American Medical Directors Association (AMDA): Long Term Care Medicine-2011

TAMPA – The treatment of osteoporosis is in flux because of a variety of forces, including a substantial increase in the number of aging patients deemed eligible for treatments, a leading geriatrician said. Just as baby boomers begin reaching senior status, a recently developed tool for assessing people’s fracture risk is increasing the number of patients considered suitable for preventive therapy.

Meanwhile, those therapy options are multiplying, and emerging evidence suggests that one, bisphosphonates, is associated with an increased risk for atypical fractures, although the absolute risk appears to be low, Dr. Barbara Messinger-Rapport, said at the AMDA Dedicated to Long Term Care Medicine annual meeting.

The assessment tool making a difference is the Web-based Fracture Risk Assessment Tool (FRAX), released by the World Health Organization in 2008. FRAX guides clinicians to consider drug therapy for patients with T scores (deviations from healthy bone density) of –2.5 or lower at the femoral neck or spine, a T score between –1.0 and –2.5 as well as a 3% or higher calculated risk for hip fracture over 10 years, or a 20% or greater risk of major osteoporosis-related fracture.

Even if a person’s T score never reaches –2.5, his or her hip fracture risk can climb to 3% or higher, said Dr. Messinger-Rapport, director of the Center for Geriatric Medicine at the Cleveland Clinic and medical director of the Fairfax Health Care Center Nursing Home, also in Cleveland. "This could widen the number of people who could be put on treatment."

Bisphosphonates remain the most-common treatment strategy, but optimal duration of therapy, timing of drug holidays, and how age and gender play into risk for adverse events remains unclear, she said.

A newer option, the monoclonal antibody denosumab (Prolia, Amgen), significantly reduced vertebral fractures compared with a placebo in published studies. Administered as a subcutaneous injection every 6 months, denosumab also may be more convenient than agents requiring infusion, Dr. Messinger-Rapport said.

Higher cost is a consideration, however. Wholesale cost of denosumab is approximately $850/60-mg subcutaneous injection. In contrast, generic alendronate costs $100-$200/year; brand-name oral bisphosphonate costs up to $1,000/year; and zoledronic acid, delivered via intravenous infusion, is approximately $1,100/year, she said.

Denosumab’s impact on clinical care is not yet know, Dr. Messinger-Rapport said. She suggested that clinicians consider this agent in high-risk elders, women or men with osteoporosis, men with prostate cancer with androgen deprivation, patients with metastatic prostate or breast cancer, and possibly patients with renal impairment (denosumab clearance is not renal). Also consider denosumab for patients who cannot tolerate a bisphosphonate either orally or by infusion, she added.

Researchers showed a 68% decrease in vertebral fractures, a 40% decline in hip fractures, and a 20% decrease in nonvertebral fractures with denosumab versus placebo in the FREEDOM study of osteoporotic women treated for 36 months (N. Engl. J. Med. 2009;361:756-65). A similar 62% decrease in vertebral fractures with denosumab, compared with placebo, was observed in a 24-month study of men with androgen deprivation for prostate cancer (N. Engl. J. Med. 2009;361:745-55).

Researchers also have examined reports of atypical femoral fractures associated with bisphosphonate use and found an association. For example, in a study published last year, 17 of 20 atypical femoral fractures occurred in patients taking oral bisphosphonates (N. Engl. J. Med. 2010;363:1848-9). In a New England Journal letter (N. Engl. J. Med. 2010;362:1848-9), the researchers stated that although they found the association, "overall the anti-fracture effects of bisphosphonates far outweigh their potential risks."

More recently, other investigators found an increased risk of subtrochanteric and femoral shaft fractures in women treated for 5 years or more with oral bisphosphonates (JAMA 2011;305:783-9). The authors stated that the absolute risk of the atypical fractures is low, however.

Dr. Messinger-Rapport listed contraindications to bisphosphonates as a prior allergic reaction, vitamin D depletion (less than 30 ng/mL), hypocalcemia, dysphagia, esophageal disorders, and severe gastroesophageal reflux disorder.

A person attending the meeting asked if it is appropriate to continue bisphosphonate therapy after a patient’s T score improves. "Yes, even if the T score only improves by a few percentage points," Dr. Messinger-Rapport replied, because there is a disproportionate benefit in terms of fracture risk reduction.

Dr. Messinger-Rapport disclosed that she is an editorial board member for the National Osteoporosis Foundation.

TAMPA – The treatment of osteoporosis is in flux because of a variety of forces, including a substantial increase in the number of aging patients deemed eligible for treatments, a leading geriatrician said. Just as baby boomers begin reaching senior status, a recently developed tool for assessing people’s fracture risk is increasing the number of patients considered suitable for preventive therapy.

Meanwhile, those therapy options are multiplying, and emerging evidence suggests that one, bisphosphonates, is associated with an increased risk for atypical fractures, although the absolute risk appears to be low, Dr. Barbara Messinger-Rapport, said at the AMDA Dedicated to Long Term Care Medicine annual meeting.

The assessment tool making a difference is the Web-based Fracture Risk Assessment Tool (FRAX), released by the World Health Organization in 2008. FRAX guides clinicians to consider drug therapy for patients with T scores (deviations from healthy bone density) of –2.5 or lower at the femoral neck or spine, a T score between –1.0 and –2.5 as well as a 3% or higher calculated risk for hip fracture over 10 years, or a 20% or greater risk of major osteoporosis-related fracture.

Even if a person’s T score never reaches –2.5, his or her hip fracture risk can climb to 3% or higher, said Dr. Messinger-Rapport, director of the Center for Geriatric Medicine at the Cleveland Clinic and medical director of the Fairfax Health Care Center Nursing Home, also in Cleveland. "This could widen the number of people who could be put on treatment."

Bisphosphonates remain the most-common treatment strategy, but optimal duration of therapy, timing of drug holidays, and how age and gender play into risk for adverse events remains unclear, she said.

A newer option, the monoclonal antibody denosumab (Prolia, Amgen), significantly reduced vertebral fractures compared with a placebo in published studies. Administered as a subcutaneous injection every 6 months, denosumab also may be more convenient than agents requiring infusion, Dr. Messinger-Rapport said.

Higher cost is a consideration, however. Wholesale cost of denosumab is approximately $850/60-mg subcutaneous injection. In contrast, generic alendronate costs $100-$200/year; brand-name oral bisphosphonate costs up to $1,000/year; and zoledronic acid, delivered via intravenous infusion, is approximately $1,100/year, she said.

Denosumab’s impact on clinical care is not yet know, Dr. Messinger-Rapport said. She suggested that clinicians consider this agent in high-risk elders, women or men with osteoporosis, men with prostate cancer with androgen deprivation, patients with metastatic prostate or breast cancer, and possibly patients with renal impairment (denosumab clearance is not renal). Also consider denosumab for patients who cannot tolerate a bisphosphonate either orally or by infusion, she added.

Researchers showed a 68% decrease in vertebral fractures, a 40% decline in hip fractures, and a 20% decrease in nonvertebral fractures with denosumab versus placebo in the FREEDOM study of osteoporotic women treated for 36 months (N. Engl. J. Med. 2009;361:756-65). A similar 62% decrease in vertebral fractures with denosumab, compared with placebo, was observed in a 24-month study of men with androgen deprivation for prostate cancer (N. Engl. J. Med. 2009;361:745-55).

Researchers also have examined reports of atypical femoral fractures associated with bisphosphonate use and found an association. For example, in a study published last year, 17 of 20 atypical femoral fractures occurred in patients taking oral bisphosphonates (N. Engl. J. Med. 2010;363:1848-9). In a New England Journal letter (N. Engl. J. Med. 2010;362:1848-9), the researchers stated that although they found the association, "overall the anti-fracture effects of bisphosphonates far outweigh their potential risks."

More recently, other investigators found an increased risk of subtrochanteric and femoral shaft fractures in women treated for 5 years or more with oral bisphosphonates (JAMA 2011;305:783-9). The authors stated that the absolute risk of the atypical fractures is low, however.

Dr. Messinger-Rapport listed contraindications to bisphosphonates as a prior allergic reaction, vitamin D depletion (less than 30 ng/mL), hypocalcemia, dysphagia, esophageal disorders, and severe gastroesophageal reflux disorder.

A person attending the meeting asked if it is appropriate to continue bisphosphonate therapy after a patient’s T score improves. "Yes, even if the T score only improves by a few percentage points," Dr. Messinger-Rapport replied, because there is a disproportionate benefit in terms of fracture risk reduction.

Dr. Messinger-Rapport disclosed that she is an editorial board member for the National Osteoporosis Foundation.

TAMPA – The treatment of osteoporosis is in flux because of a variety of forces, including a substantial increase in the number of aging patients deemed eligible for treatments, a leading geriatrician said. Just as baby boomers begin reaching senior status, a recently developed tool for assessing people’s fracture risk is increasing the number of patients considered suitable for preventive therapy.

Meanwhile, those therapy options are multiplying, and emerging evidence suggests that one, bisphosphonates, is associated with an increased risk for atypical fractures, although the absolute risk appears to be low, Dr. Barbara Messinger-Rapport, said at the AMDA Dedicated to Long Term Care Medicine annual meeting.

The assessment tool making a difference is the Web-based Fracture Risk Assessment Tool (FRAX), released by the World Health Organization in 2008. FRAX guides clinicians to consider drug therapy for patients with T scores (deviations from healthy bone density) of –2.5 or lower at the femoral neck or spine, a T score between –1.0 and –2.5 as well as a 3% or higher calculated risk for hip fracture over 10 years, or a 20% or greater risk of major osteoporosis-related fracture.

Even if a person’s T score never reaches –2.5, his or her hip fracture risk can climb to 3% or higher, said Dr. Messinger-Rapport, director of the Center for Geriatric Medicine at the Cleveland Clinic and medical director of the Fairfax Health Care Center Nursing Home, also in Cleveland. "This could widen the number of people who could be put on treatment."

Bisphosphonates remain the most-common treatment strategy, but optimal duration of therapy, timing of drug holidays, and how age and gender play into risk for adverse events remains unclear, she said.

A newer option, the monoclonal antibody denosumab (Prolia, Amgen), significantly reduced vertebral fractures compared with a placebo in published studies. Administered as a subcutaneous injection every 6 months, denosumab also may be more convenient than agents requiring infusion, Dr. Messinger-Rapport said.

Higher cost is a consideration, however. Wholesale cost of denosumab is approximately $850/60-mg subcutaneous injection. In contrast, generic alendronate costs $100-$200/year; brand-name oral bisphosphonate costs up to $1,000/year; and zoledronic acid, delivered via intravenous infusion, is approximately $1,100/year, she said.

Denosumab’s impact on clinical care is not yet know, Dr. Messinger-Rapport said. She suggested that clinicians consider this agent in high-risk elders, women or men with osteoporosis, men with prostate cancer with androgen deprivation, patients with metastatic prostate or breast cancer, and possibly patients with renal impairment (denosumab clearance is not renal). Also consider denosumab for patients who cannot tolerate a bisphosphonate either orally or by infusion, she added.

Researchers showed a 68% decrease in vertebral fractures, a 40% decline in hip fractures, and a 20% decrease in nonvertebral fractures with denosumab versus placebo in the FREEDOM study of osteoporotic women treated for 36 months (N. Engl. J. Med. 2009;361:756-65). A similar 62% decrease in vertebral fractures with denosumab, compared with placebo, was observed in a 24-month study of men with androgen deprivation for prostate cancer (N. Engl. J. Med. 2009;361:745-55).

Researchers also have examined reports of atypical femoral fractures associated with bisphosphonate use and found an association. For example, in a study published last year, 17 of 20 atypical femoral fractures occurred in patients taking oral bisphosphonates (N. Engl. J. Med. 2010;363:1848-9). In a New England Journal letter (N. Engl. J. Med. 2010;362:1848-9), the researchers stated that although they found the association, "overall the anti-fracture effects of bisphosphonates far outweigh their potential risks."

More recently, other investigators found an increased risk of subtrochanteric and femoral shaft fractures in women treated for 5 years or more with oral bisphosphonates (JAMA 2011;305:783-9). The authors stated that the absolute risk of the atypical fractures is low, however.

Dr. Messinger-Rapport listed contraindications to bisphosphonates as a prior allergic reaction, vitamin D depletion (less than 30 ng/mL), hypocalcemia, dysphagia, esophageal disorders, and severe gastroesophageal reflux disorder.

A person attending the meeting asked if it is appropriate to continue bisphosphonate therapy after a patient’s T score improves. "Yes, even if the T score only improves by a few percentage points," Dr. Messinger-Rapport replied, because there is a disproportionate benefit in terms of fracture risk reduction.

Dr. Messinger-Rapport disclosed that she is an editorial board member for the National Osteoporosis Foundation.

TAMPA – The treatment of osteoporosis is in flux because of a variety of forces, including a substantial increase in the number of aging patients deemed eligible for treatments, a leading geriatrician said. Just as baby boomers begin reaching senior status, a recently developed tool for assessing people’s fracture risk is increasing the number of patients considered suitable for preventive therapy.

Meanwhile, those therapy options are multiplying, and emerging evidence suggests that one, bisphosphonates, is associated with an increased risk for atypical fractures, although the absolute risk appears to be low, Dr. Barbara Messinger-Rapport, said at the AMDA Dedicated to Long Term Care Medicine annual meeting.

