MAGNIFY in relapsed/refractory mantle cell lymphoma

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MAGNIFY is a phase IIIB randomized trial actively recruiting patients with relapsed/refractory mantle cell lymphoma, based on studies posted at ClinicalTrials.gov.

MAGNIFY (NCT01996865) is a study of lenalidomide (CC-5013) plus rituximab maintenance therapy, followed by lenalidomide single-agent maintenance therapy, versus rituximab. Sponsored by Celgene, the maker of lenalidomide (Revlimid), the trial’s primary outcome measure is progression-free survival at up to 8 years.

The MAGNIFY trial includes patients with grades 1-3b or transformed follicular lymphoma, marginal zone lymphoma, or mantle cell lymphoma who had received at least one prior therapy and had stage I-IV measurable disease. About 500 patients are planned to enroll in 12 cycles of R2 induction, and slightly more than 300 patients are projected to be randomized after induction to the two maintenance arms. Induction includes oral lenalidomide 20 mg/day, days 1-21 per 28-day cycle; plus intravenous rituximab 375 mg/m2 on days 1, 8, 15, and 22 of cycle 1 and day 1 of cycles 3, 5, 7, 9, and 11 (28-day cycles).

Patients will then be randomized to maintenance lenalidomide 10 mg/day, given on days 1-21 per 28-day cycle for cycles 13-30; plus rituximab 375 mg/m2, given on day 1 of cycles 13, 15, 17, 19, 21, 23, 25, 27, and 29 (R2, Arm A), or rituximab alone (same schedule, Arm B). Patients receiving R2 maintenance after 18 cycles may continue maintenance lenalidomide monotherapy at 10 mg/day, days 1-21 per 28-day cycle, at the discretion of the patient and/or investigator, until disease progression as tolerated.

The primary endpoint is progression-free survival. Secondary endpoints include safety, overall survival, response rates, duration of response, and quality of life. Patients will be followed for at least 5 years after the last patient-initiated induction therapy. Enrollment in MAGNIFY began in March 2014; as of January 2016, 133 patients are enrolled, according to the study page at ClinicalTrials.gov.
 

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MAGNIFY is a phase IIIB randomized trial actively recruiting patients with relapsed/refractory mantle cell lymphoma, based on studies posted at ClinicalTrials.gov.

MAGNIFY (NCT01996865) is a study of lenalidomide (CC-5013) plus rituximab maintenance therapy, followed by lenalidomide single-agent maintenance therapy, versus rituximab. Sponsored by Celgene, the maker of lenalidomide (Revlimid), the trial’s primary outcome measure is progression-free survival at up to 8 years.

The MAGNIFY trial includes patients with grades 1-3b or transformed follicular lymphoma, marginal zone lymphoma, or mantle cell lymphoma who had received at least one prior therapy and had stage I-IV measurable disease. About 500 patients are planned to enroll in 12 cycles of R2 induction, and slightly more than 300 patients are projected to be randomized after induction to the two maintenance arms. Induction includes oral lenalidomide 20 mg/day, days 1-21 per 28-day cycle; plus intravenous rituximab 375 mg/m2 on days 1, 8, 15, and 22 of cycle 1 and day 1 of cycles 3, 5, 7, 9, and 11 (28-day cycles).

Patients will then be randomized to maintenance lenalidomide 10 mg/day, given on days 1-21 per 28-day cycle for cycles 13-30; plus rituximab 375 mg/m2, given on day 1 of cycles 13, 15, 17, 19, 21, 23, 25, 27, and 29 (R2, Arm A), or rituximab alone (same schedule, Arm B). Patients receiving R2 maintenance after 18 cycles may continue maintenance lenalidomide monotherapy at 10 mg/day, days 1-21 per 28-day cycle, at the discretion of the patient and/or investigator, until disease progression as tolerated.

The primary endpoint is progression-free survival. Secondary endpoints include safety, overall survival, response rates, duration of response, and quality of life. Patients will be followed for at least 5 years after the last patient-initiated induction therapy. Enrollment in MAGNIFY began in March 2014; as of January 2016, 133 patients are enrolled, according to the study page at ClinicalTrials.gov.
 

 

MAGNIFY is a phase IIIB randomized trial actively recruiting patients with relapsed/refractory mantle cell lymphoma, based on studies posted at ClinicalTrials.gov.

MAGNIFY (NCT01996865) is a study of lenalidomide (CC-5013) plus rituximab maintenance therapy, followed by lenalidomide single-agent maintenance therapy, versus rituximab. Sponsored by Celgene, the maker of lenalidomide (Revlimid), the trial’s primary outcome measure is progression-free survival at up to 8 years.

The MAGNIFY trial includes patients with grades 1-3b or transformed follicular lymphoma, marginal zone lymphoma, or mantle cell lymphoma who had received at least one prior therapy and had stage I-IV measurable disease. About 500 patients are planned to enroll in 12 cycles of R2 induction, and slightly more than 300 patients are projected to be randomized after induction to the two maintenance arms. Induction includes oral lenalidomide 20 mg/day, days 1-21 per 28-day cycle; plus intravenous rituximab 375 mg/m2 on days 1, 8, 15, and 22 of cycle 1 and day 1 of cycles 3, 5, 7, 9, and 11 (28-day cycles).

Patients will then be randomized to maintenance lenalidomide 10 mg/day, given on days 1-21 per 28-day cycle for cycles 13-30; plus rituximab 375 mg/m2, given on day 1 of cycles 13, 15, 17, 19, 21, 23, 25, 27, and 29 (R2, Arm A), or rituximab alone (same schedule, Arm B). Patients receiving R2 maintenance after 18 cycles may continue maintenance lenalidomide monotherapy at 10 mg/day, days 1-21 per 28-day cycle, at the discretion of the patient and/or investigator, until disease progression as tolerated.

The primary endpoint is progression-free survival. Secondary endpoints include safety, overall survival, response rates, duration of response, and quality of life. Patients will be followed for at least 5 years after the last patient-initiated induction therapy. Enrollment in MAGNIFY began in March 2014; as of January 2016, 133 patients are enrolled, according to the study page at ClinicalTrials.gov.
 

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Neoadjuvant chemoradiation may give transplant the edge over resection in biliary cancer

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Wed, 05/26/2021 - 13:52

 

– Survival for patients with hilar cholangiocarcinoma was similar between those who underwent transplantation and those who underwent resection, but neoadjuvant therapy may give transplant strategy the edge, findings of a study and meta-analysis suggest.

Comstock/Thinkstock
None of the resection patients in the meta-analysis received neoadjuvant therapy; all of the participants in two of the orthotopic liver transplantation studies, however, started with neoadjuvant chemoradiation. These patients experienced 59% and 82% 5-year survival rates, the longest reported among the nine studies in the meta-analysis.

“We found survival in the group that received neoadjuvant chemoradiation therapy and transplant had a statistically significantly better outcome compared to a control group of resection,” Dr. Gage said. More importantly, patients who received a transplant without neoadjuvant therapy had a statistically significant worse outcome than patients who got resection alone.”

The investigators noted that patient selection for neoadjuvant therapy might also be a factor contributing to superior overall survival. In a multicenter study of 147 patients undergoing liver transplantation for hilar cholangiocarcinoma, a subgroup of patients who met the selection criteria of the Mayo Clinic protocol but had not undergone neoadjuvant therapy had a 59% 5-year survival rate (PLoS One. 2016:11:e0156127).

Study discussant Maria B. Majella Doyle, MD, a general surgeon at Washington University in St. Louis, agreed that patient selection for transplantation is a likely factor.

Dr. Doyle then asked Dr. Gage how she accounts for the heterogeneity among studies performed over a 20-year period.

“That is why we did subgroup analysis of neoadjuvant versus no neoadjuvant therapy,” Dr. Gage replied.

In the future, an intent-to-treat analysis might be more accurate, Dr. Majella Doyle said, because more patients are placed on a liver transplant list than typically have the procedure.

Dr. Gage noted that 28%-48% of patients started on neoadjuvant therapy in the two studies that offered both neoadjuvant therapy and a transplant in the meta-analysis never made it to transplantation. When they were included, overall survival dropped to approximately 35% in one study and 44% in the other.

In the primary meta-analysis (before the subanalysis looking at neoadjuvant therapy), 398 patients underwent resection and another 200 underwent liver transplantation between 1996 and 2106. Patient demographics were similar between groups, including more men than women, except the average age in the resection group was older, Dr. Gage said.

Overall survival favored the transplant group at each time point: 78% versus 70% with resection at 1 year; 56% versus 42% at 3 years; and 46% versus 29% at 5 years. The odds ratios, respectively, were 1.27, 1.49 and 1.83, but the findings were not statistically significant at a 95% confidence interval.

Margin involvement was 9% in the transplant patients versus 32% in the resection patients, Dr. Gage said. The best chance of cure is R0 resection, but half of patients with hilar cholangiocarcinoma, the most common cancer of the biliary tract, are unresectable, she added.

Six of the nine studies in the meta-analysis reported margin status. Of the 344 patients in these studies, 79% achieved R0 status overall.

“The goal of treatment is R0 resection,” Dr. Gage said in response to a question about when neoadjuvant therapy is warranted. “In the patients who are resectable, I think the correct answer would be to proceed with resection. However, for those patients who are borderline resectable, it would be reasonable to consider neoadjuvant therapy.”

“One of the major things that is undervalued is neoadjuvant therapy allows better patient selection,” said session moderator Eric Jensen, MD, FACS, of University of Minnesota Health in Minneapolis. “When you say an obviously resectable tumor, when you look at the data – we’re wrong 30% of the time. So I’m in favor of neoadjuvant therapy for everybody, but that is just my bias.”

The small number of studies is a limitation of the study, Dr. Gage said. Also, all the studies were nonrandomized and retrospective, and some research spanned many years, which could introduce bias because of changes in practice over time, she added.

Based on their findings, the investigators proposed that future studies explore routine administration of neoadjuvant therapy prior to resection.

Dr. Gage and Dr. Majella Doyle had no relevant financial disclosures.

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– Survival for patients with hilar cholangiocarcinoma was similar between those who underwent transplantation and those who underwent resection, but neoadjuvant therapy may give transplant strategy the edge, findings of a study and meta-analysis suggest.

Comstock/Thinkstock
None of the resection patients in the meta-analysis received neoadjuvant therapy; all of the participants in two of the orthotopic liver transplantation studies, however, started with neoadjuvant chemoradiation. These patients experienced 59% and 82% 5-year survival rates, the longest reported among the nine studies in the meta-analysis.

“We found survival in the group that received neoadjuvant chemoradiation therapy and transplant had a statistically significantly better outcome compared to a control group of resection,” Dr. Gage said. More importantly, patients who received a transplant without neoadjuvant therapy had a statistically significant worse outcome than patients who got resection alone.”

The investigators noted that patient selection for neoadjuvant therapy might also be a factor contributing to superior overall survival. In a multicenter study of 147 patients undergoing liver transplantation for hilar cholangiocarcinoma, a subgroup of patients who met the selection criteria of the Mayo Clinic protocol but had not undergone neoadjuvant therapy had a 59% 5-year survival rate (PLoS One. 2016:11:e0156127).

Study discussant Maria B. Majella Doyle, MD, a general surgeon at Washington University in St. Louis, agreed that patient selection for transplantation is a likely factor.

Dr. Doyle then asked Dr. Gage how she accounts for the heterogeneity among studies performed over a 20-year period.

“That is why we did subgroup analysis of neoadjuvant versus no neoadjuvant therapy,” Dr. Gage replied.

In the future, an intent-to-treat analysis might be more accurate, Dr. Majella Doyle said, because more patients are placed on a liver transplant list than typically have the procedure.

Dr. Gage noted that 28%-48% of patients started on neoadjuvant therapy in the two studies that offered both neoadjuvant therapy and a transplant in the meta-analysis never made it to transplantation. When they were included, overall survival dropped to approximately 35% in one study and 44% in the other.

In the primary meta-analysis (before the subanalysis looking at neoadjuvant therapy), 398 patients underwent resection and another 200 underwent liver transplantation between 1996 and 2106. Patient demographics were similar between groups, including more men than women, except the average age in the resection group was older, Dr. Gage said.

Overall survival favored the transplant group at each time point: 78% versus 70% with resection at 1 year; 56% versus 42% at 3 years; and 46% versus 29% at 5 years. The odds ratios, respectively, were 1.27, 1.49 and 1.83, but the findings were not statistically significant at a 95% confidence interval.

Margin involvement was 9% in the transplant patients versus 32% in the resection patients, Dr. Gage said. The best chance of cure is R0 resection, but half of patients with hilar cholangiocarcinoma, the most common cancer of the biliary tract, are unresectable, she added.

Six of the nine studies in the meta-analysis reported margin status. Of the 344 patients in these studies, 79% achieved R0 status overall.

“The goal of treatment is R0 resection,” Dr. Gage said in response to a question about when neoadjuvant therapy is warranted. “In the patients who are resectable, I think the correct answer would be to proceed with resection. However, for those patients who are borderline resectable, it would be reasonable to consider neoadjuvant therapy.”

“One of the major things that is undervalued is neoadjuvant therapy allows better patient selection,” said session moderator Eric Jensen, MD, FACS, of University of Minnesota Health in Minneapolis. “When you say an obviously resectable tumor, when you look at the data – we’re wrong 30% of the time. So I’m in favor of neoadjuvant therapy for everybody, but that is just my bias.”

The small number of studies is a limitation of the study, Dr. Gage said. Also, all the studies were nonrandomized and retrospective, and some research spanned many years, which could introduce bias because of changes in practice over time, she added.

Based on their findings, the investigators proposed that future studies explore routine administration of neoadjuvant therapy prior to resection.

Dr. Gage and Dr. Majella Doyle had no relevant financial disclosures.

 

– Survival for patients with hilar cholangiocarcinoma was similar between those who underwent transplantation and those who underwent resection, but neoadjuvant therapy may give transplant strategy the edge, findings of a study and meta-analysis suggest.

Comstock/Thinkstock
None of the resection patients in the meta-analysis received neoadjuvant therapy; all of the participants in two of the orthotopic liver transplantation studies, however, started with neoadjuvant chemoradiation. These patients experienced 59% and 82% 5-year survival rates, the longest reported among the nine studies in the meta-analysis.

“We found survival in the group that received neoadjuvant chemoradiation therapy and transplant had a statistically significantly better outcome compared to a control group of resection,” Dr. Gage said. More importantly, patients who received a transplant without neoadjuvant therapy had a statistically significant worse outcome than patients who got resection alone.”

The investigators noted that patient selection for neoadjuvant therapy might also be a factor contributing to superior overall survival. In a multicenter study of 147 patients undergoing liver transplantation for hilar cholangiocarcinoma, a subgroup of patients who met the selection criteria of the Mayo Clinic protocol but had not undergone neoadjuvant therapy had a 59% 5-year survival rate (PLoS One. 2016:11:e0156127).

