimen for the treatment of gonorrhea: dual treatment with a single intramuscular dose of 250 mg of ceftriaxone (Rocephin) plus 1 g of azithromycin in a single dose.
“There have already been some cases of ceftriaxone-resistant gonorrhea reported in Japan, Spain, and other parts of Europe. And we’re now seeing azithromycin-resistant gonorrhea throughout the U.K., which is a problem. So we are really worried that we will end up with untreatable gonorrhea within a couple of years,” Dr. O’Mahony said.
The evolving antimicrobial resistance scenario is reminiscent of the quinolone experience, he added.
“In 1992, I published the first reported case of quinolone-resistant gonorrhea in Liverpool. Five years later we had to stop using quinolones because more than 10% of gonorrhea was resistant,” the venereologist said.
In mid-2016 the CDC published the first-ever comprehensive data from its Gonococcal Isolate Surveillance Project. An analysis of more than 5,000 N. gonorrhoeae isolates obtained from men with gonococcal urethritis presenting at U.S. STD clinics showed that 25.3% of samples were resistant to tetracycline, 19.2% to ciprofloxacin, and 16.2% to penicillin. The prevalence of reduced azithromycin susceptibility jumped from 0.6% in 2013 to 2.5% in 2014. Reduced ceftriaxone susceptibility doubled from 0.4% in 2013 to 0.8% the following year. Antimicrobial susceptibility patterns varied by geographic region, with the highest rates of reduced susceptibility being seen in the Midwest and among MSM (MMWR Surveill Summ. 2016;65[No. SS-7]:1–19. doi: 10.15585/mmwr.ss6507a1).
Dr. O’Mahony reported having no relevant financial conflicts.
VIENNA – , Colm O’Mahony, MD, said at the annual congress of the European Academy of Dermatology and Venereology.
“We think pharyngeal gonorrhea is now the most important factor in this continuing epidemic,” according to Dr. O’Mahony, professor of medicine and a venereologist at the University of Chester (England).
Recent studies have shown that men can carry Neisseria gonorrhoeae in their throats for weeks or months without symptoms and can readily spread the infection through unprotected oral sex.
Also, surveys of men who have sex with men (MSM) indicate that saliva is commonly used as a lubricant for anal sex. Australian investigators have estimated that about half of rectal gonorrhea in MSM would be eliminated if they stopped using their partner’s saliva for this purpose (Sex Trans Infect. 2016 Mar 3. pii:sextrans-2015-052502. doi: 10.1136/sextrans-2015-052502).
And then there is French kissing.
“Men don’t go out to a nightclub and have indiscriminate anal sex anymore. It’s not like that,” according to Dr. O’Mahony. “But they do kiss quite a lot of other men over the course of an evening, and it’s deep kissing. They may French kiss 15-20 other young men. And we think there’s actually a significant risk of transmission of gonorrhea from this simple deep kissing.”
Indeed, Australian investigators are now conducting a study examining whether having young gay men take a bottle of mouthwash with them when they go clubbing so they can take a good swish in between kissing will protect against N. gonorrhoeae infection.
“Apparently gonorrhea is quite sensitive to mouthwashes like Listerine. So we await those study results with interest,” he continued.
Dr. O’Mahony warned that the problem of multidrug-resistant gonorrhea is further along than most noninfectious disease experts realize. That’s a frightening prospect, given that an estimated 800,000 cases of gonorrhea occur annually in the United States alone. Because of well-documented treatment failures with cefixime and other oral cephalosporins, the Centers for Disease Control and Prevention now recommends only one regimen for the treatment of gonorrhea: dual treatment with a single intramuscular dose of 250 mg of ceftriaxone (Rocephin) plus 1 g of azithromycin in a single dose.
“There have already been some cases of ceftriaxone-resistant gonorrhea reported in Japan, Spain, and other parts of Europe. And we’re now seeing azithromycin-resistant gonorrhea throughout the U.K., which is a problem. So we are really worried that we will end up with untreatable gonorrhea within a couple of years,” Dr. O’Mahony said.
The evolving antimicrobial resistance scenario is reminiscent of the quinolone experience, he added.
“In 1992, I published the first reported case of quinolone-resistant gonorrhea in Liverpool. Five years later we had to stop using quinolones because more than 10% of gonorrhea was resistant,” the venereologist said.
In mid-2016 the CDC published the first-ever comprehensive data from its Gonococcal Isolate Surveillance Project. An analysis of more than 5,000 N. gonorrhoeae isolates obtained from men with gonococcal urethritis presenting at U.S. STD clinics showed that 25.3% of samples were resistant to tetracycline, 19.2% to ciprofloxacin, and 16.2% to penicillin. The prevalence of reduced azithromycin susceptibility jumped from 0.6% in 2013 to 2.5% in 2014. Reduced ceftriaxone susceptibility doubled from 0.4% in 2013 to 0.8% the following year. Antimicrobial susceptibility patterns varied by geographic region, with the highest rates of reduced susceptibility being seen in the Midwest and among MSM (MMWR Surveill Summ. 2016;65[No. SS-7]:1–19. doi: 10.15585/mmwr.ss6507a1).
Dr. O’Mahony reported having no relevant financial conflicts.
VIENNA – , Colm O’Mahony, MD, said at the annual congress of the European Academy of Dermatology and Venereology.
“We think pharyngeal gonorrhea is now the most important factor in this continuing epidemic,” according to Dr. O’Mahony, professor of medicine and a venereologist at the University of Chester (England).
Recent studies have shown that men can carry Neisseria gonorrhoeae in their throats for weeks or months without symptoms and can readily spread the infection through unprotected oral sex.
Also, surveys of men who have sex with men (MSM) indicate that saliva is commonly used as a lubricant for anal sex. Australian investigators have estimated that about half of rectal gonorrhea in MSM would be eliminated if they stopped using their partner’s saliva for this purpose (Sex Trans Infect. 2016 Mar 3. pii:sextrans-2015-052502. doi: 10.1136/sextrans-2015-052502).
And then there is French kissing.
“Men don’t go out to a nightclub and have indiscriminate anal sex anymore. It’s not like that,” according to Dr. O’Mahony. “But they do kiss quite a lot of other men over the course of an evening, and it’s deep kissing. They may French kiss 15-20 other young men. And we think there’s actually a significant risk of transmission of gonorrhea from this simple deep kissing.”