The assessment tool making a difference is the Web-based Fracture Risk Assessment Tool (FRAX), released by the World Health Organization in 2008. FRAX guides clinicians to consider drug therapy for patients with T scores (deviations from healthy bone density) of –2.5 or lower at the femoral neck or spine, a T score between –1.0 and –2.5 as well as a 3% or higher calculated risk for hip fracture over 10 years, or a 20% or greater risk of major osteoporosis-related fracture.

Even if a person’s T score never reaches –2.5, his or her hip fracture risk can climb to 3% or higher, said Dr. Messinger-Rapport, director of the Center for Geriatric Medicine at the Cleveland Clinic and medical director of the Fairfax Health Care Center Nursing Home, also in Cleveland. "This could widen the number of people who could be put on treatment."

Bisphosphonates remain the most-common treatment strategy, but optimal duration of therapy, timing of drug holidays, and how age and gender play into risk for adverse events remains unclear, she said.

A newer option, the monoclonal antibody denosumab (Prolia, Amgen), significantly reduced vertebral fractures compared with a placebo in published studies. Administered as a subcutaneous injection every 6 months, denosumab also may be more convenient than agents requiring infusion, Dr. Messinger-Rapport said.

Higher cost is a consideration, however. Wholesale cost of denosumab is approximately $850/60-mg subcutaneous injection. In contrast, generic alendronate costs $100-$200/year; brand-name oral bisphosphonate costs up to $1,000/year; and zoledronic acid, delivered via intravenous infusion, is approximately $1,100/year, she said.

Denosumab’s impact on clinical care is not yet know, Dr. Messinger-Rapport said. She suggested that clinicians consider this agent in high-risk elders, women or men with osteoporosis, men with prostate cancer with androgen deprivation, patients with metastatic prostate or breast cancer, and possibly patients with renal impairment (denosumab clearance is not renal). Also consider denosumab for patients who cannot tolerate a bisphosphonate either orally or by infusion, she added.

Researchers showed a 68% decrease in vertebral fractures, a 40% decline in hip fractures, and a 20% decrease in nonvertebral fractures with denosumab versus placebo in the FREEDOM study of osteoporotic women treated for 36 months (N. Engl. J. Med. 2009;361:756-65). A similar 62% decrease in vertebral fractures with denosumab, compared with placebo, was observed in a 24-month study of men with androgen deprivation for prostate cancer (N. Engl. J. Med. 2009;361:745-55).

Researchers also have examined reports of atypical femoral fractures associated with bisphosphonate use and found an association. For example, in a study published last year, 17 of 20 atypical femoral fractures occurred in patients taking oral bisphosphonates (N. Engl. J. Med. 2010;363:1848-9). In a New England Journal letter (N. Engl. J. Med. 2010;362:1848-9), the researchers stated that although they found the association, "overall the anti-fracture effects of bisphosphonates far outweigh their potential risks."

More recently, other investigators found an increased risk of subtrochanteric and femoral shaft fractures in women treated for 5 years or more with oral bisphosphonates (JAMA 2011;305:783-9). The authors stated that the absolute risk of the atypical fractures is low, however.

Dr. Messinger-Rapport listed contraindications to bisphosphonates as a prior allergic reaction, vitamin D depletion (less than 30 ng/mL), hypocalcemia, dysphagia, esophageal disorders, and severe gastroesophageal reflux disorder.

A person attending the meeting asked if it is appropriate to continue bisphosphonate therapy after a patient’s T score improves. "Yes, even if the T score only improves by a few percentage points," Dr. Messinger-Rapport replied, because there is a disproportionate benefit in terms of fracture risk reduction.

Dr. Messinger-Rapport disclosed that she is an editorial board member for the National Osteoporosis Foundation.

TAMPA – The treatment of osteoporosis is in flux because of a variety of forces, including a substantial increase in the number of aging patients deemed eligible for treatments, a leading geriatrician said. Just as baby boomers begin reaching senior status, a recently developed tool for assessing people’s fracture risk is increasing the number of patients considered suitable for preventive therapy.

Meanwhile, those therapy options are multiplying, and emerging evidence suggests that one, bisphosphonates, is associated with an increased risk for atypical fractures, although the absolute risk appears to be low, Dr. Barbara Messinger-Rapport, said at the AMDA Dedicated to Long Term Care Medicine annual meeting.

The assessment tool making a difference is the Web-based Fracture Risk Assessment Tool (FRAX), released by the World Health Organization in 2008. FRAX guides clinicians to consider drug therapy for patients with T scores (deviations from healthy bone density) of –2.5 or lower at the femoral neck or spine, a T score between –1.0 and –2.5 as well as a 3% or higher calculated risk for hip fracture over 10 years, or a 20% or greater risk of major osteoporosis-related fracture.

Even if a person’s T score never reaches –2.5, his or her hip fracture risk can climb to 3% or higher, said Dr. Messinger-Rapport, director of the Center for Geriatric Medicine at the Cleveland Clinic and medical director of the Fairfax Health Care Center Nursing Home, also in Cleveland. "This could widen the number of people who could be put on treatment."

Bisphosphonates remain the most-common treatment strategy, but optimal duration of therapy, timing of drug holidays, and how age and gender play into risk for adverse events remains unclear, she said.

A newer option, the monoclonal antibody denosumab (Prolia, Amgen), significantly reduced vertebral fractures compared with a placebo in published studies. Administered as a subcutaneous injection every 6 months, denosumab also may be more convenient than agents requiring infusion, Dr. Messinger-Rapport said.

Higher cost is a consideration, however. Wholesale cost of denosumab is approximately $850/60-mg subcutaneous injection. In contrast, generic alendronate costs $100-$200/year; brand-name oral bisphosphonate costs up to $1,000/year; and zoledronic acid, delivered via intravenous infusion, is approximately $1,100/year, she said.

Denosumab’s impact on clinical care is not yet know, Dr. Messinger-Rapport said. She suggested that clinicians consider this agent in high-risk elders, women or men with osteoporosis, men with prostate cancer with androgen deprivation, patients with metastatic prostate or breast cancer, and possibly patients with renal impairment (denosumab clearance is not renal). Also consider denosumab for patients who cannot tolerate a bisphosphonate either orally or by infusion, she added.

Researchers showed a 68% decrease in vertebral fractures, a 40% decline in hip fractures, and a 20% decrease in nonvertebral fractures with denosumab versus placebo in the FREEDOM study of osteoporotic women treated for 36 months (N. Engl. J. Med. 2009;361:756-65). A similar 62% decrease in vertebral fractures with denosumab, compared with placebo, was observed in a 24-month study of men with androgen deprivation for prostate cancer (N. Engl. J. Med. 2009;361:745-55).

Researchers also have examined reports of atypical femoral fractures associated with bisphosphonate use and found an association. For example, in a study published last year, 17 of 20 atypical femoral fractures occurred in patients taking oral bisphosphonates (N. Engl. J. Med. 2010;363:1848-9). In a New England Journal letter (N. Engl. J. Med. 2010;362:1848-9), the researchers stated that although they found the association, "overall the anti-fracture effects of bisphosphonates far outweigh their potential risks."

More recently, other investigators found an increased risk of subtrochanteric and femoral shaft fractures in women treated for 5 years or more with oral bisphosphonates (JAMA 2011;305:783-9). The authors stated that the absolute risk of the atypical fractures is low, however.

Dr. Messinger-Rapport listed contraindications to bisphosphonates as a prior allergic reaction, vitamin D depletion (less than 30 ng/mL), hypocalcemia, dysphagia, esophageal disorders, and severe gastroesophageal reflux disorder.

A person attending the meeting asked if it is appropriate to continue bisphosphonate therapy after a patient’s T score improves. "Yes, even if the T score only improves by a few percentage points," Dr. Messinger-Rapport replied, because there is a disproportionate benefit in terms of fracture risk reduction.

Dr. Messinger-Rapport disclosed that she is an editorial board member for the National Osteoporosis Foundation.

TAMPA – The treatment of osteoporosis is in flux because of a variety of forces, including a substantial increase in the number of aging patients deemed eligible for treatments, a leading geriatrician said. Just as baby boomers begin reaching senior status, a recently developed tool for assessing people’s fracture risk is increasing the number of patients considered suitable for preventive therapy.

Meanwhile, those therapy options are multiplying, and emerging evidence suggests that one, bisphosphonates, is associated with an increased risk for atypical fractures, although the absolute risk appears to be low, Dr. Barbara Messinger-Rapport, said at the AMDA Dedicated to Long Term Care Medicine annual meeting.

The assessment tool making a difference is the Web-based Fracture Risk Assessment Tool (FRAX), released by the World Health Organization in 2008. FRAX guides clinicians to consider drug therapy for patients with T scores (deviations from healthy bone density) of –2.5 or lower at the femoral neck or spine, a T score between –1.0 and –2.5 as well as a 3% or higher calculated risk for hip fracture over 10 years, or a 20% or greater risk of major osteoporosis-related fracture.

Even if a person’s T score never reaches –2.5, his or her hip fracture risk can climb to 3% or higher, said Dr. Messinger-Rapport, director of the Center for Geriatric Medicine at the Cleveland Clinic and medical director of the Fairfax Health Care Center Nursing Home, also in Cleveland. "This could widen the number of people who could be put on treatment."

Bisphosphonates remain the most-common treatment strategy, but optimal duration of therapy, timing of drug holidays, and how age and gender play into risk for adverse events remains unclear, she said.

A newer option, the monoclonal antibody denosumab (Prolia, Amgen), significantly reduced vertebral fractures compared with a placebo in published studies. Administered as a subcutaneous injection every 6 months, denosumab also may be more convenient than agents requiring infusion, Dr. Messinger-Rapport said.

Higher cost is a consideration, however. Wholesale cost of denosumab is approximately $850/60-mg subcutaneous injection. In contrast, generic alendronate costs $100-$200/year; brand-name oral bisphosphonate costs up to $1,000/year; and zoledronic acid, delivered via intravenous infusion, is approximately $1,100/year, she said.

Denosumab’s impact on clinical care is not yet know, Dr. Messinger-Rapport said. She suggested that clinicians consider this agent in high-risk elders, women or men with osteoporosis, men with prostate cancer with androgen deprivation, patients with metastatic prostate or breast cancer, and possibly patients with renal impairment (denosumab clearance is not renal). Also consider denosumab for patients who cannot tolerate a bisphosphonate either orally or by infusion, she added.

Researchers showed a 68% decrease in vertebral fractures, a 40% decline in hip fractures, and a 20% decrease in nonvertebral fractures with denosumab versus placebo in the FREEDOM study of osteoporotic women treated for 36 months (N. Engl. J. Med. 2009;361:756-65). A similar 62% decrease in vertebral fractures with denosumab, compared with placebo, was observed in a 24-month study of men with androgen deprivation for prostate cancer (N. Engl. J. Med. 2009;361:745-55).

Researchers also have examined reports of atypical femoral fractures associated with bisphosphonate use and found an association. For example, in a study published last year, 17 of 20 atypical femoral fractures occurred in patients taking oral bisphosphonates (N. Engl. J. Med. 2010;363:1848-9). In a New England Journal letter (N. Engl. J. Med. 2010;362:1848-9), the researchers stated that although they found the association, "overall the anti-fracture effects of bisphosphonates far outweigh their potential risks."

More recently, other investigators found an increased risk of subtrochanteric and femoral shaft fractures in women treated for 5 years or more with oral bisphosphonates (JAMA 2011;305:783-9). The authors stated that the absolute risk of the atypical fractures is low, however.

Dr. Messinger-Rapport listed contraindications to bisphosphonates as a prior allergic reaction, vitamin D depletion (less than 30 ng/mL), hypocalcemia, dysphagia, esophageal disorders, and severe gastroesophageal reflux disorder.

A person attending the meeting asked if it is appropriate to continue bisphosphonate therapy after a patient’s T score improves. "Yes, even if the T score only improves by a few percentage points," Dr. Messinger-Rapport replied, because there is a disproportionate benefit in terms of fracture risk reduction.

Dr. Messinger-Rapport disclosed that she is an editorial board member for the National Osteoporosis Foundation.

TAMPA – Sharing bad news with patients might not be easy, but it’s a skill physicians can learn and as important as knowing how to ready an EKG or an x-ray, James A. Avery, MD, CMD, said.

"What I am proposing is that giving bad news well is a fundamental long-term care physician skill, and competence in this area is critical," Dr. Avery said at this year’s AMDA – Dedicated to Long Term Medicine annual meeting.

"Giving bad news ... takes desire, courage, and practice," said Dr. Avery. "Patients deserve to get bad news delivered with compassion, hope, and integrity."

Plan ahead for the conversation; start with what the patient knows and wants to know; and develop a compassionate tone, said Dr. Avery, chief medical officer at Golden Living in Washington, a corporation that focuses on skilled nursing, assisted living, and rehabilitation therapy. Also, always provide an appropriate prognosis. "It’s your obligation to bring this up. Patients and families may be afraid to ask."

What can happen if the conversation is not done correctly? "If bad news is given poorly, it can rob hope and create distress, confusion, and anxiety. It can weaken the patient’s faith and set off a chain of events that adversely affects the survivors for years," said Dr. Avery.

"I was particularly bad at giving bad news at first," he said. A pulmonologist by training, he also worked for years in hospice care in both Florida and New York. He spoke with patients who transitioned to hospice from Memorial Sloan-Kettering Cancer Center, for example.

