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VIDEO: Adipogenic genes upregulated in high-BMI sucralose users
CHICAGO – , there was significant upregulation of genes that promote intracellular glucose transport. Genes known to be adipogenic and those governing sweet taste receptors also were significantly upregulated with sucralose exposure.
“Effects of sucralose are particularly more detrimental in obese individuals who are prediabetic or diabetic, rather than nonobese consumers of low-calorie sweetener,” said Sabyasachi Sen, MD, during a press conference at the annual meeting of the Endocrine Society.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
These new findings, together with in vitro examination of human adipose-derived mesenchymal stromal cells (MSCs) exposed to sucralose, are helping solve the puzzle of how a sweetener that delivers no energy may contribute to metabolic derangement, said Dr. Sen, professor of endocrinology at George Washington University in Washington.
Dr. Sen and his collaborators first exposed the MSCs to concentrations of sucralose ranging from 0 mM to 0.2 mM – a physiologic level for high sucralose consumers – to the supraphysiologic concentration of 1 mM.
The adipogenic genes CEBPa and FABP4 were upregulated in the sucralose-exposed MSCs, which also showed more intracellular fat droplet accumulation. Reactive oxygen species increased in the MSCs in a dose-dependent fashion as well, said Dr. Sen in a video interview.
All of this upregulation, said Dr. Sen, was pushing the MSCs toward becoming fat cells. “At the same time, we saw that there are certain genes that were upregulating that were allowing more glucose to enter the cell.” The increase in reactive oxygen species paralleled what was seen in a similar model that used glucose rather than sucralose, he said.
The investigators then took subcutaneous fat biopsies from four normal-weight individuals (body mass index, 23.4-24.8 kg/m2), and from 14 obese individuals (BMI, 32-64 kg/m2). Each group had sucralose users and nonusers. Using mRNA gene expression profiles, they saw that glucose transporter genes, adipogenic genes, and antioxidant genes were upregulated among sucralose consumers with obesity, significantly more than for the normal-weight participants.
The pattern, said Dr. Sen, was strikingly similar to what had been seen with the MSC-sucralose exposure findings. “The upregulation that we saw in the petri dish could now be seen in the human fat samples,” he said.
“We think that the sucralose is … allowing more glucose to enter the cell,” said Dr. Sen. “We think that we actually have figured out a mechanism.” He and his colleagues next plan to tag glucose molecules to follow what actually happens as they enter cells in the presence of sucralose.
When Dr. Sen’s patients ask whether they should switch to low-calorie sweetened beverages, he answers with an emphatic “no.” “I say, ‘It’s not going to do you any good, because it still may allow glucose to enter the cells … you’re going to come back to the same status quo’ ” in the context of obesity and insulin resistance, he said.
Dr. Sen reported that he has no relevant disclosures.
SOURCE: Sen S et al. ENDO 2018, Abstract SUN-071.
CHICAGO – , there was significant upregulation of genes that promote intracellular glucose transport. Genes known to be adipogenic and those governing sweet taste receptors also were significantly upregulated with sucralose exposure.
“Effects of sucralose are particularly more detrimental in obese individuals who are prediabetic or diabetic, rather than nonobese consumers of low-calorie sweetener,” said Sabyasachi Sen, MD, during a press conference at the annual meeting of the Endocrine Society.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
These new findings, together with in vitro examination of human adipose-derived mesenchymal stromal cells (MSCs) exposed to sucralose, are helping solve the puzzle of how a sweetener that delivers no energy may contribute to metabolic derangement, said Dr. Sen, professor of endocrinology at George Washington University in Washington.
Dr. Sen and his collaborators first exposed the MSCs to concentrations of sucralose ranging from 0 mM to 0.2 mM – a physiologic level for high sucralose consumers – to the supraphysiologic concentration of 1 mM.
The adipogenic genes CEBPa and FABP4 were upregulated in the sucralose-exposed MSCs, which also showed more intracellular fat droplet accumulation. Reactive oxygen species increased in the MSCs in a dose-dependent fashion as well, said Dr. Sen in a video interview.
All of this upregulation, said Dr. Sen, was pushing the MSCs toward becoming fat cells. “At the same time, we saw that there are certain genes that were upregulating that were allowing more glucose to enter the cell.” The increase in reactive oxygen species paralleled what was seen in a similar model that used glucose rather than sucralose, he said.
The investigators then took subcutaneous fat biopsies from four normal-weight individuals (body mass index, 23.4-24.8 kg/m2), and from 14 obese individuals (BMI, 32-64 kg/m2). Each group had sucralose users and nonusers. Using mRNA gene expression profiles, they saw that glucose transporter genes, adipogenic genes, and antioxidant genes were upregulated among sucralose consumers with obesity, significantly more than for the normal-weight participants.
The pattern, said Dr. Sen, was strikingly similar to what had been seen with the MSC-sucralose exposure findings. “The upregulation that we saw in the petri dish could now be seen in the human fat samples,” he said.
“We think that the sucralose is … allowing more glucose to enter the cell,” said Dr. Sen. “We think that we actually have figured out a mechanism.” He and his colleagues next plan to tag glucose molecules to follow what actually happens as they enter cells in the presence of sucralose.
When Dr. Sen’s patients ask whether they should switch to low-calorie sweetened beverages, he answers with an emphatic “no.” “I say, ‘It’s not going to do you any good, because it still may allow glucose to enter the cells … you’re going to come back to the same status quo’ ” in the context of obesity and insulin resistance, he said.
Dr. Sen reported that he has no relevant disclosures.
SOURCE: Sen S et al. ENDO 2018, Abstract SUN-071.
CHICAGO – , there was significant upregulation of genes that promote intracellular glucose transport. Genes known to be adipogenic and those governing sweet taste receptors also were significantly upregulated with sucralose exposure.
“Effects of sucralose are particularly more detrimental in obese individuals who are prediabetic or diabetic, rather than nonobese consumers of low-calorie sweetener,” said Sabyasachi Sen, MD, during a press conference at the annual meeting of the Endocrine Society.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
These new findings, together with in vitro examination of human adipose-derived mesenchymal stromal cells (MSCs) exposed to sucralose, are helping solve the puzzle of how a sweetener that delivers no energy may contribute to metabolic derangement, said Dr. Sen, professor of endocrinology at George Washington University in Washington.
Dr. Sen and his collaborators first exposed the MSCs to concentrations of sucralose ranging from 0 mM to 0.2 mM – a physiologic level for high sucralose consumers – to the supraphysiologic concentration of 1 mM.
The adipogenic genes CEBPa and FABP4 were upregulated in the sucralose-exposed MSCs, which also showed more intracellular fat droplet accumulation. Reactive oxygen species increased in the MSCs in a dose-dependent fashion as well, said Dr. Sen in a video interview.
All of this upregulation, said Dr. Sen, was pushing the MSCs toward becoming fat cells. “At the same time, we saw that there are certain genes that were upregulating that were allowing more glucose to enter the cell.” The increase in reactive oxygen species paralleled what was seen in a similar model that used glucose rather than sucralose, he said.
The investigators then took subcutaneous fat biopsies from four normal-weight individuals (body mass index, 23.4-24.8 kg/m2), and from 14 obese individuals (BMI, 32-64 kg/m2). Each group had sucralose users and nonusers. Using mRNA gene expression profiles, they saw that glucose transporter genes, adipogenic genes, and antioxidant genes were upregulated among sucralose consumers with obesity, significantly more than for the normal-weight participants.
The pattern, said Dr. Sen, was strikingly similar to what had been seen with the MSC-sucralose exposure findings. “The upregulation that we saw in the petri dish could now be seen in the human fat samples,” he said.
“We think that the sucralose is … allowing more glucose to enter the cell,” said Dr. Sen. “We think that we actually have figured out a mechanism.” He and his colleagues next plan to tag glucose molecules to follow what actually happens as they enter cells in the presence of sucralose.
When Dr. Sen’s patients ask whether they should switch to low-calorie sweetened beverages, he answers with an emphatic “no.” “I say, ‘It’s not going to do you any good, because it still may allow glucose to enter the cells … you’re going to come back to the same status quo’ ” in the context of obesity and insulin resistance, he said.
Dr. Sen reported that he has no relevant disclosures.
SOURCE: Sen S et al. ENDO 2018, Abstract SUN-071.
REPORTING FROM ENDO 2018
Insomnia – going beyond sleep hygiene
Difficulties with sleep are prevalent and significant across the developmental spectrum. Not only does poor sleep affect daytime functioning in relation to mood, focus, appetite, and emotional regulation, but ineffective bedtime routines can cause significant distress for youth and caregivers, as well. The American Academy of Sleep Medicine describes insomnia as “repeated difficulty with sleep initiation, duration, consolidation, or quality that occurs despite age-appropriate time and opportunity for sleep and results in daytime functional impairment for the child and/or family.’’1
Pediatric providers likely are familiar already with initial steps in the evaluation and treatment of insomnia. The emphasis here is assessment and intervention approaches beyond the foundational use of sleep hygiene recommendations.
In working with a patient such as Katie who comes laden with diagnoses and medications, stepping back to reconsider the assessment is an important starting point. Problems related to sleep are rife in psychiatric conditions, from depression, anxiety, and PTSD to bipolar disorder, ADHD, and autism.2
Next is see if there are external factors engendering insomnia. Sleep hygiene focuses on these, but sometimes recent stressors or familial conflict are overlooked, which may be linchpins to improving sleep patterns. Commonly prescribed medications (steroids, bupropion, and stimulants) and intoxication or withdrawal symptoms from substance use can contribute to wakefulness and deserve consideration. It can be useful to track sleep for a while to identify contributing factors, impediments to sleep, and ineffective patterns (see tools at sleepfoundation.org or the free app CBT-I Coach).
After assessment, the bulk of the evidence for pediatric insomnia is for behavioral treatments, mostly for infants and young children. This may be familiar territory, and it offers a good time to assess the level of motivation. Are the patient and family aware of how insomnia affects their lives on a day-to-day basis and is this problem a priority?
For adolescents who are convinced of the life-changing properties of a good night’s sleep, cognitive-behavioral therapy for insomnia (CBT-i) is developing a strong evidence base for insomnia in adolescents.3 CBT-i adds to the usual interventions for addressing insomnia in infants and young children by additionally training adolescents relaxation techniques, by addressing cognitive distortions about sleep, and by actually restricting sleep. This last technique involves initially reducing the amount of sleep in order to build a tight association between sleep and the bedroom, improve sleep efficiency, and increase sleep drive.
In general, medications are considered when other appropriate interventions have proven inadequate. There is very little evidence for using pharmacologic interventions for pediatric insomnia, so even if a medication is selected, behavioral approaches should remain a mainstay.4 Patients and caregivers should agree to specific short-term goals ahead of time when using sleep medicine, given the limited effectiveness and recommended short duration of use. Many medications change sleep architecture, and none have been clearly shown to sustainably improve sleep quality or quantity or reduce daytime symptoms of insomnia.
Prescribing guidelines for insomnia suggest selecting an agent matched to the symptoms and relevant to any comorbidities. Melatonin may be most helpful in shifting the sleep phase rather than for direct hypnotic effects; thus adolescents or patients with ADHD whose sleep schedule has naturally shifted later may benefit from a small dose of melatonin (1-3 mg) several hours before bedtime to prime their system. Beware that melatonin is not regulated by the Food and Drug Administration and animal studies have shown significant alterations of the gonadal hormone axis, although this has not been examined in human trials. Alpha-2 agonists – such as clonidine and guanfacine – may be helpful for sleep initiation, especially in populations with comorbid ADHD, aggression, or tics, where these medications might be otherwise indicated. Prazosin, an alpha-1 antagonist, has some limited evidence as a treatment for nightmares and PTSD symptoms, so it may be a good choice for children with trauma-related hypervigilance.
In patients with depression, low doses of trazodone (12.5-50 mg) or mirtazapine (7.5-15 mg) may be effective. Although short-acting benzodiazepines may be useful in the short-term, particularly for sleep-onset difficulties, they generally are not recommended because of the risks of abuse, diversion, withdrawal, cognitive side effects, disinhibition, development of tolerance, and contraindication with such comorbidities as sleep apnea. However, the benzodiazepine receptor agonists such as zaleplon, zolpidem, and eszopiclone, while lacking evidence in the pediatric population, may be worthwhile considerations as their varying half-lives allow for specificity in treating sleep-onset vs. sleep-maintenance problems. Caregivers should be warned about the potential for sleepwalking or other complex sleep-related behaviors with this class of medicines.
Avoid tricyclic antidepressants because of the potential for anticholinergic effects and cardiotoxicity. Atypical antipsychotics generally are not worth the risk of serious and rapid side effects associated with this class of medications, which include metabolic syndrome.
The assessment and treatment of pediatric insomnia may require several visits to complete. But, given growing knowledge of how much sleep contributes to learning, longevity, and well-being, and the consequences of sleep deprivation with regard to safety, irritability, poor concentration, disordered metabolism and appetite, etc., the potential benefits seem well worth the time.