Indeed, Australian investigators are now conducting a study examining whether having young gay men take a bottle of mouthwash with them when they go clubbing so they can take a good swish in between kissing will protect against N. gonorrhoeae infection.
“Apparently gonorrhea is quite sensitive to mouthwashes like Listerine. So we await those study results with interest,” he continued.
Dr. O’Mahony warned that the problem of multidrug-resistant gonorrhea is further along than most noninfectious disease experts realize. That’s a frightening prospect, given that an estimated 800,000 cases of gonorrhea occur annually in the United States alone. Because of well-documented treatment failures with cefixime and other oral cephalosporins, the Centers for Disease Control and Prevention now recommends only one regimen for the treatment of gonorrhea: dual treatment with a single intramuscular dose of 250 mg of ceftriaxone (Rocephin) plus 1 g of azithromycin in a single dose.
“There have already been some cases of ceftriaxone-resistant gonorrhea reported in Japan, Spain, and other parts of Europe. And we’re now seeing azithromycin-resistant gonorrhea throughout the U.K., which is a problem. So we are really worried that we will end up with untreatable gonorrhea within a couple of years,” Dr. O’Mahony said.
The evolving antimicrobial resistance scenario is reminiscent of the quinolone experience, he added.
“In 1992, I published the first reported case of quinolone-resistant gonorrhea in Liverpool. Five years later we had to stop using quinolones because more than 10% of gonorrhea was resistant,” the venereologist said.
In mid-2016 the CDC published the first-ever comprehensive data from its Gonococcal Isolate Surveillance Project. An analysis of more than 5,000 N. gonorrhoeae isolates obtained from men with gonococcal urethritis presenting at U.S. STD clinics showed that 25.3% of samples were resistant to tetracycline, 19.2% to ciprofloxacin, and 16.2% to penicillin. The prevalence of reduced azithromycin susceptibility jumped from 0.6% in 2013 to 2.5% in 2014. Reduced ceftriaxone susceptibility doubled from 0.4% in 2013 to 0.8% the following year. Antimicrobial susceptibility patterns varied by geographic region, with the highest rates of reduced susceptibility being seen in the Midwest and among MSM (MMWR Surveill Summ. 2016;65[No. SS-7]:1–19. doi: 10.15585/mmwr.ss6507a1).
Dr. O’Mahony reported having no relevant financial conflicts.
EXPERT ANALYSIS FROM THE EADV CONGRESS
Rate of mosaicism in parents of children with epileptic encephalopathy likely underestimated
HOUSTON – The rate of parental mosaicism in children with sporadic cases of epileptic encephalopathy and an apparent de novo mutation is believed to be at least 10%, which is much higher than previously thought.
The discovery, which was revealed with advanced genetic testing methods, underscores the need to rethink how parents of children with epileptic encephalopathy are counseled with regard to family planning, lead study author Candace T. Myers, PhD, said in an interview in advance of the annual meeting of the American Epilepsy Society. “Generally, families are counseled with a recurrence risk of 1%-3%, but we found that in 10% of our families their recurrence risk is much higher because we’re able to see the genetic mutation in either blood or saliva of an unaffected parent,” said Dr. Myers of the division of genetic medicine in the department of pediatrics at the University of Washington, Seattle. “If we’re able to detect it in either of those tissues that means that the level in their gametes is much higher than just a single cell or a handful of cells, which is usually how people think about de novo mutations. What we’re finding is that in 10% of cases these mutations happen during embryonic development of the parent.”
Dr. Myers reported that of the 109 families screened, 10 cases of low-level somatic mosaicism were identified: 6 in fathers and 4 in mothers. The fraction of mutant alleles identified ranged from 3%-25%, which are levels that would pass undetected by traditional Sanger sequencing methods. In three families where a mosaic parent was identified, there were multiple affected children. The finding “opens up more questions for families that are thinking about future pregnancies,” she said. “I think we should have more genetic counselors working with pediatric neurologists to facilitate those discussions.”
She acknowledged certain limitations of the study, including the fact that DNA samples were extracted only from blood and saliva. “If the mutation is not present or detected in those particular tissues, it is still possible for the parent to be a germline carrier,” Dr. Myers said. “The most relevant tissue type for us to be testing would be the sex cells. We’ll have to look for families to see if they’re willing to donate [those cells] for future studies.”
The study was funded by the National Institute of Neurological Disorders and Stroke. Dr. Myers is supported by a postdoctoral fellowship provided by the Lennox-Gastaut Syndrome Foundation and by the American Epilepsy Society. She reported having no financial disclosures.
HOUSTON – The rate of parental mosaicism in children with sporadic cases of epileptic encephalopathy and an apparent de novo mutation is believed to be at least 10%, which is much higher than previously thought.
The discovery, which was revealed with advanced genetic testing methods, underscores the need to rethink how parents of children with epileptic encephalopathy are counseled with regard to family planning, lead study author Candace T. Myers, PhD, said in an interview in advance of the annual meeting of the American Epilepsy Society. “Generally, families are counseled with a recurrence risk of 1%-3%, but we found that in 10% of our families their recurrence risk is much higher because we’re able to see the genetic mutation in either blood or saliva of an unaffected parent,” said Dr. Myers of the division of genetic medicine in the department of pediatrics at the University of Washington, Seattle. “If we’re able to detect it in either of those tissues that means that the level in their gametes is much higher than just a single cell or a handful of cells, which is usually how people think about de novo mutations. What we’re finding is that in 10% of cases these mutations happen during embryonic development of the parent.”
Dr. Myers reported that of the 109 families screened, 10 cases of low-level somatic mosaicism were identified: 6 in fathers and 4 in mothers. The fraction of mutant alleles identified ranged from 3%-25%, which are levels that would pass undetected by traditional Sanger sequencing methods. In three families where a mosaic parent was identified, there were multiple affected children. The finding “opens up more questions for families that are thinking about future pregnancies,” she said. “I think we should have more genetic counselors working with pediatric neurologists to facilitate those discussions.”