"I learned quickly that if I was going to give bad news, not to schedule the patient for midmorning on a Monday. It is too chaotic," Dr. Avery said. Schedule the patient for the first appointment after lunch or at the end of the day. Allow sufficient time and create a comfortable, private place with tissues available, he added.

Next, determine where each patient is in terms of understanding his or her illness. "Explore and ask," Dr. Avery said. Good questions include:

• Is there anyone else you want to have in the conversation?
• How do you understand what has happened to you medically?
• What have doctors told you about this illness?
• What do you think caused this illness?

"I cannot tell you how many patients with colon cancer thought they had it because they took too many antacids," Dr. Avery said. "Also, I had one woman with breast cancer who responded ‘Burger King.’ She had read an article that fatty foods caused breast cancer. She had guilt that she was leaving her family because she ate burgers instead of salads."

Also, determine how much the patient wants to know. "About 90% of patients want full information [about their condition], but everyone wants to know everything about treatment." Physicians also can be instrumental in allaying end-of-life fears, Dr. Avery said. Regardless of illness, most patients think some symptom is going to get worse and worse and crescendo in pain before they die. "How do people with [chronic obstructive pulmonary disease] die? Yes, the symptoms get worse, but with COPD, they get COPD narcosis, get sleepy, and drift away."

Intentionally develop and use a compassionate tone, Dr. Avery said. This is important because patients surveyed after they received bad news said the attitude of the person who spoke with them was the most important factor. The clarity of the message and privacy were also important, but they ranked far behind clinician attitude, he said.

Allow for silence. Let the message to sink in. "Give the patient plenty of time to react, respond, and ask questions." Also allow tears – "That can be a real problem for a lot of doctors."

A challenge for physicians is to be empathetic without breaking down completely, Dr. Avery said. When working in hospice care in New York, he frequently spent the day traveling by subway to clients’ residences. "Am I going to travel around weeping? No. You have to somehow try to meet where they are, but you cannot go there completely. It would be self-destructive."

"One reason physicians think they do not give bad news well is they fear their own response; that they will break down," Dr. Avery said. Try to determine the patient’s attitude and reflect it back to them. "This is what you do when things get emotional. And they will correct you if you’re wrong. If you say ‘You sound angry,’ they might say ‘No, I’m upset.’"

Another important thing to ask patients is "Have the doctors told you how long you have?" An accurate prognosis will help patients and family prepare, Dr. Avery said. "You have to tell them. If you don’t, they will seek a second opinion and/or leave the long-term care setting, because no one has told them." Less-experienced doctors and doctors who have had long and strong relationship with a patient can be especially poor at prognostication, he said.

Be completely honest and avoid stating a precise amount of time, such as "3 months." "I say, ‘It could be weeks instead of months,’ or, ‘It could be months instead of years.’ If they ask for a more precise prognosis, tell them it’s difficult to say, because it is," Dr. Avery said.

If you still do not feel comfortable giving a patient bad news, refer the patient to someone who does. "Call in hospice, call in palliative care. If you cannot give that bad news, you are obligated to do this," Dr. Avery said.

If your attitude is right and you’re speaking with a compassionate tone, what else should you keep in mind when giving a patient bad news?

Watch your body language, because about 90% of communication is nonverbal, Dr. Avery said. Make eye contact, for example.

Do not sound matter of fact. "Patients will say the doctor appears bored," Dr. Avery explained. At the same time, avoid rambling, he advised. A good way to do this is intentionally pause on a frequent basis. Develop a technique to slow yourself down. Dr. Avery said he silently counts backward from 10 to slow himself down, for example.

Provide information in small chunks. This is better than "the information dump," which is a tendency to disclose every detail to a patient when initial bad news is shared.

"I tell the patient she can raise her hand and stop me if it’s too much information at any point," he said.

Never say, ‘There is nothing more I can do for you," Dr. Avery advised. He said he often tells patients that there is nothing more he can do for their dementia or their cancer, "but there is a lot I can do for you as a person. ... Otherwise, you are referring to them as a lung cancer, and you’ve reduced them to an organ with a disease."

You also can admit the limitations of medicine, Dr. Avery said. "You can say, for example, ‘I wish we had more effective therapy for your condition,’ or ‘I wish I had a magic pill or magic wand I could use it to take away your cancer.’ "

Dr. Avery said that he had no relevant financial conflict of interest.

TAMPA – Sharing bad news with patients might not be easy, but it’s a skill physicians can learn and as important as knowing how to ready an EKG or an x-ray, James A. Avery, MD, CMD, said.

"What I am proposing is that giving bad news well is a fundamental long-term care physician skill, and competence in this area is critical," Dr. Avery said at this year’s AMDA – Dedicated to Long Term Medicine annual meeting.

"Giving bad news ... takes desire, courage, and practice," said Dr. Avery. "Patients deserve to get bad news delivered with compassion, hope, and integrity."

Plan ahead for the conversation; start with what the patient knows and wants to know; and develop a compassionate tone, said Dr. Avery, chief medical officer at Golden Living in Washington, a corporation that focuses on skilled nursing, assisted living, and rehabilitation therapy. Also, always provide an appropriate prognosis. "It’s your obligation to bring this up. Patients and families may be afraid to ask."

What can happen if the conversation is not done correctly? "If bad news is given poorly, it can rob hope and create distress, confusion, and anxiety. It can weaken the patient’s faith and set off a chain of events that adversely affects the survivors for years," said Dr. Avery.

"I was particularly bad at giving bad news at first," he said. A pulmonologist by training, he also worked for years in hospice care in both Florida and New York. He spoke with patients who transitioned to hospice from Memorial Sloan-Kettering Cancer Center, for example.

"I learned quickly that if I was going to give bad news, not to schedule the patient for midmorning on a Monday. It is too chaotic," Dr. Avery said. Schedule the patient for the first appointment after lunch or at the end of the day. Allow sufficient time and create a comfortable, private place with tissues available, he added.

Next, determine where each patient is in terms of understanding his or her illness. "Explore and ask," Dr. Avery said. Good questions include:

• Is there anyone else you want to have in the conversation?
• How do you understand what has happened to you medically?
• What have doctors told you about this illness?
• What do you think caused this illness?

"I cannot tell you how many patients with colon cancer thought they had it because they took too many antacids," Dr. Avery said. "Also, I had one woman with breast cancer who responded ‘Burger King.’ She had read an article that fatty foods caused breast cancer. She had guilt that she was leaving her family because she ate burgers instead of salads."

Also, determine how much the patient wants to know. "About 90% of patients want full information [about their condition], but everyone wants to know everything about treatment." Physicians also can be instrumental in allaying end-of-life fears, Dr. Avery said. Regardless of illness, most patients think some symptom is going to get worse and worse and crescendo in pain before they die. "How do people with [chronic obstructive pulmonary disease] die? Yes, the symptoms get worse, but with COPD, they get COPD narcosis, get sleepy, and drift away."

Intentionally develop and use a compassionate tone, Dr. Avery said. This is important because patients surveyed after they received bad news said the attitude of the person who spoke with them was the most important factor. The clarity of the message and privacy were also important, but they ranked far behind clinician attitude, he said.

Allow for silence. Let the message to sink in. "Give the patient plenty of time to react, respond, and ask questions." Also allow tears – "That can be a real problem for a lot of doctors."

A challenge for physicians is to be empathetic without breaking down completely, Dr. Avery said. When working in hospice care in New York, he frequently spent the day traveling by subway to clients’ residences. "Am I going to travel around weeping? No. You have to somehow try to meet where they are, but you cannot go there completely. It would be self-destructive."

"One reason physicians think they do not give bad news well is they fear their own response; that they will break down," Dr. Avery said. Try to determine the patient’s attitude and reflect it back to them. "This is what you do when things get emotional. And they will correct you if you’re wrong. If you say ‘You sound angry,’ they might say ‘No, I’m upset.’"

Another important thing to ask patients is "Have the doctors told you how long you have?" An accurate prognosis will help patients and family prepare, Dr. Avery said. "You have to tell them. If you don’t, they will seek a second opinion and/or leave the long-term care setting, because no one has told them." Less-experienced doctors and doctors who have had long and strong relationship with a patient can be especially poor at prognostication, he said.

Be completely honest and avoid stating a precise amount of time, such as "3 months." "I say, ‘It could be weeks instead of months,’ or, ‘It could be months instead of years.’ If they ask for a more precise prognosis, tell them it’s difficult to say, because it is," Dr. Avery said.

If you still do not feel comfortable giving a patient bad news, refer the patient to someone who does. "Call in hospice, call in palliative care. If you cannot give that bad news, you are obligated to do this," Dr. Avery said.

If your attitude is right and you’re speaking with a compassionate tone, what else should you keep in mind when giving a patient bad news?

Watch your body language, because about 90% of communication is nonverbal, Dr. Avery said. Make eye contact, for example.

Do not sound matter of fact. "Patients will say the doctor appears bored," Dr. Avery explained. At the same time, avoid rambling, he advised. A good way to do this is intentionally pause on a frequent basis. Develop a technique to slow yourself down. Dr. Avery said he silently counts backward from 10 to slow himself down, for example.

Provide information in small chunks. This is better than "the information dump," which is a tendency to disclose every detail to a patient when initial bad news is shared.

"I tell the patient she can raise her hand and stop me if it’s too much information at any point," he said.

Never say, ‘There is nothing more I can do for you," Dr. Avery advised. He said he often tells patients that there is nothing more he can do for their dementia or their cancer, "but there is a lot I can do for you as a person. ... Otherwise, you are referring to them as a lung cancer, and you’ve reduced them to an organ with a disease."

You also can admit the limitations of medicine, Dr. Avery said. "You can say, for example, ‘I wish we had more effective therapy for your condition,’ or ‘I wish I had a magic pill or magic wand I could use it to take away your cancer.’ "

Dr. Avery said that he had no relevant financial conflict of interest.

TAMPA – Sharing bad news with patients might not be easy, but it’s a skill physicians can learn and as important as knowing how to ready an EKG or an x-ray, James A. Avery, MD, CMD, said.

"What I am proposing is that giving bad news well is a fundamental long-term care physician skill, and competence in this area is critical," Dr. Avery said at this year’s AMDA – Dedicated to Long Term Medicine annual meeting.

"Giving bad news ... takes desire, courage, and practice," said Dr. Avery. "Patients deserve to get bad news delivered with compassion, hope, and integrity."

Plan ahead for the conversation; start with what the patient knows and wants to know; and develop a compassionate tone, said Dr. Avery, chief medical officer at Golden Living in Washington, a corporation that focuses on skilled nursing, assisted living, and rehabilitation therapy. Also, always provide an appropriate prognosis. "It’s your obligation to bring this up. Patients and families may be afraid to ask."

What can happen if the conversation is not done correctly? "If bad news is given poorly, it can rob hope and create distress, confusion, and anxiety. It can weaken the patient’s faith and set off a chain of events that adversely affects the survivors for years," said Dr. Avery.

"I was particularly bad at giving bad news at first," he said. A pulmonologist by training, he also worked for years in hospice care in both Florida and New York. He spoke with patients who transitioned to hospice from Memorial Sloan-Kettering Cancer Center, for example.

"I learned quickly that if I was going to give bad news, not to schedule the patient for midmorning on a Monday. It is too chaotic," Dr. Avery said. Schedule the patient for the first appointment after lunch or at the end of the day. Allow sufficient time and create a comfortable, private place with tissues available, he added.

Next, determine where each patient is in terms of understanding his or her illness. "Explore and ask," Dr. Avery said. Good questions include:

• Is there anyone else you want to have in the conversation?
• How do you understand what has happened to you medically?
• What have doctors told you about this illness?
• What do you think caused this illness?

"I cannot tell you how many patients with colon cancer thought they had it because they took too many antacids," Dr. Avery said. "Also, I had one woman with breast cancer who responded ‘Burger King.’ She had read an article that fatty foods caused breast cancer. She had guilt that she was leaving her family because she ate burgers instead of salads."

Also, determine how much the patient wants to know. "About 90% of patients want full information [about their condition], but everyone wants to know everything about treatment." Physicians also can be instrumental in allaying end-of-life fears, Dr. Avery said. Regardless of illness, most patients think some symptom is going to get worse and worse and crescendo in pain before they die. "How do people with [chronic obstructive pulmonary disease] die? Yes, the symptoms get worse, but with COPD, they get COPD narcosis, get sleepy, and drift away."

Intentionally develop and use a compassionate tone, Dr. Avery said. This is important because patients surveyed after they received bad news said the attitude of the person who spoke with them was the most important factor. The clarity of the message and privacy were also important, but they ranked far behind clinician attitude, he said.

Allow for silence. Let the message to sink in. "Give the patient plenty of time to react, respond, and ask questions." Also allow tears – "That can be a real problem for a lot of doctors."

A challenge for physicians is to be empathetic without breaking down completely, Dr. Avery said. When working in hospice care in New York, he frequently spent the day traveling by subway to clients’ residences. "Am I going to travel around weeping? No. You have to somehow try to meet where they are, but you cannot go there completely. It would be self-destructive."

"One reason physicians think they do not give bad news well is they fear their own response; that they will break down," Dr. Avery said. Try to determine the patient’s attitude and reflect it back to them. "This is what you do when things get emotional. And they will correct you if you’re wrong. If you say ‘You sound angry,’ they might say ‘No, I’m upset.’"