Dr. Rosenfeld is assistant professor of psychiatry at Vermont Center for Children, Youth & Families, at the University of Vermont Medical Center, and the University of Vermont, Burlington. He has received honorarium from Oakstone Publishing for contributing board review course content on human development.
References
1. International Classification of Sleep Disorders: Diagnostic & Coding Manual. 2nd edition. (Westchester: American Academy of Sleep Medicine, 2005).
2. Child Adolesc Psychiatr Clin N Am. 2009 Oct;18(4):979-1000
3. J Child Psychol Psychiatry. 2017, Oct 20. doi: 10.1111/jcpp.12834.
4. Child Adolesc Psychiatric Clin N Am. 2009, Oct;18(4):1001-16.
Difficulties with sleep are prevalent and significant across the developmental spectrum. Not only does poor sleep affect daytime functioning in relation to mood, focus, appetite, and emotional regulation, but ineffective bedtime routines can cause significant distress for youth and caregivers, as well. The American Academy of Sleep Medicine describes insomnia as “repeated difficulty with sleep initiation, duration, consolidation, or quality that occurs despite age-appropriate time and opportunity for sleep and results in daytime functional impairment for the child and/or family.’’1
Pediatric providers likely are familiar already with initial steps in the evaluation and treatment of insomnia. The emphasis here is assessment and intervention approaches beyond the foundational use of sleep hygiene recommendations.
In working with a patient such as Katie who comes laden with diagnoses and medications, stepping back to reconsider the assessment is an important starting point. Problems related to sleep are rife in psychiatric conditions, from depression, anxiety, and PTSD to bipolar disorder, ADHD, and autism.2
Next is see if there are external factors engendering insomnia. Sleep hygiene focuses on these, but sometimes recent stressors or familial conflict are overlooked, which may be linchpins to improving sleep patterns. Commonly prescribed medications (steroids, bupropion, and stimulants) and intoxication or withdrawal symptoms from substance use can contribute to wakefulness and deserve consideration. It can be useful to track sleep for a while to identify contributing factors, impediments to sleep, and ineffective patterns (see tools at sleepfoundation.org or the free app CBT-I Coach).
After assessment, the bulk of the evidence for pediatric insomnia is for behavioral treatments, mostly for infants and young children. This may be familiar territory, and it offers a good time to assess the level of motivation. Are the patient and family aware of how insomnia affects their lives on a day-to-day basis and is this problem a priority?
For adolescents who are convinced of the life-changing properties of a good night’s sleep, cognitive-behavioral therapy for insomnia (CBT-i) is developing a strong evidence base for insomnia in adolescents.3 CBT-i adds to the usual interventions for addressing insomnia in infants and young children by additionally training adolescents relaxation techniques, by addressing cognitive distortions about sleep, and by actually restricting sleep. This last technique involves initially reducing the amount of sleep in order to build a tight association between sleep and the bedroom, improve sleep efficiency, and increase sleep drive.
In general, medications are considered when other appropriate interventions have proven inadequate. There is very little evidence for using pharmacologic interventions for pediatric insomnia, so even if a medication is selected, behavioral approaches should remain a mainstay.4 Patients and caregivers should agree to specific short-term goals ahead of time when using sleep medicine, given the limited effectiveness and recommended short duration of use. Many medications change sleep architecture, and none have been clearly shown to sustainably improve sleep quality or quantity or reduce daytime symptoms of insomnia.
Prescribing guidelines for insomnia suggest selecting an agent matched to the symptoms and relevant to any comorbidities. Melatonin may be most helpful in shifting the sleep phase rather than for direct hypnotic effects; thus adolescents or patients with ADHD whose sleep schedule has naturally shifted later may benefit from a small dose of melatonin (1-3 mg) several hours before bedtime to prime their system. Beware that melatonin is not regulated by the Food and Drug Administration and animal studies have shown significant alterations of the gonadal hormone axis, although this has not been examined in human trials. Alpha-2 agonists – such as clonidine and guanfacine – may be helpful for sleep initiation, especially in populations with comorbid ADHD, aggression, or tics, where these medications might be otherwise indicated. Prazosin, an alpha-1 antagonist, has some limited evidence as a treatment for nightmares and PTSD symptoms, so it may be a good choice for children with trauma-related hypervigilance.
In patients with depression, low doses of trazodone (12.5-50 mg) or mirtazapine (7.5-15 mg) may be effective. Although short-acting benzodiazepines may be useful in the short-term, particularly for sleep-onset difficulties, they generally are not recommended because of the risks of abuse, diversion, withdrawal, cognitive side effects, disinhibition, development of tolerance, and contraindication with such comorbidities as sleep apnea. However, the benzodiazepine receptor agonists such as zaleplon, zolpidem, and eszopiclone, while lacking evidence in the pediatric population, may be worthwhile considerations as their varying half-lives allow for specificity in treating sleep-onset vs. sleep-maintenance problems. Caregivers should be warned about the potential for sleepwalking or other complex sleep-related behaviors with this class of medicines.
Avoid tricyclic antidepressants because of the potential for anticholinergic effects and cardiotoxicity. Atypical antipsychotics generally are not worth the risk of serious and rapid side effects associated with this class of medications, which include metabolic syndrome.
The assessment and treatment of pediatric insomnia may require several visits to complete. But, given growing knowledge of how much sleep contributes to learning, longevity, and well-being, and the consequences of sleep deprivation with regard to safety, irritability, poor concentration, disordered metabolism and appetite, etc., the potential benefits seem well worth the time.
Dr. Rosenfeld is assistant professor of psychiatry at Vermont Center for Children, Youth & Families, at the University of Vermont Medical Center, and the University of Vermont, Burlington. He has received honorarium from Oakstone Publishing for contributing board review course content on human development.
References
1. International Classification of Sleep Disorders: Diagnostic & Coding Manual. 2nd edition. (Westchester: American Academy of Sleep Medicine, 2005).
2. Child Adolesc Psychiatr Clin N Am. 2009 Oct;18(4):979-1000
3. J Child Psychol Psychiatry. 2017, Oct 20. doi: 10.1111/jcpp.12834.
4. Child Adolesc Psychiatric Clin N Am. 2009, Oct;18(4):1001-16.
Difficulties with sleep are prevalent and significant across the developmental spectrum. Not only does poor sleep affect daytime functioning in relation to mood, focus, appetite, and emotional regulation, but ineffective bedtime routines can cause significant distress for youth and caregivers, as well. The American Academy of Sleep Medicine describes insomnia as “repeated difficulty with sleep initiation, duration, consolidation, or quality that occurs despite age-appropriate time and opportunity for sleep and results in daytime functional impairment for the child and/or family.’’1
Pediatric providers likely are familiar already with initial steps in the evaluation and treatment of insomnia. The emphasis here is assessment and intervention approaches beyond the foundational use of sleep hygiene recommendations.
In working with a patient such as Katie who comes laden with diagnoses and medications, stepping back to reconsider the assessment is an important starting point. Problems related to sleep are rife in psychiatric conditions, from depression, anxiety, and PTSD to bipolar disorder, ADHD, and autism.2
Next is see if there are external factors engendering insomnia. Sleep hygiene focuses on these, but sometimes recent stressors or familial conflict are overlooked, which may be linchpins to improving sleep patterns. Commonly prescribed medications (steroids, bupropion, and stimulants) and intoxication or withdrawal symptoms from substance use can contribute to wakefulness and deserve consideration. It can be useful to track sleep for a while to identify contributing factors, impediments to sleep, and ineffective patterns (see tools at sleepfoundation.org or the free app CBT-I Coach).
After assessment, the bulk of the evidence for pediatric insomnia is for behavioral treatments, mostly for infants and young children. This may be familiar territory, and it offers a good time to assess the level of motivation. Are the patient and family aware of how insomnia affects their lives on a day-to-day basis and is this problem a priority?
For adolescents who are convinced of the life-changing properties of a good night’s sleep, cognitive-behavioral therapy for insomnia (CBT-i) is developing a strong evidence base for insomnia in adolescents.3 CBT-i adds to the usual interventions for addressing insomnia in infants and young children by additionally training adolescents relaxation techniques, by addressing cognitive distortions about sleep, and by actually restricting sleep. This last technique involves initially reducing the amount of sleep in order to build a tight association between sleep and the bedroom, improve sleep efficiency, and increase sleep drive.
In general, medications are considered when other appropriate interventions have proven inadequate. There is very little evidence for using pharmacologic interventions for pediatric insomnia, so even if a medication is selected, behavioral approaches should remain a mainstay.4 Patients and caregivers should agree to specific short-term goals ahead of time when using sleep medicine, given the limited effectiveness and recommended short duration of use. Many medications change sleep architecture, and none have been clearly shown to sustainably improve sleep quality or quantity or reduce daytime symptoms of insomnia.
Prescribing guidelines for insomnia suggest selecting an agent matched to the symptoms and relevant to any comorbidities. Melatonin may be most helpful in shifting the sleep phase rather than for direct hypnotic effects; thus adolescents or patients with ADHD whose sleep schedule has naturally shifted later may benefit from a small dose of melatonin (1-3 mg) several hours before bedtime to prime their system. Beware that melatonin is not regulated by the Food and Drug Administration and animal studies have shown significant alterations of the gonadal hormone axis, although this has not been examined in human trials. Alpha-2 agonists – such as clonidine and guanfacine – may be helpful for sleep initiation, especially in populations with comorbid ADHD, aggression, or tics, where these medications might be otherwise indicated. Prazosin, an alpha-1 antagonist, has some limited evidence as a treatment for nightmares and PTSD symptoms, so it may be a good choice for children with trauma-related hypervigilance.
In patients with depression, low doses of trazodone (12.5-50 mg) or mirtazapine (7.5-15 mg) may be effective. Although short-acting benzodiazepines may be useful in the short-term, particularly for sleep-onset difficulties, they generally are not recommended because of the risks of abuse, diversion, withdrawal, cognitive side effects, disinhibition, development of tolerance, and contraindication with such comorbidities as sleep apnea. However, the benzodiazepine receptor agonists such as zaleplon, zolpidem, and eszopiclone, while lacking evidence in the pediatric population, may be worthwhile considerations as their varying half-lives allow for specificity in treating sleep-onset vs. sleep-maintenance problems. Caregivers should be warned about the potential for sleepwalking or other complex sleep-related behaviors with this class of medicines.
Avoid tricyclic antidepressants because of the potential for anticholinergic effects and cardiotoxicity. Atypical antipsychotics generally are not worth the risk of serious and rapid side effects associated with this class of medications, which include metabolic syndrome.
The assessment and treatment of pediatric insomnia may require several visits to complete. But, given growing knowledge of how much sleep contributes to learning, longevity, and well-being, and the consequences of sleep deprivation with regard to safety, irritability, poor concentration, disordered metabolism and appetite, etc., the potential benefits seem well worth the time.
Dr. Rosenfeld is assistant professor of psychiatry at Vermont Center for Children, Youth & Families, at the University of Vermont Medical Center, and the University of Vermont, Burlington. He has received honorarium from Oakstone Publishing for contributing board review course content on human development.
References
1. International Classification of Sleep Disorders: Diagnostic & Coding Manual. 2nd edition. (Westchester: American Academy of Sleep Medicine, 2005).
2. Child Adolesc Psychiatr Clin N Am. 2009 Oct;18(4):979-1000
3. J Child Psychol Psychiatry. 2017, Oct 20. doi: 10.1111/jcpp.12834.
4. Child Adolesc Psychiatric Clin N Am. 2009, Oct;18(4):1001-16.
Dexcom G6 gets FDA nod
from the Food and Drug Administration.
The Dexcom G6 is about 28% smaller than its predecessor, the G5, can be worn for up to 10 days – 43% longer than the G5 – and doesn’t require any finger-stick calibrations or treatment decisions. It’s the first FDA-approved integrated continuous glucose monitoring (iCGM) system that can link electronically to other compatible devices, including automated insulin dosing systems, insulin pumps, blood glucose meters, and other electronic devices used for diabetes management, the FDA said in a press statement. Its revamped sensor doesn’t interact with acetaminophen – another distinct advantage over the G5.
The device will be commercially available sometime this year, the Dexcom website noted.
The device also set a new premarketing review standard for CGM’s, which can now utilize the less-burdensome 510(k) clearance pathway. Until now, they have been treated as the highest-risk Class III medical devices.
According to the FDA statement, the agency “…recognized this as an opportunity to reduce the regulatory burden for this type of device by establishing criteria that would classify these as ‘moderate risk,’ class II medical devices with special controls.”
G6 was approved through this new pathway, dedicated to novel, low-to-moderate-risk devices that are not “substantially equivalent” to an already legally marketed device, the press statement said.