Study discussant Maria B. Majella Doyle, MD, a general surgeon at Washington University in St. Louis, agreed that patient selection for transplantation is a likely factor.

Dr. Doyle then asked Dr. Gage how she accounts for the heterogeneity among studies performed over a 20-year period.

“That is why we did subgroup analysis of neoadjuvant versus no neoadjuvant therapy,” Dr. Gage replied.

In the future, an intent-to-treat analysis might be more accurate, Dr. Majella Doyle said, because more patients are placed on a liver transplant list than typically have the procedure.

Dr. Gage noted that 28%-48% of patients started on neoadjuvant therapy in the two studies that offered both neoadjuvant therapy and a transplant in the meta-analysis never made it to transplantation. When they were included, overall survival dropped to approximately 35% in one study and 44% in the other.

In the primary meta-analysis (before the subanalysis looking at neoadjuvant therapy), 398 patients underwent resection and another 200 underwent liver transplantation between 1996 and 2106. Patient demographics were similar between groups, including more men than women, except the average age in the resection group was older, Dr. Gage said.

Overall survival favored the transplant group at each time point: 78% versus 70% with resection at 1 year; 56% versus 42% at 3 years; and 46% versus 29% at 5 years. The odds ratios, respectively, were 1.27, 1.49 and 1.83, but the findings were not statistically significant at a 95% confidence interval.

Margin involvement was 9% in the transplant patients versus 32% in the resection patients, Dr. Gage said. The best chance of cure is R0 resection, but half of patients with hilar cholangiocarcinoma, the most common cancer of the biliary tract, are unresectable, she added.

Six of the nine studies in the meta-analysis reported margin status. Of the 344 patients in these studies, 79% achieved R0 status overall.

“The goal of treatment is R0 resection,” Dr. Gage said in response to a question about when neoadjuvant therapy is warranted. “In the patients who are resectable, I think the correct answer would be to proceed with resection. However, for those patients who are borderline resectable, it would be reasonable to consider neoadjuvant therapy.”

“One of the major things that is undervalued is neoadjuvant therapy allows better patient selection,” said session moderator Eric Jensen, MD, FACS, of University of Minnesota Health in Minneapolis. “When you say an obviously resectable tumor, when you look at the data – we’re wrong 30% of the time. So I’m in favor of neoadjuvant therapy for everybody, but that is just my bias.”

The small number of studies is a limitation of the study, Dr. Gage said. Also, all the studies were nonrandomized and retrospective, and some research spanned many years, which could introduce bias because of changes in practice over time, she added.

Based on their findings, the investigators proposed that future studies explore routine administration of neoadjuvant therapy prior to resection.

Dr. Gage and Dr. Majella Doyle had no relevant financial disclosures.

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Predicting extraction of an intact uterus in robotic-assisted laparoscopic hysterectomy

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– Investigators at the University of Tennessee, Chattanooga, have come up with a simple scoring system to predict if an intact uterus can be delivered vaginally during laparoscopic hysterectomy.

Age greater than 50 years counts as 1 point and uterine length greater than 11 cm, height greater than 8 cm, and width greater than 6.9 cm each count for 3 points. A score of 4 or higher suggests the need for an alternative to vaginal extraction, they reported at the annual scientific meeting of the Society of Gynecologic Surgeons.

Dr. Shanti Mohling
“In the current environment, with morcellation under scrutiny, [this system] may enable clinicians to better anticipate the need for an alternate route of specimen delivery and counsel patients accordingly,” said Shanti Mohling, MD, the lead investigator and director of gynecology at the University of Tennessee.

The team reviewed 367 robotic-assisted total laparoscopic hysterectomies. An intact uterus was able to be extracted vaginally in 265 cases (72%); minilaparotomy was used for the rest. Uterine length, height, and width were documented from pathology reports. The scoring system correctly classified 94.6% of the cases. Sensitivity was 85.3%, specificity was 98.1%, positive predictive value was 94.57%, and negative predictive value was 94.55%.

Factoring in parity, uterine weight, body mass index, procedure indications, tobacco use, and comorbidities did not statistically influence the predictive power.

Gynecologic surgeons “are trying to get specimens out intact” and want to know ahead of time if it’s possible, Dr. Mohling said. “I wanted to create a model that was very reproducible.”

The general benchmark for vaginal delivery of an intact uterus is size below 12 weeks pregnancy, but the University of Tennessee model is more precise, according to Dr. Mohling. “I’ve added this to my counseling,” she said.

There was no external funding for the work and the investigators reported having no relevant financial disclosures.

* The meeting sponsor information was updated 6/9/2017.

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– Investigators at the University of Tennessee, Chattanooga, have come up with a simple scoring system to predict if an intact uterus can be delivered vaginally during laparoscopic hysterectomy.

Age greater than 50 years counts as 1 point and uterine length greater than 11 cm, height greater than 8 cm, and width greater than 6.9 cm each count for 3 points. A score of 4 or higher suggests the need for an alternative to vaginal extraction, they reported at the annual scientific meeting of the Society of Gynecologic Surgeons.

Dr. Shanti Mohling
“In the current environment, with morcellation under scrutiny, [this system] may enable clinicians to better anticipate the need for an alternate route of specimen delivery and counsel patients accordingly,” said Shanti Mohling, MD, the lead investigator and director of gynecology at the University of Tennessee.

The team reviewed 367 robotic-assisted total laparoscopic hysterectomies. An intact uterus was able to be extracted vaginally in 265 cases (72%); minilaparotomy was used for the rest. Uterine length, height, and width were documented from pathology reports. The scoring system correctly classified 94.6% of the cases. Sensitivity was 85.3%, specificity was 98.1%, positive predictive value was 94.57%, and negative predictive value was 94.55%.

Factoring in parity, uterine weight, body mass index, procedure indications, tobacco use, and comorbidities did not statistically influence the predictive power.

Gynecologic surgeons “are trying to get specimens out intact” and want to know ahead of time if it’s possible, Dr. Mohling said. “I wanted to create a model that was very reproducible.”

The general benchmark for vaginal delivery of an intact uterus is size below 12 weeks pregnancy, but the University of Tennessee model is more precise, according to Dr. Mohling. “I’ve added this to my counseling,” she said.

There was no external funding for the work and the investigators reported having no relevant financial disclosures.

* The meeting sponsor information was updated 6/9/2017.

 

– Investigators at the University of Tennessee, Chattanooga, have come up with a simple scoring system to predict if an intact uterus can be delivered vaginally during laparoscopic hysterectomy.

Age greater than 50 years counts as 1 point and uterine length greater than 11 cm, height greater than 8 cm, and width greater than 6.9 cm each count for 3 points. A score of 4 or higher suggests the need for an alternative to vaginal extraction, they reported at the annual scientific meeting of the Society of Gynecologic Surgeons.

Dr. Shanti Mohling
“In the current environment, with morcellation under scrutiny, [this system] may enable clinicians to better anticipate the need for an alternate route of specimen delivery and counsel patients accordingly,” said Shanti Mohling, MD, the lead investigator and director of gynecology at the University of Tennessee.

The team reviewed 367 robotic-assisted total laparoscopic hysterectomies. An intact uterus was able to be extracted vaginally in 265 cases (72%); minilaparotomy was used for the rest. Uterine length, height, and width were documented from pathology reports. The scoring system correctly classified 94.6% of the cases. Sensitivity was 85.3%, specificity was 98.1%, positive predictive value was 94.57%, and negative predictive value was 94.55%.

Factoring in parity, uterine weight, body mass index, procedure indications, tobacco use, and comorbidities did not statistically influence the predictive power.

Gynecologic surgeons “are trying to get specimens out intact” and want to know ahead of time if it’s possible, Dr. Mohling said. “I wanted to create a model that was very reproducible.”

The general benchmark for vaginal delivery of an intact uterus is size below 12 weeks pregnancy, but the University of Tennessee model is more precise, according to Dr. Mohling. “I’ve added this to my counseling,” she said.

There was no external funding for the work and the investigators reported having no relevant financial disclosures.

* The meeting sponsor information was updated 6/9/2017.

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Key clinical point: A 10-point scoring system helps to predict vaginal extraction of an intact uterus in laparoscopic hysterectomy.

Major finding: The sensitivity of the scoring system was 85.3%, specificity was 98.1%, positive predictive value was 94.57%, and negative predictive value was 94.55%.

Data source: Single-center review of 367 robotic total laparoscopic hysterectomies during 2012-2015.

Disclosures: There was no external funding for the work, and the investigators reported having no relevant financial disclosures.

Don’t ask

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Fri, 01/18/2019 - 16:40

 

You walk into an examining room and discover a 3-year-old in his underpants wearing a fireman’s hat and what must be his older sister’s rubber boots. You have to ask: “Are you going to be a firefighter when you grow up?” If he is a sensitive kid he will resist answering, “What do you think, Dr. Obvious?” and instead he politely replies, “Yes, and an EMT [emergency medical technician] too.”

Adults, even ones who have devoted their professional lives to the care of children, can’t seem to stifle the urge ask every young person they meet about his or her career plans. It is a strange sort of obsession, and may simply reflect the fact that most adults are at a loss for conversation starters when it comes to talking with young people. Children don’t seem to have much concern about the weather. And most of them don’t have opinions about the current political situation. They don’t have stories about their grandchildren they would love to bore you with. You could ask if the child has a pet, but that may be picking the scab of an unresolved family issue.

Dr. William G. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years.
Dr. William G. Wilkoff


Most adults realize that their career plans prior to adolescence have no relationship to their present situation. Thinking back on this disconnect in their own lives may provide them with a good chuckle. But they also may hope to store away the child’s naive answer as ammunition for a future embarrassing challenge. “Do you remember that you once told me you were going to be a forest ranger?”

It may be that the child’s answer will give the adults an opportunity to share their “wisdom” based on their own career decisions. How lucky for the child who has stumbled on an unsolicited life coach.

For the most part, these interrogations about career planning are just idle banter. But as children get older, reality begins shining its harsh light on choices and decisions. What was once a seemingly harmless question about the distant future may no longer be so innocuous. I try to sound apologetic when I say to high school juniors and seniors, “I’m sure everyone is asking you, but what about college?” However, after reading a story in The Wall Street Journal, I now wonder whether I should be skipping the apology and just simply not raising the subject of college (“What’s Worse Than Waiting to Hear From Colleges? Getting Interrogated About It,” by Sue Shellenbarger, March 8, 2017).

In communities where most high school graduates have been on a college track since middle school, tension and anxiety hangs over the older adolescents like a cloud that darkens as application deadlines herald the long and painful wait for acceptance/rejection letters and emails. High school seniors are tired of thinking about the process and certainly don’t want to talk about. They consider questions about their future an invasion of their privacy. Redbubble, an online marketplace based in Australia, is seeing rising sales of T-shirts that read “Don’t ask me about college. Thanks.”

The unwelcome interrogations don’t stop with college acceptance. Adults want to know, “Have you chosen a major?” And as college graduation nears they can’t resist asking, “Do you have any job offers?”

Most adolescents and many 20-somethings don’t seem to have a career goal. It may be that they are afraid that the process of setting a goal will make them more vulnerable to failure. It also may be that revealing, “I’ve always wanted to be a ...” will label them as being a bit childish and weird.

Where does all this adolescent discomfort with the near future leave us pediatricians? The complete evaluation of a high school–age patient should include a question or questions about how our patient is weathering the college and career planning process. The challenge is how to present those questions in a manner that makes it clear that we aren’t just another one of those career-obsessed nosy adults.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

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You walk into an examining room and discover a 3-year-old in his underpants wearing a fireman’s hat and what must be his older sister’s rubber boots. You have to ask: “Are you going to be a firefighter when you grow up?” If he is a sensitive kid he will resist answering, “What do you think, Dr. Obvious?” and instead he politely replies, “Yes, and an EMT [emergency medical technician] too.”

Adults, even ones who have devoted their professional lives to the care of children, can’t seem to stifle the urge ask every young person they meet about his or her career plans. It is a strange sort of obsession, and may simply reflect the fact that most adults are at a loss for conversation starters when it comes to talking with young people. Children don’t seem to have much concern about the weather. And most of them don’t have opinions about the current political situation. They don’t have stories about their grandchildren they would love to bore you with. You could ask if the child has a pet, but that may be picking the scab of an unresolved family issue.

Dr. William G. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years.
Dr. William G. Wilkoff


Most adults realize that their career plans prior to adolescence have no relationship to their present situation. Thinking back on this disconnect in their own lives may provide them with a good chuckle. But they also may hope to store away the child’s naive answer as ammunition for a future embarrassing challenge. “Do you remember that you once told me you were going to be a forest ranger?”

It may be that the child’s answer will give the adults an opportunity to share their “wisdom” based on their own career decisions. How lucky for the child who has stumbled on an unsolicited life coach.

For the most part, these interrogations about career planning are just idle banter. But as children get older, reality begins shining its harsh light on choices and decisions. What was once a seemingly harmless question about the distant future may no longer be so innocuous. I try to sound apologetic when I say to high school juniors and seniors, “I’m sure everyone is asking you, but what about college?” However, after reading a story in The Wall Street Journal, I now wonder whether I should be skipping the apology and just simply not raising the subject of college (“What’s Worse Than Waiting to Hear From Colleges? Getting Interrogated About It,” by Sue Shellenbarger, March 8, 2017).

In communities where most high school graduates have been on a college track since middle school, tension and anxiety hangs over the older adolescents like a cloud that darkens as application deadlines herald the long and painful wait for acceptance/rejection letters and emails. High school seniors are tired of thinking about the process and certainly don’t want to talk about. They consider questions about their future an invasion of their privacy. Redbubble, an online marketplace based in Australia, is seeing rising sales of T-shirts that read “Don’t ask me about college. Thanks.”

The unwelcome interrogations don’t stop with college acceptance. Adults want to know, “Have you chosen a major?” And as college graduation nears they can’t resist asking, “Do you have any job offers?”

Most adolescents and many 20-somethings don’t seem to have a career goal. It may be that they are afraid that the process of setting a goal will make them more vulnerable to failure. It also may be that revealing, “I’ve always wanted to be a ...” will label them as being a bit childish and weird.

Where does all this adolescent discomfort with the near future leave us pediatricians? The complete evaluation of a high school–age patient should include a question or questions about how our patient is weathering the college and career planning process. The challenge is how to present those questions in a manner that makes it clear that we aren’t just another one of those career-obsessed nosy adults.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

 

You walk into an examining room and discover a 3-year-old in his underpants wearing a fireman’s hat and what must be his older sister’s rubber boots. You have to ask: “Are you going to be a firefighter when you grow up?” If he is a sensitive kid he will resist answering, “What do you think, Dr. Obvious?” and instead he politely replies, “Yes, and an EMT [emergency medical technician] too.”