She acknowledged certain limitations of the study, including the fact that DNA samples were extracted only from blood and saliva. “If the mutation is not present or detected in those particular tissues, it is still possible for the parent to be a germline carrier,” Dr. Myers said. “The most relevant tissue type for us to be testing would be the sex cells. We’ll have to look for families to see if they’re willing to donate [those cells] for future studies.”
The study was funded by the National Institute of Neurological Disorders and Stroke. Dr. Myers is supported by a postdoctoral fellowship provided by the Lennox-Gastaut Syndrome Foundation and by the American Epilepsy Society. She reported having no financial disclosures.
HOUSTON – The rate of parental mosaicism in children with sporadic cases of epileptic encephalopathy and an apparent de novo mutation is believed to be at least 10%, which is much higher than previously thought.
The discovery, which was revealed with advanced genetic testing methods, underscores the need to rethink how parents of children with epileptic encephalopathy are counseled with regard to family planning, lead study author Candace T. Myers, PhD, said in an interview in advance of the annual meeting of the American Epilepsy Society. “Generally, families are counseled with a recurrence risk of 1%-3%, but we found that in 10% of our families their recurrence risk is much higher because we’re able to see the genetic mutation in either blood or saliva of an unaffected parent,” said Dr. Myers of the division of genetic medicine in the department of pediatrics at the University of Washington, Seattle. “If we’re able to detect it in either of those tissues that means that the level in their gametes is much higher than just a single cell or a handful of cells, which is usually how people think about de novo mutations. What we’re finding is that in 10% of cases these mutations happen during embryonic development of the parent.”
Dr. Myers reported that of the 109 families screened, 10 cases of low-level somatic mosaicism were identified: 6 in fathers and 4 in mothers. The fraction of mutant alleles identified ranged from 3%-25%, which are levels that would pass undetected by traditional Sanger sequencing methods. In three families where a mosaic parent was identified, there were multiple affected children. The finding “opens up more questions for families that are thinking about future pregnancies,” she said. “I think we should have more genetic counselors working with pediatric neurologists to facilitate those discussions.”
She acknowledged certain limitations of the study, including the fact that DNA samples were extracted only from blood and saliva. “If the mutation is not present or detected in those particular tissues, it is still possible for the parent to be a germline carrier,” Dr. Myers said. “The most relevant tissue type for us to be testing would be the sex cells. We’ll have to look for families to see if they’re willing to donate [those cells] for future studies.”
The study was funded by the National Institute of Neurological Disorders and Stroke. Dr. Myers is supported by a postdoctoral fellowship provided by the Lennox-Gastaut Syndrome Foundation and by the American Epilepsy Society. She reported having no financial disclosures.
AT AES 2016
Key clinical point:
Major finding: Of 109 families screened, 10 cases of low-level somatic mosaicism were identified: 6 in fathers and 4 in mothers.
Data source: Screening of 109 families where the affected child’s epileptic encephalopathy was attributed to a substitution or small indel in 1 of 31 established epilepsy genes and reported as “de novo” by either clinical or research analysis of parental DNA.
Disclosures: The study was funded by National Institute of Neurological Disorders and Stroke. Dr. Myers is supported by a postdoctoral fellowship provided by the Lennox-Gastaut Syndrome Foundation and by the American Epilepsy Society. She reported having no financial disclosures.
VIDEO: Addition of antibody drug conjugate produces deep AML remissions
SAN DIEGO – After more than four decades of near stagnation in the treatment of patients with acute myeloid leukemia (AML), investigators are beginning to identify drugs that can produce rapid and deep complete remissions, which recent evidence suggests are associated with prolonged survival.
In this video interview at the annual meeting of the American Society of Hematology, Harry P. Erba, MD, PhD, professor of medicine, University of Alabama, Birmingham, describes the early results of one such agent, a novel antibody drug conjugate called vadastuximab talirine, or 33A for short. In the phase Ib clinical trial of induction therapy for newly diagnosed AML, a combination of standard 7+3 induction chemotherapy with cytarabine and daunorubicin plus 33A was associated with a 76% composite rate of complete remissions or complete remissions with incomplete recovery of platelets.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
SAN DIEGO – After more than four decades of near stagnation in the treatment of patients with acute myeloid leukemia (AML), investigators are beginning to identify drugs that can produce rapid and deep complete remissions, which recent evidence suggests are associated with prolonged survival.
In this video interview at the annual meeting of the American Society of Hematology, Harry P. Erba, MD, PhD, professor of medicine, University of Alabama, Birmingham, describes the early results of one such agent, a novel antibody drug conjugate called vadastuximab talirine, or 33A for short. In the phase Ib clinical trial of induction therapy for newly diagnosed AML, a combination of standard 7+3 induction chemotherapy with cytarabine and daunorubicin plus 33A was associated with a 76% composite rate of complete remissions or complete remissions with incomplete recovery of platelets.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
SAN DIEGO – After more than four decades of near stagnation in the treatment of patients with acute myeloid leukemia (AML), investigators are beginning to identify drugs that can produce rapid and deep complete remissions, which recent evidence suggests are associated with prolonged survival.