The FDA evaluated data from two clinical studies of the Dexcom G6, which included 324 adults and children aged 2 years and older with diabetes. Both studies included multiple clinical visits within a 10-day period where system readings were compared to a laboratory test method that measures blood glucose values. No serious adverse events were reported during the studies.
from the Food and Drug Administration.
The Dexcom G6 is about 28% smaller than its predecessor, the G5, can be worn for up to 10 days – 43% longer than the G5 – and doesn’t require any finger-stick calibrations or treatment decisions. It’s the first FDA-approved integrated continuous glucose monitoring (iCGM) system that can link electronically to other compatible devices, including automated insulin dosing systems, insulin pumps, blood glucose meters, and other electronic devices used for diabetes management, the FDA said in a press statement. Its revamped sensor doesn’t interact with acetaminophen – another distinct advantage over the G5.
The device will be commercially available sometime this year, the Dexcom website noted.
The device also set a new premarketing review standard for CGM’s, which can now utilize the less-burdensome 510(k) clearance pathway. Until now, they have been treated as the highest-risk Class III medical devices.
According to the FDA statement, the agency “…recognized this as an opportunity to reduce the regulatory burden for this type of device by establishing criteria that would classify these as ‘moderate risk,’ class II medical devices with special controls.”
G6 was approved through this new pathway, dedicated to novel, low-to-moderate-risk devices that are not “substantially equivalent” to an already legally marketed device, the press statement said.
The FDA evaluated data from two clinical studies of the Dexcom G6, which included 324 adults and children aged 2 years and older with diabetes. Both studies included multiple clinical visits within a 10-day period where system readings were compared to a laboratory test method that measures blood glucose values. No serious adverse events were reported during the studies.
from the Food and Drug Administration.
The Dexcom G6 is about 28% smaller than its predecessor, the G5, can be worn for up to 10 days – 43% longer than the G5 – and doesn’t require any finger-stick calibrations or treatment decisions. It’s the first FDA-approved integrated continuous glucose monitoring (iCGM) system that can link electronically to other compatible devices, including automated insulin dosing systems, insulin pumps, blood glucose meters, and other electronic devices used for diabetes management, the FDA said in a press statement. Its revamped sensor doesn’t interact with acetaminophen – another distinct advantage over the G5.
The device will be commercially available sometime this year, the Dexcom website noted.
The device also set a new premarketing review standard for CGM’s, which can now utilize the less-burdensome 510(k) clearance pathway. Until now, they have been treated as the highest-risk Class III medical devices.
According to the FDA statement, the agency “…recognized this as an opportunity to reduce the regulatory burden for this type of device by establishing criteria that would classify these as ‘moderate risk,’ class II medical devices with special controls.”
G6 was approved through this new pathway, dedicated to novel, low-to-moderate-risk devices that are not “substantially equivalent” to an already legally marketed device, the press statement said.
The FDA evaluated data from two clinical studies of the Dexcom G6, which included 324 adults and children aged 2 years and older with diabetes. Both studies included multiple clinical visits within a 10-day period where system readings were compared to a laboratory test method that measures blood glucose values. No serious adverse events were reported during the studies.
The Prevention and Treatment of Femoral Trial Head Loss in Total Hip Arthroplasty
ABSTRACT
This article aims to provide the information necessary to prevent femoral trial head loss and to offer information regarding retrieval of the trial head if it is lost within the surgical field. These techniques can be used to help guide practice in the future. A review of the literature was conducted using a computerized search of PubMed in regard to this issue to investigate how such an occurrence can be prevented and what steps can be taken if preventative measures fail.
Continue to: Total hip arthroplasty...
Total hip arthroplasty (THA) is becoming an increasingly common procedure. Although this procedure is frequently performed, intraoperative complications still arise; therefore, methods of preventing and ameliorating these complications must be devised. One such complication is the loss of the femoral trial head component within the patient.
Loss of the trial head has been documented in THA cases that have used a number of different surgical approaches.1 Although it is uncommon to lose the trial within the pelvis, it is not an entirely unlikely phenomenon. The possibility of such an event makes prevention important, especially given the associated morbidity that loss of the component could cause. Fortunately, there are preventative measures that can be taken to minimize the probability of losing the femoral trial head, in addition to techniques that can be utilized if prevention fails.
SURGICAL TECHNIQUE
PREVENTION
Firstly, it is important to avoid the use of worn-out femoral trial components. It is thought that the incidence of femoral trial head loss is increased when the trunnion is older and has been used repeatedly.2,3 Therefore, it is advised that the use of worn femoral trial stems and other older trial components be avoided.
When the femoral trial head disengages anteriorly, it has the potential to enter the pelvis/retroperitoneal space.2,4 The femoral trial head may move more freely in the absence of resistance offered by the anterior capsule.4 Therefore, when extensive anterior capsular dissection has taken place, such as during extensive capsulectomy, caution should be exercised when manipulating the hip. This emphasizes the necessity to closely monitor the head during any manipulation, particularly in the presence of significant anterior capsule disruption.
Modular hip arthroplasty prosthetics allow for various intraoperative changes to be made to the femoral component, providing greater specificity to the prosthesis.5 However, the modularity of the femoral component has been described as a factor contributing to loss of the femoral trial head.4 This also has been discussed with respect to the implantable prosthetic femoral head itself because of disengagement from the femoral stem during reduction and dislocation.4
Continue to: Case reports have cited...
Case reports have cited the tension of the soft tissues as a definitive factor in trial head loss.1,4,6 These reports discuss the notion that more tension within the soft tissue can increase the likelihood that the trial head will dislodge during reduction or dislocation. Surgeons should therefore consider taking special care when manipulating the trial joint when the soft tissues are particularly tight and offer significant resistance. It has been suggested that the incision be packed with gauze during reductions when the soft tissue is under significant tension in order to keep the femoral trial head from entering the pelvis.6
A simple technique that can be utilized in the prevention of femoral trial head loss is the placement of a suture through the apical hole in the trial head to aid in the retrieval of the implant if it is lost.1 Madsen and colleagues1 suggest the placement of a No.1 (or thicker) suture through this hole. Although this takes some time to perform, it could prove useful in the prevention of complicated implant loss.
Lastly, and perhaps most importantly, it is essential that there is communication and understanding between the surgeon and any assistants. This has been noted to be particularly important during posterior or lateral surgical approaches when the trial head can be lost during attempts at reduction with traction and internal rotation.2 Given the possibility of losing the trial head during this reduction maneuver, communication between the team during the reduction is instrumental.
RETRIEVAL
If the femoral trial head dissociates from the trunnion of the femoral trial manipulation, there are some techniques that can be used to aid in retrieval. It has been described that when the trial head is lost within the surgical wound, it can travel underneath the rectus femoris muscle and cross the pelvic brim, subsequently entering the pelvis along the psoas tendon, as the psoas bursa offers little resistance to the smooth femoral trial head.1 The trial head has been found to follow this path along the psoas tendon until it is located in the posterior pelvis within the retroperitoneal space.1,7 What follows is a compilation of techniques for approaching loss of the femoral trial head when it occurs.
The femoral trial head is round and smooth, which complicates its retrieval. If the surgeon tries to simply grab the component with fingers, it may slip away into the pelvis. When trialing the hip to assess for anterior stability, if the femoral trial head is lost, the leg should not be moved.7 At this point, a manual attempt to recover the trial head before it moves into the pelvis along the psoas tendon should be made.7 It is possible that the femoral trial head may spin when trying to retrieve it, however this should still be attempted before a formal additional surgical approach is employed.7 It has also been noted that one can manually simultaneously press down on the hypogastrium toward the iliac fossa in order to inhibit the movement of the disarticulated trial head from advancing proximally.3 After performing this maneuver, the femoral trial head can be retrieved through the inguinal canal.3
Continue to: Additional surgical approaches...
Additional surgical approaches can also be utilized for retrieval of the femoral trial head if other measures fail. Callaghan and colleagues7 describe a separate surgical approach that can be used to retrieve the trial component after losing the trial head during a posterolateral approach for THA. This technique is commenced by making a 6-cm to 7-cm incision along the iliac crest to the anteromedial aspect of the anterior superior iliac spine.7 The interval between the iliacus and the inner table of the iliac wing is developed, and an attempt is made to locate the femoral trial head and guide it distally along the pelvis toward the hip. Fingers or napkin forceps can be used to accomplish this advancement of the trial head distally toward the hip, and once reaching surgical site, the trial can then be retrieved.7 Further extension of the incision can be made distally if this limited approach is unsuccessful.7 In the event the femoral trial head is still unable to be retrieved, the authors suggest considering a dedicated retroperitoneal approach for trial retrieval after the arthroplasty procedure has been completed.7
Another method for retrieval of the femoral trial head has been described specifically in the setting of a direct lateral approach.8 Kalra and colleagues8 describe a case in which the trial femoral head dislocated anteriorly, and although it was unable to be visualized, the component was able to be palpated posterior to the superior pubic ramus. With the trial head still disassociated within the pelvis, the final implants were implanted. Although the trial was unable to be viewed, using the same incision for the direct lateral approach, the trial femoral head was guided posteriorly toward the sciatic notch. A posterior approach to the hip was then performed using the same initial direct lateral incision used. Subsequent exposure and release of the external rotators and posterior capsule was performed, as was release of the insertion of the gluteus maximus in order to facilitate better visualization and to prevent excessive tension on the sciatic nerve. Blunt finger dissection of the soft tissues was then performed, and the trial head was retrieved from the sciatic notch with a Kocher clamp.8
Madsen and colleagues1 highlight two different cases in which the trial head was lost into the pelvis when using an anterolateral (modified Watson-Jones) approach to the hip to perform THA. As previously alluded to, the trial heads traveled along the patients’ psoas muscle and stopped directly anterior to their sacroiliac joint. In both cases, the trial head was retrieved using a large Satinsky aortic clamp, which enabled the surgeons to drag the trial head to the pelvic brim where it could be removed with a hemostat.1
Multiple authors have discussed the decision to leave the component within the pelvis if the femoral trial head cannot be retrieved.2,4,7 Batouk and colleagues4 noted that in a case of loss of the femoral trial head, the component would be unlikely to disrupt any of the structures within the pelvis, and in the absence of compression of any vital structures, leaving the implant in the patient could be considered. Although the short-term follow-up of 3 months noted in this particular case did not yield any obvious detriment to the patient in regard to symptomatology, the authors note that the long-term effects of such a practice is unclear.4 In another case, in which the decision was made to leave the femoral trial head, the patient at postoperative week 6 began to hear clicking in the hip with an associated loss of range of motion.7 This subsequently prompted removal of the trial component.
DISCUSSION
Although not a particularly common complication, loss of the femoral trial head can occur; therefore, a plan of action should be in place to prevent its loss or to retrieve it if prevention is ineffective. Given the modularity of various arthroplasty systems in regard to the different trial components or even the final implantable prosthetic devices, component loss is a possibility. An understanding of this complication and the appropriate steps to approaching it could aid in preventing patient morbidity. Because of this, it is imperative that surgeons who perform THA be aware of the potential complications and the measures that can be taken to address them.
Continue to: CONCLUSION
CONCLUSION
The femoral trial head often can be quickly and easily recovered; however, trial component recovery can sometimes be more complicated. Loss of the trial femoral head could potentially occur during dislocation, reduction, or any of the trial positions. An example of a more complicated recovery is when the femoral trial head is lost into the retroperitoneal space, which could occur when trialing the hip in extension to assess the anterior stability of the hip. Loss of the femoral trial head is an avoidable occurrence, and it has the potential to cause a number of complications as well as the need for additional incisions/surgery to retrieve the femoral trial head. The subsequent issues that could arise after loss occurs can not only lead to extensive surgical complications, but can also foster patient dissatisfaction regarding surgical outcomes. Therefore, consistent attempts to utilize preventative techniques are essential. As discussed, simple measures such as placement of a suture through the apical hole of the trial component and adequate communication between those involved in reduction and trialing maneuvers, can serve to avert femoral trial head loss.
1. Madsen WY, Mitchell BS, Kates SL. Successful intraoperative retrieval of dislocated femoral trial head during total hip arthroplasty. J Arthroplasty. 2012;27(5):820.e9-e11. doi:10.1016/j.arth.2011.08.006.
2. Ozkan K, Ugutmen E, Altintas F, Eren A, Mahirogullari M. Intraoperative dislocation of the prosthetic femoral head into the pelvis during total hip arthroplasty. Acta Orthop Belg. 2008;74(4):553-555.
3. Rachbauer F, Nogler M, Krismer M, Moritz M. Intraoperative migration of the trial femoral head into the pelvis during total hip arthroplasty: prevention and retrieval. J Bone Joint Surg Am. 2002;84-A(5):881-882.
4. Batouk O, Gilbart M, Jain R. Intraoperative dislocation of the trial femoral head into the pelvis during total hip arthroplasty: a case report. J Bone Joint Surg Am. 2001;83-A(10):1549-1551.