Another important thing to ask patients is "Have the doctors told you how long you have?" An accurate prognosis will help patients and family prepare, Dr. Avery said. "You have to tell them. If you don’t, they will seek a second opinion and/or leave the long-term care setting, because no one has told them." Less-experienced doctors and doctors who have had long and strong relationship with a patient can be especially poor at prognostication, he said.

Be completely honest and avoid stating a precise amount of time, such as "3 months." "I say, ‘It could be weeks instead of months,’ or, ‘It could be months instead of years.’ If they ask for a more precise prognosis, tell them it’s difficult to say, because it is," Dr. Avery said.

If you still do not feel comfortable giving a patient bad news, refer the patient to someone who does. "Call in hospice, call in palliative care. If you cannot give that bad news, you are obligated to do this," Dr. Avery said.

If your attitude is right and you’re speaking with a compassionate tone, what else should you keep in mind when giving a patient bad news?

Watch your body language, because about 90% of communication is nonverbal, Dr. Avery said. Make eye contact, for example.

Do not sound matter of fact. "Patients will say the doctor appears bored," Dr. Avery explained. At the same time, avoid rambling, he advised. A good way to do this is intentionally pause on a frequent basis. Develop a technique to slow yourself down. Dr. Avery said he silently counts backward from 10 to slow himself down, for example.

Provide information in small chunks. This is better than "the information dump," which is a tendency to disclose every detail to a patient when initial bad news is shared.

"I tell the patient she can raise her hand and stop me if it’s too much information at any point," he said.

Never say, ‘There is nothing more I can do for you," Dr. Avery advised. He said he often tells patients that there is nothing more he can do for their dementia or their cancer, "but there is a lot I can do for you as a person. ... Otherwise, you are referring to them as a lung cancer, and you’ve reduced them to an organ with a disease."

You also can admit the limitations of medicine, Dr. Avery said. "You can say, for example, ‘I wish we had more effective therapy for your condition,’ or ‘I wish I had a magic pill or magic wand I could use it to take away your cancer.’ "

Dr. Avery said that he had no relevant financial conflict of interest.

TAMPA – Sharing bad news with patients might not be easy, but it’s a skill physicians can learn and as important as knowing how to ready an EKG or an x-ray, James A. Avery, MD, CMD, said.

"What I am proposing is that giving bad news well is a fundamental long-term care physician skill, and competence in this area is critical," Dr. Avery said at this year’s AMDA – Dedicated to Long Term Medicine annual meeting.

"Giving bad news ... takes desire, courage, and practice," said Dr. Avery. "Patients deserve to get bad news delivered with compassion, hope, and integrity."

Plan ahead for the conversation; start with what the patient knows and wants to know; and develop a compassionate tone, said Dr. Avery, chief medical officer at Golden Living in Washington, a corporation that focuses on skilled nursing, assisted living, and rehabilitation therapy. Also, always provide an appropriate prognosis. "It’s your obligation to bring this up. Patients and families may be afraid to ask."

What can happen if the conversation is not done correctly? "If bad news is given poorly, it can rob hope and create distress, confusion, and anxiety. It can weaken the patient’s faith and set off a chain of events that adversely affects the survivors for years," said Dr. Avery.

"I was particularly bad at giving bad news at first," he said. A pulmonologist by training, he also worked for years in hospice care in both Florida and New York. He spoke with patients who transitioned to hospice from Memorial Sloan-Kettering Cancer Center, for example.

"I learned quickly that if I was going to give bad news, not to schedule the patient for midmorning on a Monday. It is too chaotic," Dr. Avery said. Schedule the patient for the first appointment after lunch or at the end of the day. Allow sufficient time and create a comfortable, private place with tissues available, he added.

Next, determine where each patient is in terms of understanding his or her illness. "Explore and ask," Dr. Avery said. Good questions include:

• Is there anyone else you want to have in the conversation?
• How do you understand what has happened to you medically?
• What have doctors told you about this illness?
• What do you think caused this illness?

"I cannot tell you how many patients with colon cancer thought they had it because they took too many antacids," Dr. Avery said. "Also, I had one woman with breast cancer who responded ‘Burger King.’ She had read an article that fatty foods caused breast cancer. She had guilt that she was leaving her family because she ate burgers instead of salads."

Also, determine how much the patient wants to know. "About 90% of patients want full information [about their condition], but everyone wants to know everything about treatment." Physicians also can be instrumental in allaying end-of-life fears, Dr. Avery said. Regardless of illness, most patients think some symptom is going to get worse and worse and crescendo in pain before they die. "How do people with [chronic obstructive pulmonary disease] die? Yes, the symptoms get worse, but with COPD, they get COPD narcosis, get sleepy, and drift away."

Intentionally develop and use a compassionate tone, Dr. Avery said. This is important because patients surveyed after they received bad news said the attitude of the person who spoke with them was the most important factor. The clarity of the message and privacy were also important, but they ranked far behind clinician attitude, he said.

Allow for silence. Let the message to sink in. "Give the patient plenty of time to react, respond, and ask questions." Also allow tears – "That can be a real problem for a lot of doctors."

A challenge for physicians is to be empathetic without breaking down completely, Dr. Avery said. When working in hospice care in New York, he frequently spent the day traveling by subway to clients’ residences. "Am I going to travel around weeping? No. You have to somehow try to meet where they are, but you cannot go there completely. It would be self-destructive."

"One reason physicians think they do not give bad news well is they fear their own response; that they will break down," Dr. Avery said. Try to determine the patient’s attitude and reflect it back to them. "This is what you do when things get emotional. And they will correct you if you’re wrong. If you say ‘You sound angry,’ they might say ‘No, I’m upset.’"

Another important thing to ask patients is "Have the doctors told you how long you have?" An accurate prognosis will help patients and family prepare, Dr. Avery said. "You have to tell them. If you don’t, they will seek a second opinion and/or leave the long-term care setting, because no one has told them." Less-experienced doctors and doctors who have had long and strong relationship with a patient can be especially poor at prognostication, he said.

Be completely honest and avoid stating a precise amount of time, such as "3 months." "I say, ‘It could be weeks instead of months,’ or, ‘It could be months instead of years.’ If they ask for a more precise prognosis, tell them it’s difficult to say, because it is," Dr. Avery said.

If you still do not feel comfortable giving a patient bad news, refer the patient to someone who does. "Call in hospice, call in palliative care. If you cannot give that bad news, you are obligated to do this," Dr. Avery said.

If your attitude is right and you’re speaking with a compassionate tone, what else should you keep in mind when giving a patient bad news?

Watch your body language, because about 90% of communication is nonverbal, Dr. Avery said. Make eye contact, for example.

Do not sound matter of fact. "Patients will say the doctor appears bored," Dr. Avery explained. At the same time, avoid rambling, he advised. A good way to do this is intentionally pause on a frequent basis. Develop a technique to slow yourself down. Dr. Avery said he silently counts backward from 10 to slow himself down, for example.

Provide information in small chunks. This is better than "the information dump," which is a tendency to disclose every detail to a patient when initial bad news is shared.

"I tell the patient she can raise her hand and stop me if it’s too much information at any point," he said.

Never say, ‘There is nothing more I can do for you," Dr. Avery advised. He said he often tells patients that there is nothing more he can do for their dementia or their cancer, "but there is a lot I can do for you as a person. ... Otherwise, you are referring to them as a lung cancer, and you’ve reduced them to an organ with a disease."

You also can admit the limitations of medicine, Dr. Avery said. "You can say, for example, ‘I wish we had more effective therapy for your condition,’ or ‘I wish I had a magic pill or magic wand I could use it to take away your cancer.’ "

Dr. Avery said that he had no relevant financial conflict of interest.

TAMPA – Sharing bad news with patients might not be easy, but it’s a skill physicians can learn and as important as knowing how to ready an EKG or an x-ray, James A. Avery, MD, CMD, said.

"What I am proposing is that giving bad news well is a fundamental long-term care physician skill, and competence in this area is critical," Dr. Avery said at this year’s AMDA – Dedicated to Long Term Medicine annual meeting.

"Giving bad news ... takes desire, courage, and practice," said Dr. Avery. "Patients deserve to get bad news delivered with compassion, hope, and integrity."

Plan ahead for the conversation; start with what the patient knows and wants to know; and develop a compassionate tone, said Dr. Avery, chief medical officer at Golden Living in Washington, a corporation that focuses on skilled nursing, assisted living, and rehabilitation therapy. Also, always provide an appropriate prognosis. "It’s your obligation to bring this up. Patients and families may be afraid to ask."

What can happen if the conversation is not done correctly? "If bad news is given poorly, it can rob hope and create distress, confusion, and anxiety. It can weaken the patient’s faith and set off a chain of events that adversely affects the survivors for years," said Dr. Avery.

"I was particularly bad at giving bad news at first," he said. A pulmonologist by training, he also worked for years in hospice care in both Florida and New York. He spoke with patients who transitioned to hospice from Memorial Sloan-Kettering Cancer Center, for example.

"I learned quickly that if I was going to give bad news, not to schedule the patient for midmorning on a Monday. It is too chaotic," Dr. Avery said. Schedule the patient for the first appointment after lunch or at the end of the day. Allow sufficient time and create a comfortable, private place with tissues available, he added.

Next, determine where each patient is in terms of understanding his or her illness. "Explore and ask," Dr. Avery said. Good questions include:

• Is there anyone else you want to have in the conversation?
• How do you understand what has happened to you medically?
• What have doctors told you about this illness?
• What do you think caused this illness?

"I cannot tell you how many patients with colon cancer thought they had it because they took too many antacids," Dr. Avery said. "Also, I had one woman with breast cancer who responded ‘Burger King.’ She had read an article that fatty foods caused breast cancer. She had guilt that she was leaving her family because she ate burgers instead of salads."

Also, determine how much the patient wants to know. "About 90% of patients want full information [about their condition], but everyone wants to know everything about treatment." Physicians also can be instrumental in allaying end-of-life fears, Dr. Avery said. Regardless of illness, most patients think some symptom is going to get worse and worse and crescendo in pain before they die. "How do people with [chronic obstructive pulmonary disease] die? Yes, the symptoms get worse, but with COPD, they get COPD narcosis, get sleepy, and drift away."

Intentionally develop and use a compassionate tone, Dr. Avery said. This is important because patients surveyed after they received bad news said the attitude of the person who spoke with them was the most important factor. The clarity of the message and privacy were also important, but they ranked far behind clinician attitude, he said.

Allow for silence. Let the message to sink in. "Give the patient plenty of time to react, respond, and ask questions." Also allow tears – "That can be a real problem for a lot of doctors."

A challenge for physicians is to be empathetic without breaking down completely, Dr. Avery said. When working in hospice care in New York, he frequently spent the day traveling by subway to clients’ residences. "Am I going to travel around weeping? No. You have to somehow try to meet where they are, but you cannot go there completely. It would be self-destructive."

"One reason physicians think they do not give bad news well is they fear their own response; that they will break down," Dr. Avery said. Try to determine the patient’s attitude and reflect it back to them. "This is what you do when things get emotional. And they will correct you if you’re wrong. If you say ‘You sound angry,’ they might say ‘No, I’m upset.’"

Another important thing to ask patients is "Have the doctors told you how long you have?" An accurate prognosis will help patients and family prepare, Dr. Avery said. "You have to tell them. If you don’t, they will seek a second opinion and/or leave the long-term care setting, because no one has told them." Less-experienced doctors and doctors who have had long and strong relationship with a patient can be especially poor at prognostication, he said.

Be completely honest and avoid stating a precise amount of time, such as "3 months." "I say, ‘It could be weeks instead of months,’ or, ‘It could be months instead of years.’ If they ask for a more precise prognosis, tell them it’s difficult to say, because it is," Dr. Avery said.

If you still do not feel comfortable giving a patient bad news, refer the patient to someone who does. "Call in hospice, call in palliative care. If you cannot give that bad news, you are obligated to do this," Dr. Avery said.

If your attitude is right and you’re speaking with a compassionate tone, what else should you keep in mind when giving a patient bad news?

Watch your body language, because about 90% of communication is nonverbal, Dr. Avery said. Make eye contact, for example.

Do not sound matter of fact. "Patients will say the doctor appears bored," Dr. Avery explained. At the same time, avoid rambling, he advised. A good way to do this is intentionally pause on a frequent basis. Develop a technique to slow yourself down. Dr. Avery said he silently counts backward from 10 to slow himself down, for example.

Provide information in small chunks. This is better than "the information dump," which is a tendency to disclose every detail to a patient when initial bad news is shared.

"I tell the patient she can raise her hand and stop me if it’s too much information at any point," he said.

Never say, ‘There is nothing more I can do for you," Dr. Avery advised. He said he often tells patients that there is nothing more he can do for their dementia or their cancer, "but there is a lot I can do for you as a person. ... Otherwise, you are referring to them as a lung cancer, and you’ve reduced them to an organ with a disease."

You also can admit the limitations of medicine, Dr. Avery said. "You can say, for example, ‘I wish we had more effective therapy for your condition,’ or ‘I wish I had a magic pill or magic wand I could use it to take away your cancer.’ "

Dr. Avery said that he had no relevant financial conflict of interest.

TAMPA – Sharing bad news with patients might not be easy, but it’s a skill physicians can learn and as important as knowing how to ready an EKG or an x-ray, James A. Avery, MD, CMD, said.