Adults, even ones who have devoted their professional lives to the care of children, can’t seem to stifle the urge ask every young person they meet about his or her career plans. It is a strange sort of obsession, and may simply reflect the fact that most adults are at a loss for conversation starters when it comes to talking with young people. Children don’t seem to have much concern about the weather. And most of them don’t have opinions about the current political situation. They don’t have stories about their grandchildren they would love to bore you with. You could ask if the child has a pet, but that may be picking the scab of an unresolved family issue.

Dr. William G. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years.
Dr. William G. Wilkoff


Most adults realize that their career plans prior to adolescence have no relationship to their present situation. Thinking back on this disconnect in their own lives may provide them with a good chuckle. But they also may hope to store away the child’s naive answer as ammunition for a future embarrassing challenge. “Do you remember that you once told me you were going to be a forest ranger?”

It may be that the child’s answer will give the adults an opportunity to share their “wisdom” based on their own career decisions. How lucky for the child who has stumbled on an unsolicited life coach.

For the most part, these interrogations about career planning are just idle banter. But as children get older, reality begins shining its harsh light on choices and decisions. What was once a seemingly harmless question about the distant future may no longer be so innocuous. I try to sound apologetic when I say to high school juniors and seniors, “I’m sure everyone is asking you, but what about college?” However, after reading a story in The Wall Street Journal, I now wonder whether I should be skipping the apology and just simply not raising the subject of college (“What’s Worse Than Waiting to Hear From Colleges? Getting Interrogated About It,” by Sue Shellenbarger, March 8, 2017).

In communities where most high school graduates have been on a college track since middle school, tension and anxiety hangs over the older adolescents like a cloud that darkens as application deadlines herald the long and painful wait for acceptance/rejection letters and emails. High school seniors are tired of thinking about the process and certainly don’t want to talk about. They consider questions about their future an invasion of their privacy. Redbubble, an online marketplace based in Australia, is seeing rising sales of T-shirts that read “Don’t ask me about college. Thanks.”

The unwelcome interrogations don’t stop with college acceptance. Adults want to know, “Have you chosen a major?” And as college graduation nears they can’t resist asking, “Do you have any job offers?”

Most adolescents and many 20-somethings don’t seem to have a career goal. It may be that they are afraid that the process of setting a goal will make them more vulnerable to failure. It also may be that revealing, “I’ve always wanted to be a ...” will label them as being a bit childish and weird.

Where does all this adolescent discomfort with the near future leave us pediatricians? The complete evaluation of a high school–age patient should include a question or questions about how our patient is weathering the college and career planning process. The challenge is how to present those questions in a manner that makes it clear that we aren’t just another one of those career-obsessed nosy adults.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

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Number of U.S. Zika-infected pregnancies tops 5,100

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Fri, 01/18/2019 - 16:40

 

Almost 200 cases of pregnant women with Zika virus infection were reported in the United States during the 2 weeks ending March 28, with the number split evenly between the territories and the 50 states and Washington, D.C., according to the Centers for Disease Control and Prevention.

These latest 197 cases – 98 in the territories and 99 in the states/D.C. – bring the U.S. total since the beginning of 2016 to 5,177 pregnant women with laboratory evidence of Zika virus infection: 3,461 in the U.S. territories and 1,716 in the states/D.C., the CDC reported on April 6.

Of those 1,716 pregnancies in the states/D.C., 1,311 have been completed, with Zika-related birth defects reported in 56 liveborn infants (2 in the last 2 weeks) and 7 pregnancy losses (none in the last 2 weeks), according to data from the U.S. Zika Pregnancy Registry. The CDC stopped reporting adverse pregnancy outcomes in Puerto Rico and the other U.S. territories in October because of differences in inclusion criteria.

Since Jan. 1, 2015, a total of 41,701 cases of Zika virus infection have been reported among all Americans: 5,197 in the states/D.C. and 36,504 in the territories. Almost all of the territorial cases (97%) have occurred in Puerto Rico, while Florida (21%), New York (20%), and California (9%) together have accounted for half of the cases in the states/D.C., the CDC said.

These are not real-time data and reflect only pregnancy outcomes for women with any laboratory evidence of possible Zika virus infection, although it is not known if Zika virus was the cause of the poor outcomes. Zika-related birth defects recorded by the CDC could include microcephaly, calcium deposits in the brain indicating possible brain damage, excess fluid in the brain cavities and surrounding the brain, absent or poorly formed brain structures, abnormal eye development, or other problems resulting from brain damage that affect nerves, muscles, and bones. The pregnancy losses encompass any miscarriage, stillbirth, or termination with evidence of birth defects.

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Almost 200 cases of pregnant women with Zika virus infection were reported in the United States during the 2 weeks ending March 28, with the number split evenly between the territories and the 50 states and Washington, D.C., according to the Centers for Disease Control and Prevention.

These latest 197 cases – 98 in the territories and 99 in the states/D.C. – bring the U.S. total since the beginning of 2016 to 5,177 pregnant women with laboratory evidence of Zika virus infection: 3,461 in the U.S. territories and 1,716 in the states/D.C., the CDC reported on April 6.

Of those 1,716 pregnancies in the states/D.C., 1,311 have been completed, with Zika-related birth defects reported in 56 liveborn infants (2 in the last 2 weeks) and 7 pregnancy losses (none in the last 2 weeks), according to data from the U.S. Zika Pregnancy Registry. The CDC stopped reporting adverse pregnancy outcomes in Puerto Rico and the other U.S. territories in October because of differences in inclusion criteria.

Since Jan. 1, 2015, a total of 41,701 cases of Zika virus infection have been reported among all Americans: 5,197 in the states/D.C. and 36,504 in the territories. Almost all of the territorial cases (97%) have occurred in Puerto Rico, while Florida (21%), New York (20%), and California (9%) together have accounted for half of the cases in the states/D.C., the CDC said.

These are not real-time data and reflect only pregnancy outcomes for women with any laboratory evidence of possible Zika virus infection, although it is not known if Zika virus was the cause of the poor outcomes. Zika-related birth defects recorded by the CDC could include microcephaly, calcium deposits in the brain indicating possible brain damage, excess fluid in the brain cavities and surrounding the brain, absent or poorly formed brain structures, abnormal eye development, or other problems resulting from brain damage that affect nerves, muscles, and bones. The pregnancy losses encompass any miscarriage, stillbirth, or termination with evidence of birth defects.

 

Almost 200 cases of pregnant women with Zika virus infection were reported in the United States during the 2 weeks ending March 28, with the number split evenly between the territories and the 50 states and Washington, D.C., according to the Centers for Disease Control and Prevention.

These latest 197 cases – 98 in the territories and 99 in the states/D.C. – bring the U.S. total since the beginning of 2016 to 5,177 pregnant women with laboratory evidence of Zika virus infection: 3,461 in the U.S. territories and 1,716 in the states/D.C., the CDC reported on April 6.

Of those 1,716 pregnancies in the states/D.C., 1,311 have been completed, with Zika-related birth defects reported in 56 liveborn infants (2 in the last 2 weeks) and 7 pregnancy losses (none in the last 2 weeks), according to data from the U.S. Zika Pregnancy Registry. The CDC stopped reporting adverse pregnancy outcomes in Puerto Rico and the other U.S. territories in October because of differences in inclusion criteria.

Since Jan. 1, 2015, a total of 41,701 cases of Zika virus infection have been reported among all Americans: 5,197 in the states/D.C. and 36,504 in the territories. Almost all of the territorial cases (97%) have occurred in Puerto Rico, while Florida (21%), New York (20%), and California (9%) together have accounted for half of the cases in the states/D.C., the CDC said.

These are not real-time data and reflect only pregnancy outcomes for women with any laboratory evidence of possible Zika virus infection, although it is not known if Zika virus was the cause of the poor outcomes. Zika-related birth defects recorded by the CDC could include microcephaly, calcium deposits in the brain indicating possible brain damage, excess fluid in the brain cavities and surrounding the brain, absent or poorly formed brain structures, abnormal eye development, or other problems resulting from brain damage that affect nerves, muscles, and bones. The pregnancy losses encompass any miscarriage, stillbirth, or termination with evidence of birth defects.

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Evidence for medical marijuana largely up in smoke

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SAN DIEGO – Despite the popularity of medical marijuana, robust evidence for its use is limited or nonexistent for most medical conditions.

“This is a tough subject to study,” Ellie Grossman, MD, said at the annual meeting of the American College of Physicians. “There is federal money that can only be used in very limited ways to study it. Our science is way behind the times in terms of what our patients are doing and using.”

Typical limitations of marijuana studies include self-report of quantity/duration used and the fact that biochemical/quantifiable measures are lacking. “For inhaled marijuana, there is variability in how much is inhaled and how deeply it’s being inhaled,” said Dr. Grossman, an internist who practices in Somerville, Mass.

Dr. Ellie Grossman


Then there’s the issue of recall bias and the question as to whether oral cannabinoids equate to the plant-derived forms of medical marijuana that patients obtain from their local dispensaries.

That matters, because the majority of published studies on the topic have evaluated oral cannabinoids, not the plant form. “So, what we’re studying is vastly different from what our patients are using,” she said.

The most solid indication clinicians have for recommending medical marijuana is for chronic pain, and the most common condition studied has been neuropathy.

“Most evidence compares cannabinoid to placebo,” said Dr. Grossman, primary care lead for behavioral health integration at Cambridge (Mass.) Health Alliance. “There’s almost nothing out there comparing cannabinoid to any other pain-relieving agent that a patient might choose to use.

“A lot of the literature comes from oral synthesized agents,” she continued. “There’s a little bit of science about inhaled forms, but a lot of this is very different from what my patient got last week in a medical marijuana dispensary in Massachusetts.”

Results from a systematic review of 79 studies of cannabinoids for medical use in 6,462 study participants showed that, compared with placebo, cannabinoids were associated with a greater average number of patients showing a complete nausea and vomiting response (47% vs. 20%; odds ratio, 3.82), reduction in pain (37% vs. 31%; OR, 1.41), a greater average reduction in numerical rating scale pain assessment (on a 0- to 10-point scale; weighted mean difference of –0.46), and average reduction in the Ashworth spasticity scale (–0.36) (JAMA 2015 Jun 23-30;313[24]:2456-73).

A separate meta-analysis of studies compared inhaled cannabis sativa to placebo for chronic painful neuropathy. The researchers found that those patients who used inhaled cannabis sativa were 3.2 times more likely to achieve a 30% or greater reduction in pain, compared with those in the placebo group (J. Pain 2015 Dec;16[12]:1221-32).

However, Dr. Grossman cautioned that the number of patients studied was fewer than 200, “so, you could argue that this is a body of knowledge where the jury is still out.”

According to a 2017 report from the National Academy of Sciences titled, “The Health Effects of Cannabis and Cannabinoids,” another area in which the knowledge base is less solid is the use of oral cannabinoids for chemotherapy-induced nausea and vomiting.

“There’s a reasonable amount of evidence showing that some of these are better than placebo for relief of these symptoms,” Dr. Grossman said. “That said, the jury’s out as to whether they are any better than our other antiemetic agents. And there are no studies comparing them to neurokinin-1 inhibitors, which are the newest class of drug often used by oncologists for this indication. There is also no good evidence about inhaled plant cannabis.”

Studies of oral cannabinoids for multiple-sclerosis–related spasticity have demonstrated a small improvement on patient-reported spasticity (less than 1 point on a 10-point scale), but there was no improvement in clinician-reported outcomes. At the same time, their use for weight loss/anorexia in HIV “is very limited, and there are no studies of plant-derived cannabis,” Dr. Grossman said.

According to the National Academy of Sciences report, some evidence supports the use of oral cannabinoids for short-term sleep outcomes in patients with chronic diseases such as fibromyalgia and MS. One small study of oral cannabinoid for anxiety found that it improved social anxiety symptoms on the public speaking test, but there have been no studies using inhaled cannabinoids/marijuana.

The health risks of medical marijuana are largely unknown, Dr. Grossman said, noting that most evidence on longer‐term health risks comes from epidemiologic studies of recreational cannabis users.

“Medical marijuana users tend to be older and tend to be sicker,” she said. “We don’t know anything about the long-term effects in that sicker population.”

Among healthier people, Dr. Grossman continued, cannabis use is associated with increased risk of cough, wheeze, and sputum/phlegm. “There’s also an increased risk of motor vehicle accidents,” she said. “That is certainly a concern in places where they’re legalizing marijuana.”

Cannabis use is associated with lower neonatal birth weight, case reports/series of unintentional pediatric ingestions, and a possible increase in suicidal ideation, suicide attempts, and completed suicides.

“The evidence is very limited regarding associations with myocardial infarction, stroke, COPD, and mortality,” she added. “We don’t really know.”

Dr. Grossman reported having no financial disclosures.

 

 

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SAN DIEGO – Despite the popularity of medical marijuana, robust evidence for its use is limited or nonexistent for most medical conditions.

“This is a tough subject to study,” Ellie Grossman, MD, said at the annual meeting of the American College of Physicians. “There is federal money that can only be used in very limited ways to study it. Our science is way behind the times in terms of what our patients are doing and using.”

Typical limitations of marijuana studies include self-report of quantity/duration used and the fact that biochemical/quantifiable measures are lacking. “For inhaled marijuana, there is variability in how much is inhaled and how deeply it’s being inhaled,” said Dr. Grossman, an internist who practices in Somerville, Mass.

Dr. Ellie Grossman


Then there’s the issue of recall bias and the question as to whether oral cannabinoids equate to the plant-derived forms of medical marijuana that patients obtain from their local dispensaries.

That matters, because the majority of published studies on the topic have evaluated oral cannabinoids, not the plant form. “So, what we’re studying is vastly different from what our patients are using,” she said.

The most solid indication clinicians have for recommending medical marijuana is for chronic pain, and the most common condition studied has been neuropathy.

“Most evidence compares cannabinoid to placebo,” said Dr. Grossman, primary care lead for behavioral health integration at Cambridge (Mass.) Health Alliance. “There’s almost nothing out there comparing cannabinoid to any other pain-relieving agent that a patient might choose to use.

“A lot of the literature comes from oral synthesized agents,” she continued. “There’s a little bit of science about inhaled forms, but a lot of this is very different from what my patient got last week in a medical marijuana dispensary in Massachusetts.”

Results from a systematic review of 79 studies of cannabinoids for medical use in 6,462 study participants showed that, compared with placebo, cannabinoids were associated with a greater average number of patients showing a complete nausea and vomiting response (47% vs. 20%; odds ratio, 3.82), reduction in pain (37% vs. 31%; OR, 1.41), a greater average reduction in numerical rating scale pain assessment (on a 0- to 10-point scale; weighted mean difference of –0.46), and average reduction in the Ashworth spasticity scale (–0.36) (JAMA 2015 Jun 23-30;313[24]:2456-73).