5. Srinivasan A, Jung E, Levine BR. Modularity of the femoral component in total hip arthroplasty. J Am Acad Orthop Surg. 2012;20(4):214-222. doi:10.5435/JAAOS-20-04-214.
6. Princep A. Intraoperative migration of the trial femoral head into the pelvis during total hip arthroplasty: prevention and retrieval. J Bone Joint Surg Am. 2002;84-A(5):880-881.
7. Callaghan JJ, McAndrew C, Boese CK, Forest E. Intrapelvic migration of the trial femoral head during total hip arthroplasty: is retrieval necessary? A report of four cases. Iowa Orthop J. 2006;26:60-62.
8. Kalra K, Ries MD, Bozic KJ. Intrapelvic displacement of a trial femoral head during total hip arthroplasty and a method to retrieve it. J Arthroplasty 2011;26(2):338.e21-e23. doi:10.1016/j.arth.2009.12.005.
ABSTRACT
This article aims to provide the information necessary to prevent femoral trial head loss and to offer information regarding retrieval of the trial head if it is lost within the surgical field. These techniques can be used to help guide practice in the future. A review of the literature was conducted using a computerized search of PubMed in regard to this issue to investigate how such an occurrence can be prevented and what steps can be taken if preventative measures fail.
Continue to: Total hip arthroplasty...
Total hip arthroplasty (THA) is becoming an increasingly common procedure. Although this procedure is frequently performed, intraoperative complications still arise; therefore, methods of preventing and ameliorating these complications must be devised. One such complication is the loss of the femoral trial head component within the patient.
Loss of the trial head has been documented in THA cases that have used a number of different surgical approaches.1 Although it is uncommon to lose the trial within the pelvis, it is not an entirely unlikely phenomenon. The possibility of such an event makes prevention important, especially given the associated morbidity that loss of the component could cause. Fortunately, there are preventative measures that can be taken to minimize the probability of losing the femoral trial head, in addition to techniques that can be utilized if prevention fails.
SURGICAL TECHNIQUE
PREVENTION
Firstly, it is important to avoid the use of worn-out femoral trial components. It is thought that the incidence of femoral trial head loss is increased when the trunnion is older and has been used repeatedly.2,3 Therefore, it is advised that the use of worn femoral trial stems and other older trial components be avoided.
When the femoral trial head disengages anteriorly, it has the potential to enter the pelvis/retroperitoneal space.2,4 The femoral trial head may move more freely in the absence of resistance offered by the anterior capsule.4 Therefore, when extensive anterior capsular dissection has taken place, such as during extensive capsulectomy, caution should be exercised when manipulating the hip. This emphasizes the necessity to closely monitor the head during any manipulation, particularly in the presence of significant anterior capsule disruption.
Modular hip arthroplasty prosthetics allow for various intraoperative changes to be made to the femoral component, providing greater specificity to the prosthesis.5 However, the modularity of the femoral component has been described as a factor contributing to loss of the femoral trial head.4 This also has been discussed with respect to the implantable prosthetic femoral head itself because of disengagement from the femoral stem during reduction and dislocation.4
Continue to: Case reports have cited...
Case reports have cited the tension of the soft tissues as a definitive factor in trial head loss.1,4,6 These reports discuss the notion that more tension within the soft tissue can increase the likelihood that the trial head will dislodge during reduction or dislocation. Surgeons should therefore consider taking special care when manipulating the trial joint when the soft tissues are particularly tight and offer significant resistance. It has been suggested that the incision be packed with gauze during reductions when the soft tissue is under significant tension in order to keep the femoral trial head from entering the pelvis.6
A simple technique that can be utilized in the prevention of femoral trial head loss is the placement of a suture through the apical hole in the trial head to aid in the retrieval of the implant if it is lost.1 Madsen and colleagues1 suggest the placement of a No.1 (or thicker) suture through this hole. Although this takes some time to perform, it could prove useful in the prevention of complicated implant loss.
Lastly, and perhaps most importantly, it is essential that there is communication and understanding between the surgeon and any assistants. This has been noted to be particularly important during posterior or lateral surgical approaches when the trial head can be lost during attempts at reduction with traction and internal rotation.2 Given the possibility of losing the trial head during this reduction maneuver, communication between the team during the reduction is instrumental.
RETRIEVAL
If the femoral trial head dissociates from the trunnion of the femoral trial manipulation, there are some techniques that can be used to aid in retrieval. It has been described that when the trial head is lost within the surgical wound, it can travel underneath the rectus femoris muscle and cross the pelvic brim, subsequently entering the pelvis along the psoas tendon, as the psoas bursa offers little resistance to the smooth femoral trial head.1 The trial head has been found to follow this path along the psoas tendon until it is located in the posterior pelvis within the retroperitoneal space.1,7 What follows is a compilation of techniques for approaching loss of the femoral trial head when it occurs.
The femoral trial head is round and smooth, which complicates its retrieval. If the surgeon tries to simply grab the component with fingers, it may slip away into the pelvis. When trialing the hip to assess for anterior stability, if the femoral trial head is lost, the leg should not be moved.7 At this point, a manual attempt to recover the trial head before it moves into the pelvis along the psoas tendon should be made.7 It is possible that the femoral trial head may spin when trying to retrieve it, however this should still be attempted before a formal additional surgical approach is employed.7 It has also been noted that one can manually simultaneously press down on the hypogastrium toward the iliac fossa in order to inhibit the movement of the disarticulated trial head from advancing proximally.3 After performing this maneuver, the femoral trial head can be retrieved through the inguinal canal.3
Continue to: Additional surgical approaches...
Additional surgical approaches can also be utilized for retrieval of the femoral trial head if other measures fail. Callaghan and colleagues7 describe a separate surgical approach that can be used to retrieve the trial component after losing the trial head during a posterolateral approach for THA. This technique is commenced by making a 6-cm to 7-cm incision along the iliac crest to the anteromedial aspect of the anterior superior iliac spine.7 The interval between the iliacus and the inner table of the iliac wing is developed, and an attempt is made to locate the femoral trial head and guide it distally along the pelvis toward the hip. Fingers or napkin forceps can be used to accomplish this advancement of the trial head distally toward the hip, and once reaching surgical site, the trial can then be retrieved.7 Further extension of the incision can be made distally if this limited approach is unsuccessful.7 In the event the femoral trial head is still unable to be retrieved, the authors suggest considering a dedicated retroperitoneal approach for trial retrieval after the arthroplasty procedure has been completed.7
Another method for retrieval of the femoral trial head has been described specifically in the setting of a direct lateral approach.8 Kalra and colleagues8 describe a case in which the trial femoral head dislocated anteriorly, and although it was unable to be visualized, the component was able to be palpated posterior to the superior pubic ramus. With the trial head still disassociated within the pelvis, the final implants were implanted. Although the trial was unable to be viewed, using the same incision for the direct lateral approach, the trial femoral head was guided posteriorly toward the sciatic notch. A posterior approach to the hip was then performed using the same initial direct lateral incision used. Subsequent exposure and release of the external rotators and posterior capsule was performed, as was release of the insertion of the gluteus maximus in order to facilitate better visualization and to prevent excessive tension on the sciatic nerve. Blunt finger dissection of the soft tissues was then performed, and the trial head was retrieved from the sciatic notch with a Kocher clamp.8
Madsen and colleagues1 highlight two different cases in which the trial head was lost into the pelvis when using an anterolateral (modified Watson-Jones) approach to the hip to perform THA. As previously alluded to, the trial heads traveled along the patients’ psoas muscle and stopped directly anterior to their sacroiliac joint. In both cases, the trial head was retrieved using a large Satinsky aortic clamp, which enabled the surgeons to drag the trial head to the pelvic brim where it could be removed with a hemostat.1
Multiple authors have discussed the decision to leave the component within the pelvis if the femoral trial head cannot be retrieved.2,4,7 Batouk and colleagues4 noted that in a case of loss of the femoral trial head, the component would be unlikely to disrupt any of the structures within the pelvis, and in the absence of compression of any vital structures, leaving the implant in the patient could be considered. Although the short-term follow-up of 3 months noted in this particular case did not yield any obvious detriment to the patient in regard to symptomatology, the authors note that the long-term effects of such a practice is unclear.4 In another case, in which the decision was made to leave the femoral trial head, the patient at postoperative week 6 began to hear clicking in the hip with an associated loss of range of motion.7 This subsequently prompted removal of the trial component.
DISCUSSION
Although not a particularly common complication, loss of the femoral trial head can occur; therefore, a plan of action should be in place to prevent its loss or to retrieve it if prevention is ineffective. Given the modularity of various arthroplasty systems in regard to the different trial components or even the final implantable prosthetic devices, component loss is a possibility. An understanding of this complication and the appropriate steps to approaching it could aid in preventing patient morbidity. Because of this, it is imperative that surgeons who perform THA be aware of the potential complications and the measures that can be taken to address them.
Continue to: CONCLUSION
CONCLUSION
The femoral trial head often can be quickly and easily recovered; however, trial component recovery can sometimes be more complicated. Loss of the trial femoral head could potentially occur during dislocation, reduction, or any of the trial positions. An example of a more complicated recovery is when the femoral trial head is lost into the retroperitoneal space, which could occur when trialing the hip in extension to assess the anterior stability of the hip. Loss of the femoral trial head is an avoidable occurrence, and it has the potential to cause a number of complications as well as the need for additional incisions/surgery to retrieve the femoral trial head. The subsequent issues that could arise after loss occurs can not only lead to extensive surgical complications, but can also foster patient dissatisfaction regarding surgical outcomes. Therefore, consistent attempts to utilize preventative techniques are essential. As discussed, simple measures such as placement of a suture through the apical hole of the trial component and adequate communication between those involved in reduction and trialing maneuvers, can serve to avert femoral trial head loss.
ABSTRACT
This article aims to provide the information necessary to prevent femoral trial head loss and to offer information regarding retrieval of the trial head if it is lost within the surgical field. These techniques can be used to help guide practice in the future. A review of the literature was conducted using a computerized search of PubMed in regard to this issue to investigate how such an occurrence can be prevented and what steps can be taken if preventative measures fail.
Continue to: Total hip arthroplasty...
Total hip arthroplasty (THA) is becoming an increasingly common procedure. Although this procedure is frequently performed, intraoperative complications still arise; therefore, methods of preventing and ameliorating these complications must be devised. One such complication is the loss of the femoral trial head component within the patient.
Loss of the trial head has been documented in THA cases that have used a number of different surgical approaches.1 Although it is uncommon to lose the trial within the pelvis, it is not an entirely unlikely phenomenon. The possibility of such an event makes prevention important, especially given the associated morbidity that loss of the component could cause. Fortunately, there are preventative measures that can be taken to minimize the probability of losing the femoral trial head, in addition to techniques that can be utilized if prevention fails.
SURGICAL TECHNIQUE
PREVENTION
Firstly, it is important to avoid the use of worn-out femoral trial components. It is thought that the incidence of femoral trial head loss is increased when the trunnion is older and has been used repeatedly.2,3 Therefore, it is advised that the use of worn femoral trial stems and other older trial components be avoided.
When the femoral trial head disengages anteriorly, it has the potential to enter the pelvis/retroperitoneal space.2,4 The femoral trial head may move more freely in the absence of resistance offered by the anterior capsule.4 Therefore, when extensive anterior capsular dissection has taken place, such as during extensive capsulectomy, caution should be exercised when manipulating the hip. This emphasizes the necessity to closely monitor the head during any manipulation, particularly in the presence of significant anterior capsule disruption.
Modular hip arthroplasty prosthetics allow for various intraoperative changes to be made to the femoral component, providing greater specificity to the prosthesis.5 However, the modularity of the femoral component has been described as a factor contributing to loss of the femoral trial head.4 This also has been discussed with respect to the implantable prosthetic femoral head itself because of disengagement from the femoral stem during reduction and dislocation.4
Continue to: Case reports have cited...
Case reports have cited the tension of the soft tissues as a definitive factor in trial head loss.1,4,6 These reports discuss the notion that more tension within the soft tissue can increase the likelihood that the trial head will dislodge during reduction or dislocation. Surgeons should therefore consider taking special care when manipulating the trial joint when the soft tissues are particularly tight and offer significant resistance. It has been suggested that the incision be packed with gauze during reductions when the soft tissue is under significant tension in order to keep the femoral trial head from entering the pelvis.6
A simple technique that can be utilized in the prevention of femoral trial head loss is the placement of a suture through the apical hole in the trial head to aid in the retrieval of the implant if it is lost.1 Madsen and colleagues1 suggest the placement of a No.1 (or thicker) suture through this hole. Although this takes some time to perform, it could prove useful in the prevention of complicated implant loss.
Lastly, and perhaps most importantly, it is essential that there is communication and understanding between the surgeon and any assistants. This has been noted to be particularly important during posterior or lateral surgical approaches when the trial head can be lost during attempts at reduction with traction and internal rotation.2 Given the possibility of losing the trial head during this reduction maneuver, communication between the team during the reduction is instrumental.