In this video interview at the annual meeting of the American Society of Hematology, Harry P. Erba, MD, PhD, professor of medicine, University of Alabama, Birmingham, describes the early results of one such agent, a novel antibody drug conjugate called vadastuximab talirine, or 33A for short. In the phase Ib clinical trial of induction therapy for newly diagnosed AML, a combination of standard 7+3 induction chemotherapy with cytarabine and daunorubicin plus 33A was associated with a 76% composite rate of complete remissions or complete remissions with incomplete recovery of platelets.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
AT ASH 2016
Psoriasis and Internal Disease: Report From the Mount Sinai Winter Symposium
At the 19th Annual Mount Sinai Winter Symposium, Dr. Jashin J. Wu spoke about psoriasis and internal disease. He discussed psoriasis and noncardiovascular comorbidities as well as cardiovascular comorbidities. Dr. Wu also addressed if treating psoriasis can improve cardiovascular disease.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
At the 19th Annual Mount Sinai Winter Symposium, Dr. Jashin J. Wu spoke about psoriasis and internal disease. He discussed psoriasis and noncardiovascular comorbidities as well as cardiovascular comorbidities. Dr. Wu also addressed if treating psoriasis can improve cardiovascular disease.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
At the 19th Annual Mount Sinai Winter Symposium, Dr. Jashin J. Wu spoke about psoriasis and internal disease. He discussed psoriasis and noncardiovascular comorbidities as well as cardiovascular comorbidities. Dr. Wu also addressed if treating psoriasis can improve cardiovascular disease.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
Mycotic Septic Arthritis of the Ankle Joint
Septic arthritis is a common orthopedic emergency. The most common causative organism is Staphylococcus aureus. Mycotic infections, such as those involving Candida organisms, are much less common but just as debilitating. Delayed diagnosis of septic arthritis caused by Candida infection may result in increased morbidity, making treatment more challenging. Here we report a case of Candida albicans septic arthritis of the ankle and subtalar joint in a patient with diabetes mellitus (DM) and rheumatoid arthritis (RA). The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 52-year-old woman with type 2 DM (requiring subcutaneous insulin analogue therapy) and RA presented to a local emergency department with a 3-day history of right ankle pain after having the subtalar joint injected with steroid by a rheumatologist 4 weeks earlier. For about 2 weeks, there was purulent discharge from the peroneal sheath. The patient’s RA was being treated with prednisolone (maintenance therapy). Physical examination revealed low-grade pyrexia (37.8°C) and difficulty bearing full weight on the ankle. Clinically, the joint was not erythematous, but active and passive movements were painful. Blood tests revealed a C-reactive protein level of 98 mg/dL and a white blood cell (WBC) count of 11.3 × 109/L. Erythrocyte sedimentation rate (ESR) was not checked. The ankle underwent magnetic resonance imaging (Figures A-D).
Mycotic screening of the fluid was positive for C albicans. The patient was referred to the orthopedic team, which performed urgent arthroscopic surgical débridement, biopsy, and washout of the subtalar joint. After surgery, a 6-week course of antifungal therapy with anidulafungin was started, per specialist microbiology advice.
The septic ankle was successfully managed with arthroscopic surgical débridement followed by treatment with anidulafungin. The patient continued to make good progress and was weight-bearing when discharged home from the orthopedic unit.
Discussion
Worldwide, about 1 in 6 people has arthritis, which affects daily lifestyle and reduces quality of life. Degenerative, inflammatory, and septic arthritis each has its management challenges.1
Septic arthritis is an acute infection of the joint, usually of bacterial etiology. It can present as a polyarticular arthropathy (~15% of cases),2,3 but a monoarthropathy of the hip, knee, or ankle is more common.4The Kocher criteria are often applied to cases of suspected septic arthritis of joints, even though they were initially used to distinguish septic arthritis from transient synovitis in pediatric hip joints.5 Kocher and colleagues5 reported 4 key clinical criteria: inability to bear weight, WBC count over 12 × 109/L, ESR over 40 mm/h, and temperature over 38.5°C. When all 4 criteria are met, the predictive value is 99.6%. These criteria are now widely applied to adult joints, and not only the hips.
In septic arthritis, the most common causative pathogen is S aureus.3,6Streptococcus, Neisseria, and Pseudomonas also are common.7 Although much rarer, Candida variants and other mycotic pathogens have been implicated as well.8C albicans is a well-known fungus that colonizes mucosal surfaces. Research indicates increased oral C albicans colonization in rheumatoid patients.9 Although most Candida septic arthritis cases are caused by C albicans, there is no large body of data showing the true incidence of fungal pathogens in septic arthritis.
Our literature search yielded 2 case reports on Candida septic arthritis involving the ankle, but the causative organisms were Candida parapsilosis and Candida glabrata.9,10 Cases of Candida septic arthritis involving the knee or shoulder have also been reported.11-15 Case reports demonstrate that Candida fungal arthritis is extremely rare.9 Etiology reportedly includes direct intra-articular inoculation by surgery or secondary to hematogenous seeding, particularly in immunocompromised patients.10 Risk factors include immunosuppression and joint suppression. DM and RA are common comorbidities in patients with septic arthritis.6,16 The pathophysiology of RA is inflammatory pannus formation of the periarticular surface with subsequent articular cartilage destruction and erosion, as well as progressive deformity and functional debilitation.1Patients with DM are at increased risk for developing fungal and other infections. Factors increasing this risk include disruption of skin-barrier integrity; reduced peripheral oxygen and blood supply, which also disrupts antibiotic delivery; and hyperglycemia-induced reduction in antibody function and disruption of phagocytosis and chemotaxis.17Fungi are eukaryotic, and infections caused by these organisms are difficult to treat.18 As fungal infections are more prevalent among immunosuppressed patients, they often result in prolonged treatment without guarantee of eradication, as spores may persist subclinically.
Literature on C albicans septic arthritis is lacking in general but especially in rheumatoid patients. Delayed diagnosis and suboptimal treatment may result in fungal osteomyelitis. There is little evidence on treating this rare fungal complication, and outcomes historically have been poor.19In an animal model, Marijnissen and colleagues20 found that C albicans infection can increase destruction in an arthritic joint by cytokine environment modification. The result was advanced destruction of the joint and debilitation. For disease management, the authors considered these essential: early diagnosis, prompt treatment, and, as indicated, surgical débridement.
Treatment of Candida septic arthritis largely involves use of antifungal medication, either with surgical débridement, as in our patient’s case, or without. Which antifungal medication to use should be based on sensitivities, identified from wound aspirate, and microbiology advice about treatment duration. The antibiotic should be a broad-spectrum antifungal cover, in keeping with local antibiotic prescribing guidelines, which can be refined once definitive organism culture and sensitivity results are known. However, early aggressive treatment is essential. Periprosthetic fungal infection is rarely resolved without implant removal.21
Conclusion
This case reflects the complexities of septic arthritis caused by atypical pathogens and highlights the need for clinical vigilance in the setting of comorbidities, such as DM and RA. Failure to consider the diagnosis early on might result in delayed and inadequate treatment, increased joint destruction, and, potentially, osteomyelitis with subsequent increased morbidity. Early diagnosis (based on joint aspirate findings), surgical débridement, and prolonged aggressive treatment with antifungal medication are the mainstays of treatment.
Am J Orthop. 2016;45(7):E478-E480. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Auday BC, Buratovich MA, Marrocco, GF, Moglia P, eds. Magill’s Medical Guide. 7th ed. Ipswich, MA: Salem Press; 2014.