"What I am proposing is that giving bad news well is a fundamental long-term care physician skill, and competence in this area is critical," Dr. Avery said at this year’s AMDA – Dedicated to Long Term Medicine annual meeting.

"Giving bad news ... takes desire, courage, and practice," said Dr. Avery. "Patients deserve to get bad news delivered with compassion, hope, and integrity."

Plan ahead for the conversation; start with what the patient knows and wants to know; and develop a compassionate tone, said Dr. Avery, chief medical officer at Golden Living in Washington, a corporation that focuses on skilled nursing, assisted living, and rehabilitation therapy. Also, always provide an appropriate prognosis. "It’s your obligation to bring this up. Patients and families may be afraid to ask."

What can happen if the conversation is not done correctly? "If bad news is given poorly, it can rob hope and create distress, confusion, and anxiety. It can weaken the patient’s faith and set off a chain of events that adversely affects the survivors for years," said Dr. Avery.

"I was particularly bad at giving bad news at first," he said. A pulmonologist by training, he also worked for years in hospice care in both Florida and New York. He spoke with patients who transitioned to hospice from Memorial Sloan-Kettering Cancer Center, for example.

"I learned quickly that if I was going to give bad news, not to schedule the patient for midmorning on a Monday. It is too chaotic," Dr. Avery said. Schedule the patient for the first appointment after lunch or at the end of the day. Allow sufficient time and create a comfortable, private place with tissues available, he added.

Next, determine where each patient is in terms of understanding his or her illness. "Explore and ask," Dr. Avery said. Good questions include:

• Is there anyone else you want to have in the conversation?
• How do you understand what has happened to you medically?
• What have doctors told you about this illness?
• What do you think caused this illness?

"I cannot tell you how many patients with colon cancer thought they had it because they took too many antacids," Dr. Avery said. "Also, I had one woman with breast cancer who responded ‘Burger King.’ She had read an article that fatty foods caused breast cancer. She had guilt that she was leaving her family because she ate burgers instead of salads."

Also, determine how much the patient wants to know. "About 90% of patients want full information [about their condition], but everyone wants to know everything about treatment." Physicians also can be instrumental in allaying end-of-life fears, Dr. Avery said. Regardless of illness, most patients think some symptom is going to get worse and worse and crescendo in pain before they die. "How do people with [chronic obstructive pulmonary disease] die? Yes, the symptoms get worse, but with COPD, they get COPD narcosis, get sleepy, and drift away."

Intentionally develop and use a compassionate tone, Dr. Avery said. This is important because patients surveyed after they received bad news said the attitude of the person who spoke with them was the most important factor. The clarity of the message and privacy were also important, but they ranked far behind clinician attitude, he said.

Allow for silence. Let the message to sink in. "Give the patient plenty of time to react, respond, and ask questions." Also allow tears – "That can be a real problem for a lot of doctors."

A challenge for physicians is to be empathetic without breaking down completely, Dr. Avery said. When working in hospice care in New York, he frequently spent the day traveling by subway to clients’ residences. "Am I going to travel around weeping? No. You have to somehow try to meet where they are, but you cannot go there completely. It would be self-destructive."

"One reason physicians think they do not give bad news well is they fear their own response; that they will break down," Dr. Avery said. Try to determine the patient’s attitude and reflect it back to them. "This is what you do when things get emotional. And they will correct you if you’re wrong. If you say ‘You sound angry,’ they might say ‘No, I’m upset.’"

Another important thing to ask patients is "Have the doctors told you how long you have?" An accurate prognosis will help patients and family prepare, Dr. Avery said. "You have to tell them. If you don’t, they will seek a second opinion and/or leave the long-term care setting, because no one has told them." Less-experienced doctors and doctors who have had long and strong relationship with a patient can be especially poor at prognostication, he said.

Be completely honest and avoid stating a precise amount of time, such as "3 months." "I say, ‘It could be weeks instead of months,’ or, ‘It could be months instead of years.’ If they ask for a more precise prognosis, tell them it’s difficult to say, because it is," Dr. Avery said.

If you still do not feel comfortable giving a patient bad news, refer the patient to someone who does. "Call in hospice, call in palliative care. If you cannot give that bad news, you are obligated to do this," Dr. Avery said.

If your attitude is right and you’re speaking with a compassionate tone, what else should you keep in mind when giving a patient bad news?

Watch your body language, because about 90% of communication is nonverbal, Dr. Avery said. Make eye contact, for example.

Do not sound matter of fact. "Patients will say the doctor appears bored," Dr. Avery explained. At the same time, avoid rambling, he advised. A good way to do this is intentionally pause on a frequent basis. Develop a technique to slow yourself down. Dr. Avery said he silently counts backward from 10 to slow himself down, for example.

Provide information in small chunks. This is better than "the information dump," which is a tendency to disclose every detail to a patient when initial bad news is shared.

"I tell the patient she can raise her hand and stop me if it’s too much information at any point," he said.

Never say, ‘There is nothing more I can do for you," Dr. Avery advised. He said he often tells patients that there is nothing more he can do for their dementia or their cancer, "but there is a lot I can do for you as a person. ... Otherwise, you are referring to them as a lung cancer, and you’ve reduced them to an organ with a disease."

You also can admit the limitations of medicine, Dr. Avery said. "You can say, for example, ‘I wish we had more effective therapy for your condition,’ or ‘I wish I had a magic pill or magic wand I could use it to take away your cancer.’ "

Dr. Avery said that he had no relevant financial conflict of interest.

TAMPA – Sharing bad news with patients might not be easy, but it’s a skill physicians can learn and as important as knowing how to ready an EKG or an x-ray, James A. Avery, MD, CMD, said.

"What I am proposing is that giving bad news well is a fundamental long-term care physician skill, and competence in this area is critical," Dr. Avery said at this year’s AMDA – Dedicated to Long Term Medicine annual meeting.

"Giving bad news ... takes desire, courage, and practice," said Dr. Avery. "Patients deserve to get bad news delivered with compassion, hope, and integrity."

Plan ahead for the conversation; start with what the patient knows and wants to know; and develop a compassionate tone, said Dr. Avery, chief medical officer at Golden Living in Washington, a corporation that focuses on skilled nursing, assisted living, and rehabilitation therapy. Also, always provide an appropriate prognosis. "It’s your obligation to bring this up. Patients and families may be afraid to ask."

What can happen if the conversation is not done correctly? "If bad news is given poorly, it can rob hope and create distress, confusion, and anxiety. It can weaken the patient’s faith and set off a chain of events that adversely affects the survivors for years," said Dr. Avery.

"I was particularly bad at giving bad news at first," he said. A pulmonologist by training, he also worked for years in hospice care in both Florida and New York. He spoke with patients who transitioned to hospice from Memorial Sloan-Kettering Cancer Center, for example.

"I learned quickly that if I was going to give bad news, not to schedule the patient for midmorning on a Monday. It is too chaotic," Dr. Avery said. Schedule the patient for the first appointment after lunch or at the end of the day. Allow sufficient time and create a comfortable, private place with tissues available, he added.

Next, determine where each patient is in terms of understanding his or her illness. "Explore and ask," Dr. Avery said. Good questions include:

• Is there anyone else you want to have in the conversation?
• How do you understand what has happened to you medically?
• What have doctors told you about this illness?
• What do you think caused this illness?

"I cannot tell you how many patients with colon cancer thought they had it because they took too many antacids," Dr. Avery said. "Also, I had one woman with breast cancer who responded ‘Burger King.’ She had read an article that fatty foods caused breast cancer. She had guilt that she was leaving her family because she ate burgers instead of salads."

Also, determine how much the patient wants to know. "About 90% of patients want full information [about their condition], but everyone wants to know everything about treatment." Physicians also can be instrumental in allaying end-of-life fears, Dr. Avery said. Regardless of illness, most patients think some symptom is going to get worse and worse and crescendo in pain before they die. "How do people with [chronic obstructive pulmonary disease] die? Yes, the symptoms get worse, but with COPD, they get COPD narcosis, get sleepy, and drift away."

Intentionally develop and use a compassionate tone, Dr. Avery said. This is important because patients surveyed after they received bad news said the attitude of the person who spoke with them was the most important factor. The clarity of the message and privacy were also important, but they ranked far behind clinician attitude, he said.

Allow for silence. Let the message to sink in. "Give the patient plenty of time to react, respond, and ask questions." Also allow tears – "That can be a real problem for a lot of doctors."

A challenge for physicians is to be empathetic without breaking down completely, Dr. Avery said. When working in hospice care in New York, he frequently spent the day traveling by subway to clients’ residences. "Am I going to travel around weeping? No. You have to somehow try to meet where they are, but you cannot go there completely. It would be self-destructive."

"One reason physicians think they do not give bad news well is they fear their own response; that they will break down," Dr. Avery said. Try to determine the patient’s attitude and reflect it back to them. "This is what you do when things get emotional. And they will correct you if you’re wrong. If you say ‘You sound angry,’ they might say ‘No, I’m upset.’"

Another important thing to ask patients is "Have the doctors told you how long you have?" An accurate prognosis will help patients and family prepare, Dr. Avery said. "You have to tell them. If you don’t, they will seek a second opinion and/or leave the long-term care setting, because no one has told them." Less-experienced doctors and doctors who have had long and strong relationship with a patient can be especially poor at prognostication, he said.

Be completely honest and avoid stating a precise amount of time, such as "3 months." "I say, ‘It could be weeks instead of months,’ or, ‘It could be months instead of years.’ If they ask for a more precise prognosis, tell them it’s difficult to say, because it is," Dr. Avery said.

If you still do not feel comfortable giving a patient bad news, refer the patient to someone who does. "Call in hospice, call in palliative care. If you cannot give that bad news, you are obligated to do this," Dr. Avery said.

If your attitude is right and you’re speaking with a compassionate tone, what else should you keep in mind when giving a patient bad news?

Watch your body language, because about 90% of communication is nonverbal, Dr. Avery said. Make eye contact, for example.

Do not sound matter of fact. "Patients will say the doctor appears bored," Dr. Avery explained. At the same time, avoid rambling, he advised. A good way to do this is intentionally pause on a frequent basis. Develop a technique to slow yourself down. Dr. Avery said he silently counts backward from 10 to slow himself down, for example.

Provide information in small chunks. This is better than "the information dump," which is a tendency to disclose every detail to a patient when initial bad news is shared.

"I tell the patient she can raise her hand and stop me if it’s too much information at any point," he said.

Never say, ‘There is nothing more I can do for you," Dr. Avery advised. He said he often tells patients that there is nothing more he can do for their dementia or their cancer, "but there is a lot I can do for you as a person. ... Otherwise, you are referring to them as a lung cancer, and you’ve reduced them to an organ with a disease."

You also can admit the limitations of medicine, Dr. Avery said. "You can say, for example, ‘I wish we had more effective therapy for your condition,’ or ‘I wish I had a magic pill or magic wand I could use it to take away your cancer.’ "

Dr. Avery said that he had no relevant financial conflict of interest.

TAMPA – Sharing bad news with patients might not be easy, but it’s a skill physicians can learn and as important as knowing how to ready an EKG or an x-ray, James A. Avery, MD, CMD, said.

"What I am proposing is that giving bad news well is a fundamental long-term care physician skill, and competence in this area is critical," Dr. Avery said at this year’s AMDA – Dedicated to Long Term Medicine annual meeting.

"Giving bad news ... takes desire, courage, and practice," said Dr. Avery. "Patients deserve to get bad news delivered with compassion, hope, and integrity."

Plan ahead for the conversation; start with what the patient knows and wants to know; and develop a compassionate tone, said Dr. Avery, chief medical officer at Golden Living in Washington, a corporation that focuses on skilled nursing, assisted living, and rehabilitation therapy. Also, always provide an appropriate prognosis. "It’s your obligation to bring this up. Patients and families may be afraid to ask."

What can happen if the conversation is not done correctly? "If bad news is given poorly, it can rob hope and create distress, confusion, and anxiety. It can weaken the patient’s faith and set off a chain of events that adversely affects the survivors for years," said Dr. Avery.

"I was particularly bad at giving bad news at first," he said. A pulmonologist by training, he also worked for years in hospice care in both Florida and New York. He spoke with patients who transitioned to hospice from Memorial Sloan-Kettering Cancer Center, for example.

"I learned quickly that if I was going to give bad news, not to schedule the patient for midmorning on a Monday. It is too chaotic," Dr. Avery said. Schedule the patient for the first appointment after lunch or at the end of the day. Allow sufficient time and create a comfortable, private place with tissues available, he added.

Next, determine where each patient is in terms of understanding his or her illness. "Explore and ask," Dr. Avery said. Good questions include:

• Is there anyone else you want to have in the conversation?
• How do you understand what has happened to you medically?
• What have doctors told you about this illness?
• What do you think caused this illness?

"I cannot tell you how many patients with colon cancer thought they had it because they took too many antacids," Dr. Avery said. "Also, I had one woman with breast cancer who responded ‘Burger King.’ She had read an article that fatty foods caused breast cancer. She had guilt that she was leaving her family because she ate burgers instead of salads."