RETRIEVAL
If the femoral trial head dissociates from the trunnion of the femoral trial manipulation, there are some techniques that can be used to aid in retrieval. It has been described that when the trial head is lost within the surgical wound, it can travel underneath the rectus femoris muscle and cross the pelvic brim, subsequently entering the pelvis along the psoas tendon, as the psoas bursa offers little resistance to the smooth femoral trial head.1 The trial head has been found to follow this path along the psoas tendon until it is located in the posterior pelvis within the retroperitoneal space.1,7 What follows is a compilation of techniques for approaching loss of the femoral trial head when it occurs.
The femoral trial head is round and smooth, which complicates its retrieval. If the surgeon tries to simply grab the component with fingers, it may slip away into the pelvis. When trialing the hip to assess for anterior stability, if the femoral trial head is lost, the leg should not be moved.7 At this point, a manual attempt to recover the trial head before it moves into the pelvis along the psoas tendon should be made.7 It is possible that the femoral trial head may spin when trying to retrieve it, however this should still be attempted before a formal additional surgical approach is employed.7 It has also been noted that one can manually simultaneously press down on the hypogastrium toward the iliac fossa in order to inhibit the movement of the disarticulated trial head from advancing proximally.3 After performing this maneuver, the femoral trial head can be retrieved through the inguinal canal.3
Continue to: Additional surgical approaches...
Additional surgical approaches can also be utilized for retrieval of the femoral trial head if other measures fail. Callaghan and colleagues7 describe a separate surgical approach that can be used to retrieve the trial component after losing the trial head during a posterolateral approach for THA. This technique is commenced by making a 6-cm to 7-cm incision along the iliac crest to the anteromedial aspect of the anterior superior iliac spine.7 The interval between the iliacus and the inner table of the iliac wing is developed, and an attempt is made to locate the femoral trial head and guide it distally along the pelvis toward the hip. Fingers or napkin forceps can be used to accomplish this advancement of the trial head distally toward the hip, and once reaching surgical site, the trial can then be retrieved.7 Further extension of the incision can be made distally if this limited approach is unsuccessful.7 In the event the femoral trial head is still unable to be retrieved, the authors suggest considering a dedicated retroperitoneal approach for trial retrieval after the arthroplasty procedure has been completed.7
Another method for retrieval of the femoral trial head has been described specifically in the setting of a direct lateral approach.8 Kalra and colleagues8 describe a case in which the trial femoral head dislocated anteriorly, and although it was unable to be visualized, the component was able to be palpated posterior to the superior pubic ramus. With the trial head still disassociated within the pelvis, the final implants were implanted. Although the trial was unable to be viewed, using the same incision for the direct lateral approach, the trial femoral head was guided posteriorly toward the sciatic notch. A posterior approach to the hip was then performed using the same initial direct lateral incision used. Subsequent exposure and release of the external rotators and posterior capsule was performed, as was release of the insertion of the gluteus maximus in order to facilitate better visualization and to prevent excessive tension on the sciatic nerve. Blunt finger dissection of the soft tissues was then performed, and the trial head was retrieved from the sciatic notch with a Kocher clamp.8
Madsen and colleagues1 highlight two different cases in which the trial head was lost into the pelvis when using an anterolateral (modified Watson-Jones) approach to the hip to perform THA. As previously alluded to, the trial heads traveled along the patients’ psoas muscle and stopped directly anterior to their sacroiliac joint. In both cases, the trial head was retrieved using a large Satinsky aortic clamp, which enabled the surgeons to drag the trial head to the pelvic brim where it could be removed with a hemostat.1
Multiple authors have discussed the decision to leave the component within the pelvis if the femoral trial head cannot be retrieved.2,4,7 Batouk and colleagues4 noted that in a case of loss of the femoral trial head, the component would be unlikely to disrupt any of the structures within the pelvis, and in the absence of compression of any vital structures, leaving the implant in the patient could be considered. Although the short-term follow-up of 3 months noted in this particular case did not yield any obvious detriment to the patient in regard to symptomatology, the authors note that the long-term effects of such a practice is unclear.4 In another case, in which the decision was made to leave the femoral trial head, the patient at postoperative week 6 began to hear clicking in the hip with an associated loss of range of motion.7 This subsequently prompted removal of the trial component.
DISCUSSION
Although not a particularly common complication, loss of the femoral trial head can occur; therefore, a plan of action should be in place to prevent its loss or to retrieve it if prevention is ineffective. Given the modularity of various arthroplasty systems in regard to the different trial components or even the final implantable prosthetic devices, component loss is a possibility. An understanding of this complication and the appropriate steps to approaching it could aid in preventing patient morbidity. Because of this, it is imperative that surgeons who perform THA be aware of the potential complications and the measures that can be taken to address them.
Continue to: CONCLUSION
CONCLUSION
The femoral trial head often can be quickly and easily recovered; however, trial component recovery can sometimes be more complicated. Loss of the trial femoral head could potentially occur during dislocation, reduction, or any of the trial positions. An example of a more complicated recovery is when the femoral trial head is lost into the retroperitoneal space, which could occur when trialing the hip in extension to assess the anterior stability of the hip. Loss of the femoral trial head is an avoidable occurrence, and it has the potential to cause a number of complications as well as the need for additional incisions/surgery to retrieve the femoral trial head. The subsequent issues that could arise after loss occurs can not only lead to extensive surgical complications, but can also foster patient dissatisfaction regarding surgical outcomes. Therefore, consistent attempts to utilize preventative techniques are essential. As discussed, simple measures such as placement of a suture through the apical hole of the trial component and adequate communication between those involved in reduction and trialing maneuvers, can serve to avert femoral trial head loss.
1. Madsen WY, Mitchell BS, Kates SL. Successful intraoperative retrieval of dislocated femoral trial head during total hip arthroplasty. J Arthroplasty. 2012;27(5):820.e9-e11. doi:10.1016/j.arth.2011.08.006.
2. Ozkan K, Ugutmen E, Altintas F, Eren A, Mahirogullari M. Intraoperative dislocation of the prosthetic femoral head into the pelvis during total hip arthroplasty. Acta Orthop Belg. 2008;74(4):553-555.
3. Rachbauer F, Nogler M, Krismer M, Moritz M. Intraoperative migration of the trial femoral head into the pelvis during total hip arthroplasty: prevention and retrieval. J Bone Joint Surg Am. 2002;84-A(5):881-882.
4. Batouk O, Gilbart M, Jain R. Intraoperative dislocation of the trial femoral head into the pelvis during total hip arthroplasty: a case report. J Bone Joint Surg Am. 2001;83-A(10):1549-1551.
5. Srinivasan A, Jung E, Levine BR. Modularity of the femoral component in total hip arthroplasty. J Am Acad Orthop Surg. 2012;20(4):214-222. doi:10.5435/JAAOS-20-04-214.
6. Princep A. Intraoperative migration of the trial femoral head into the pelvis during total hip arthroplasty: prevention and retrieval. J Bone Joint Surg Am. 2002;84-A(5):880-881.
7. Callaghan JJ, McAndrew C, Boese CK, Forest E. Intrapelvic migration of the trial femoral head during total hip arthroplasty: is retrieval necessary? A report of four cases. Iowa Orthop J. 2006;26:60-62.
8. Kalra K, Ries MD, Bozic KJ. Intrapelvic displacement of a trial femoral head during total hip arthroplasty and a method to retrieve it. J Arthroplasty 2011;26(2):338.e21-e23. doi:10.1016/j.arth.2009.12.005.
1. Madsen WY, Mitchell BS, Kates SL. Successful intraoperative retrieval of dislocated femoral trial head during total hip arthroplasty. J Arthroplasty. 2012;27(5):820.e9-e11. doi:10.1016/j.arth.2011.08.006.
2. Ozkan K, Ugutmen E, Altintas F, Eren A, Mahirogullari M. Intraoperative dislocation of the prosthetic femoral head into the pelvis during total hip arthroplasty. Acta Orthop Belg. 2008;74(4):553-555.
3. Rachbauer F, Nogler M, Krismer M, Moritz M. Intraoperative migration of the trial femoral head into the pelvis during total hip arthroplasty: prevention and retrieval. J Bone Joint Surg Am. 2002;84-A(5):881-882.
4. Batouk O, Gilbart M, Jain R. Intraoperative dislocation of the trial femoral head into the pelvis during total hip arthroplasty: a case report. J Bone Joint Surg Am. 2001;83-A(10):1549-1551.
5. Srinivasan A, Jung E, Levine BR. Modularity of the femoral component in total hip arthroplasty. J Am Acad Orthop Surg. 2012;20(4):214-222. doi:10.5435/JAAOS-20-04-214.
6. Princep A. Intraoperative migration of the trial femoral head into the pelvis during total hip arthroplasty: prevention and retrieval. J Bone Joint Surg Am. 2002;84-A(5):880-881.
7. Callaghan JJ, McAndrew C, Boese CK, Forest E. Intrapelvic migration of the trial femoral head during total hip arthroplasty: is retrieval necessary? A report of four cases. Iowa Orthop J. 2006;26:60-62.
8. Kalra K, Ries MD, Bozic KJ. Intrapelvic displacement of a trial femoral head during total hip arthroplasty and a method to retrieve it. J Arthroplasty 2011;26(2):338.e21-e23. doi:10.1016/j.arth.2009.12.005.
TAKE-HOME POINTS
- Femoral head trial loss is a complication that can occur during THA.
- This event can be a source of avoidable morbidity.
- Preventative measures can be taken to avoid this complication.
- If preventative measures fail, retrieval of the femoral trial head can be performed.
- A thorough understanding of preventative and retrieval methods is essential for surgeons that perform THA.
VIDEO: Digital innovation, consumer point of view can solve clinical problems
BOSTON – Carla E. Small, MBA, senior director of innovation at Boston Children’s Hospital, addressed digital health care in a video interview at the AGA Tech Summit, sponsored by the AGA Center for GI Innovation and Technology. It is really just providing health care to patients in a digital world, she said, adding that she prefers the term “tech-enabled health care.” One up-and-coming example of this is the use of Alexa-type voice devices to do work and solve small clinical problems. Her program did a nationwide survey of pediatricians and found that half were interested in using voice technology. Artificial intelligence is another area of technology that Boston Children’s is using – in particular, they have created algorithms that help pediatricians analyze brain scans of young children, because so few pediatricians are trained in this area. The innovation program also has taken the digital world to pediatric patients in a program called Health Voyager in which children can take a virtual journey through their own diseased intestinal system.
BOSTON – Carla E. Small, MBA, senior director of innovation at Boston Children’s Hospital, addressed digital health care in a video interview at the AGA Tech Summit, sponsored by the AGA Center for GI Innovation and Technology. It is really just providing health care to patients in a digital world, she said, adding that she prefers the term “tech-enabled health care.” One up-and-coming example of this is the use of Alexa-type voice devices to do work and solve small clinical problems. Her program did a nationwide survey of pediatricians and found that half were interested in using voice technology. Artificial intelligence is another area of technology that Boston Children’s is using – in particular, they have created algorithms that help pediatricians analyze brain scans of young children, because so few pediatricians are trained in this area. The innovation program also has taken the digital world to pediatric patients in a program called Health Voyager in which children can take a virtual journey through their own diseased intestinal system.
BOSTON – Carla E. Small, MBA, senior director of innovation at Boston Children’s Hospital, addressed digital health care in a video interview at the AGA Tech Summit, sponsored by the AGA Center for GI Innovation and Technology. It is really just providing health care to patients in a digital world, she said, adding that she prefers the term “tech-enabled health care.” One up-and-coming example of this is the use of Alexa-type voice devices to do work and solve small clinical problems. Her program did a nationwide survey of pediatricians and found that half were interested in using voice technology. Artificial intelligence is another area of technology that Boston Children’s is using – in particular, they have created algorithms that help pediatricians analyze brain scans of young children, because so few pediatricians are trained in this area. The innovation program also has taken the digital world to pediatric patients in a program called Health Voyager in which children can take a virtual journey through their own diseased intestinal system.
FROM THE 20I8 AGA TECH SUMMIT
Thousands mistakenly enrolled during state’s Medicaid expansion, feds find
California signed up an estimated 450,000 people under Medicaid expansion who may not have been eligible for coverage, according to a report by the Health & Human Services’ chief watchdog.
In a Feb. 21 report, the HHS’s inspector general estimated that California spent $738.2 million on 366,078 expansion beneficiaries who were ineligible. It spent an additional $416.5 million for 79,055 expansion enrollees who were “potentially” ineligible, auditors found.
Auditors said nearly 90% of the $1.15 billion in questionable payments involved federal money, while the rest came from the state’s Medicaid program, known as Medi-Cal. They examined a 6-month period from Oct. 1, 2014, to March 31, 2015, when Medicaid payments of $6.2 billion were made related to 1.9 million newly eligible enrollees.