A separate meta-analysis of studies compared inhaled cannabis sativa to placebo for chronic painful neuropathy. The researchers found that those patients who used inhaled cannabis sativa were 3.2 times more likely to achieve a 30% or greater reduction in pain, compared with those in the placebo group (J. Pain 2015 Dec;16[12]:1221-32).

However, Dr. Grossman cautioned that the number of patients studied was fewer than 200, “so, you could argue that this is a body of knowledge where the jury is still out.”

According to a 2017 report from the National Academy of Sciences titled, “The Health Effects of Cannabis and Cannabinoids,” another area in which the knowledge base is less solid is the use of oral cannabinoids for chemotherapy-induced nausea and vomiting.

“There’s a reasonable amount of evidence showing that some of these are better than placebo for relief of these symptoms,” Dr. Grossman said. “That said, the jury’s out as to whether they are any better than our other antiemetic agents. And there are no studies comparing them to neurokinin-1 inhibitors, which are the newest class of drug often used by oncologists for this indication. There is also no good evidence about inhaled plant cannabis.”

Studies of oral cannabinoids for multiple-sclerosis–related spasticity have demonstrated a small improvement on patient-reported spasticity (less than 1 point on a 10-point scale), but there was no improvement in clinician-reported outcomes. At the same time, their use for weight loss/anorexia in HIV “is very limited, and there are no studies of plant-derived cannabis,” Dr. Grossman said.

According to the National Academy of Sciences report, some evidence supports the use of oral cannabinoids for short-term sleep outcomes in patients with chronic diseases such as fibromyalgia and MS. One small study of oral cannabinoid for anxiety found that it improved social anxiety symptoms on the public speaking test, but there have been no studies using inhaled cannabinoids/marijuana.

The health risks of medical marijuana are largely unknown, Dr. Grossman said, noting that most evidence on longer‐term health risks comes from epidemiologic studies of recreational cannabis users.

“Medical marijuana users tend to be older and tend to be sicker,” she said. “We don’t know anything about the long-term effects in that sicker population.”

Among healthier people, Dr. Grossman continued, cannabis use is associated with increased risk of cough, wheeze, and sputum/phlegm. “There’s also an increased risk of motor vehicle accidents,” she said. “That is certainly a concern in places where they’re legalizing marijuana.”

Cannabis use is associated with lower neonatal birth weight, case reports/series of unintentional pediatric ingestions, and a possible increase in suicidal ideation, suicide attempts, and completed suicides.

“The evidence is very limited regarding associations with myocardial infarction, stroke, COPD, and mortality,” she added. “We don’t really know.”

Dr. Grossman reported having no financial disclosures.

 

 

 

SAN DIEGO – Despite the popularity of medical marijuana, robust evidence for its use is limited or nonexistent for most medical conditions.

“This is a tough subject to study,” Ellie Grossman, MD, said at the annual meeting of the American College of Physicians. “There is federal money that can only be used in very limited ways to study it. Our science is way behind the times in terms of what our patients are doing and using.”

Typical limitations of marijuana studies include self-report of quantity/duration used and the fact that biochemical/quantifiable measures are lacking. “For inhaled marijuana, there is variability in how much is inhaled and how deeply it’s being inhaled,” said Dr. Grossman, an internist who practices in Somerville, Mass.

Dr. Ellie Grossman


Then there’s the issue of recall bias and the question as to whether oral cannabinoids equate to the plant-derived forms of medical marijuana that patients obtain from their local dispensaries.

That matters, because the majority of published studies on the topic have evaluated oral cannabinoids, not the plant form. “So, what we’re studying is vastly different from what our patients are using,” she said.

The most solid indication clinicians have for recommending medical marijuana is for chronic pain, and the most common condition studied has been neuropathy.

“Most evidence compares cannabinoid to placebo,” said Dr. Grossman, primary care lead for behavioral health integration at Cambridge (Mass.) Health Alliance. “There’s almost nothing out there comparing cannabinoid to any other pain-relieving agent that a patient might choose to use.

“A lot of the literature comes from oral synthesized agents,” she continued. “There’s a little bit of science about inhaled forms, but a lot of this is very different from what my patient got last week in a medical marijuana dispensary in Massachusetts.”

Results from a systematic review of 79 studies of cannabinoids for medical use in 6,462 study participants showed that, compared with placebo, cannabinoids were associated with a greater average number of patients showing a complete nausea and vomiting response (47% vs. 20%; odds ratio, 3.82), reduction in pain (37% vs. 31%; OR, 1.41), a greater average reduction in numerical rating scale pain assessment (on a 0- to 10-point scale; weighted mean difference of –0.46), and average reduction in the Ashworth spasticity scale (–0.36) (JAMA 2015 Jun 23-30;313[24]:2456-73).

A separate meta-analysis of studies compared inhaled cannabis sativa to placebo for chronic painful neuropathy. The researchers found that those patients who used inhaled cannabis sativa were 3.2 times more likely to achieve a 30% or greater reduction in pain, compared with those in the placebo group (J. Pain 2015 Dec;16[12]:1221-32).

However, Dr. Grossman cautioned that the number of patients studied was fewer than 200, “so, you could argue that this is a body of knowledge where the jury is still out.”

According to a 2017 report from the National Academy of Sciences titled, “The Health Effects of Cannabis and Cannabinoids,” another area in which the knowledge base is less solid is the use of oral cannabinoids for chemotherapy-induced nausea and vomiting.

“There’s a reasonable amount of evidence showing that some of these are better than placebo for relief of these symptoms,” Dr. Grossman said. “That said, the jury’s out as to whether they are any better than our other antiemetic agents. And there are no studies comparing them to neurokinin-1 inhibitors, which are the newest class of drug often used by oncologists for this indication. There is also no good evidence about inhaled plant cannabis.”

Studies of oral cannabinoids for multiple-sclerosis–related spasticity have demonstrated a small improvement on patient-reported spasticity (less than 1 point on a 10-point scale), but there was no improvement in clinician-reported outcomes. At the same time, their use for weight loss/anorexia in HIV “is very limited, and there are no studies of plant-derived cannabis,” Dr. Grossman said.

According to the National Academy of Sciences report, some evidence supports the use of oral cannabinoids for short-term sleep outcomes in patients with chronic diseases such as fibromyalgia and MS. One small study of oral cannabinoid for anxiety found that it improved social anxiety symptoms on the public speaking test, but there have been no studies using inhaled cannabinoids/marijuana.

The health risks of medical marijuana are largely unknown, Dr. Grossman said, noting that most evidence on longer‐term health risks comes from epidemiologic studies of recreational cannabis users.

“Medical marijuana users tend to be older and tend to be sicker,” she said. “We don’t know anything about the long-term effects in that sicker population.”

Among healthier people, Dr. Grossman continued, cannabis use is associated with increased risk of cough, wheeze, and sputum/phlegm. “There’s also an increased risk of motor vehicle accidents,” she said. “That is certainly a concern in places where they’re legalizing marijuana.”

Cannabis use is associated with lower neonatal birth weight, case reports/series of unintentional pediatric ingestions, and a possible increase in suicidal ideation, suicide attempts, and completed suicides.

“The evidence is very limited regarding associations with myocardial infarction, stroke, COPD, and mortality,” she added. “We don’t really know.”

Dr. Grossman reported having no financial disclosures.

 

 

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Rumors about the death of tPA are exaggerated

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Where do we go from here?

More than 20 years after IV tissue plasminogen activator was officially approved for use in acute ischemic stroke, now data suggest mechanical thrombectomy is superior, regardless of whether tPA is given.

Granted, these are preliminary trials, and a lot more research needs to be done: randomized studies, determinations of which patients are the best candidates, which devices are most useful, etc.

Dr. Allan M. Block, a neurologist in Scottsdale, Arizona.
Dr. Allan M. Block
This led to an email exchange between another neurologist and me recently, wondering if we should be notifying the interventionalists, too, as soon as a nonhemorrhagic stroke is rolled in. Why should we have all the fun? Heck, why bother me at all? If they’re better at it, call the interventionalists and let me sleep.

Of course, it’s not that simple. The data thus far suggest thrombectomy is best when used in anterior circulation strokes, with a National Institutes of Health Stroke Scale score of greater than 6, so obviously we shouldn’t be calling them in on every case.

You have to balance that against legal issues. It certainly isn’t too far-fetched to imagine being sued because you didn’t call an interventionalist, or another neurologist testifying that you fell below the standard of care by not doing so. The right person will say that about anything, regardless of clinical data.

This is still up in the air right now, as I doubt the interventionalists want to take acute ischemic stroke off our hands, nor do we want to give it up, either. It’s a disorder of the brain, and that is what we deal with, isn’t it?

The bottom line is that rumors about the death of tPA in acute ischemic stroke are greatly exaggerated. Only time will tell.

Medicine, for better or worse, is an inexact science. No one can predict outcomes, adverse reactions, or complications with 100% certainty. Which treatment will work best for which patient is never known. That’s why we need controlled trials to know which odds are best overall, and take it from there. Preliminary trials can be very helpful at pointing us in the right directions, but are for from definitive. As with so many other things, your mileage may vary.
 

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

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Where do we go from here?

More than 20 years after IV tissue plasminogen activator was officially approved for use in acute ischemic stroke, now data suggest mechanical thrombectomy is superior, regardless of whether tPA is given.

Granted, these are preliminary trials, and a lot more research needs to be done: randomized studies, determinations of which patients are the best candidates, which devices are most useful, etc.

Dr. Allan M. Block, a neurologist in Scottsdale, Arizona.
Dr. Allan M. Block
This led to an email exchange between another neurologist and me recently, wondering if we should be notifying the interventionalists, too, as soon as a nonhemorrhagic stroke is rolled in. Why should we have all the fun? Heck, why bother me at all? If they’re better at it, call the interventionalists and let me sleep.

Of course, it’s not that simple. The data thus far suggest thrombectomy is best when used in anterior circulation strokes, with a National Institutes of Health Stroke Scale score of greater than 6, so obviously we shouldn’t be calling them in on every case.

You have to balance that against legal issues. It certainly isn’t too far-fetched to imagine being sued because you didn’t call an interventionalist, or another neurologist testifying that you fell below the standard of care by not doing so. The right person will say that about anything, regardless of clinical data.

This is still up in the air right now, as I doubt the interventionalists want to take acute ischemic stroke off our hands, nor do we want to give it up, either. It’s a disorder of the brain, and that is what we deal with, isn’t it?

The bottom line is that rumors about the death of tPA in acute ischemic stroke are greatly exaggerated. Only time will tell.

Medicine, for better or worse, is an inexact science. No one can predict outcomes, adverse reactions, or complications with 100% certainty. Which treatment will work best for which patient is never known. That’s why we need controlled trials to know which odds are best overall, and take it from there. Preliminary trials can be very helpful at pointing us in the right directions, but are for from definitive. As with so many other things, your mileage may vary.
 

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

 

Where do we go from here?

More than 20 years after IV tissue plasminogen activator was officially approved for use in acute ischemic stroke, now data suggest mechanical thrombectomy is superior, regardless of whether tPA is given.

Granted, these are preliminary trials, and a lot more research needs to be done: randomized studies, determinations of which patients are the best candidates, which devices are most useful, etc.

Dr. Allan M. Block, a neurologist in Scottsdale, Arizona.
Dr. Allan M. Block
This led to an email exchange between another neurologist and me recently, wondering if we should be notifying the interventionalists, too, as soon as a nonhemorrhagic stroke is rolled in. Why should we have all the fun? Heck, why bother me at all? If they’re better at it, call the interventionalists and let me sleep.

Of course, it’s not that simple. The data thus far suggest thrombectomy is best when used in anterior circulation strokes, with a National Institutes of Health Stroke Scale score of greater than 6, so obviously we shouldn’t be calling them in on every case.

You have to balance that against legal issues. It certainly isn’t too far-fetched to imagine being sued because you didn’t call an interventionalist, or another neurologist testifying that you fell below the standard of care by not doing so. The right person will say that about anything, regardless of clinical data.

This is still up in the air right now, as I doubt the interventionalists want to take acute ischemic stroke off our hands, nor do we want to give it up, either. It’s a disorder of the brain, and that is what we deal with, isn’t it?

The bottom line is that rumors about the death of tPA in acute ischemic stroke are greatly exaggerated. Only time will tell.

Medicine, for better or worse, is an inexact science. No one can predict outcomes, adverse reactions, or complications with 100% certainty. Which treatment will work best for which patient is never known. That’s why we need controlled trials to know which odds are best overall, and take it from there. Preliminary trials can be very helpful at pointing us in the right directions, but are for from definitive. As with so many other things, your mileage may vary.
 

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

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Pardon the interruption?

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Fri, 01/18/2019 - 16:40

 

Your first patient of the afternoon is a 9-year-old boy who moved to town several months ago. Mercifully, the second patient of the afternoon has canceled, giving you a few more minutes to get acquainted with this young man whose chief complaint is listed as “behavior problem.” You learn quickly that this family has relocated from a town just 20 miles away because they are seeking a school that is a “better fit” for your new patient.

Due to some miscommunications, the child’s old records have not arrived at your office. The mother says that her son is not taking any medication, and she isn’t sure if he has ever been given a diagnosis. You learn that he likes to argue and is prone to violent temper tantrums. Your initial brief exam does not suggest any cognitive deficits, but he exudes an aura of anger and discontent. You tell his mother that you will be glad to try to help, but you will need his old records and another longer visit before you can make any recommendations.

Dr. William G. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years.
Dr. William G. Wilkoff


Two days later you see a fourth-grader you have known since birth. He rarely comes to the office with problems, but you understand that he is a good student, a competent athlete, and socially engaged. His chief complaint for this visit is “hair loss,” but you soon discover that he has trichotillomania and has recently begun having nightmares and experiencing enuresis. All of these symptoms began a month ago with arrival of a new student in his class whose violent outbursts have become increasingly more physical. I have borrowed this child’s scenario from a similar case study in a recent supplement to the Journal of Developmental & Behavioral Pediatrics titled, “Behavioral Changes Associated with a Disruptive New Student in the Classroom,” (J Dev Behav Pediatr. Feb/Mar 2017. doi: 10.1097/DBP.0000000000000175).

The afternoon following your visit with the hair-pulling fourth-grader, you receive the new patient’s records for which you have been waiting. The circle is completed as you read that this is his third school in 18 months, and the reports of his behavior make it clear that your two patients are classmates. This scenario of coincidence could easily have occurred in a small town like Brunswick, Maine, where I practiced, but I have manufactured it to raise several questions about social priorities and professional ethics.