Also, determine how much the patient wants to know. "About 90% of patients want full information [about their condition], but everyone wants to know everything about treatment." Physicians also can be instrumental in allaying end-of-life fears, Dr. Avery said. Regardless of illness, most patients think some symptom is going to get worse and worse and crescendo in pain before they die. "How do people with [chronic obstructive pulmonary disease] die? Yes, the symptoms get worse, but with COPD, they get COPD narcosis, get sleepy, and drift away."

Intentionally develop and use a compassionate tone, Dr. Avery said. This is important because patients surveyed after they received bad news said the attitude of the person who spoke with them was the most important factor. The clarity of the message and privacy were also important, but they ranked far behind clinician attitude, he said.

Allow for silence. Let the message to sink in. "Give the patient plenty of time to react, respond, and ask questions." Also allow tears – "That can be a real problem for a lot of doctors."

A challenge for physicians is to be empathetic without breaking down completely, Dr. Avery said. When working in hospice care in New York, he frequently spent the day traveling by subway to clients’ residences. "Am I going to travel around weeping? No. You have to somehow try to meet where they are, but you cannot go there completely. It would be self-destructive."

"One reason physicians think they do not give bad news well is they fear their own response; that they will break down," Dr. Avery said. Try to determine the patient’s attitude and reflect it back to them. "This is what you do when things get emotional. And they will correct you if you’re wrong. If you say ‘You sound angry,’ they might say ‘No, I’m upset.’"

Another important thing to ask patients is "Have the doctors told you how long you have?" An accurate prognosis will help patients and family prepare, Dr. Avery said. "You have to tell them. If you don’t, they will seek a second opinion and/or leave the long-term care setting, because no one has told them." Less-experienced doctors and doctors who have had long and strong relationship with a patient can be especially poor at prognostication, he said.

Be completely honest and avoid stating a precise amount of time, such as "3 months." "I say, ‘It could be weeks instead of months,’ or, ‘It could be months instead of years.’ If they ask for a more precise prognosis, tell them it’s difficult to say, because it is," Dr. Avery said.

If you still do not feel comfortable giving a patient bad news, refer the patient to someone who does. "Call in hospice, call in palliative care. If you cannot give that bad news, you are obligated to do this," Dr. Avery said.

If your attitude is right and you’re speaking with a compassionate tone, what else should you keep in mind when giving a patient bad news?

Watch your body language, because about 90% of communication is nonverbal, Dr. Avery said. Make eye contact, for example.

Do not sound matter of fact. "Patients will say the doctor appears bored," Dr. Avery explained. At the same time, avoid rambling, he advised. A good way to do this is intentionally pause on a frequent basis. Develop a technique to slow yourself down. Dr. Avery said he silently counts backward from 10 to slow himself down, for example.

Provide information in small chunks. This is better than "the information dump," which is a tendency to disclose every detail to a patient when initial bad news is shared.

"I tell the patient she can raise her hand and stop me if it’s too much information at any point," he said.

Never say, ‘There is nothing more I can do for you," Dr. Avery advised. He said he often tells patients that there is nothing more he can do for their dementia or their cancer, "but there is a lot I can do for you as a person. ... Otherwise, you are referring to them as a lung cancer, and you’ve reduced them to an organ with a disease."

You also can admit the limitations of medicine, Dr. Avery said. "You can say, for example, ‘I wish we had more effective therapy for your condition,’ or ‘I wish I had a magic pill or magic wand I could use it to take away your cancer.’ "

Dr. Avery said that he had no relevant financial conflict of interest.

TAMPA – Sharing bad news with patients might not be easy, but it’s a skill physicians can learn and as important as knowing how to ready an EKG or an x-ray, James A. Avery, MD, CMD, said.

"What I am proposing is that giving bad news well is a fundamental long-term care physician skill, and competence in this area is critical," Dr. Avery said at this year’s AMDA – Dedicated to Long Term Medicine annual meeting.

"Giving bad news ... takes desire, courage, and practice," said Dr. Avery. "Patients deserve to get bad news delivered with compassion, hope, and integrity."

Plan ahead for the conversation; start with what the patient knows and wants to know; and develop a compassionate tone, said Dr. Avery, chief medical officer at Golden Living in Washington, a corporation that focuses on skilled nursing, assisted living, and rehabilitation therapy. Also, always provide an appropriate prognosis. "It’s your obligation to bring this up. Patients and families may be afraid to ask."

What can happen if the conversation is not done correctly? "If bad news is given poorly, it can rob hope and create distress, confusion, and anxiety. It can weaken the patient’s faith and set off a chain of events that adversely affects the survivors for years," said Dr. Avery.

"I was particularly bad at giving bad news at first," he said. A pulmonologist by training, he also worked for years in hospice care in both Florida and New York. He spoke with patients who transitioned to hospice from Memorial Sloan-Kettering Cancer Center, for example.

"I learned quickly that if I was going to give bad news, not to schedule the patient for midmorning on a Monday. It is too chaotic," Dr. Avery said. Schedule the patient for the first appointment after lunch or at the end of the day. Allow sufficient time and create a comfortable, private place with tissues available, he added.

Next, determine where each patient is in terms of understanding his or her illness. "Explore and ask," Dr. Avery said. Good questions include:

• Is there anyone else you want to have in the conversation?
• How do you understand what has happened to you medically?
• What have doctors told you about this illness?
• What do you think caused this illness?

"I cannot tell you how many patients with colon cancer thought they had it because they took too many antacids," Dr. Avery said. "Also, I had one woman with breast cancer who responded ‘Burger King.’ She had read an article that fatty foods caused breast cancer. She had guilt that she was leaving her family because she ate burgers instead of salads."

Also, determine how much the patient wants to know. "About 90% of patients want full information [about their condition], but everyone wants to know everything about treatment." Physicians also can be instrumental in allaying end-of-life fears, Dr. Avery said. Regardless of illness, most patients think some symptom is going to get worse and worse and crescendo in pain before they die. "How do people with [chronic obstructive pulmonary disease] die? Yes, the symptoms get worse, but with COPD, they get COPD narcosis, get sleepy, and drift away."

Intentionally develop and use a compassionate tone, Dr. Avery said. This is important because patients surveyed after they received bad news said the attitude of the person who spoke with them was the most important factor. The clarity of the message and privacy were also important, but they ranked far behind clinician attitude, he said.

Allow for silence. Let the message to sink in. "Give the patient plenty of time to react, respond, and ask questions." Also allow tears – "That can be a real problem for a lot of doctors."

A challenge for physicians is to be empathetic without breaking down completely, Dr. Avery said. When working in hospice care in New York, he frequently spent the day traveling by subway to clients’ residences. "Am I going to travel around weeping? No. You have to somehow try to meet where they are, but you cannot go there completely. It would be self-destructive."

"One reason physicians think they do not give bad news well is they fear their own response; that they will break down," Dr. Avery said. Try to determine the patient’s attitude and reflect it back to them. "This is what you do when things get emotional. And they will correct you if you’re wrong. If you say ‘You sound angry,’ they might say ‘No, I’m upset.’"

Another important thing to ask patients is "Have the doctors told you how long you have?" An accurate prognosis will help patients and family prepare, Dr. Avery said. "You have to tell them. If you don’t, they will seek a second opinion and/or leave the long-term care setting, because no one has told them." Less-experienced doctors and doctors who have had long and strong relationship with a patient can be especially poor at prognostication, he said.

Be completely honest and avoid stating a precise amount of time, such as "3 months." "I say, ‘It could be weeks instead of months,’ or, ‘It could be months instead of years.’ If they ask for a more precise prognosis, tell them it’s difficult to say, because it is," Dr. Avery said.

If you still do not feel comfortable giving a patient bad news, refer the patient to someone who does. "Call in hospice, call in palliative care. If you cannot give that bad news, you are obligated to do this," Dr. Avery said.

If your attitude is right and you’re speaking with a compassionate tone, what else should you keep in mind when giving a patient bad news?

Watch your body language, because about 90% of communication is nonverbal, Dr. Avery said. Make eye contact, for example.

Do not sound matter of fact. "Patients will say the doctor appears bored," Dr. Avery explained. At the same time, avoid rambling, he advised. A good way to do this is intentionally pause on a frequent basis. Develop a technique to slow yourself down. Dr. Avery said he silently counts backward from 10 to slow himself down, for example.

Provide information in small chunks. This is better than "the information dump," which is a tendency to disclose every detail to a patient when initial bad news is shared.

"I tell the patient she can raise her hand and stop me if it’s too much information at any point," he said.

Never say, ‘There is nothing more I can do for you," Dr. Avery advised. He said he often tells patients that there is nothing more he can do for their dementia or their cancer, "but there is a lot I can do for you as a person. ... Otherwise, you are referring to them as a lung cancer, and you’ve reduced them to an organ with a disease."

You also can admit the limitations of medicine, Dr. Avery said. "You can say, for example, ‘I wish we had more effective therapy for your condition,’ or ‘I wish I had a magic pill or magic wand I could use it to take away your cancer.’ "

Dr. Avery said that he had no relevant financial conflict of interest.

TAMPA – Why would two patients respond so differently the same medication? Although the reasons are several, recent advances support a prominent role for genetic differences in drug metabolism, according to a panel at the AMDA – Dedicated to Long Term Care Medicine annual meeting.

The good news is that this is not theoretical science. Some variations in patient response can be predicted using commercially available genetic assays, said the genetics and long-term care experts.

One strategy is to test patients for variations in genes for cytochrome P450 enzymes. Before prescribing an antidepressant, for example, you can test a patient for variations in their 2D6, 2C9, and 2C19 enzymes, which metabolize psychoactive medications and many others.

Depending on a patient’s genetics, in other words, he or she might be a poor, intermediate, or ultrarapid metabolizer of a particular medication, which can dramatically increase or decrease efficacy and side effects. Slow or poor metabolizers can experience a build-up of particular drug and extra side effects, whereas a rapid metabolizer might not get a full therapeutic benefit because of a drug’s quick clearance.

"If I have someone who is a 2D6-poor metabolizer, Paxil [paroxetine] is going to be at sky-high level, so instead I might try something like Luvox [fluvoxamine] or Celexa [citalopram]," said Dr. Joel Winner, medical director of Assure Rx Health, a laboratory service offering pharmacogenomics. "I am a clinician as well. I see patients and I use this technology," said Dr. Winner, who also is a private practice psychiatrist in Boulder, Colo.

He estimated that 60% of his patients undergo some form of genetic testing to help him make treatment decisions. "Fifty percent of depressed patients prescribed drugs are nonresponders," Dr. Winner said.

The ability to predict response versus waiting up to 8 weeks to judge a drug’s efficacy is an advantage, said Dr. Amita R. Patel, a geriatric psychiatrist at Wright State University, Dayton, Ohio.

Minimizing side effects is another goal of genetic testing, she added. "Drug-induced side effects, unfortunately, are very, very common and lead to noncompliance," Dr. Patel said. As an example, she described a woman not responding well to duloxetine [Cymbalta]. The patient felt sad, unmotivated, restless, anxious, and worried and reported sleep disturbances and daytime fatigue. Her Patient Health Questionnaire (PHQ-9) depression score was 15. Eight weeks after she switched to desvenlafaxine [Pristiq], her PHG-9 improved to a 5. (Desvenlafaxine and clonazepam are her current regimen.)

"She was not responding well to Cymbalta ... because her serum levels were too low. She was an ultrarapid metabolizer," Dr. Patel said. The patient also was taking insulin and omeprazole, two medications that were lowering her response to antidepressants.

"We are continuing to look at genes that predict weight gain, metabolic syndrome, or other issues relevant to psychiatry," Dr. Winner said.

A 60-year-old patient with treatment-resistant depression is another example. History revealed that the patient was unresponsive to escitalopram and budeprion XL. A switch to nortriptyline (Pamelor) did not significantly improve symptoms. When low-dose fluoxetine (Prozac) was added, the patient developed sedation and experienced a fall.

Subsequent genetic testing showed that the patient had impaired metabolism affected by 2D6, which metabolizes nortriptyline and fluoxetine. "So pharmacogenomic testing is very useful in our practice," Dr. Patel said. "We really need to look at a patient’s 2D6 whenever it is possible."

"Sometimes when we cannot figure out why a patient is oversedated at a low dose, [genetic testing] is something that can answer that question," said Manju T. Beier, PharmD, who is a senior partner for Geriatric Consultant Resources and on the pharmacy faculty at the University of Michigan, Ann Arbor.

Dr. Beier explained that metabolism of prodrugs works counterintuitively. "You need an enzyme to metabolize it to active compound, so you will get higher adverse events if you are a rapid metabolizer and inefficacy if you are a poor metabolizer."

A 79-year-old woman hospitalized with pneumonia was treated with antibiotics and codeine for her cough, for example. She was found unresponsive on day 2 of admission. She was transferred to critical care, intubated, put on a respirator, and given supportive care.

She recovered fully, but genetic testing revealed that the patient "was an ultrarapid metabolizer ... and she converted that small amount of codeine [a prodrug] to large amounts of morphine rapidly," Dr. Beier said.

If a depressed patient also takes tamoxifen and is a poor metabolizer through 2D6, he or she will not convert as much tamoxifen to its active metabolite endoxifen, Dr. Patel said. When choosing an antidepressant for this type of patient, consider mirtazapine or venlafaxine (which do not strongly inhibit 2D6) vs. paroxetine or fluoxetine, she added.

The enzyme 2C9 metabolizes more than 90% of active S-warfarin, Dr. Beier said, and testing for variation in metabolism is clinically relevant with about 2 million patients started on warfarin each year. Testing for 2C9 and other genetic variations can explain up to 40% of the difference in current warfarin dosing, she added.