2. Dhaliwal S, LeBel ME. Rapidly progressing polyarticular septic arthritis in a patient with rheumatoid arthritis. Am J Orthop. 2012;41(7):E100-E101.
3. Mateo Soria L, Olivé Marqués A, García Casares E, García Melchor E, Holgado Pérez S, Tena Marsà X. Polyarticular septic arthritis: analysis of 19 cases [in Spanish]. Reumatol Clin. 2009;5(1):18-22.
4. Caksen H, Oztürk MK, Uzüm K, Yüksel S, Ustünbaş HB, Per H. Septic arthritis in childhood. Pediatr Int. 2000;42(5):534-540.
5. Kocher MS, Zurakowski D, Kasser JR. Differentiating between septic arthritis and transient synovitis of the hip in children: an evidence-based clinical prediction algorithm. J Bone Joint Surg Am. 1999;81(12):1662-1670.
6. Madruga Dias J, Costa MM, Pereira da Silva JA, Viana de Queiroz M. Septic arthritis: patients with or without isolated infectious agents have similar characteristics. Infection. 2014;42(2):385-391.
7. Louthrenoo W, Kasitanon N, Wangkaew S, Hongsongkiat S, Sukitawut W, Wichainun R. Streptococcus agalactiae: an emerging cause of septic arthritis. J Clin Rheumatol. 2014;20(2):74-78.
8. Zmierczak H, Goemaere S, Mielants H, Verbruggen G, Veys EM. Candida glabrata arthritis: case report and review of the literature of Candida arthritis. Clin Rheumatol. 1999;18(5):406-409.
9. Bishu S, Su EW, Wilkerson ER, et al. Rheumatoid arthritis patients exhibit impaired Candida albicans–specific Th17 responses. Arthritis Res Ther. 2014;16(1):R50.
10. Legout L, Assal M, Rohner P, Lew D, Bernard L, Hoffmeyer P. Successful treatment of Candida parapsilosis (fluconazole-resistant) osteomyelitis with caspofungin in a HIV patient. Scand J Infect Dis. 2006;38(8):728-730.
11. Sung J, Chun K. Candida parapsilosis arthritis involving the ankle in a diabetes patient. J Korean Soc Radiol. 2011;64:587-591.
12. Marmor L, Peter JB. Candida arthritis of the knee joint. Clin Orthop Relat Res. 1976;(118):133-135.
13. Turgut B, Vural O, Demir M, Kaldir M. Candida arthritis in a patient with chronic myelogenous leukemia (CML) in blastic transformation, unresponsive to fluconazole, but treated effectively with liposomal amphotericin B. Ann Hematol. 2002;81(9):529-531.
14. Christensson B, Ryd L, Dahlberg L, Lohmander S. Candida albicans arthritis in a nonimmunocompromised patient. Complication of placebo intraarticular injections. Acta Orthop Scand. 1993;64(6):695-698.
15. Jeong YM, Cho HY, Lee SW, Hwang YM, Kim YK. Candida septic arthritis with rice body formation: a case report and review of literature. Korean J Radiol. 2013;14(3):465-469.
16. Favero M, Schiavon R, Riato L, Carraro V, Punzi L. Septic arthritis: a 12 years retrospective study in a rheumatological university clinic [in Italian]. Reumatismo. 2008;60(4):260-267.
17. Leslie D, Lansang C, Coppack S, Kennedy L. Diabetes: Clinician’s Desk Reference. Boca Raton, FL: CRC Press; 2012.
18. Silva PM, Gonçalves S, Santos NC. Defensins: antifungal lesions from eukaryotes. Front Microbiol. 2014;5:97.
19. Bariteau JT, Waryasz GR, McDonnell M, Fischer SA, Hayda RA, Born CT. Fungal osteomyelitis and septic arthritis. J Am Acad Orthop Surg. 2014;22(6):390-401.
20. Marijnissen RJ, Koenders MI, van de Veerdonk FL, et al. Exposure to Candida albicans polarizes a T-cell driven arthritis model towards Th17 responses, resulting in a more destructive arthritis. PLoS One. 2012;7(6):e38889.
21. International Consensus on Periprosthetic Joint Infection. Musculoskeletal Infection Society website. http://www.msis-na.org/international-consensus. Published August 1, 2013. Accessed October 16, 2016.
Septic arthritis is a common orthopedic emergency. The most common causative organism is Staphylococcus aureus. Mycotic infections, such as those involving Candida organisms, are much less common but just as debilitating. Delayed diagnosis of septic arthritis caused by Candida infection may result in increased morbidity, making treatment more challenging. Here we report a case of Candida albicans septic arthritis of the ankle and subtalar joint in a patient with diabetes mellitus (DM) and rheumatoid arthritis (RA). The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 52-year-old woman with type 2 DM (requiring subcutaneous insulin analogue therapy) and RA presented to a local emergency department with a 3-day history of right ankle pain after having the subtalar joint injected with steroid by a rheumatologist 4 weeks earlier. For about 2 weeks, there was purulent discharge from the peroneal sheath. The patient’s RA was being treated with prednisolone (maintenance therapy). Physical examination revealed low-grade pyrexia (37.8°C) and difficulty bearing full weight on the ankle. Clinically, the joint was not erythematous, but active and passive movements were painful. Blood tests revealed a C-reactive protein level of 98 mg/dL and a white blood cell (WBC) count of 11.3 × 109/L. Erythrocyte sedimentation rate (ESR) was not checked. The ankle underwent magnetic resonance imaging (Figures A-D).
Mycotic screening of the fluid was positive for C albicans. The patient was referred to the orthopedic team, which performed urgent arthroscopic surgical débridement, biopsy, and washout of the subtalar joint. After surgery, a 6-week course of antifungal therapy with anidulafungin was started, per specialist microbiology advice.
The septic ankle was successfully managed with arthroscopic surgical débridement followed by treatment with anidulafungin. The patient continued to make good progress and was weight-bearing when discharged home from the orthopedic unit.