Forty years ago, institutions housing individuals with Down syndrome started closing and the process of integrating children with a variety of cognitive and physical disabilities into traditional classrooms began. To the surprise of some people, this mainstreaming has generally gone well. Unfortunately, funding hasn’t always caught up with the demand for services. For the most part, children readily accept their challenged classmates who look, move, and sound different. The flailing and grunting of the child with spastic choreoathetosis using a wheelchair isn’t considered an interruption because “that’s just the way she is.”

However, there seems to be an invisible line that separates those children who seem to be incapable of stopping their potentially disruptive behavior from those children we assume “ought to know better” or whose parents we believe have failed at instilling even the most basic discipline. You can certainly question the validity of those assumptions. But it is clear that your new patient’s disruptive behavior is interfering with his classmates’ education, and in some cases threatening their health. Your patient with trichotillomania is probably the canary in a very unsettled mine.

Your dilemma as the pediatrician for these two boys is the same we face as a society. How do you effectively advocate for a positive educational atmosphere for children with a variety of special needs, some of which seem to be in direct conflict? You can ask the school system to be patient as you help the disruptive child get connected with the services he needs. But you know that could take several months at a minimum. Meanwhile your hair-pulling patient and his classmates are losing valuable educational opportunities by the day.

I don’t have the answer, but I suspect that somehow it is going to come down to affordability. Counseling, psychiatrists, and one on one classroom aids don’t come cheap, nor does the tuition for a special school in another school district. But we can’t discount the value of an education free of disruption.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected]

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Your first patient of the afternoon is a 9-year-old boy who moved to town several months ago. Mercifully, the second patient of the afternoon has canceled, giving you a few more minutes to get acquainted with this young man whose chief complaint is listed as “behavior problem.” You learn quickly that this family has relocated from a town just 20 miles away because they are seeking a school that is a “better fit” for your new patient.

Due to some miscommunications, the child’s old records have not arrived at your office. The mother says that her son is not taking any medication, and she isn’t sure if he has ever been given a diagnosis. You learn that he likes to argue and is prone to violent temper tantrums. Your initial brief exam does not suggest any cognitive deficits, but he exudes an aura of anger and discontent. You tell his mother that you will be glad to try to help, but you will need his old records and another longer visit before you can make any recommendations.

Dr. William G. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years.
Dr. William G. Wilkoff


Two days later you see a fourth-grader you have known since birth. He rarely comes to the office with problems, but you understand that he is a good student, a competent athlete, and socially engaged. His chief complaint for this visit is “hair loss,” but you soon discover that he has trichotillomania and has recently begun having nightmares and experiencing enuresis. All of these symptoms began a month ago with arrival of a new student in his class whose violent outbursts have become increasingly more physical. I have borrowed this child’s scenario from a similar case study in a recent supplement to the Journal of Developmental & Behavioral Pediatrics titled, “Behavioral Changes Associated with a Disruptive New Student in the Classroom,” (J Dev Behav Pediatr. Feb/Mar 2017. doi: 10.1097/DBP.0000000000000175).

The afternoon following your visit with the hair-pulling fourth-grader, you receive the new patient’s records for which you have been waiting. The circle is completed as you read that this is his third school in 18 months, and the reports of his behavior make it clear that your two patients are classmates. This scenario of coincidence could easily have occurred in a small town like Brunswick, Maine, where I practiced, but I have manufactured it to raise several questions about social priorities and professional ethics.

Forty years ago, institutions housing individuals with Down syndrome started closing and the process of integrating children with a variety of cognitive and physical disabilities into traditional classrooms began. To the surprise of some people, this mainstreaming has generally gone well. Unfortunately, funding hasn’t always caught up with the demand for services. For the most part, children readily accept their challenged classmates who look, move, and sound different. The flailing and grunting of the child with spastic choreoathetosis using a wheelchair isn’t considered an interruption because “that’s just the way she is.”

However, there seems to be an invisible line that separates those children who seem to be incapable of stopping their potentially disruptive behavior from those children we assume “ought to know better” or whose parents we believe have failed at instilling even the most basic discipline. You can certainly question the validity of those assumptions. But it is clear that your new patient’s disruptive behavior is interfering with his classmates’ education, and in some cases threatening their health. Your patient with trichotillomania is probably the canary in a very unsettled mine.

Your dilemma as the pediatrician for these two boys is the same we face as a society. How do you effectively advocate for a positive educational atmosphere for children with a variety of special needs, some of which seem to be in direct conflict? You can ask the school system to be patient as you help the disruptive child get connected with the services he needs. But you know that could take several months at a minimum. Meanwhile your hair-pulling patient and his classmates are losing valuable educational opportunities by the day.

I don’t have the answer, but I suspect that somehow it is going to come down to affordability. Counseling, psychiatrists, and one on one classroom aids don’t come cheap, nor does the tuition for a special school in another school district. But we can’t discount the value of an education free of disruption.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected]

 

Your first patient of the afternoon is a 9-year-old boy who moved to town several months ago. Mercifully, the second patient of the afternoon has canceled, giving you a few more minutes to get acquainted with this young man whose chief complaint is listed as “behavior problem.” You learn quickly that this family has relocated from a town just 20 miles away because they are seeking a school that is a “better fit” for your new patient.

Due to some miscommunications, the child’s old records have not arrived at your office. The mother says that her son is not taking any medication, and she isn’t sure if he has ever been given a diagnosis. You learn that he likes to argue and is prone to violent temper tantrums. Your initial brief exam does not suggest any cognitive deficits, but he exudes an aura of anger and discontent. You tell his mother that you will be glad to try to help, but you will need his old records and another longer visit before you can make any recommendations.

Dr. William G. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years.
Dr. William G. Wilkoff


Two days later you see a fourth-grader you have known since birth. He rarely comes to the office with problems, but you understand that he is a good student, a competent athlete, and socially engaged. His chief complaint for this visit is “hair loss,” but you soon discover that he has trichotillomania and has recently begun having nightmares and experiencing enuresis. All of these symptoms began a month ago with arrival of a new student in his class whose violent outbursts have become increasingly more physical. I have borrowed this child’s scenario from a similar case study in a recent supplement to the Journal of Developmental & Behavioral Pediatrics titled, “Behavioral Changes Associated with a Disruptive New Student in the Classroom,” (J Dev Behav Pediatr. Feb/Mar 2017. doi: 10.1097/DBP.0000000000000175).

The afternoon following your visit with the hair-pulling fourth-grader, you receive the new patient’s records for which you have been waiting. The circle is completed as you read that this is his third school in 18 months, and the reports of his behavior make it clear that your two patients are classmates. This scenario of coincidence could easily have occurred in a small town like Brunswick, Maine, where I practiced, but I have manufactured it to raise several questions about social priorities and professional ethics.

Forty years ago, institutions housing individuals with Down syndrome started closing and the process of integrating children with a variety of cognitive and physical disabilities into traditional classrooms began. To the surprise of some people, this mainstreaming has generally gone well. Unfortunately, funding hasn’t always caught up with the demand for services. For the most part, children readily accept their challenged classmates who look, move, and sound different. The flailing and grunting of the child with spastic choreoathetosis using a wheelchair isn’t considered an interruption because “that’s just the way she is.”

However, there seems to be an invisible line that separates those children who seem to be incapable of stopping their potentially disruptive behavior from those children we assume “ought to know better” or whose parents we believe have failed at instilling even the most basic discipline. You can certainly question the validity of those assumptions. But it is clear that your new patient’s disruptive behavior is interfering with his classmates’ education, and in some cases threatening their health. Your patient with trichotillomania is probably the canary in a very unsettled mine.

Your dilemma as the pediatrician for these two boys is the same we face as a society. How do you effectively advocate for a positive educational atmosphere for children with a variety of special needs, some of which seem to be in direct conflict? You can ask the school system to be patient as you help the disruptive child get connected with the services he needs. But you know that could take several months at a minimum. Meanwhile your hair-pulling patient and his classmates are losing valuable educational opportunities by the day.

I don’t have the answer, but I suspect that somehow it is going to come down to affordability. Counseling, psychiatrists, and one on one classroom aids don’t come cheap, nor does the tuition for a special school in another school district. But we can’t discount the value of an education free of disruption.
 

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected]

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How’s your postacute network doing?

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Fri, 09/14/2018 - 12:00
Hospitalists should understand who is in, and the selection criteria

By now, nearly all hospitals are developing networks of postacute facilities for some or all of their patients, such as those in ACOs, bundled payments, or other value-based programs. Commonly referred to as preferred providers, performance networks, narrow networks, or similar, these networks of skilled nursing facilities (SNFs) and other entities that provide postacute care (like home health agencies) are usually chosen because they have demonstrated that they provide high quality, cost-effective care for patients after they leave the hospital.

 

While case managers are often the ones who counsel patients and caregivers on the details of the network, hospitalists should have at least a high-level grasp of which facilities are on the list and what the network selection criteria are. I would argue that hospitalists should lead the discussion with patients on postacute facility selection as it relates to which facilities are in the network and why going to a network facility is advantageous. Why? Because as hospitalist practices begin to share clinical and financial risk for patients, or at least become eligible to share in savings as MACRA encourages, they will have a vested interest in network facilities’ performance.
 

Postacute care network selection criteria

There is a range of criteria – usually incorporating measures of quality and efficiency – for including providers like SNFs in networks. In terms of quality, criteria can include physician/provider availability, star ratings on Nursing Home Compare, care transitions measures, Department of Public Health inspection survey scores, Joint Commission accreditation, etc.

Dr. Win Whitcomb
The most notable efficiency measures include readmission rates (we won’t debate here whether this should be a quality measure), cost, and length of stay in the facility. Another key driver of inclusion can be ownership status. If a SNF or other postacute provider is owned by the hospital, it may be included for that reason alone. Also, if the hospitalist group is creating the network, it may include facilities that are staffed by the group or by affiliated physicians/providers.

A few caveats regarding specific selection criteria:

Star ratings on Nursing Home Compare

These are derived from nursing staffing ratios, health inspections, and 16 quality measures. More than half of the quality measures pertain to long-stay residents who typically are not in the ACO or bundled payment program for which the network was created (these are usually short-stay patients).

SNF length of stay

High readmission rates from a SNF can actually lower its length of stay, so including “balancing” measures such as readmissions should be considered.
 

What about patient choice?

Narrow postacute networks are not only becoming the norm, but there is also broad recognition from CMS, MedPAC, and industry leaders that value-based payment programs require such networks to succeed. That said, case managers and other discharge planners may still resist networks on the grounds that they might be perceived as restricting patient choice. One approach to balancing differing views on patient choice is to give patients the traditional longer list of available postacute providers, and also furnish the shorter network list accompanied by an explanation of why certain SNFs are in the network. Thankfully, as ACOs and bundles become widespread, resistance to narrow networks is dying down.

What role should hospitalists play in network referrals?

High functioning hospitalist practices should lead the discussion with patients and the health care team on referrals to network SNFs. Why? Patients are looking for their doctors to guide them on such decisions. Only if the physician opts not to have the discussion will patients look to the case manager for direction on which postacute facility to choose. A better option still would be for the hospitalists to partner with case managers to have the conversation with patients. In such a scenario, the hospitalist can begin the discussion and cover the major points, and the case manager can follow with more detailed information. For less mature hospitalist practices, the case manager can play a larger role in the discussion. In any case, as value-based models become ubiquitous, and shared savings become a driver of hospitalist revenue, hospitalists’ knowledge of and active participation in conversations around narrow networks and referrals will be necessary.

Dr. Whitcomb is chief medical officer at Remedy Partners in Darien, Conn. He is a cofounder and past president of SHM.

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Hospitalists should understand who is in, and the selection criteria
Hospitalists should understand who is in, and the selection criteria

By now, nearly all hospitals are developing networks of postacute facilities for some or all of their patients, such as those in ACOs, bundled payments, or other value-based programs. Commonly referred to as preferred providers, performance networks, narrow networks, or similar, these networks of skilled nursing facilities (SNFs) and other entities that provide postacute care (like home health agencies) are usually chosen because they have demonstrated that they provide high quality, cost-effective care for patients after they leave the hospital.

 

While case managers are often the ones who counsel patients and caregivers on the details of the network, hospitalists should have at least a high-level grasp of which facilities are on the list and what the network selection criteria are. I would argue that hospitalists should lead the discussion with patients on postacute facility selection as it relates to which facilities are in the network and why going to a network facility is advantageous. Why? Because as hospitalist practices begin to share clinical and financial risk for patients, or at least become eligible to share in savings as MACRA encourages, they will have a vested interest in network facilities’ performance.
 

Postacute care network selection criteria

There is a range of criteria – usually incorporating measures of quality and efficiency – for including providers like SNFs in networks. In terms of quality, criteria can include physician/provider availability, star ratings on Nursing Home Compare, care transitions measures, Department of Public Health inspection survey scores, Joint Commission accreditation, etc.

Dr. Win Whitcomb
The most notable efficiency measures include readmission rates (we won’t debate here whether this should be a quality measure), cost, and length of stay in the facility. Another key driver of inclusion can be ownership status. If a SNF or other postacute provider is owned by the hospital, it may be included for that reason alone. Also, if the hospitalist group is creating the network, it may include facilities that are staffed by the group or by affiliated physicians/providers.

A few caveats regarding specific selection criteria:

Star ratings on Nursing Home Compare

These are derived from nursing staffing ratios, health inspections, and 16 quality measures. More than half of the quality measures pertain to long-stay residents who typically are not in the ACO or bundled payment program for which the network was created (these are usually short-stay patients).

SNF length of stay

High readmission rates from a SNF can actually lower its length of stay, so including “balancing” measures such as readmissions should be considered.
 

What about patient choice?

Narrow postacute networks are not only becoming the norm, but there is also broad recognition from CMS, MedPAC, and industry leaders that value-based payment programs require such networks to succeed. That said, case managers and other discharge planners may still resist networks on the grounds that they might be perceived as restricting patient choice. One approach to balancing differing views on patient choice is to give patients the traditional longer list of available postacute providers, and also furnish the shorter network list accompanied by an explanation of why certain SNFs are in the network. Thankfully, as ACOs and bundles become widespread, resistance to narrow networks is dying down.

What role should hospitalists play in network referrals?

High functioning hospitalist practices should lead the discussion with patients and the health care team on referrals to network SNFs. Why? Patients are looking for their doctors to guide them on such decisions. Only if the physician opts not to have the discussion will patients look to the case manager for direction on which postacute facility to choose. A better option still would be for the hospitalists to partner with case managers to have the conversation with patients. In such a scenario, the hospitalist can begin the discussion and cover the major points, and the case manager can follow with more detailed information. For less mature hospitalist practices, the case manager can play a larger role in the discussion. In any case, as value-based models become ubiquitous, and shared savings become a driver of hospitalist revenue, hospitalists’ knowledge of and active participation in conversations around narrow networks and referrals will be necessary.