There were limitations to the California review, however. The audit extrapolated from a sample of 150 beneficiaries. The authors reported a 90% confidence level in their results – whereas 95% would be more common. That meant that the number of those ineligible could have been as low as 260,000 or as high as 630,000.
“If HHS has a strong reason to believe that California is systematically making enrollment errors, it would be helpful to show that in a more robust analysis,” said Ben Ippolito, a health care economist at the American Enterprise Institute, a conservative think tank. “The federal government should ensure that states are being good stewards of federal money.”
Nonetheless, the audit highlighted weaknesses in California’s Medicaid program, the largest in the nation with 13.4 million enrollees and an annual budget topping $100 billion, counting federal and state money. Medicaid covers one in three Californians.
The inspector general found deficiencies in the state’s computer system for verifying eligibility and discovered errors by caseworkers. The Medicaid payments cited in the report covered people in the state’s fee-for-service system, managed-care plans, drug treatment programs, and those receiving mental health services.
California’s Department of Health Care Services, which runs Medi-Cal, said in a statement that it agreed with nearly all of the auditors’ recommendations and that the agency “has taken steps to address all of the findings.”
In a written response to the inspector general, California officials said several computer upgrades were made after the audit period and before publication of the report that should improve the accuracy of eligibility decisions.
Among the 150 expansion enrollees analyzed in detail, 75%, or 112, were deemed eligible for the Medicaid program in California. Auditors discovered a variety of problems with the other 38 enrollees.
During the audit period, 12 enrollees in the sample group had incomes above 138% of the federal poverty level, making them ineligible financially for public assistance, according to the report.
In other instances, beneficiaries were already enrolled in Medicare, the federal health insurance for people 65 and older or who have severe disabilities, and did not qualify for Medi-Cal. One woman indicated she didn’t want Medi-Cal but was enrolled anyway.
In 2014, the state struggled to clear a massive backlog of Medi-Cal applications, which reached about 900,000 at one point. Many people complained about being mistakenly rejected for coverage or that their applications were lost in the state or county computer systems.
California was one of 31 states to expand Medicaid under the 2010 Affordable Care Act. The health law established a higher federal reimbursement for these newly eligible patients, primarily low-income adults without children. After expansion started in 2014, the HHS inspector general’s office began reviewing whether states were determining eligibility correctly and spending taxpayer dollars appropriately.
In a similar audit released in January, the inspector general estimated that New York spent $26.2 million in federal Medicaid money on 47,271 expansion enrollees who were ineligible for coverage. (The sample size there was 130 enrollees.) Overall, New York had far fewer expansion enrollees and related spending, compared with California.
Audits of other states’ records are planned
“It is inevitable that in a big rollout of new eligibility for any public program there are going to be glitches in implementation,” said Kathy Hempstead, a health-policy expert and senior adviser at the Robert Wood Johnson Foundation. “The inspector general wants to make sure that states are being sufficiently careful.”
Nationwide, Medicaid, the state-federal health insurance program designed for the poor, is the country’s largest health insurance program, covering 74 million Americans. In the past year, Republican efforts to reduce Medicaid funding and enrollment have sparked intense political debates and loud protests over the size and scope of the public program.
The federal government footed the entire cost of Medicaid expansion during the first three years, instead of taking the usual approach of splitting the costs with states. Now, states are picking up more of the bill. Their share of the costs will grow to 10 percent by 2020.
The California audit didn’t request a specific repayment from the state, but the findings were sent to the Centers for Medicare & Medicaid Services for review. CMS officials didn’t return a request for comment.
Donald White, a spokesman for the inspector general’s office, said the agency stood by the report’s findings and declined to comment further.
This story was produced by Kaiser Health News, which publishes California Healthline, an editorially independent service of the California Health Care Foundation. Kaiser Health News is a nonprofit news service covering health issues. It is an editorially independent program of the Kaiser Family Foundation that is not affiliated with Kaiser Permanente.
California signed up an estimated 450,000 people under Medicaid expansion who may not have been eligible for coverage, according to a report by the Health & Human Services’ chief watchdog.
In a Feb. 21 report, the HHS’s inspector general estimated that California spent $738.2 million on 366,078 expansion beneficiaries who were ineligible. It spent an additional $416.5 million for 79,055 expansion enrollees who were “potentially” ineligible, auditors found.
Auditors said nearly 90% of the $1.15 billion in questionable payments involved federal money, while the rest came from the state’s Medicaid program, known as Medi-Cal. They examined a 6-month period from Oct. 1, 2014, to March 31, 2015, when Medicaid payments of $6.2 billion were made related to 1.9 million newly eligible enrollees.
There were limitations to the California review, however. The audit extrapolated from a sample of 150 beneficiaries. The authors reported a 90% confidence level in their results – whereas 95% would be more common. That meant that the number of those ineligible could have been as low as 260,000 or as high as 630,000.
“If HHS has a strong reason to believe that California is systematically making enrollment errors, it would be helpful to show that in a more robust analysis,” said Ben Ippolito, a health care economist at the American Enterprise Institute, a conservative think tank. “The federal government should ensure that states are being good stewards of federal money.”
Nonetheless, the audit highlighted weaknesses in California’s Medicaid program, the largest in the nation with 13.4 million enrollees and an annual budget topping $100 billion, counting federal and state money. Medicaid covers one in three Californians.
The inspector general found deficiencies in the state’s computer system for verifying eligibility and discovered errors by caseworkers. The Medicaid payments cited in the report covered people in the state’s fee-for-service system, managed-care plans, drug treatment programs, and those receiving mental health services.
California’s Department of Health Care Services, which runs Medi-Cal, said in a statement that it agreed with nearly all of the auditors’ recommendations and that the agency “has taken steps to address all of the findings.”
In a written response to the inspector general, California officials said several computer upgrades were made after the audit period and before publication of the report that should improve the accuracy of eligibility decisions.
Among the 150 expansion enrollees analyzed in detail, 75%, or 112, were deemed eligible for the Medicaid program in California. Auditors discovered a variety of problems with the other 38 enrollees.
During the audit period, 12 enrollees in the sample group had incomes above 138% of the federal poverty level, making them ineligible financially for public assistance, according to the report.
In other instances, beneficiaries were already enrolled in Medicare, the federal health insurance for people 65 and older or who have severe disabilities, and did not qualify for Medi-Cal. One woman indicated she didn’t want Medi-Cal but was enrolled anyway.
In 2014, the state struggled to clear a massive backlog of Medi-Cal applications, which reached about 900,000 at one point. Many people complained about being mistakenly rejected for coverage or that their applications were lost in the state or county computer systems.
California was one of 31 states to expand Medicaid under the 2010 Affordable Care Act. The health law established a higher federal reimbursement for these newly eligible patients, primarily low-income adults without children. After expansion started in 2014, the HHS inspector general’s office began reviewing whether states were determining eligibility correctly and spending taxpayer dollars appropriately.
In a similar audit released in January, the inspector general estimated that New York spent $26.2 million in federal Medicaid money on 47,271 expansion enrollees who were ineligible for coverage. (The sample size there was 130 enrollees.) Overall, New York had far fewer expansion enrollees and related spending, compared with California.
Audits of other states’ records are planned
“It is inevitable that in a big rollout of new eligibility for any public program there are going to be glitches in implementation,” said Kathy Hempstead, a health-policy expert and senior adviser at the Robert Wood Johnson Foundation. “The inspector general wants to make sure that states are being sufficiently careful.”
Nationwide, Medicaid, the state-federal health insurance program designed for the poor, is the country’s largest health insurance program, covering 74 million Americans. In the past year, Republican efforts to reduce Medicaid funding and enrollment have sparked intense political debates and loud protests over the size and scope of the public program.
The federal government footed the entire cost of Medicaid expansion during the first three years, instead of taking the usual approach of splitting the costs with states. Now, states are picking up more of the bill. Their share of the costs will grow to 10 percent by 2020.
The California audit didn’t request a specific repayment from the state, but the findings were sent to the Centers for Medicare & Medicaid Services for review. CMS officials didn’t return a request for comment.
Donald White, a spokesman for the inspector general’s office, said the agency stood by the report’s findings and declined to comment further.
This story was produced by Kaiser Health News, which publishes California Healthline, an editorially independent service of the California Health Care Foundation. Kaiser Health News is a nonprofit news service covering health issues. It is an editorially independent program of the Kaiser Family Foundation that is not affiliated with Kaiser Permanente.
California signed up an estimated 450,000 people under Medicaid expansion who may not have been eligible for coverage, according to a report by the Health & Human Services’ chief watchdog.
In a Feb. 21 report, the HHS’s inspector general estimated that California spent $738.2 million on 366,078 expansion beneficiaries who were ineligible. It spent an additional $416.5 million for 79,055 expansion enrollees who were “potentially” ineligible, auditors found.
Auditors said nearly 90% of the $1.15 billion in questionable payments involved federal money, while the rest came from the state’s Medicaid program, known as Medi-Cal. They examined a 6-month period from Oct. 1, 2014, to March 31, 2015, when Medicaid payments of $6.2 billion were made related to 1.9 million newly eligible enrollees.
There were limitations to the California review, however. The audit extrapolated from a sample of 150 beneficiaries. The authors reported a 90% confidence level in their results – whereas 95% would be more common. That meant that the number of those ineligible could have been as low as 260,000 or as high as 630,000.
“If HHS has a strong reason to believe that California is systematically making enrollment errors, it would be helpful to show that in a more robust analysis,” said Ben Ippolito, a health care economist at the American Enterprise Institute, a conservative think tank. “The federal government should ensure that states are being good stewards of federal money.”
Nonetheless, the audit highlighted weaknesses in California’s Medicaid program, the largest in the nation with 13.4 million enrollees and an annual budget topping $100 billion, counting federal and state money. Medicaid covers one in three Californians.
The inspector general found deficiencies in the state’s computer system for verifying eligibility and discovered errors by caseworkers. The Medicaid payments cited in the report covered people in the state’s fee-for-service system, managed-care plans, drug treatment programs, and those receiving mental health services.
California’s Department of Health Care Services, which runs Medi-Cal, said in a statement that it agreed with nearly all of the auditors’ recommendations and that the agency “has taken steps to address all of the findings.”
In a written response to the inspector general, California officials said several computer upgrades were made after the audit period and before publication of the report that should improve the accuracy of eligibility decisions.
Among the 150 expansion enrollees analyzed in detail, 75%, or 112, were deemed eligible for the Medicaid program in California. Auditors discovered a variety of problems with the other 38 enrollees.
During the audit period, 12 enrollees in the sample group had incomes above 138% of the federal poverty level, making them ineligible financially for public assistance, according to the report.
In other instances, beneficiaries were already enrolled in Medicare, the federal health insurance for people 65 and older or who have severe disabilities, and did not qualify for Medi-Cal. One woman indicated she didn’t want Medi-Cal but was enrolled anyway.
In 2014, the state struggled to clear a massive backlog of Medi-Cal applications, which reached about 900,000 at one point. Many people complained about being mistakenly rejected for coverage or that their applications were lost in the state or county computer systems.
California was one of 31 states to expand Medicaid under the 2010 Affordable Care Act. The health law established a higher federal reimbursement for these newly eligible patients, primarily low-income adults without children. After expansion started in 2014, the HHS inspector general’s office began reviewing whether states were determining eligibility correctly and spending taxpayer dollars appropriately.
In a similar audit released in January, the inspector general estimated that New York spent $26.2 million in federal Medicaid money on 47,271 expansion enrollees who were ineligible for coverage. (The sample size there was 130 enrollees.) Overall, New York had far fewer expansion enrollees and related spending, compared with California.
Audits of other states’ records are planned
“It is inevitable that in a big rollout of new eligibility for any public program there are going to be glitches in implementation,” said Kathy Hempstead, a health-policy expert and senior adviser at the Robert Wood Johnson Foundation. “The inspector general wants to make sure that states are being sufficiently careful.”
Nationwide, Medicaid, the state-federal health insurance program designed for the poor, is the country’s largest health insurance program, covering 74 million Americans. In the past year, Republican efforts to reduce Medicaid funding and enrollment have sparked intense political debates and loud protests over the size and scope of the public program.
The federal government footed the entire cost of Medicaid expansion during the first three years, instead of taking the usual approach of splitting the costs with states. Now, states are picking up more of the bill. Their share of the costs will grow to 10 percent by 2020.
The California audit didn’t request a specific repayment from the state, but the findings were sent to the Centers for Medicare & Medicaid Services for review. CMS officials didn’t return a request for comment.
Donald White, a spokesman for the inspector general’s office, said the agency stood by the report’s findings and declined to comment further.
This story was produced by Kaiser Health News, which publishes California Healthline, an editorially independent service of the California Health Care Foundation. Kaiser Health News is a nonprofit news service covering health issues. It is an editorially independent program of the Kaiser Family Foundation that is not affiliated with Kaiser Permanente.