Discussion
Worldwide, about 1 in 6 people has arthritis, which affects daily lifestyle and reduces quality of life. Degenerative, inflammatory, and septic arthritis each has its management challenges.1
Septic arthritis is an acute infection of the joint, usually of bacterial etiology. It can present as a polyarticular arthropathy (~15% of cases),2,3 but a monoarthropathy of the hip, knee, or ankle is more common.4The Kocher criteria are often applied to cases of suspected septic arthritis of joints, even though they were initially used to distinguish septic arthritis from transient synovitis in pediatric hip joints.5 Kocher and colleagues5 reported 4 key clinical criteria: inability to bear weight, WBC count over 12 × 109/L, ESR over 40 mm/h, and temperature over 38.5°C. When all 4 criteria are met, the predictive value is 99.6%. These criteria are now widely applied to adult joints, and not only the hips.
In septic arthritis, the most common causative pathogen is S aureus.3,6Streptococcus, Neisseria, and Pseudomonas also are common.7 Although much rarer, Candida variants and other mycotic pathogens have been implicated as well.8C albicans is a well-known fungus that colonizes mucosal surfaces. Research indicates increased oral C albicans colonization in rheumatoid patients.9 Although most Candida septic arthritis cases are caused by C albicans, there is no large body of data showing the true incidence of fungal pathogens in septic arthritis.
Our literature search yielded 2 case reports on Candida septic arthritis involving the ankle, but the causative organisms were Candida parapsilosis and Candida glabrata.9,10 Cases of Candida septic arthritis involving the knee or shoulder have also been reported.11-15 Case reports demonstrate that Candida fungal arthritis is extremely rare.9 Etiology reportedly includes direct intra-articular inoculation by surgery or secondary to hematogenous seeding, particularly in immunocompromised patients.10 Risk factors include immunosuppression and joint suppression. DM and RA are common comorbidities in patients with septic arthritis.6,16 The pathophysiology of RA is inflammatory pannus formation of the periarticular surface with subsequent articular cartilage destruction and erosion, as well as progressive deformity and functional debilitation.1Patients with DM are at increased risk for developing fungal and other infections. Factors increasing this risk include disruption of skin-barrier integrity; reduced peripheral oxygen and blood supply, which also disrupts antibiotic delivery; and hyperglycemia-induced reduction in antibody function and disruption of phagocytosis and chemotaxis.17Fungi are eukaryotic, and infections caused by these organisms are difficult to treat.18 As fungal infections are more prevalent among immunosuppressed patients, they often result in prolonged treatment without guarantee of eradication, as spores may persist subclinically.
Literature on C albicans septic arthritis is lacking in general but especially in rheumatoid patients. Delayed diagnosis and suboptimal treatment may result in fungal osteomyelitis. There is little evidence on treating this rare fungal complication, and outcomes historically have been poor.19In an animal model, Marijnissen and colleagues20 found that C albicans infection can increase destruction in an arthritic joint by cytokine environment modification. The result was advanced destruction of the joint and debilitation. For disease management, the authors considered these essential: early diagnosis, prompt treatment, and, as indicated, surgical débridement.
Treatment of Candida septic arthritis largely involves use of antifungal medication, either with surgical débridement, as in our patient’s case, or without. Which antifungal medication to use should be based on sensitivities, identified from wound aspirate, and microbiology advice about treatment duration. The antibiotic should be a broad-spectrum antifungal cover, in keeping with local antibiotic prescribing guidelines, which can be refined once definitive organism culture and sensitivity results are known. However, early aggressive treatment is essential. Periprosthetic fungal infection is rarely resolved without implant removal.21
Conclusion
This case reflects the complexities of septic arthritis caused by atypical pathogens and highlights the need for clinical vigilance in the setting of comorbidities, such as DM and RA. Failure to consider the diagnosis early on might result in delayed and inadequate treatment, increased joint destruction, and, potentially, osteomyelitis with subsequent increased morbidity. Early diagnosis (based on joint aspirate findings), surgical débridement, and prolonged aggressive treatment with antifungal medication are the mainstays of treatment.
Am J Orthop. 2016;45(7):E478-E480. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
Septic arthritis is a common orthopedic emergency. The most common causative organism is Staphylococcus aureus. Mycotic infections, such as those involving Candida organisms, are much less common but just as debilitating. Delayed diagnosis of septic arthritis caused by Candida infection may result in increased morbidity, making treatment more challenging. Here we report a case of Candida albicans septic arthritis of the ankle and subtalar joint in a patient with diabetes mellitus (DM) and rheumatoid arthritis (RA). The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 52-year-old woman with type 2 DM (requiring subcutaneous insulin analogue therapy) and RA presented to a local emergency department with a 3-day history of right ankle pain after having the subtalar joint injected with steroid by a rheumatologist 4 weeks earlier. For about 2 weeks, there was purulent discharge from the peroneal sheath. The patient’s RA was being treated with prednisolone (maintenance therapy). Physical examination revealed low-grade pyrexia (37.8°C) and difficulty bearing full weight on the ankle. Clinically, the joint was not erythematous, but active and passive movements were painful. Blood tests revealed a C-reactive protein level of 98 mg/dL and a white blood cell (WBC) count of 11.3 × 109/L. Erythrocyte sedimentation rate (ESR) was not checked. The ankle underwent magnetic resonance imaging (Figures A-D).
Mycotic screening of the fluid was positive for C albicans. The patient was referred to the orthopedic team, which performed urgent arthroscopic surgical débridement, biopsy, and washout of the subtalar joint. After surgery, a 6-week course of antifungal therapy with anidulafungin was started, per specialist microbiology advice.
The septic ankle was successfully managed with arthroscopic surgical débridement followed by treatment with anidulafungin. The patient continued to make good progress and was weight-bearing when discharged home from the orthopedic unit.
Discussion
Worldwide, about 1 in 6 people has arthritis, which affects daily lifestyle and reduces quality of life. Degenerative, inflammatory, and septic arthritis each has its management challenges.1
Septic arthritis is an acute infection of the joint, usually of bacterial etiology. It can present as a polyarticular arthropathy (~15% of cases),2,3 but a monoarthropathy of the hip, knee, or ankle is more common.4The Kocher criteria are often applied to cases of suspected septic arthritis of joints, even though they were initially used to distinguish septic arthritis from transient synovitis in pediatric hip joints.5 Kocher and colleagues5 reported 4 key clinical criteria: inability to bear weight, WBC count over 12 × 109/L, ESR over 40 mm/h, and temperature over 38.5°C. When all 4 criteria are met, the predictive value is 99.6%. These criteria are now widely applied to adult joints, and not only the hips.