Dr. Whitcomb is chief medical officer at Remedy Partners in Darien, Conn. He is a cofounder and past president of SHM.

By now, nearly all hospitals are developing networks of postacute facilities for some or all of their patients, such as those in ACOs, bundled payments, or other value-based programs. Commonly referred to as preferred providers, performance networks, narrow networks, or similar, these networks of skilled nursing facilities (SNFs) and other entities that provide postacute care (like home health agencies) are usually chosen because they have demonstrated that they provide high quality, cost-effective care for patients after they leave the hospital.

 

While case managers are often the ones who counsel patients and caregivers on the details of the network, hospitalists should have at least a high-level grasp of which facilities are on the list and what the network selection criteria are. I would argue that hospitalists should lead the discussion with patients on postacute facility selection as it relates to which facilities are in the network and why going to a network facility is advantageous. Why? Because as hospitalist practices begin to share clinical and financial risk for patients, or at least become eligible to share in savings as MACRA encourages, they will have a vested interest in network facilities’ performance.
 

Postacute care network selection criteria

There is a range of criteria – usually incorporating measures of quality and efficiency – for including providers like SNFs in networks. In terms of quality, criteria can include physician/provider availability, star ratings on Nursing Home Compare, care transitions measures, Department of Public Health inspection survey scores, Joint Commission accreditation, etc.

Dr. Win Whitcomb
The most notable efficiency measures include readmission rates (we won’t debate here whether this should be a quality measure), cost, and length of stay in the facility. Another key driver of inclusion can be ownership status. If a SNF or other postacute provider is owned by the hospital, it may be included for that reason alone. Also, if the hospitalist group is creating the network, it may include facilities that are staffed by the group or by affiliated physicians/providers.

A few caveats regarding specific selection criteria:

Star ratings on Nursing Home Compare

These are derived from nursing staffing ratios, health inspections, and 16 quality measures. More than half of the quality measures pertain to long-stay residents who typically are not in the ACO or bundled payment program for which the network was created (these are usually short-stay patients).

SNF length of stay

High readmission rates from a SNF can actually lower its length of stay, so including “balancing” measures such as readmissions should be considered.
 

What about patient choice?

Narrow postacute networks are not only becoming the norm, but there is also broad recognition from CMS, MedPAC, and industry leaders that value-based payment programs require such networks to succeed. That said, case managers and other discharge planners may still resist networks on the grounds that they might be perceived as restricting patient choice. One approach to balancing differing views on patient choice is to give patients the traditional longer list of available postacute providers, and also furnish the shorter network list accompanied by an explanation of why certain SNFs are in the network. Thankfully, as ACOs and bundles become widespread, resistance to narrow networks is dying down.

What role should hospitalists play in network referrals?

High functioning hospitalist practices should lead the discussion with patients and the health care team on referrals to network SNFs. Why? Patients are looking for their doctors to guide them on such decisions. Only if the physician opts not to have the discussion will patients look to the case manager for direction on which postacute facility to choose. A better option still would be for the hospitalists to partner with case managers to have the conversation with patients. In such a scenario, the hospitalist can begin the discussion and cover the major points, and the case manager can follow with more detailed information. For less mature hospitalist practices, the case manager can play a larger role in the discussion. In any case, as value-based models become ubiquitous, and shared savings become a driver of hospitalist revenue, hospitalists’ knowledge of and active participation in conversations around narrow networks and referrals will be necessary.

Dr. Whitcomb is chief medical officer at Remedy Partners in Darien, Conn. He is a cofounder and past president of SHM.

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Hypoperfusion Retinopathy

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Thu, 04/26/2018 - 08:46
By identifying ocular manifestations of cardiovascular conditions, physicians can avoid potentially serious outcomes in patients.

Cardiovascular diseases are some of the most common conditions found in the geriatric population. Ocular manifestations of systemic cardiovascular conditions often are the initial presentation of the systemic disease. Identifying these findings help reveal the underlying disease and prevent more serious visual and systemic complications or even death.

Hypoperfusion retinopathy can occur as an early manifestation of carotid occlusive disease. It results from poor arterial perfusion pressure secondary to significant or complete carotid artery blockage resulting in retinal changes. Atherosclerotic disease is generally the main culprit. Early manifestations can be seen as midperipheral retinal hemorrhages, dilated often nontortuous veins, and retinal neovascularization. Untreated or advanced cases of carotid occlusive disease can lead to a more serious ocular ischemic syndrome, which encompasses a panocular ischemia and can result in severe vision loss and neovascular glaucoma. Restoration of arterial perfusion pressure is the main goal for managing this condition.

 

Case Report

A 71-year-old white male was referred by his primary care physician (PCP) to the eye clinic for a routine comprehensive eye exam. The patient reported that his current progressive lenses, prescribed 2 years prior, were not strong enough at both distance and near, and that his eyes often felt dry. The symptoms were gradual in onset since his prior exam with no reported flashes, floaters, loss of vision, headaches, or ocular irritations.

The patient’s medical history was significant for morbid obesity, hypertension, borderline diabetes mellitus, and obstructive sleep apnea. His ocular history included recurrent conjunctivitis. At the time of the visit, the patient’s medications included 81 mg aspirin, 10 mg benazepril, 1,000 mg fish oil, 80 mg simvastatin, and use of a continuous positive airway pressure machine.

Best-corrected Snellen visual acuity was stable to his last eye exam at 20/25+2 right eye and 20/25-1 left eye with a manifest refraction of +2.25-0.75 × 077, and +2.75-1.25 × 096 in the right and left eye, respectively. Pupils were equally round and reactive to light with no afferent pupillary defect. Extraocular motility and finger counting fields were unremarkable. Anterior segment evaluation revealed lax bilateral upper lid apposition and mild cataracts in both eyes but were otherwise unremarkable (Figure 1). Dilated fundus examination revealed extensive hemorrhaging in the midperipheral retina of the right eye only (Figure 2). The left eye retina showed no abnormalities.

At this point the patient declined any additional symptoms, including eye pain, headache, transient vision loss, jaw claudication, and stroke signs. A complete blood count and hemoglobin A1c (HbA1c) was ordered, and all findings were unremarkable with no evidence of blood dyscrasia and with a HbA1c of 6.0. A carotid ultrasound (CUS) was also performed and revealed severe narrowing of the proximal section of the right internal carotid artery (ICA) with a trickle flow (Figure 3). The peak systolic velocity (PSV) at this level was 508 cm/s. There also was severe narrowing and turbulent flow in both the mid and distal portions of the right ICA. The patient was sent for a vascular evaluation 2 days following the CUS.

Based on the ocular findings and CUS results, the diagnosis of hypoperfusion retinopathy secondary to carotid occlusive disease was made. Because the patient was asymptomatic with no additional ocular sequelae, he was scheduled for an eye clinic follow-up in 2 months. The electrocardiogram, chest X-ray, and exercise stress test results were negative for acute cardiopulmonary disease, ischemia, or arrhythmias. A computed tomography angiography was performed and confirmed a high-grade lesion of the right ICA of > 95%. The vascular surgeon reported an 11% risk of stroke within 5 years and a 1% risk of stroke with surgery. Based on these results the patient underwent a right carotid endarterectomy (CEA) 2 weeks later. A follow-up CUS was performed 1 month post-CEA and revealed no abnormal fluid or significant plaque with a PSV of 92 cm/s (prior to surgery PSV was 508 cm/s) (Figure 3).

The patient returned to the eye clinic 1 month after the CEA. Gonioscopy revealed no neovascularization of the iris or angle and the dilated eye exam showed resolution of the midperipheral blot hemorrhages in his right eye with no evidence of retinal neovascularization.

Discussion

Hypoperfusion retinopathy is characterized by posterior retinal changes secondary to chronic ocular ischemia from decreased arterial perfusion related to significant or complete carotid artery stenosis.1-5 Early literature referred to this condition as venous stasis retinopathy; however, this term is misleading as the condition results from a reduction in arterial perfusion pressure and the term describes venous outflow obstruction.6 The terms carotid ischemic retinopathy, ischemic oculopathy, and hypotensive retinopathy also have been used interchangeably when describing hypoperfusion retinopathy.6

 

 

Incidence of hypoperfusion retinopathy is twice as high in males as it is in females due to a higher prevalence of cardiovascular disease.7 Hypoperfusion retinopathy rarely presents before the age of 50 years, with the average age of onset around 65 years.7 The exact rate of occurrence is unknown as this condition often is underdiagnosed because it mimics other vascular conditions, such as venous occlusive disease and diabetic retinopathy.1,7 Patients can present asymptomatically where findings are incidental on a dilated eye exam, or they may present with vision loss that can be gradual, sudden, or transient in nature.5,6,8

Gradual vision loss can follow a period of weeks to months and can occur secondary to posterior ischemia, macular edema, or choroidal hypoperfusion.1,3,8,9 Sudden vision loss can occur from severe hypoperfusion, creating an acute inner layer retinal ischemia. This type of vision loss often is accompanied by a cherry red spot in the macula and can be caused by an embolic plaque.1,8 Transient vision loss (TVL) also can be secondary to a plaque emboli or light induced. Patients with light-induced TVL report poor to blurry vision or prolonged after image when exposed to bright lights. In theory when the retina is exposed to light, there is an increase in metabolic demand that is unmet in those with choroidal vascular insufficiency from significant carotid stenosis.3,8,10

The clinical presentation most often is unilateral. Early stages of the disease generally affect the midperipheral retina but can be found in the posterior pole with chronicity. Early findings include microaneurysms, nerve fiber layer and inner retinal layer hemorrhages, and dilated, but generally not tortuous, veins.5 Chronic stage findings include arteriolar narrowing, extreme venous dilation, occasionally macular edema, and neovascularization of the disc and or retina.5 Disc edema or collaterals usually are not present.5

The mechanism behind hypoperfusion retinopathy results from an overall ischemic cascade and starts with comorbid cardiovascular conditions, such as hypertension, hypercholesterolemia, diabetes, heart disease, and history of smoking.1,2,5 These conditions play a role in creating atherosclerotic buildup in the arterial lumen leading to chronic narrowing and a decrease in arterial perfusion pressure. Over time, a low-grade hypoxic situation is formed, generating vascular endothelial cell damage and pericytes cell loss, thus causing leakage of fluid.1,2,5 With these chronic hypoxic states, angiogenic factor release eventually leads to posterior neovascularization.1,2,5 Further chronicity of carotid occlusive disease can create a panocular ischemia that also involves anterior structures, including iris, conjunctiva, episclera, or cornea. At this point, hypoperfusion retinopathy progresses to a more severe condition called ocular ischemic syndrome (OIS).2,5

Ocular ischemic syndrome can be associated with a 40% mortality rate within 5 years of onset as it is generally found in those with overall poor health.5 Along with posterior neovascularization, anterior structures also are involved. Sixty-seven percent of cases have iris or angle neovascularization of which 35% go on to develop neovascular glaucoma and its complications.1,8 With OIS, 90% of cases have some type of vision loss, and 40% report ipsilateral ocular pain.1,8 Visual loss can be gradual, sudden, or transient. The pain can occur from ocular ischemia, ruptured corneal epithelial microcysts secondary to acute glaucoma, elevated intraocular pressure (IOP) with neovascular glaucoma, or from ipsilateral dural ischemia.1,5,6,8 Fluorescein angiography is commonly used to diagnose and manage OIS, because it allows for the visualization of retinal and choroidal circulation and the detection of neovascular proliferation and ischemic areas.

Diagnostic Imaging

Several diagnostic testing strategies are available to evaluate for carotid occlusive disease. Carotid ultrasonography is a noninvasive, safe, and inexpensive screening tool to evaluate for high-grade stenosis. However, it can sometimes overestimate the degree of stenosis and is not reliable with severe calcifications.8 Computed tomography angiography and magnetic resonance angiography are minimally invasive tools that can be used to screen or confirm the degree of stenosis.8 These can be used in addition or instead of ultrasonography, especially in instances where patients have a short neck or high carotid bifurcation that may affect reliability. Both are contraindicated in those with renal failure as both modalities require the use of a contrast dye. Magnetic resonance angiography is far more expensive, time consuming, and not readily available.8 Carotid angiography is considered the gold standard for imaging the entire carotid artery system because it allows for the evaluation of plaque morphology, atherosclerotic disease, and collateral circulations.8 The disadvantages to this invasive and high-cost procedure include a risk of mortality that can occur secondary to an embolic stroke, myocardial infarction (MI), carotid artery dissection, or arterial thrombosis.8

Treatment

Treatment and management for carotid artery stenosis is focused on combined effort with the patient’s PCP and other specialists, including cardiologist, neurologist, and vascular surgeons.11 Treatment of comorbid conditions, education on healthy lifestyle, and smoking cessation are all imperative to the patient’s well-being. Managing ocular sequelae is based on specific findings and can include intravitreal antivascular edothelial growth factor or steroidal injections, pan retinal photocoagulation, or hypotensive drops.6,7

 

 

Restoration of arterial perfusion pressure is the main goal of treatment, and this can be done through CEA or carotid artery stents. Surgical intervention by CEA is determined based on each patient and his or her overall health. A full cardiac workup is required due to surgical risks. The North American Symptomatic Carotid Endarterectomy Trial evaluated symptomatic stenosis and the effectiveness of surgical intervention on stroke prevention. The trial reported that CEA was beneficial in symptomatic patients with 55% to 99% stenosis and especially in those with higher grade stenosis (> 70% up to 95%).5,7,8,12 With regard to asymptomatic patients with high-grade stenosis, CEA has been found to reduce the risk of stroke if there is at least 60% stenosis.5,7,8

Carotid artery stents can be used as an alternative when CEA is not effective or contraindicated due to a history of previous CEA, neck radiation, unstable angina, congestive heart failure, or recent MI.5,7,8 Neither CEA nor stenting is considered effective in complete occlusions due to the high risk of thromboembolism formation.5,7,8

Conclusion

Hypoperfusion retinopathy describes posterior retinal findings that occur secondary to poor arterial perfusion caused by carotid occlusive disease. Early intervention and restoration of this pressure can prevent the risk of developing a more serious condition characterized by a panocular ischemia called OIS. Unlike hypoperfusion retinopathy, OIS also includes anterior segment findings such as iris neovascularization, which may lead to neovascular glaucoma, whereas hypoperfusion retinopathy is localized to the posterior pole. Patients that develop OIS are at a 40% risk of mortality within 5 years due to poor overall health. Understanding the patient’s signs and symptoms can aid in the diagnosis of both conditions. Collaborative management with the patient’s PCP and specialists in treating comorbid conditions is vital to the patients’ well-being.