Another discovery of impaired metabolism led the Food and Drug Administration to require a black box warning for the anticlotting agent clopidogrel (Plavix) in 2010. The agency announced a reduced effectiveness of clopidogrel in patients who are poor metabolizers. Clopidogrel is another prodrug that has to be metabolized before it is biologically active, this time through the 2C19 enzyme pathway.

Available tests for such genetic differences in drug metabolism can cost $300-$700 and often are paid for out of pocket by patients, according to the panel. Dr. Beier recommended www.23andme.com for information on less expensive genetic testing. "I love this site. For $199, you can get a genome analysis. You can have your whole family spit in a cup, just not the same cup." (According to the Web site, the price is now $99.).

Full genome sequencing costs approximately $10,000. "When it comes down to a couple thousand dollars, it will be more affordable," Dr. Winner said, "but what are you going to do with the information?"

Dr. Winner is medical director for a genetic testing firm but had no other relevant disclosures. Dr. Patel and Dr. Beier disclosed no conflict of interest.

TAMPA – Why would two patients respond so differently the same medication? Although the reasons are several, recent advances support a prominent role for genetic differences in drug metabolism, according to a panel at the AMDA – Dedicated to Long Term Care Medicine annual meeting.

The good news is that this is not theoretical science. Some variations in patient response can be predicted using commercially available genetic assays, said the genetics and long-term care experts.

One strategy is to test patients for variations in genes for cytochrome P450 enzymes. Before prescribing an antidepressant, for example, you can test a patient for variations in their 2D6, 2C9, and 2C19 enzymes, which metabolize psychoactive medications and many others.

Depending on a patient’s genetics, in other words, he or she might be a poor, intermediate, or ultrarapid metabolizer of a particular medication, which can dramatically increase or decrease efficacy and side effects. Slow or poor metabolizers can experience a build-up of particular drug and extra side effects, whereas a rapid metabolizer might not get a full therapeutic benefit because of a drug’s quick clearance.

"If I have someone who is a 2D6-poor metabolizer, Paxil [paroxetine] is going to be at sky-high level, so instead I might try something like Luvox [fluvoxamine] or Celexa [citalopram]," said Dr. Joel Winner, medical director of Assure Rx Health, a laboratory service offering pharmacogenomics. "I am a clinician as well. I see patients and I use this technology," said Dr. Winner, who also is a private practice psychiatrist in Boulder, Colo.

He estimated that 60% of his patients undergo some form of genetic testing to help him make treatment decisions. "Fifty percent of depressed patients prescribed drugs are nonresponders," Dr. Winner said.

The ability to predict response versus waiting up to 8 weeks to judge a drug’s efficacy is an advantage, said Dr. Amita R. Patel, a geriatric psychiatrist at Wright State University, Dayton, Ohio.

Minimizing side effects is another goal of genetic testing, she added. "Drug-induced side effects, unfortunately, are very, very common and lead to noncompliance," Dr. Patel said. As an example, she described a woman not responding well to duloxetine [Cymbalta]. The patient felt sad, unmotivated, restless, anxious, and worried and reported sleep disturbances and daytime fatigue. Her Patient Health Questionnaire (PHQ-9) depression score was 15. Eight weeks after she switched to desvenlafaxine [Pristiq], her PHG-9 improved to a 5. (Desvenlafaxine and clonazepam are her current regimen.)

"She was not responding well to Cymbalta ... because her serum levels were too low. She was an ultrarapid metabolizer," Dr. Patel said. The patient also was taking insulin and omeprazole, two medications that were lowering her response to antidepressants.

"We are continuing to look at genes that predict weight gain, metabolic syndrome, or other issues relevant to psychiatry," Dr. Winner said.

A 60-year-old patient with treatment-resistant depression is another example. History revealed that the patient was unresponsive to escitalopram and budeprion XL. A switch to nortriptyline (Pamelor) did not significantly improve symptoms. When low-dose fluoxetine (Prozac) was added, the patient developed sedation and experienced a fall.

Subsequent genetic testing showed that the patient had impaired metabolism affected by 2D6, which metabolizes nortriptyline and fluoxetine. "So pharmacogenomic testing is very useful in our practice," Dr. Patel said. "We really need to look at a patient’s 2D6 whenever it is possible."

"Sometimes when we cannot figure out why a patient is oversedated at a low dose, [genetic testing] is something that can answer that question," said Manju T. Beier, PharmD, who is a senior partner for Geriatric Consultant Resources and on the pharmacy faculty at the University of Michigan, Ann Arbor.

Dr. Beier explained that metabolism of prodrugs works counterintuitively. "You need an enzyme to metabolize it to active compound, so you will get higher adverse events if you are a rapid metabolizer and inefficacy if you are a poor metabolizer."

A 79-year-old woman hospitalized with pneumonia was treated with antibiotics and codeine for her cough, for example. She was found unresponsive on day 2 of admission. She was transferred to critical care, intubated, put on a respirator, and given supportive care.

She recovered fully, but genetic testing revealed that the patient "was an ultrarapid metabolizer ... and she converted that small amount of codeine [a prodrug] to large amounts of morphine rapidly," Dr. Beier said.

If a depressed patient also takes tamoxifen and is a poor metabolizer through 2D6, he or she will not convert as much tamoxifen to its active metabolite endoxifen, Dr. Patel said. When choosing an antidepressant for this type of patient, consider mirtazapine or venlafaxine (which do not strongly inhibit 2D6) vs. paroxetine or fluoxetine, she added.

The enzyme 2C9 metabolizes more than 90% of active S-warfarin, Dr. Beier said, and testing for variation in metabolism is clinically relevant with about 2 million patients started on warfarin each year. Testing for 2C9 and other genetic variations can explain up to 40% of the difference in current warfarin dosing, she added.

Another discovery of impaired metabolism led the Food and Drug Administration to require a black box warning for the anticlotting agent clopidogrel (Plavix) in 2010. The agency announced a reduced effectiveness of clopidogrel in patients who are poor metabolizers. Clopidogrel is another prodrug that has to be metabolized before it is biologically active, this time through the 2C19 enzyme pathway.

Available tests for such genetic differences in drug metabolism can cost $300-$700 and often are paid for out of pocket by patients, according to the panel. Dr. Beier recommended www.23andme.com for information on less expensive genetic testing. "I love this site. For $199, you can get a genome analysis. You can have your whole family spit in a cup, just not the same cup." (According to the Web site, the price is now $99.).

Full genome sequencing costs approximately $10,000. "When it comes down to a couple thousand dollars, it will be more affordable," Dr. Winner said, "but what are you going to do with the information?"

Dr. Winner is medical director for a genetic testing firm but had no other relevant disclosures. Dr. Patel and Dr. Beier disclosed no conflict of interest.

TAMPA – Why would two patients respond so differently the same medication? Although the reasons are several, recent advances support a prominent role for genetic differences in drug metabolism, according to a panel at the AMDA – Dedicated to Long Term Care Medicine annual meeting.

The good news is that this is not theoretical science. Some variations in patient response can be predicted using commercially available genetic assays, said the genetics and long-term care experts.

One strategy is to test patients for variations in genes for cytochrome P450 enzymes. Before prescribing an antidepressant, for example, you can test a patient for variations in their 2D6, 2C9, and 2C19 enzymes, which metabolize psychoactive medications and many others.

Depending on a patient’s genetics, in other words, he or she might be a poor, intermediate, or ultrarapid metabolizer of a particular medication, which can dramatically increase or decrease efficacy and side effects. Slow or poor metabolizers can experience a build-up of particular drug and extra side effects, whereas a rapid metabolizer might not get a full therapeutic benefit because of a drug’s quick clearance.

"If I have someone who is a 2D6-poor metabolizer, Paxil [paroxetine] is going to be at sky-high level, so instead I might try something like Luvox [fluvoxamine] or Celexa [citalopram]," said Dr. Joel Winner, medical director of Assure Rx Health, a laboratory service offering pharmacogenomics. "I am a clinician as well. I see patients and I use this technology," said Dr. Winner, who also is a private practice psychiatrist in Boulder, Colo.

He estimated that 60% of his patients undergo some form of genetic testing to help him make treatment decisions. "Fifty percent of depressed patients prescribed drugs are nonresponders," Dr. Winner said.

The ability to predict response versus waiting up to 8 weeks to judge a drug’s efficacy is an advantage, said Dr. Amita R. Patel, a geriatric psychiatrist at Wright State University, Dayton, Ohio.

Minimizing side effects is another goal of genetic testing, she added. "Drug-induced side effects, unfortunately, are very, very common and lead to noncompliance," Dr. Patel said. As an example, she described a woman not responding well to duloxetine [Cymbalta]. The patient felt sad, unmotivated, restless, anxious, and worried and reported sleep disturbances and daytime fatigue. Her Patient Health Questionnaire (PHQ-9) depression score was 15. Eight weeks after she switched to desvenlafaxine [Pristiq], her PHG-9 improved to a 5. (Desvenlafaxine and clonazepam are her current regimen.)

"She was not responding well to Cymbalta ... because her serum levels were too low. She was an ultrarapid metabolizer," Dr. Patel said. The patient also was taking insulin and omeprazole, two medications that were lowering her response to antidepressants.

"We are continuing to look at genes that predict weight gain, metabolic syndrome, or other issues relevant to psychiatry," Dr. Winner said.

A 60-year-old patient with treatment-resistant depression is another example. History revealed that the patient was unresponsive to escitalopram and budeprion XL. A switch to nortriptyline (Pamelor) did not significantly improve symptoms. When low-dose fluoxetine (Prozac) was added, the patient developed sedation and experienced a fall.

Subsequent genetic testing showed that the patient had impaired metabolism affected by 2D6, which metabolizes nortriptyline and fluoxetine. "So pharmacogenomic testing is very useful in our practice," Dr. Patel said. "We really need to look at a patient’s 2D6 whenever it is possible."

"Sometimes when we cannot figure out why a patient is oversedated at a low dose, [genetic testing] is something that can answer that question," said Manju T. Beier, PharmD, who is a senior partner for Geriatric Consultant Resources and on the pharmacy faculty at the University of Michigan, Ann Arbor.

Dr. Beier explained that metabolism of prodrugs works counterintuitively. "You need an enzyme to metabolize it to active compound, so you will get higher adverse events if you are a rapid metabolizer and inefficacy if you are a poor metabolizer."

A 79-year-old woman hospitalized with pneumonia was treated with antibiotics and codeine for her cough, for example. She was found unresponsive on day 2 of admission. She was transferred to critical care, intubated, put on a respirator, and given supportive care.

She recovered fully, but genetic testing revealed that the patient "was an ultrarapid metabolizer ... and she converted that small amount of codeine [a prodrug] to large amounts of morphine rapidly," Dr. Beier said.

If a depressed patient also takes tamoxifen and is a poor metabolizer through 2D6, he or she will not convert as much tamoxifen to its active metabolite endoxifen, Dr. Patel said. When choosing an antidepressant for this type of patient, consider mirtazapine or venlafaxine (which do not strongly inhibit 2D6) vs. paroxetine or fluoxetine, she added.

The enzyme 2C9 metabolizes more than 90% of active S-warfarin, Dr. Beier said, and testing for variation in metabolism is clinically relevant with about 2 million patients started on warfarin each year. Testing for 2C9 and other genetic variations can explain up to 40% of the difference in current warfarin dosing, she added.

Another discovery of impaired metabolism led the Food and Drug Administration to require a black box warning for the anticlotting agent clopidogrel (Plavix) in 2010. The agency announced a reduced effectiveness of clopidogrel in patients who are poor metabolizers. Clopidogrel is another prodrug that has to be metabolized before it is biologically active, this time through the 2C19 enzyme pathway.

Available tests for such genetic differences in drug metabolism can cost $300-$700 and often are paid for out of pocket by patients, according to the panel. Dr. Beier recommended www.23andme.com for information on less expensive genetic testing. "I love this site. For $199, you can get a genome analysis. You can have your whole family spit in a cup, just not the same cup." (According to the Web site, the price is now $99.).

Full genome sequencing costs approximately $10,000. "When it comes down to a couple thousand dollars, it will be more affordable," Dr. Winner said, "but what are you going to do with the information?"

Dr. Winner is medical director for a genetic testing firm but had no other relevant disclosures. Dr. Patel and Dr. Beier disclosed no conflict of interest.

TAMPA – Why would two patients respond so differently the same medication? Although the reasons are several, recent advances support a prominent role for genetic differences in drug metabolism, according to a panel at the AMDA – Dedicated to Long Term Care Medicine annual meeting.

The good news is that this is not theoretical science. Some variations in patient response can be predicted using commercially available genetic assays, said the genetics and long-term care experts.

One strategy is to test patients for variations in genes for cytochrome P450 enzymes. Before prescribing an antidepressant, for example, you can test a patient for variations in their 2D6, 2C9, and 2C19 enzymes, which metabolize psychoactive medications and many others.

Depending on a patient’s genetics, in other words, he or she might be a poor, intermediate, or ultrarapid metabolizer of a particular medication, which can dramatically increase or decrease efficacy and side effects. Slow or poor metabolizers can experience a build-up of particular drug and extra side effects, whereas a rapid metabolizer might not get a full therapeutic benefit because of a drug’s quick clearance.