VIDEO: In 2018, the AGA Center for GI Innovation and Technology is going strong
BOSTON – The AGA Center for GI Innovation and Technology (CGIT) was founded 9 years ago to foster innovation in GI disease, according to Sri Komanduri, MD, AGAF, and V. Raman Muthusamy, MD, the current cochairs. The mandate is still the same, with the idea that CGIT will continue to provide support and resources to a wide variety of stakeholders throughout the daunting process of getting a new technology or product through funding and approval to reimbursement and adoption. Dr. Komanduri, the medical director of the GI laboratory and director of interventional endoscopy at Northwestern University in Chicago, emphasized the need to support the entire process from idea to adoption as a continuum that should not be handled by different silos – CGIT should be there every step of the way.
CGIT will concentrate on six main areas now, although Dr. Muthusamy, director of interventional endoscopy and general GI endoscopy at the University of California, Los Angeles, said in a video interview that they are flexible enough to work with any GI-applicable technology that will help practicing clinicians. These six areas are endoscopy for bariatric treatments, endoscopy for resection in place of surgery, endoscope reprocessing, interventional endoscopy, endoscopic reflux technology, and endoscopic diagnostic colorectal advances.
BOSTON – The AGA Center for GI Innovation and Technology (CGIT) was founded 9 years ago to foster innovation in GI disease, according to Sri Komanduri, MD, AGAF, and V. Raman Muthusamy, MD, the current cochairs. The mandate is still the same, with the idea that CGIT will continue to provide support and resources to a wide variety of stakeholders throughout the daunting process of getting a new technology or product through funding and approval to reimbursement and adoption. Dr. Komanduri, the medical director of the GI laboratory and director of interventional endoscopy at Northwestern University in Chicago, emphasized the need to support the entire process from idea to adoption as a continuum that should not be handled by different silos – CGIT should be there every step of the way.
CGIT will concentrate on six main areas now, although Dr. Muthusamy, director of interventional endoscopy and general GI endoscopy at the University of California, Los Angeles, said in a video interview that they are flexible enough to work with any GI-applicable technology that will help practicing clinicians. These six areas are endoscopy for bariatric treatments, endoscopy for resection in place of surgery, endoscope reprocessing, interventional endoscopy, endoscopic reflux technology, and endoscopic diagnostic colorectal advances.
BOSTON – The AGA Center for GI Innovation and Technology (CGIT) was founded 9 years ago to foster innovation in GI disease, according to Sri Komanduri, MD, AGAF, and V. Raman Muthusamy, MD, the current cochairs. The mandate is still the same, with the idea that CGIT will continue to provide support and resources to a wide variety of stakeholders throughout the daunting process of getting a new technology or product through funding and approval to reimbursement and adoption. Dr. Komanduri, the medical director of the GI laboratory and director of interventional endoscopy at Northwestern University in Chicago, emphasized the need to support the entire process from idea to adoption as a continuum that should not be handled by different silos – CGIT should be there every step of the way.
CGIT will concentrate on six main areas now, although Dr. Muthusamy, director of interventional endoscopy and general GI endoscopy at the University of California, Los Angeles, said in a video interview that they are flexible enough to work with any GI-applicable technology that will help practicing clinicians. These six areas are endoscopy for bariatric treatments, endoscopy for resection in place of surgery, endoscope reprocessing, interventional endoscopy, endoscopic reflux technology, and endoscopic diagnostic colorectal advances.
FROM THE 2018 AGA TECH SUMMIT
VIDEO: It’s all about improving the patient experience
BOSTON – “When I assess a new technology,” said V. Raman Muthusamy, MD, chair of the AGA Center for GI Innovation and Technology (CGIT), “I look for three things” – it should allow us to do something we couldn’t do before, give better outcomes and/or do the procedure less invasively, or provide cost savings. Ideally, he said during an interview at the AGA Tech Summit, it should do all three. Dr. Muthusamy, director of interventional endoscopy and general GI endoscopy at the University of California, Los Angeles, said one of the goals of the CGIT is to keep physicians up to date on new technologies, but he recommends all physicians assess the data on new technologies and weigh the advantages before incorporating a new device into their practice. Better diagnostic tools and novel therapeutics should improve the patient experience.
BOSTON – “When I assess a new technology,” said V. Raman Muthusamy, MD, chair of the AGA Center for GI Innovation and Technology (CGIT), “I look for three things” – it should allow us to do something we couldn’t do before, give better outcomes and/or do the procedure less invasively, or provide cost savings. Ideally, he said during an interview at the AGA Tech Summit, it should do all three. Dr. Muthusamy, director of interventional endoscopy and general GI endoscopy at the University of California, Los Angeles, said one of the goals of the CGIT is to keep physicians up to date on new technologies, but he recommends all physicians assess the data on new technologies and weigh the advantages before incorporating a new device into their practice. Better diagnostic tools and novel therapeutics should improve the patient experience.
BOSTON – “When I assess a new technology,” said V. Raman Muthusamy, MD, chair of the AGA Center for GI Innovation and Technology (CGIT), “I look for three things” – it should allow us to do something we couldn’t do before, give better outcomes and/or do the procedure less invasively, or provide cost savings. Ideally, he said during an interview at the AGA Tech Summit, it should do all three. Dr. Muthusamy, director of interventional endoscopy and general GI endoscopy at the University of California, Los Angeles, said one of the goals of the CGIT is to keep physicians up to date on new technologies, but he recommends all physicians assess the data on new technologies and weigh the advantages before incorporating a new device into their practice. Better diagnostic tools and novel therapeutics should improve the patient experience.
FROM THE 2018 AGA TECH SUMMIT
Irritability, depressive mood tied to higher suicidality risk in adolescence
Children who are particularly irritable, depressive, and anxious might be at greater risk of suicidality in adolescence, according to a population-based cohort study.
Researchers enrolled 1,430 participants from the Québec Longitudinal Study of Child Development, aged 6-12 years, and performed yearly or biyearly assessments over a follow-up of 5 months to 17 years, according to a study published online March 28 in JAMA Psychiatry (doi: 10.1001/jamapsychiatry.2018.0174).
They found that girls who rated highly for irritability and for the depressive/anxious mood profile on the Behavior Questionnaire, a measure created for Canada’s National Longitudinal Study of Children and Youth, had a threefold higher risk of suicidality (odds ratio, 3.07; 95% confidence interval, 1.54-6.12). Meanwhile, boys had a twofold higher risk (OR, 2.13; 95% CI, 0.95-4.78), compared with children with low irritability and depressive/anxious mood.
“Exploratory analyses by sex indicated that this association was more important for girls than boys, as indicated by the need to prevent the exposure among 5 girls to avoid 1 case of suicidality,” wrote Massimiliano Orri, PhD, and his associates.
The rates of suicidality in children with high irritability and high depressive/anxious mood were 16.4%, compared with 11% in the group with the lowest symptom levels.
Even in children with only moderate irritability and low depressive/anxious mood, a significant increase was found in the odds of showing suicidality, compared with the reference group (OR, 1.51; 95% CI, 1.02-2.25).
“Although previous studies reported associations between irritability during childhood and adolescence and later depression, anxiety, and suicidality, we found that even moderate levels of irritability may contribute to suicidal risk,” wrote Dr. Orri of Bordeaux Population Health Research Centre, at the Institut National de la Santé et de la Recherche Medicale in France. “Such results indicate that .”
Children with a high depressive/anxious mood profile showed the same odds of suicidality as those of the reference group.
The authors noted that there was considerably stability in developmental profiles, so children who showed the highest levels of symptoms at age 6 were likely to exhibit those same high levels at age 12.
They also commented on their study’s use of an “innovative, person-centered approach” to describe the joint course of these moods over the time course of the study.
The investigators cited several limitations. One is that the assessment of childhood symptoms were based on teachers only, so depressive/anxious mood might have been underrated compared with irritability “because internalizing symptoms may be more difficult to observe in a school setting than externalized symptoms.”
Dr. Orri and two associates reported receiving support from the Canadian Institutes of Health Research. The other researchers cited funding from the National Alliance for Research on Schizophrenia and Depression and the Fonds de Recherche du Québec. No other financial disclosures were reported. The Québec Longitudinal Study of Child Development was supported by several entities, including the Québec Government’s Ministry of Health, Ministry of Education, and Ministry of Family Affairs.
SOURCE: Orri M et al. JAMA Psychiatry. 2018 Mar 28. doi: 10.1001/jamapsychiatry.2018.0174.
Children who are particularly irritable, depressive, and anxious might be at greater risk of suicidality in adolescence, according to a population-based cohort study.
Researchers enrolled 1,430 participants from the Québec Longitudinal Study of Child Development, aged 6-12 years, and performed yearly or biyearly assessments over a follow-up of 5 months to 17 years, according to a study published online March 28 in JAMA Psychiatry (doi: 10.1001/jamapsychiatry.2018.0174).
They found that girls who rated highly for irritability and for the depressive/anxious mood profile on the Behavior Questionnaire, a measure created for Canada’s National Longitudinal Study of Children and Youth, had a threefold higher risk of suicidality (odds ratio, 3.07; 95% confidence interval, 1.54-6.12). Meanwhile, boys had a twofold higher risk (OR, 2.13; 95% CI, 0.95-4.78), compared with children with low irritability and depressive/anxious mood.
“Exploratory analyses by sex indicated that this association was more important for girls than boys, as indicated by the need to prevent the exposure among 5 girls to avoid 1 case of suicidality,” wrote Massimiliano Orri, PhD, and his associates.
The rates of suicidality in children with high irritability and high depressive/anxious mood were 16.4%, compared with 11% in the group with the lowest symptom levels.
Even in children with only moderate irritability and low depressive/anxious mood, a significant increase was found in the odds of showing suicidality, compared with the reference group (OR, 1.51; 95% CI, 1.02-2.25).
“Although previous studies reported associations between irritability during childhood and adolescence and later depression, anxiety, and suicidality, we found that even moderate levels of irritability may contribute to suicidal risk,” wrote Dr. Orri of Bordeaux Population Health Research Centre, at the Institut National de la Santé et de la Recherche Medicale in France. “Such results indicate that .”
Children with a high depressive/anxious mood profile showed the same odds of suicidality as those of the reference group.
The authors noted that there was considerably stability in developmental profiles, so children who showed the highest levels of symptoms at age 6 were likely to exhibit those same high levels at age 12.
They also commented on their study’s use of an “innovative, person-centered approach” to describe the joint course of these moods over the time course of the study.
The investigators cited several limitations. One is that the assessment of childhood symptoms were based on teachers only, so depressive/anxious mood might have been underrated compared with irritability “because internalizing symptoms may be more difficult to observe in a school setting than externalized symptoms.”
Dr. Orri and two associates reported receiving support from the Canadian Institutes of Health Research. The other researchers cited funding from the National Alliance for Research on Schizophrenia and Depression and the Fonds de Recherche du Québec. No other financial disclosures were reported. The Québec Longitudinal Study of Child Development was supported by several entities, including the Québec Government’s Ministry of Health, Ministry of Education, and Ministry of Family Affairs.
SOURCE: Orri M et al. JAMA Psychiatry. 2018 Mar 28. doi: 10.1001/jamapsychiatry.2018.0174.
Children who are particularly irritable, depressive, and anxious might be at greater risk of suicidality in adolescence, according to a population-based cohort study.
Researchers enrolled 1,430 participants from the Québec Longitudinal Study of Child Development, aged 6-12 years, and performed yearly or biyearly assessments over a follow-up of 5 months to 17 years, according to a study published online March 28 in JAMA Psychiatry (doi: 10.1001/jamapsychiatry.2018.0174).
They found that girls who rated highly for irritability and for the depressive/anxious mood profile on the Behavior Questionnaire, a measure created for Canada’s National Longitudinal Study of Children and Youth, had a threefold higher risk of suicidality (odds ratio, 3.07; 95% confidence interval, 1.54-6.12). Meanwhile, boys had a twofold higher risk (OR, 2.13; 95% CI, 0.95-4.78), compared with children with low irritability and depressive/anxious mood.
“Exploratory analyses by sex indicated that this association was more important for girls than boys, as indicated by the need to prevent the exposure among 5 girls to avoid 1 case of suicidality,” wrote Massimiliano Orri, PhD, and his associates.
The rates of suicidality in children with high irritability and high depressive/anxious mood were 16.4%, compared with 11% in the group with the lowest symptom levels.
Even in children with only moderate irritability and low depressive/anxious mood, a significant increase was found in the odds of showing suicidality, compared with the reference group (OR, 1.51; 95% CI, 1.02-2.25).
“Although previous studies reported associations between irritability during childhood and adolescence and later depression, anxiety, and suicidality, we found that even moderate levels of irritability may contribute to suicidal risk,” wrote Dr. Orri of Bordeaux Population Health Research Centre, at the Institut National de la Santé et de la Recherche Medicale in France. “Such results indicate that .”