References

1. Brown GC, Magargal LE. The ocular ischemic syndrome. Int Ophthalmol. 1988;11(4):239-251.

2. Dahlman AH, McCormack D, Harrison RJ. Bilateral hypoperfuion retinopathy. J R Soc Med. 2001; 94(6):298-299.

3. Dugan JD Jr, Green WR. Ophthalmologic manifestations of carotid occlusive disease. Eye (Lond). 1991;5(pt 2):226-238.

4. Klijn CJ, Kappelle LJ, Tulleken CAF, van Gijn J. Symptomatic carotid artery occlusion. A reappraisal of hemodynamic factors. Stroke. 1997;28(10):2084-2093.

5. McCrary JA III. Venous stasis retinopathy of stenotic or occlusive caroid origin. J Clin Neuroophthalmol. 1989;9(3):195-199.

6. Sanborn GE, Magargal LE. Arterial obstructive disease of the eye. In: Tasman W, Jaeger EA, eds. Duane’s Ophthalmology. 12th ed. Vol 3. Riverwoods, IL: Lippincott Williams & Wilkins; 2013:chap 14.

7. Terelak-Borys B, Skonieczna K, Grabska-Liberek I. Ocular ischemic syndrome–a systematic review. Med Sci Monit. 2012;18(8):RA138-RA144.

8. Atebara NH, Brown GC. The ocular ischemic syndrome. In: Tasman W, Jaeger EA, eds. Duane’s Ophthalmology. 12th ed. Vol 3. Riverwoods, IL: Lippincott Williams & Wilkins; 2013:chap 12.

9. Ho AC, Lieb WE, Flaharty PM, et al. Color Doppler imaging of the ocular ischaemic syndrome. Ophthalmology. 1992;99(9):1453-1462.

10. Kahn M, Green WR, Knox DL, Miller NR. Ocular features of carotid occlusive disease. Retina. 1986;6(4):239-252.

11. Mizener JB, Podhajsky P, Hayreh SS. Ocular ischemic syndrome. Ophthalmology. 1997;104(5):859-864.

12. Ferguson GG, Eliasziw M, Barr HW, et al. The North American Symptomatic Carotid Endarterectomy Trial: surgical results in 1415 patients. Stroke. 1999;30(9):1751-1758.

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Dr. Patel was a primary care and ocular disease resident at the time this article was submitted, and Dr. Chih is the residency in primary eye care program coordinator, both at William V. Chappell, Jr. VA Satellite Outpatient Clinic in Daytona Beach, Florida. Dr. Patel currently is an optometrist at the Magruder Eye Institute in Orlando, Florida.

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The authors report no actual or potential conflicts of interest with regard to this article.

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Author disclosures
The authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of
Federal Practitioner, Frontline Medical Communications Inc., the U.S. Government, or any of its agencies.

Author and Disclosure Information

Dr. Patel was a primary care and ocular disease resident at the time this article was submitted, and Dr. Chih is the residency in primary eye care program coordinator, both at William V. Chappell, Jr. VA Satellite Outpatient Clinic in Daytona Beach, Florida. Dr. Patel currently is an optometrist at the Magruder Eye Institute in Orlando, Florida.

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Related Articles
By identifying ocular manifestations of cardiovascular conditions, physicians can avoid potentially serious outcomes in patients.
By identifying ocular manifestations of cardiovascular conditions, physicians can avoid potentially serious outcomes in patients.

Cardiovascular diseases are some of the most common conditions found in the geriatric population. Ocular manifestations of systemic cardiovascular conditions often are the initial presentation of the systemic disease. Identifying these findings help reveal the underlying disease and prevent more serious visual and systemic complications or even death.

Hypoperfusion retinopathy can occur as an early manifestation of carotid occlusive disease. It results from poor arterial perfusion pressure secondary to significant or complete carotid artery blockage resulting in retinal changes. Atherosclerotic disease is generally the main culprit. Early manifestations can be seen as midperipheral retinal hemorrhages, dilated often nontortuous veins, and retinal neovascularization. Untreated or advanced cases of carotid occlusive disease can lead to a more serious ocular ischemic syndrome, which encompasses a panocular ischemia and can result in severe vision loss and neovascular glaucoma. Restoration of arterial perfusion pressure is the main goal for managing this condition.

 

Case Report

A 71-year-old white male was referred by his primary care physician (PCP) to the eye clinic for a routine comprehensive eye exam. The patient reported that his current progressive lenses, prescribed 2 years prior, were not strong enough at both distance and near, and that his eyes often felt dry. The symptoms were gradual in onset since his prior exam with no reported flashes, floaters, loss of vision, headaches, or ocular irritations.

The patient’s medical history was significant for morbid obesity, hypertension, borderline diabetes mellitus, and obstructive sleep apnea. His ocular history included recurrent conjunctivitis. At the time of the visit, the patient’s medications included 81 mg aspirin, 10 mg benazepril, 1,000 mg fish oil, 80 mg simvastatin, and use of a continuous positive airway pressure machine.

Best-corrected Snellen visual acuity was stable to his last eye exam at 20/25+2 right eye and 20/25-1 left eye with a manifest refraction of +2.25-0.75 × 077, and +2.75-1.25 × 096 in the right and left eye, respectively. Pupils were equally round and reactive to light with no afferent pupillary defect. Extraocular motility and finger counting fields were unremarkable. Anterior segment evaluation revealed lax bilateral upper lid apposition and mild cataracts in both eyes but were otherwise unremarkable (Figure 1). Dilated fundus examination revealed extensive hemorrhaging in the midperipheral retina of the right eye only (Figure 2). The left eye retina showed no abnormalities.

At this point the patient declined any additional symptoms, including eye pain, headache, transient vision loss, jaw claudication, and stroke signs. A complete blood count and hemoglobin A1c (HbA1c) was ordered, and all findings were unremarkable with no evidence of blood dyscrasia and with a HbA1c of 6.0. A carotid ultrasound (CUS) was also performed and revealed severe narrowing of the proximal section of the right internal carotid artery (ICA) with a trickle flow (Figure 3). The peak systolic velocity (PSV) at this level was 508 cm/s. There also was severe narrowing and turbulent flow in both the mid and distal portions of the right ICA. The patient was sent for a vascular evaluation 2 days following the CUS.

Based on the ocular findings and CUS results, the diagnosis of hypoperfusion retinopathy secondary to carotid occlusive disease was made. Because the patient was asymptomatic with no additional ocular sequelae, he was scheduled for an eye clinic follow-up in 2 months. The electrocardiogram, chest X-ray, and exercise stress test results were negative for acute cardiopulmonary disease, ischemia, or arrhythmias. A computed tomography angiography was performed and confirmed a high-grade lesion of the right ICA of > 95%. The vascular surgeon reported an 11% risk of stroke within 5 years and a 1% risk of stroke with surgery. Based on these results the patient underwent a right carotid endarterectomy (CEA) 2 weeks later. A follow-up CUS was performed 1 month post-CEA and revealed no abnormal fluid or significant plaque with a PSV of 92 cm/s (prior to surgery PSV was 508 cm/s) (Figure 3).

The patient returned to the eye clinic 1 month after the CEA. Gonioscopy revealed no neovascularization of the iris or angle and the dilated eye exam showed resolution of the midperipheral blot hemorrhages in his right eye with no evidence of retinal neovascularization.

Discussion

Hypoperfusion retinopathy is characterized by posterior retinal changes secondary to chronic ocular ischemia from decreased arterial perfusion related to significant or complete carotid artery stenosis.1-5 Early literature referred to this condition as venous stasis retinopathy; however, this term is misleading as the condition results from a reduction in arterial perfusion pressure and the term describes venous outflow obstruction.6 The terms carotid ischemic retinopathy, ischemic oculopathy, and hypotensive retinopathy also have been used interchangeably when describing hypoperfusion retinopathy.6

 

 

Incidence of hypoperfusion retinopathy is twice as high in males as it is in females due to a higher prevalence of cardiovascular disease.7 Hypoperfusion retinopathy rarely presents before the age of 50 years, with the average age of onset around 65 years.7 The exact rate of occurrence is unknown as this condition often is underdiagnosed because it mimics other vascular conditions, such as venous occlusive disease and diabetic retinopathy.1,7 Patients can present asymptomatically where findings are incidental on a dilated eye exam, or they may present with vision loss that can be gradual, sudden, or transient in nature.5,6,8

Gradual vision loss can follow a period of weeks to months and can occur secondary to posterior ischemia, macular edema, or choroidal hypoperfusion.1,3,8,9 Sudden vision loss can occur from severe hypoperfusion, creating an acute inner layer retinal ischemia. This type of vision loss often is accompanied by a cherry red spot in the macula and can be caused by an embolic plaque.1,8 Transient vision loss (TVL) also can be secondary to a plaque emboli or light induced. Patients with light-induced TVL report poor to blurry vision or prolonged after image when exposed to bright lights. In theory when the retina is exposed to light, there is an increase in metabolic demand that is unmet in those with choroidal vascular insufficiency from significant carotid stenosis.3,8,10

The clinical presentation most often is unilateral. Early stages of the disease generally affect the midperipheral retina but can be found in the posterior pole with chronicity. Early findings include microaneurysms, nerve fiber layer and inner retinal layer hemorrhages, and dilated, but generally not tortuous, veins.5 Chronic stage findings include arteriolar narrowing, extreme venous dilation, occasionally macular edema, and neovascularization of the disc and or retina.5 Disc edema or collaterals usually are not present.5

The mechanism behind hypoperfusion retinopathy results from an overall ischemic cascade and starts with comorbid cardiovascular conditions, such as hypertension, hypercholesterolemia, diabetes, heart disease, and history of smoking.1,2,5 These conditions play a role in creating atherosclerotic buildup in the arterial lumen leading to chronic narrowing and a decrease in arterial perfusion pressure. Over time, a low-grade hypoxic situation is formed, generating vascular endothelial cell damage and pericytes cell loss, thus causing leakage of fluid.1,2,5 With these chronic hypoxic states, angiogenic factor release eventually leads to posterior neovascularization.1,2,5 Further chronicity of carotid occlusive disease can create a panocular ischemia that also involves anterior structures, including iris, conjunctiva, episclera, or cornea. At this point, hypoperfusion retinopathy progresses to a more severe condition called ocular ischemic syndrome (OIS).2,5

Ocular ischemic syndrome can be associated with a 40% mortality rate within 5 years of onset as it is generally found in those with overall poor health.5 Along with posterior neovascularization, anterior structures also are involved. Sixty-seven percent of cases have iris or angle neovascularization of which 35% go on to develop neovascular glaucoma and its complications.1,8 With OIS, 90% of cases have some type of vision loss, and 40% report ipsilateral ocular pain.1,8 Visual loss can be gradual, sudden, or transient. The pain can occur from ocular ischemia, ruptured corneal epithelial microcysts secondary to acute glaucoma, elevated intraocular pressure (IOP) with neovascular glaucoma, or from ipsilateral dural ischemia.1,5,6,8 Fluorescein angiography is commonly used to diagnose and manage OIS, because it allows for the visualization of retinal and choroidal circulation and the detection of neovascular proliferation and ischemic areas.

Diagnostic Imaging

Several diagnostic testing strategies are available to evaluate for carotid occlusive disease. Carotid ultrasonography is a noninvasive, safe, and inexpensive screening tool to evaluate for high-grade stenosis. However, it can sometimes overestimate the degree of stenosis and is not reliable with severe calcifications.8 Computed tomography angiography and magnetic resonance angiography are minimally invasive tools that can be used to screen or confirm the degree of stenosis.8 These can be used in addition or instead of ultrasonography, especially in instances where patients have a short neck or high carotid bifurcation that may affect reliability. Both are contraindicated in those with renal failure as both modalities require the use of a contrast dye. Magnetic resonance angiography is far more expensive, time consuming, and not readily available.8 Carotid angiography is considered the gold standard for imaging the entire carotid artery system because it allows for the evaluation of plaque morphology, atherosclerotic disease, and collateral circulations.8 The disadvantages to this invasive and high-cost procedure include a risk of mortality that can occur secondary to an embolic stroke, myocardial infarction (MI), carotid artery dissection, or arterial thrombosis.8

Treatment

Treatment and management for carotid artery stenosis is focused on combined effort with the patient’s PCP and other specialists, including cardiologist, neurologist, and vascular surgeons.11 Treatment of comorbid conditions, education on healthy lifestyle, and smoking cessation are all imperative to the patient’s well-being. Managing ocular sequelae is based on specific findings and can include intravitreal antivascular edothelial growth factor or steroidal injections, pan retinal photocoagulation, or hypotensive drops.6,7

 

 

Restoration of arterial perfusion pressure is the main goal of treatment, and this can be done through CEA or carotid artery stents. Surgical intervention by CEA is determined based on each patient and his or her overall health. A full cardiac workup is required due to surgical risks. The North American Symptomatic Carotid Endarterectomy Trial evaluated symptomatic stenosis and the effectiveness of surgical intervention on stroke prevention. The trial reported that CEA was beneficial in symptomatic patients with 55% to 99% stenosis and especially in those with higher grade stenosis (> 70% up to 95%).5,7,8,12 With regard to asymptomatic patients with high-grade stenosis, CEA has been found to reduce the risk of stroke if there is at least 60% stenosis.5,7,8

Carotid artery stents can be used as an alternative when CEA is not effective or contraindicated due to a history of previous CEA, neck radiation, unstable angina, congestive heart failure, or recent MI.5,7,8 Neither CEA nor stenting is considered effective in complete occlusions due to the high risk of thromboembolism formation.5,7,8

Conclusion

Hypoperfusion retinopathy describes posterior retinal findings that occur secondary to poor arterial perfusion caused by carotid occlusive disease. Early intervention and restoration of this pressure can prevent the risk of developing a more serious condition characterized by a panocular ischemia called OIS. Unlike hypoperfusion retinopathy, OIS also includes anterior segment findings such as iris neovascularization, which may lead to neovascular glaucoma, whereas hypoperfusion retinopathy is localized to the posterior pole. Patients that develop OIS are at a 40% risk of mortality within 5 years due to poor overall health. Understanding the patient’s signs and symptoms can aid in the diagnosis of both conditions. Collaborative management with the patient’s PCP and specialists in treating comorbid conditions is vital to the patients’ well-being.

Cardiovascular diseases are some of the most common conditions found in the geriatric population. Ocular manifestations of systemic cardiovascular conditions often are the initial presentation of the systemic disease. Identifying these findings help reveal the underlying disease and prevent more serious visual and systemic complications or even death.

Hypoperfusion retinopathy can occur as an early manifestation of carotid occlusive disease. It results from poor arterial perfusion pressure secondary to significant or complete carotid artery blockage resulting in retinal changes. Atherosclerotic disease is generally the main culprit. Early manifestations can be seen as midperipheral retinal hemorrhages, dilated often nontortuous veins, and retinal neovascularization. Untreated or advanced cases of carotid occlusive disease can lead to a more serious ocular ischemic syndrome, which encompasses a panocular ischemia and can result in severe vision loss and neovascular glaucoma. Restoration of arterial perfusion pressure is the main goal for managing this condition.