In septic arthritis, the most common causative pathogen is S aureus.3,6Streptococcus, Neisseria, and Pseudomonas also are common.7 Although much rarer, Candida variants and other mycotic pathogens have been implicated as well.8C albicans is a well-known fungus that colonizes mucosal surfaces. Research indicates increased oral C albicans colonization in rheumatoid patients.9 Although most Candida septic arthritis cases are caused by C albicans, there is no large body of data showing the true incidence of fungal pathogens in septic arthritis.
Our literature search yielded 2 case reports on Candida septic arthritis involving the ankle, but the causative organisms were Candida parapsilosis and Candida glabrata.9,10 Cases of Candida septic arthritis involving the knee or shoulder have also been reported.11-15 Case reports demonstrate that Candida fungal arthritis is extremely rare.9 Etiology reportedly includes direct intra-articular inoculation by surgery or secondary to hematogenous seeding, particularly in immunocompromised patients.10 Risk factors include immunosuppression and joint suppression. DM and RA are common comorbidities in patients with septic arthritis.6,16 The pathophysiology of RA is inflammatory pannus formation of the periarticular surface with subsequent articular cartilage destruction and erosion, as well as progressive deformity and functional debilitation.1Patients with DM are at increased risk for developing fungal and other infections. Factors increasing this risk include disruption of skin-barrier integrity; reduced peripheral oxygen and blood supply, which also disrupts antibiotic delivery; and hyperglycemia-induced reduction in antibody function and disruption of phagocytosis and chemotaxis.17Fungi are eukaryotic, and infections caused by these organisms are difficult to treat.18 As fungal infections are more prevalent among immunosuppressed patients, they often result in prolonged treatment without guarantee of eradication, as spores may persist subclinically.
Literature on C albicans septic arthritis is lacking in general but especially in rheumatoid patients. Delayed diagnosis and suboptimal treatment may result in fungal osteomyelitis. There is little evidence on treating this rare fungal complication, and outcomes historically have been poor.19In an animal model, Marijnissen and colleagues20 found that C albicans infection can increase destruction in an arthritic joint by cytokine environment modification. The result was advanced destruction of the joint and debilitation. For disease management, the authors considered these essential: early diagnosis, prompt treatment, and, as indicated, surgical débridement.
Treatment of Candida septic arthritis largely involves use of antifungal medication, either with surgical débridement, as in our patient’s case, or without. Which antifungal medication to use should be based on sensitivities, identified from wound aspirate, and microbiology advice about treatment duration. The antibiotic should be a broad-spectrum antifungal cover, in keeping with local antibiotic prescribing guidelines, which can be refined once definitive organism culture and sensitivity results are known. However, early aggressive treatment is essential. Periprosthetic fungal infection is rarely resolved without implant removal.21
Conclusion
This case reflects the complexities of septic arthritis caused by atypical pathogens and highlights the need for clinical vigilance in the setting of comorbidities, such as DM and RA. Failure to consider the diagnosis early on might result in delayed and inadequate treatment, increased joint destruction, and, potentially, osteomyelitis with subsequent increased morbidity. Early diagnosis (based on joint aspirate findings), surgical débridement, and prolonged aggressive treatment with antifungal medication are the mainstays of treatment.
Am J Orthop. 2016;45(7):E478-E480. Copyright Frontline Medical Communications Inc. 2016. All rights reserved.
1. Auday BC, Buratovich MA, Marrocco, GF, Moglia P, eds. Magill’s Medical Guide. 7th ed. Ipswich, MA: Salem Press; 2014.
2. Dhaliwal S, LeBel ME. Rapidly progressing polyarticular septic arthritis in a patient with rheumatoid arthritis. Am J Orthop. 2012;41(7):E100-E101.
3. Mateo Soria L, Olivé Marqués A, García Casares E, García Melchor E, Holgado Pérez S, Tena Marsà X. Polyarticular septic arthritis: analysis of 19 cases [in Spanish]. Reumatol Clin. 2009;5(1):18-22.
4. Caksen H, Oztürk MK, Uzüm K, Yüksel S, Ustünbaş HB, Per H. Septic arthritis in childhood. Pediatr Int. 2000;42(5):534-540.
5. Kocher MS, Zurakowski D, Kasser JR. Differentiating between septic arthritis and transient synovitis of the hip in children: an evidence-based clinical prediction algorithm. J Bone Joint Surg Am. 1999;81(12):1662-1670.
6. Madruga Dias J, Costa MM, Pereira da Silva JA, Viana de Queiroz M. Septic arthritis: patients with or without isolated infectious agents have similar characteristics. Infection. 2014;42(2):385-391.
7. Louthrenoo W, Kasitanon N, Wangkaew S, Hongsongkiat S, Sukitawut W, Wichainun R. Streptococcus agalactiae: an emerging cause of septic arthritis. J Clin Rheumatol. 2014;20(2):74-78.
8. Zmierczak H, Goemaere S, Mielants H, Verbruggen G, Veys EM. Candida glabrata arthritis: case report and review of the literature of Candida arthritis. Clin Rheumatol. 1999;18(5):406-409.
9. Bishu S, Su EW, Wilkerson ER, et al. Rheumatoid arthritis patients exhibit impaired Candida albicans–specific Th17 responses. Arthritis Res Ther. 2014;16(1):R50.
10. Legout L, Assal M, Rohner P, Lew D, Bernard L, Hoffmeyer P. Successful treatment of Candida parapsilosis (fluconazole-resistant) osteomyelitis with caspofungin in a HIV patient. Scand J Infect Dis. 2006;38(8):728-730.
11. Sung J, Chun K. Candida parapsilosis arthritis involving the ankle in a diabetes patient. J Korean Soc Radiol. 2011;64:587-591.
12. Marmor L, Peter JB. Candida arthritis of the knee joint. Clin Orthop Relat Res. 1976;(118):133-135.
13. Turgut B, Vural O, Demir M, Kaldir M. Candida arthritis in a patient with chronic myelogenous leukemia (CML) in blastic transformation, unresponsive to fluconazole, but treated effectively with liposomal amphotericin B. Ann Hematol. 2002;81(9):529-531.