Children with a high depressive/anxious mood profile showed the same odds of suicidality as those of the reference group.
The authors noted that there was considerably stability in developmental profiles, so children who showed the highest levels of symptoms at age 6 were likely to exhibit those same high levels at age 12.
They also commented on their study’s use of an “innovative, person-centered approach” to describe the joint course of these moods over the time course of the study.
The investigators cited several limitations. One is that the assessment of childhood symptoms were based on teachers only, so depressive/anxious mood might have been underrated compared with irritability “because internalizing symptoms may be more difficult to observe in a school setting than externalized symptoms.”
Dr. Orri and two associates reported receiving support from the Canadian Institutes of Health Research. The other researchers cited funding from the National Alliance for Research on Schizophrenia and Depression and the Fonds de Recherche du Québec. No other financial disclosures were reported. The Québec Longitudinal Study of Child Development was supported by several entities, including the Québec Government’s Ministry of Health, Ministry of Education, and Ministry of Family Affairs.
SOURCE: Orri M et al. JAMA Psychiatry. 2018 Mar 28. doi: 10.1001/jamapsychiatry.2018.0174.
FROM JAMA PSYCHIATRY
Key clinical point: Irritability in children may predict suicidality in adolescence.
Major finding: Girls with high irritability and depressive/anxious mood profile had a threefold higher risk of suicidality in adolescence.
Study details: A population-based cohort study involving 1,430 participants.
Disclosures: Dr. Orri and two associates reported receiving support from the Canadian Institutes of Health Research. The other researchers cited funding from the National Alliance for Research on Schizophrenia and Depression and the Fonds de Recherche du Québec. No other financial disclosures were reported. The Québec Longitudinal Study of Child Development was supported by several entities, including the Québec Government’s Ministry of Health, Ministry of Education, and Ministry of Family Affairs.
Source: Orri M et al. JAMA Psychiatry. 2018 Mar 28. doi: 10.1001/jamapsychiatry.2018.0174.
Brigadier General Carl Rogers Darnall: Saving Lives on a Massive Scale
The Carl R. Darnall Army Medical Center at Fort Hood, Texas, is named in honor of Brigadier General Carl Rogers Darnall, a Texas native and career Army physician whose active-duty service spanned 35 years. Darnall, the oldest of 7 siblings, could not have imagined the enormity of the contributions that he would make and the lives that would be saved as he pursued a career in medicine.
Born on the family farm north of Dallas on Christmas Day in 1867, Darnall attended college in nearby Bonham and graduated from Transylvania University in Kentucky. He attended Jefferson Medical College in Philadelphia, Pennsylvania, graduating in 1890. Darnall spent several years in private practice before he joined the Army Medical Corps in 1896. He completed the Army Medical School in 1897. Opened in 1893, the Army Medical School was a 4-to-6-month course for civilian physicians entering active duty. The courses introduced physicians to the duties of medical officers as well as military surgery, medicine, and hygiene. It is considered by many to be the first school of public health in the U.S.
Darnall’s first assignments in Texas were followed by deployment to Cuba during the Spanish American War and then the Philippines, where he served as an operating surgeon and pathologist aboard the hospital ship, USS Relief. Darnall later accompanied an international expeditionary force to China in response to the Boxer Rebellion. In 1902, Darnall received an assignment to the Army Medical School in Washington, DC, that would change his life and the lives of millions around the world. Detailed as instructor for sanitary chemistry and operative surgery, he also served as secretary of the faculty. Just as Major Walter Reed and others before him, Darnall used his position at the Army Medical School to pursue important clinical research.
The complete story of the purification of drinking water is beyond the scope of this short biography. In brief, as early as 1894 the addition of chlorine to water was shown to render it “germ free.” In the 1890s, there were at least 2 attempts at water purification on a large scale with chlorine in European cities. One of the first uses of chlorine in the U.S. occurred in 1908 in Jersey City, New Jersey. At the Army Medical School, Darnall discovered the value of using compressed liquefied chlorine gas to purify water. He invented a mechanical liquid chlorine purifier in 1910 that became known as a chlorinator. In November 1911, Major Darnall authored a 15-page article concerning water purification.1 Darnall also devised and patented a water filter, which the U.S. Army used for many years.
The principles of his chlorinator and use of anhydrous liquid chlorine were later applied to municipal water supplies throughout the world. The positive benefit of clean drinking water to improving public health is beyond measure. It has been said that more lives have been saved and more sickness prevented by Darnall’s contribution to sanitary water than by any other single achievement in medicine.
During World War I, Darnall was promoted to colonel and assigned to the Finance and Supply Division in the Office of the Surgeon General. After the war, he served as department surgeon in Hawaii. In 1925, he returned to the Office of the Surgeon General as executive officer. In November 1929, he was promoted to brigadier general and became the commanding general of the Army Medical Center and Walter Reed General Hospital, a position he held for 2 years until his retirement in 1931.Darnall died on January 18, 1941, at Walter Reed General Hospital just 6 days after his wife of 48 years had died at their home in Washington, DC. He is buried in Section 3 at Arlington National Cemetery. His 3 sons, Joseph Rogers, William Major, and Carl Robert, all served in some capacity in the Army.
Darnall Army Community Hospital opened in 1965, replacing the World War II-era hospital at Fort Hood. In 1984 a 5-year reconstruction project with additional floor space was completed. On May 1, 2006, the hospital was officially renamed the Carl R. Darnall Army Medical Center.
About this column
This column provides biographical sketches of the namesakes of military and VA health care facilities. To learn more about the individual your facility was named for or to offer a topic suggestion, contact us at [email protected] or on Facebook.
1. Darnall CR. The purification of water by anhydrous chlorine. J Am Public Health Assoc. 1911;1(11):783-797.
The Carl R. Darnall Army Medical Center at Fort Hood, Texas, is named in honor of Brigadier General Carl Rogers Darnall, a Texas native and career Army physician whose active-duty service spanned 35 years. Darnall, the oldest of 7 siblings, could not have imagined the enormity of the contributions that he would make and the lives that would be saved as he pursued a career in medicine.
Born on the family farm north of Dallas on Christmas Day in 1867, Darnall attended college in nearby Bonham and graduated from Transylvania University in Kentucky. He attended Jefferson Medical College in Philadelphia, Pennsylvania, graduating in 1890. Darnall spent several years in private practice before he joined the Army Medical Corps in 1896. He completed the Army Medical School in 1897. Opened in 1893, the Army Medical School was a 4-to-6-month course for civilian physicians entering active duty. The courses introduced physicians to the duties of medical officers as well as military surgery, medicine, and hygiene. It is considered by many to be the first school of public health in the U.S.
Darnall’s first assignments in Texas were followed by deployment to Cuba during the Spanish American War and then the Philippines, where he served as an operating surgeon and pathologist aboard the hospital ship, USS Relief. Darnall later accompanied an international expeditionary force to China in response to the Boxer Rebellion. In 1902, Darnall received an assignment to the Army Medical School in Washington, DC, that would change his life and the lives of millions around the world. Detailed as instructor for sanitary chemistry and operative surgery, he also served as secretary of the faculty. Just as Major Walter Reed and others before him, Darnall used his position at the Army Medical School to pursue important clinical research.
The complete story of the purification of drinking water is beyond the scope of this short biography. In brief, as early as 1894 the addition of chlorine to water was shown to render it “germ free.” In the 1890s, there were at least 2 attempts at water purification on a large scale with chlorine in European cities. One of the first uses of chlorine in the U.S. occurred in 1908 in Jersey City, New Jersey. At the Army Medical School, Darnall discovered the value of using compressed liquefied chlorine gas to purify water. He invented a mechanical liquid chlorine purifier in 1910 that became known as a chlorinator. In November 1911, Major Darnall authored a 15-page article concerning water purification.1 Darnall also devised and patented a water filter, which the U.S. Army used for many years.
The principles of his chlorinator and use of anhydrous liquid chlorine were later applied to municipal water supplies throughout the world. The positive benefit of clean drinking water to improving public health is beyond measure. It has been said that more lives have been saved and more sickness prevented by Darnall’s contribution to sanitary water than by any other single achievement in medicine.
During World War I, Darnall was promoted to colonel and assigned to the Finance and Supply Division in the Office of the Surgeon General. After the war, he served as department surgeon in Hawaii. In 1925, he returned to the Office of the Surgeon General as executive officer. In November 1929, he was promoted to brigadier general and became the commanding general of the Army Medical Center and Walter Reed General Hospital, a position he held for 2 years until his retirement in 1931.Darnall died on January 18, 1941, at Walter Reed General Hospital just 6 days after his wife of 48 years had died at their home in Washington, DC. He is buried in Section 3 at Arlington National Cemetery. His 3 sons, Joseph Rogers, William Major, and Carl Robert, all served in some capacity in the Army.
Darnall Army Community Hospital opened in 1965, replacing the World War II-era hospital at Fort Hood. In 1984 a 5-year reconstruction project with additional floor space was completed. On May 1, 2006, the hospital was officially renamed the Carl R. Darnall Army Medical Center.
About this column
This column provides biographical sketches of the namesakes of military and VA health care facilities. To learn more about the individual your facility was named for or to offer a topic suggestion, contact us at [email protected] or on Facebook.
The Carl R. Darnall Army Medical Center at Fort Hood, Texas, is named in honor of Brigadier General Carl Rogers Darnall, a Texas native and career Army physician whose active-duty service spanned 35 years. Darnall, the oldest of 7 siblings, could not have imagined the enormity of the contributions that he would make and the lives that would be saved as he pursued a career in medicine.
Born on the family farm north of Dallas on Christmas Day in 1867, Darnall attended college in nearby Bonham and graduated from Transylvania University in Kentucky. He attended Jefferson Medical College in Philadelphia, Pennsylvania, graduating in 1890. Darnall spent several years in private practice before he joined the Army Medical Corps in 1896. He completed the Army Medical School in 1897. Opened in 1893, the Army Medical School was a 4-to-6-month course for civilian physicians entering active duty. The courses introduced physicians to the duties of medical officers as well as military surgery, medicine, and hygiene. It is considered by many to be the first school of public health in the U.S.
Darnall’s first assignments in Texas were followed by deployment to Cuba during the Spanish American War and then the Philippines, where he served as an operating surgeon and pathologist aboard the hospital ship, USS Relief. Darnall later accompanied an international expeditionary force to China in response to the Boxer Rebellion. In 1902, Darnall received an assignment to the Army Medical School in Washington, DC, that would change his life and the lives of millions around the world. Detailed as instructor for sanitary chemistry and operative surgery, he also served as secretary of the faculty. Just as Major Walter Reed and others before him, Darnall used his position at the Army Medical School to pursue important clinical research.
The complete story of the purification of drinking water is beyond the scope of this short biography. In brief, as early as 1894 the addition of chlorine to water was shown to render it “germ free.” In the 1890s, there were at least 2 attempts at water purification on a large scale with chlorine in European cities. One of the first uses of chlorine in the U.S. occurred in 1908 in Jersey City, New Jersey. At the Army Medical School, Darnall discovered the value of using compressed liquefied chlorine gas to purify water. He invented a mechanical liquid chlorine purifier in 1910 that became known as a chlorinator. In November 1911, Major Darnall authored a 15-page article concerning water purification.1 Darnall also devised and patented a water filter, which the U.S. Army used for many years.
The principles of his chlorinator and use of anhydrous liquid chlorine were later applied to municipal water supplies throughout the world. The positive benefit of clean drinking water to improving public health is beyond measure. It has been said that more lives have been saved and more sickness prevented by Darnall’s contribution to sanitary water than by any other single achievement in medicine.
During World War I, Darnall was promoted to colonel and assigned to the Finance and Supply Division in the Office of the Surgeon General. After the war, he served as department surgeon in Hawaii. In 1925, he returned to the Office of the Surgeon General as executive officer. In November 1929, he was promoted to brigadier general and became the commanding general of the Army Medical Center and Walter Reed General Hospital, a position he held for 2 years until his retirement in 1931.Darnall died on January 18, 1941, at Walter Reed General Hospital just 6 days after his wife of 48 years had died at their home in Washington, DC. He is buried in Section 3 at Arlington National Cemetery. His 3 sons, Joseph Rogers, William Major, and Carl Robert, all served in some capacity in the Army.
Darnall Army Community Hospital opened in 1965, replacing the World War II-era hospital at Fort Hood. In 1984 a 5-year reconstruction project with additional floor space was completed. On May 1, 2006, the hospital was officially renamed the Carl R. Darnall Army Medical Center.
About this column
This column provides biographical sketches of the namesakes of military and VA health care facilities. To learn more about the individual your facility was named for or to offer a topic suggestion, contact us at [email protected] or on Facebook.
1. Darnall CR. The purification of water by anhydrous chlorine. J Am Public Health Assoc. 1911;1(11):783-797.
1. Darnall CR. The purification of water by anhydrous chlorine. J Am Public Health Assoc. 1911;1(11):783-797.