 

Case Report

A 71-year-old white male was referred by his primary care physician (PCP) to the eye clinic for a routine comprehensive eye exam. The patient reported that his current progressive lenses, prescribed 2 years prior, were not strong enough at both distance and near, and that his eyes often felt dry. The symptoms were gradual in onset since his prior exam with no reported flashes, floaters, loss of vision, headaches, or ocular irritations.

The patient’s medical history was significant for morbid obesity, hypertension, borderline diabetes mellitus, and obstructive sleep apnea. His ocular history included recurrent conjunctivitis. At the time of the visit, the patient’s medications included 81 mg aspirin, 10 mg benazepril, 1,000 mg fish oil, 80 mg simvastatin, and use of a continuous positive airway pressure machine.

Best-corrected Snellen visual acuity was stable to his last eye exam at 20/25+2 right eye and 20/25-1 left eye with a manifest refraction of +2.25-0.75 × 077, and +2.75-1.25 × 096 in the right and left eye, respectively. Pupils were equally round and reactive to light with no afferent pupillary defect. Extraocular motility and finger counting fields were unremarkable. Anterior segment evaluation revealed lax bilateral upper lid apposition and mild cataracts in both eyes but were otherwise unremarkable (Figure 1). Dilated fundus examination revealed extensive hemorrhaging in the midperipheral retina of the right eye only (Figure 2). The left eye retina showed no abnormalities.

At this point the patient declined any additional symptoms, including eye pain, headache, transient vision loss, jaw claudication, and stroke signs. A complete blood count and hemoglobin A1c (HbA1c) was ordered, and all findings were unremarkable with no evidence of blood dyscrasia and with a HbA1c of 6.0. A carotid ultrasound (CUS) was also performed and revealed severe narrowing of the proximal section of the right internal carotid artery (ICA) with a trickle flow (Figure 3). The peak systolic velocity (PSV) at this level was 508 cm/s. There also was severe narrowing and turbulent flow in both the mid and distal portions of the right ICA. The patient was sent for a vascular evaluation 2 days following the CUS.

Based on the ocular findings and CUS results, the diagnosis of hypoperfusion retinopathy secondary to carotid occlusive disease was made. Because the patient was asymptomatic with no additional ocular sequelae, he was scheduled for an eye clinic follow-up in 2 months. The electrocardiogram, chest X-ray, and exercise stress test results were negative for acute cardiopulmonary disease, ischemia, or arrhythmias. A computed tomography angiography was performed and confirmed a high-grade lesion of the right ICA of > 95%. The vascular surgeon reported an 11% risk of stroke within 5 years and a 1% risk of stroke with surgery. Based on these results the patient underwent a right carotid endarterectomy (CEA) 2 weeks later. A follow-up CUS was performed 1 month post-CEA and revealed no abnormal fluid or significant plaque with a PSV of 92 cm/s (prior to surgery PSV was 508 cm/s) (Figure 3).

The patient returned to the eye clinic 1 month after the CEA. Gonioscopy revealed no neovascularization of the iris or angle and the dilated eye exam showed resolution of the midperipheral blot hemorrhages in his right eye with no evidence of retinal neovascularization.

Discussion

Hypoperfusion retinopathy is characterized by posterior retinal changes secondary to chronic ocular ischemia from decreased arterial perfusion related to significant or complete carotid artery stenosis.1-5 Early literature referred to this condition as venous stasis retinopathy; however, this term is misleading as the condition results from a reduction in arterial perfusion pressure and the term describes venous outflow obstruction.6 The terms carotid ischemic retinopathy, ischemic oculopathy, and hypotensive retinopathy also have been used interchangeably when describing hypoperfusion retinopathy.6

 

 

Incidence of hypoperfusion retinopathy is twice as high in males as it is in females due to a higher prevalence of cardiovascular disease.7 Hypoperfusion retinopathy rarely presents before the age of 50 years, with the average age of onset around 65 years.7 The exact rate of occurrence is unknown as this condition often is underdiagnosed because it mimics other vascular conditions, such as venous occlusive disease and diabetic retinopathy.1,7 Patients can present asymptomatically where findings are incidental on a dilated eye exam, or they may present with vision loss that can be gradual, sudden, or transient in nature.5,6,8

Gradual vision loss can follow a period of weeks to months and can occur secondary to posterior ischemia, macular edema, or choroidal hypoperfusion.1,3,8,9 Sudden vision loss can occur from severe hypoperfusion, creating an acute inner layer retinal ischemia. This type of vision loss often is accompanied by a cherry red spot in the macula and can be caused by an embolic plaque.1,8 Transient vision loss (TVL) also can be secondary to a plaque emboli or light induced. Patients with light-induced TVL report poor to blurry vision or prolonged after image when exposed to bright lights. In theory when the retina is exposed to light, there is an increase in metabolic demand that is unmet in those with choroidal vascular insufficiency from significant carotid stenosis.3,8,10

The clinical presentation most often is unilateral. Early stages of the disease generally affect the midperipheral retina but can be found in the posterior pole with chronicity. Early findings include microaneurysms, nerve fiber layer and inner retinal layer hemorrhages, and dilated, but generally not tortuous, veins.5 Chronic stage findings include arteriolar narrowing, extreme venous dilation, occasionally macular edema, and neovascularization of the disc and or retina.5 Disc edema or collaterals usually are not present.5

The mechanism behind hypoperfusion retinopathy results from an overall ischemic cascade and starts with comorbid cardiovascular conditions, such as hypertension, hypercholesterolemia, diabetes, heart disease, and history of smoking.1,2,5 These conditions play a role in creating atherosclerotic buildup in the arterial lumen leading to chronic narrowing and a decrease in arterial perfusion pressure. Over time, a low-grade hypoxic situation is formed, generating vascular endothelial cell damage and pericytes cell loss, thus causing leakage of fluid.1,2,5 With these chronic hypoxic states, angiogenic factor release eventually leads to posterior neovascularization.1,2,5 Further chronicity of carotid occlusive disease can create a panocular ischemia that also involves anterior structures, including iris, conjunctiva, episclera, or cornea. At this point, hypoperfusion retinopathy progresses to a more severe condition called ocular ischemic syndrome (OIS).2,5

Ocular ischemic syndrome can be associated with a 40% mortality rate within 5 years of onset as it is generally found in those with overall poor health.5 Along with posterior neovascularization, anterior structures also are involved. Sixty-seven percent of cases have iris or angle neovascularization of which 35% go on to develop neovascular glaucoma and its complications.1,8 With OIS, 90% of cases have some type of vision loss, and 40% report ipsilateral ocular pain.1,8 Visual loss can be gradual, sudden, or transient. The pain can occur from ocular ischemia, ruptured corneal epithelial microcysts secondary to acute glaucoma, elevated intraocular pressure (IOP) with neovascular glaucoma, or from ipsilateral dural ischemia.1,5,6,8 Fluorescein angiography is commonly used to diagnose and manage OIS, because it allows for the visualization of retinal and choroidal circulation and the detection of neovascular proliferation and ischemic areas.

Diagnostic Imaging

Several diagnostic testing strategies are available to evaluate for carotid occlusive disease. Carotid ultrasonography is a noninvasive, safe, and inexpensive screening tool to evaluate for high-grade stenosis. However, it can sometimes overestimate the degree of stenosis and is not reliable with severe calcifications.8 Computed tomography angiography and magnetic resonance angiography are minimally invasive tools that can be used to screen or confirm the degree of stenosis.8 These can be used in addition or instead of ultrasonography, especially in instances where patients have a short neck or high carotid bifurcation that may affect reliability. Both are contraindicated in those with renal failure as both modalities require the use of a contrast dye. Magnetic resonance angiography is far more expensive, time consuming, and not readily available.8 Carotid angiography is considered the gold standard for imaging the entire carotid artery system because it allows for the evaluation of plaque morphology, atherosclerotic disease, and collateral circulations.8 The disadvantages to this invasive and high-cost procedure include a risk of mortality that can occur secondary to an embolic stroke, myocardial infarction (MI), carotid artery dissection, or arterial thrombosis.8

Treatment

Treatment and management for carotid artery stenosis is focused on combined effort with the patient’s PCP and other specialists, including cardiologist, neurologist, and vascular surgeons.11 Treatment of comorbid conditions, education on healthy lifestyle, and smoking cessation are all imperative to the patient’s well-being. Managing ocular sequelae is based on specific findings and can include intravitreal antivascular edothelial growth factor or steroidal injections, pan retinal photocoagulation, or hypotensive drops.6,7

 

 

Restoration of arterial perfusion pressure is the main goal of treatment, and this can be done through CEA or carotid artery stents. Surgical intervention by CEA is determined based on each patient and his or her overall health. A full cardiac workup is required due to surgical risks. The North American Symptomatic Carotid Endarterectomy Trial evaluated symptomatic stenosis and the effectiveness of surgical intervention on stroke prevention. The trial reported that CEA was beneficial in symptomatic patients with 55% to 99% stenosis and especially in those with higher grade stenosis (> 70% up to 95%).5,7,8,12 With regard to asymptomatic patients with high-grade stenosis, CEA has been found to reduce the risk of stroke if there is at least 60% stenosis.5,7,8

Carotid artery stents can be used as an alternative when CEA is not effective or contraindicated due to a history of previous CEA, neck radiation, unstable angina, congestive heart failure, or recent MI.5,7,8 Neither CEA nor stenting is considered effective in complete occlusions due to the high risk of thromboembolism formation.5,7,8

Conclusion

Hypoperfusion retinopathy describes posterior retinal findings that occur secondary to poor arterial perfusion caused by carotid occlusive disease. Early intervention and restoration of this pressure can prevent the risk of developing a more serious condition characterized by a panocular ischemia called OIS. Unlike hypoperfusion retinopathy, OIS also includes anterior segment findings such as iris neovascularization, which may lead to neovascular glaucoma, whereas hypoperfusion retinopathy is localized to the posterior pole. Patients that develop OIS are at a 40% risk of mortality within 5 years due to poor overall health. Understanding the patient’s signs and symptoms can aid in the diagnosis of both conditions. Collaborative management with the patient’s PCP and specialists in treating comorbid conditions is vital to the patients’ well-being.

References

1. Brown GC, Magargal LE. The ocular ischemic syndrome. Int Ophthalmol. 1988;11(4):239-251.

2. Dahlman AH, McCormack D, Harrison RJ. Bilateral hypoperfuion retinopathy. J R Soc Med. 2001; 94(6):298-299.

3. Dugan JD Jr, Green WR. Ophthalmologic manifestations of carotid occlusive disease. Eye (Lond). 1991;5(pt 2):226-238.

4. Klijn CJ, Kappelle LJ, Tulleken CAF, van Gijn J. Symptomatic carotid artery occlusion. A reappraisal of hemodynamic factors. Stroke. 1997;28(10):2084-2093.

5. McCrary JA III. Venous stasis retinopathy of stenotic or occlusive caroid origin. J Clin Neuroophthalmol. 1989;9(3):195-199.

6. Sanborn GE, Magargal LE. Arterial obstructive disease of the eye. In: Tasman W, Jaeger EA, eds. Duane’s Ophthalmology. 12th ed. Vol 3. Riverwoods, IL: Lippincott Williams & Wilkins; 2013:chap 14.

7. Terelak-Borys B, Skonieczna K, Grabska-Liberek I. Ocular ischemic syndrome–a systematic review. Med Sci Monit. 2012;18(8):RA138-RA144.

8. Atebara NH, Brown GC. The ocular ischemic syndrome. In: Tasman W, Jaeger EA, eds. Duane’s Ophthalmology. 12th ed. Vol 3. Riverwoods, IL: Lippincott Williams & Wilkins; 2013:chap 12.

9. Ho AC, Lieb WE, Flaharty PM, et al. Color Doppler imaging of the ocular ischaemic syndrome. Ophthalmology. 1992;99(9):1453-1462.

10. Kahn M, Green WR, Knox DL, Miller NR. Ocular features of carotid occlusive disease. Retina. 1986;6(4):239-252.

11. Mizener JB, Podhajsky P, Hayreh SS. Ocular ischemic syndrome. Ophthalmology. 1997;104(5):859-864.

12. Ferguson GG, Eliasziw M, Barr HW, et al. The North American Symptomatic Carotid Endarterectomy Trial: surgical results in 1415 patients. Stroke. 1999;30(9):1751-1758.

References

1. Brown GC, Magargal LE. The ocular ischemic syndrome. Int Ophthalmol. 1988;11(4):239-251.

2. Dahlman AH, McCormack D, Harrison RJ. Bilateral hypoperfuion retinopathy. J R Soc Med. 2001; 94(6):298-299.

3. Dugan JD Jr, Green WR. Ophthalmologic manifestations of carotid occlusive disease. Eye (Lond). 1991;5(pt 2):226-238.

4. Klijn CJ, Kappelle LJ, Tulleken CAF, van Gijn J. Symptomatic carotid artery occlusion. A reappraisal of hemodynamic factors. Stroke. 1997;28(10):2084-2093.

5. McCrary JA III. Venous stasis retinopathy of stenotic or occlusive caroid origin. J Clin Neuroophthalmol. 1989;9(3):195-199.

6. Sanborn GE, Magargal LE. Arterial obstructive disease of the eye. In: Tasman W, Jaeger EA, eds. Duane’s Ophthalmology. 12th ed. Vol 3. Riverwoods, IL: Lippincott Williams & Wilkins; 2013:chap 14.

7. Terelak-Borys B, Skonieczna K, Grabska-Liberek I. Ocular ischemic syndrome–a systematic review. Med Sci Monit. 2012;18(8):RA138-RA144.

8. Atebara NH, Brown GC. The ocular ischemic syndrome. In: Tasman W, Jaeger EA, eds. Duane’s Ophthalmology. 12th ed. Vol 3. Riverwoods, IL: Lippincott Williams & Wilkins; 2013:chap 12.

9. Ho AC, Lieb WE, Flaharty PM, et al. Color Doppler imaging of the ocular ischaemic syndrome. Ophthalmology. 1992;99(9):1453-1462.

10. Kahn M, Green WR, Knox DL, Miller NR. Ocular features of carotid occlusive disease. Retina. 1986;6(4):239-252.

11. Mizener JB, Podhajsky P, Hayreh SS. Ocular ischemic syndrome. Ophthalmology. 1997;104(5):859-864.

12. Ferguson GG, Eliasziw M, Barr HW, et al. The North American Symptomatic Carotid Endarterectomy Trial: surgical results in 1415 patients. Stroke. 1999;30(9):1751-1758.

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