14. Christensson B, Ryd L, Dahlberg L, Lohmander S. Candida albicans arthritis in a nonimmunocompromised patient. Complication of placebo intraarticular injections. Acta Orthop Scand. 1993;64(6):695-698.
15. Jeong YM, Cho HY, Lee SW, Hwang YM, Kim YK. Candida septic arthritis with rice body formation: a case report and review of literature. Korean J Radiol. 2013;14(3):465-469.
16. Favero M, Schiavon R, Riato L, Carraro V, Punzi L. Septic arthritis: a 12 years retrospective study in a rheumatological university clinic [in Italian]. Reumatismo. 2008;60(4):260-267.
17. Leslie D, Lansang C, Coppack S, Kennedy L. Diabetes: Clinician’s Desk Reference. Boca Raton, FL: CRC Press; 2012.
18. Silva PM, Gonçalves S, Santos NC. Defensins: antifungal lesions from eukaryotes. Front Microbiol. 2014;5:97.
19. Bariteau JT, Waryasz GR, McDonnell M, Fischer SA, Hayda RA, Born CT. Fungal osteomyelitis and septic arthritis. J Am Acad Orthop Surg. 2014;22(6):390-401.
20. Marijnissen RJ, Koenders MI, van de Veerdonk FL, et al. Exposure to Candida albicans polarizes a T-cell driven arthritis model towards Th17 responses, resulting in a more destructive arthritis. PLoS One. 2012;7(6):e38889.
21. International Consensus on Periprosthetic Joint Infection. Musculoskeletal Infection Society website. http://www.msis-na.org/international-consensus. Published August 1, 2013. Accessed October 16, 2016.
1. Auday BC, Buratovich MA, Marrocco, GF, Moglia P, eds. Magill’s Medical Guide. 7th ed. Ipswich, MA: Salem Press; 2014.
2. Dhaliwal S, LeBel ME. Rapidly progressing polyarticular septic arthritis in a patient with rheumatoid arthritis. Am J Orthop. 2012;41(7):E100-E101.
3. Mateo Soria L, Olivé Marqués A, García Casares E, García Melchor E, Holgado Pérez S, Tena Marsà X. Polyarticular septic arthritis: analysis of 19 cases [in Spanish]. Reumatol Clin. 2009;5(1):18-22.
4. Caksen H, Oztürk MK, Uzüm K, Yüksel S, Ustünbaş HB, Per H. Septic arthritis in childhood. Pediatr Int. 2000;42(5):534-540.
5. Kocher MS, Zurakowski D, Kasser JR. Differentiating between septic arthritis and transient synovitis of the hip in children: an evidence-based clinical prediction algorithm. J Bone Joint Surg Am. 1999;81(12):1662-1670.
6. Madruga Dias J, Costa MM, Pereira da Silva JA, Viana de Queiroz M. Septic arthritis: patients with or without isolated infectious agents have similar characteristics. Infection. 2014;42(2):385-391.
7. Louthrenoo W, Kasitanon N, Wangkaew S, Hongsongkiat S, Sukitawut W, Wichainun R. Streptococcus agalactiae: an emerging cause of septic arthritis. J Clin Rheumatol. 2014;20(2):74-78.
8. Zmierczak H, Goemaere S, Mielants H, Verbruggen G, Veys EM. Candida glabrata arthritis: case report and review of the literature of Candida arthritis. Clin Rheumatol. 1999;18(5):406-409.
9. Bishu S, Su EW, Wilkerson ER, et al. Rheumatoid arthritis patients exhibit impaired Candida albicans–specific Th17 responses. Arthritis Res Ther. 2014;16(1):R50.
10. Legout L, Assal M, Rohner P, Lew D, Bernard L, Hoffmeyer P. Successful treatment of Candida parapsilosis (fluconazole-resistant) osteomyelitis with caspofungin in a HIV patient. Scand J Infect Dis. 2006;38(8):728-730.
11. Sung J, Chun K. Candida parapsilosis arthritis involving the ankle in a diabetes patient. J Korean Soc Radiol. 2011;64:587-591.
12. Marmor L, Peter JB. Candida arthritis of the knee joint. Clin Orthop Relat Res. 1976;(118):133-135.
13. Turgut B, Vural O, Demir M, Kaldir M. Candida arthritis in a patient with chronic myelogenous leukemia (CML) in blastic transformation, unresponsive to fluconazole, but treated effectively with liposomal amphotericin B. Ann Hematol. 2002;81(9):529-531.
14. Christensson B, Ryd L, Dahlberg L, Lohmander S. Candida albicans arthritis in a nonimmunocompromised patient. Complication of placebo intraarticular injections. Acta Orthop Scand. 1993;64(6):695-698.
15. Jeong YM, Cho HY, Lee SW, Hwang YM, Kim YK. Candida septic arthritis with rice body formation: a case report and review of literature. Korean J Radiol. 2013;14(3):465-469.
16. Favero M, Schiavon R, Riato L, Carraro V, Punzi L. Septic arthritis: a 12 years retrospective study in a rheumatological university clinic [in Italian]. Reumatismo. 2008;60(4):260-267.
17. Leslie D, Lansang C, Coppack S, Kennedy L. Diabetes: Clinician’s Desk Reference. Boca Raton, FL: CRC Press; 2012.
18. Silva PM, Gonçalves S, Santos NC. Defensins: antifungal lesions from eukaryotes. Front Microbiol. 2014;5:97.
19. Bariteau JT, Waryasz GR, McDonnell M, Fischer SA, Hayda RA, Born CT. Fungal osteomyelitis and septic arthritis. J Am Acad Orthop Surg. 2014;22(6):390-401.
20. Marijnissen RJ, Koenders MI, van de Veerdonk FL, et al. Exposure to Candida albicans polarizes a T-cell driven arthritis model towards Th17 responses, resulting in a more destructive arthritis. PLoS One. 2012;7(6):e38889.
21. International Consensus on Periprosthetic Joint Infection. Musculoskeletal Infection Society website. http://www.msis-na.org/international-consensus. Published August 1, 2013. Accessed October 16, 2016.