"If I have someone who is a 2D6-poor metabolizer, Paxil [paroxetine] is going to be at sky-high level, so instead I might try something like Luvox [fluvoxamine] or Celexa [citalopram]," said Dr. Joel Winner, medical director of Assure Rx Health, a laboratory service offering pharmacogenomics. "I am a clinician as well. I see patients and I use this technology," said Dr. Winner, who also is a private practice psychiatrist in Boulder, Colo.

He estimated that 60% of his patients undergo some form of genetic testing to help him make treatment decisions. "Fifty percent of depressed patients prescribed drugs are nonresponders," Dr. Winner said.

The ability to predict response versus waiting up to 8 weeks to judge a drug’s efficacy is an advantage, said Dr. Amita R. Patel, a geriatric psychiatrist at Wright State University, Dayton, Ohio.

Minimizing side effects is another goal of genetic testing, she added. "Drug-induced side effects, unfortunately, are very, very common and lead to noncompliance," Dr. Patel said. As an example, she described a woman not responding well to duloxetine [Cymbalta]. The patient felt sad, unmotivated, restless, anxious, and worried and reported sleep disturbances and daytime fatigue. Her Patient Health Questionnaire (PHQ-9) depression score was 15. Eight weeks after she switched to desvenlafaxine [Pristiq], her PHG-9 improved to a 5. (Desvenlafaxine and clonazepam are her current regimen.)

"She was not responding well to Cymbalta ... because her serum levels were too low. She was an ultrarapid metabolizer," Dr. Patel said. The patient also was taking insulin and omeprazole, two medications that were lowering her response to antidepressants.

"We are continuing to look at genes that predict weight gain, metabolic syndrome, or other issues relevant to psychiatry," Dr. Winner said.

A 60-year-old patient with treatment-resistant depression is another example. History revealed that the patient was unresponsive to escitalopram and budeprion XL. A switch to nortriptyline (Pamelor) did not significantly improve symptoms. When low-dose fluoxetine (Prozac) was added, the patient developed sedation and experienced a fall.

Subsequent genetic testing showed that the patient had impaired metabolism affected by 2D6, which metabolizes nortriptyline and fluoxetine. "So pharmacogenomic testing is very useful in our practice," Dr. Patel said. "We really need to look at a patient’s 2D6 whenever it is possible."

"Sometimes when we cannot figure out why a patient is oversedated at a low dose, [genetic testing] is something that can answer that question," said Manju T. Beier, PharmD, who is a senior partner for Geriatric Consultant Resources and on the pharmacy faculty at the University of Michigan, Ann Arbor.

Dr. Beier explained that metabolism of prodrugs works counterintuitively. "You need an enzyme to metabolize it to active compound, so you will get higher adverse events if you are a rapid metabolizer and inefficacy if you are a poor metabolizer."

A 79-year-old woman hospitalized with pneumonia was treated with antibiotics and codeine for her cough, for example. She was found unresponsive on day 2 of admission. She was transferred to critical care, intubated, put on a respirator, and given supportive care.

She recovered fully, but genetic testing revealed that the patient "was an ultrarapid metabolizer ... and she converted that small amount of codeine [a prodrug] to large amounts of morphine rapidly," Dr. Beier said.

If a depressed patient also takes tamoxifen and is a poor metabolizer through 2D6, he or she will not convert as much tamoxifen to its active metabolite endoxifen, Dr. Patel said. When choosing an antidepressant for this type of patient, consider mirtazapine or venlafaxine (which do not strongly inhibit 2D6) vs. paroxetine or fluoxetine, she added.

The enzyme 2C9 metabolizes more than 90% of active S-warfarin, Dr. Beier said, and testing for variation in metabolism is clinically relevant with about 2 million patients started on warfarin each year. Testing for 2C9 and other genetic variations can explain up to 40% of the difference in current warfarin dosing, she added.

Another discovery of impaired metabolism led the Food and Drug Administration to require a black box warning for the anticlotting agent clopidogrel (Plavix) in 2010. The agency announced a reduced effectiveness of clopidogrel in patients who are poor metabolizers. Clopidogrel is another prodrug that has to be metabolized before it is biologically active, this time through the 2C19 enzyme pathway.

Available tests for such genetic differences in drug metabolism can cost $300-$700 and often are paid for out of pocket by patients, according to the panel. Dr. Beier recommended www.23andme.com for information on less expensive genetic testing. "I love this site. For $199, you can get a genome analysis. You can have your whole family spit in a cup, just not the same cup." (According to the Web site, the price is now $99.).

Full genome sequencing costs approximately $10,000. "When it comes down to a couple thousand dollars, it will be more affordable," Dr. Winner said, "but what are you going to do with the information?"

Dr. Winner is medical director for a genetic testing firm but had no other relevant disclosures. Dr. Patel and Dr. Beier disclosed no conflict of interest.

TAMPA – Why would two patients respond so differently the same medication? Although the reasons are several, recent advances support a prominent role for genetic differences in drug metabolism, according to a panel at the AMDA – Dedicated to Long Term Care Medicine annual meeting.

The good news is that this is not theoretical science. Some variations in patient response can be predicted using commercially available genetic assays, said the genetics and long-term care experts.

One strategy is to test patients for variations in genes for cytochrome P450 enzymes. Before prescribing an antidepressant, for example, you can test a patient for variations in their 2D6, 2C9, and 2C19 enzymes, which metabolize psychoactive medications and many others.

Depending on a patient’s genetics, in other words, he or she might be a poor, intermediate, or ultrarapid metabolizer of a particular medication, which can dramatically increase or decrease efficacy and side effects. Slow or poor metabolizers can experience a build-up of particular drug and extra side effects, whereas a rapid metabolizer might not get a full therapeutic benefit because of a drug’s quick clearance.

"If I have someone who is a 2D6-poor metabolizer, Paxil [paroxetine] is going to be at sky-high level, so instead I might try something like Luvox [fluvoxamine] or Celexa [citalopram]," said Dr. Joel Winner, medical director of Assure Rx Health, a laboratory service offering pharmacogenomics. "I am a clinician as well. I see patients and I use this technology," said Dr. Winner, who also is a private practice psychiatrist in Boulder, Colo.

He estimated that 60% of his patients undergo some form of genetic testing to help him make treatment decisions. "Fifty percent of depressed patients prescribed drugs are nonresponders," Dr. Winner said.

The ability to predict response versus waiting up to 8 weeks to judge a drug’s efficacy is an advantage, said Dr. Amita R. Patel, a geriatric psychiatrist at Wright State University, Dayton, Ohio.

Minimizing side effects is another goal of genetic testing, she added. "Drug-induced side effects, unfortunately, are very, very common and lead to noncompliance," Dr. Patel said. As an example, she described a woman not responding well to duloxetine [Cymbalta]. The patient felt sad, unmotivated, restless, anxious, and worried and reported sleep disturbances and daytime fatigue. Her Patient Health Questionnaire (PHQ-9) depression score was 15. Eight weeks after she switched to desvenlafaxine [Pristiq], her PHG-9 improved to a 5. (Desvenlafaxine and clonazepam are her current regimen.)

"She was not responding well to Cymbalta ... because her serum levels were too low. She was an ultrarapid metabolizer," Dr. Patel said. The patient also was taking insulin and omeprazole, two medications that were lowering her response to antidepressants.

"We are continuing to look at genes that predict weight gain, metabolic syndrome, or other issues relevant to psychiatry," Dr. Winner said.

A 60-year-old patient with treatment-resistant depression is another example. History revealed that the patient was unresponsive to escitalopram and budeprion XL. A switch to nortriptyline (Pamelor) did not significantly improve symptoms. When low-dose fluoxetine (Prozac) was added, the patient developed sedation and experienced a fall.

Subsequent genetic testing showed that the patient had impaired metabolism affected by 2D6, which metabolizes nortriptyline and fluoxetine. "So pharmacogenomic testing is very useful in our practice," Dr. Patel said. "We really need to look at a patient’s 2D6 whenever it is possible."

"Sometimes when we cannot figure out why a patient is oversedated at a low dose, [genetic testing] is something that can answer that question," said Manju T. Beier, PharmD, who is a senior partner for Geriatric Consultant Resources and on the pharmacy faculty at the University of Michigan, Ann Arbor.

Dr. Beier explained that metabolism of prodrugs works counterintuitively. "You need an enzyme to metabolize it to active compound, so you will get higher adverse events if you are a rapid metabolizer and inefficacy if you are a poor metabolizer."

A 79-year-old woman hospitalized with pneumonia was treated with antibiotics and codeine for her cough, for example. She was found unresponsive on day 2 of admission. She was transferred to critical care, intubated, put on a respirator, and given supportive care.

She recovered fully, but genetic testing revealed that the patient "was an ultrarapid metabolizer ... and she converted that small amount of codeine [a prodrug] to large amounts of morphine rapidly," Dr. Beier said.

If a depressed patient also takes tamoxifen and is a poor metabolizer through 2D6, he or she will not convert as much tamoxifen to its active metabolite endoxifen, Dr. Patel said. When choosing an antidepressant for this type of patient, consider mirtazapine or venlafaxine (which do not strongly inhibit 2D6) vs. paroxetine or fluoxetine, she added.

The enzyme 2C9 metabolizes more than 90% of active S-warfarin, Dr. Beier said, and testing for variation in metabolism is clinically relevant with about 2 million patients started on warfarin each year. Testing for 2C9 and other genetic variations can explain up to 40% of the difference in current warfarin dosing, she added.

Another discovery of impaired metabolism led the Food and Drug Administration to require a black box warning for the anticlotting agent clopidogrel (Plavix) in 2010. The agency announced a reduced effectiveness of clopidogrel in patients who are poor metabolizers. Clopidogrel is another prodrug that has to be metabolized before it is biologically active, this time through the 2C19 enzyme pathway.

Available tests for such genetic differences in drug metabolism can cost $300-$700 and often are paid for out of pocket by patients, according to the panel. Dr. Beier recommended www.23andme.com for information on less expensive genetic testing. "I love this site. For $199, you can get a genome analysis. You can have your whole family spit in a cup, just not the same cup." (According to the Web site, the price is now $99.).

Full genome sequencing costs approximately $10,000. "When it comes down to a couple thousand dollars, it will be more affordable," Dr. Winner said, "but what are you going to do with the information?"

Dr. Winner is medical director for a genetic testing firm but had no other relevant disclosures. Dr. Patel and Dr. Beier disclosed no conflict of interest.

TAMPA – Why would two patients respond so differently the same medication? Although the reasons are several, recent advances support a prominent role for genetic differences in drug metabolism, according to a panel at the AMDA – Dedicated to Long Term Care Medicine annual meeting.

The good news is that this is not theoretical science. Some variations in patient response can be predicted using commercially available genetic assays, said the genetics and long-term care experts.

One strategy is to test patients for variations in genes for cytochrome P450 enzymes. Before prescribing an antidepressant, for example, you can test a patient for variations in their 2D6, 2C9, and 2C19 enzymes, which metabolize psychoactive medications and many others.

Depending on a patient’s genetics, in other words, he or she might be a poor, intermediate, or ultrarapid metabolizer of a particular medication, which can dramatically increase or decrease efficacy and side effects. Slow or poor metabolizers can experience a build-up of particular drug and extra side effects, whereas a rapid metabolizer might not get a full therapeutic benefit because of a drug’s quick clearance.

"If I have someone who is a 2D6-poor metabolizer, Paxil [paroxetine] is going to be at sky-high level, so instead I might try something like Luvox [fluvoxamine] or Celexa [citalopram]," said Dr. Joel Winner, medical director of Assure Rx Health, a laboratory service offering pharmacogenomics. "I am a clinician as well. I see patients and I use this technology," said Dr. Winner, who also is a private practice psychiatrist in Boulder, Colo.

He estimated that 60% of his patients undergo some form of genetic testing to help him make treatment decisions. "Fifty percent of depressed patients prescribed drugs are nonresponders," Dr. Winner said.

The ability to predict response versus waiting up to 8 weeks to judge a drug’s efficacy is an advantage, said Dr. Amita R. Patel, a geriatric psychiatrist at Wright State University, Dayton, Ohio.

Minimizing side effects is another goal of genetic testing, she added. "Drug-induced side effects, unfortunately, are very, very common and lead to noncompliance," Dr. Patel said. As an example, she described a woman not responding well to duloxetine [Cymbalta]. The patient felt sad, unmotivated, restless, anxious, and worried and reported sleep disturbances and daytime fatigue. Her Patient Health Questionnaire (PHQ-9) depression score was 15. Eight weeks after she switched to desvenlafaxine [Pristiq], her PHG-9 improved to a 5. (Desvenlafaxine and clonazepam are her current regimen.)

"She was not responding well to Cymbalta ... because her serum levels were too low. She was an ultrarapid metabolizer," Dr. Patel said. The patient also was taking insulin and omeprazole, two medications that were lowering her response to antidepressants.

"We are continuing to look at genes that predict weight gain, metabolic syndrome, or other issues relevant to psychiatry," Dr. Winner said.

A 60-year-old patient with treatment-resistant depression is another example. History revealed that the patient was unresponsive to escitalopram and budeprion XL. A switch to nortriptyline (Pamelor) did not significantly improve symptoms. When low-dose fluoxetine (Prozac) was added, the patient developed sedation and experienced a fall.

Subsequent genetic testing showed that the patient had impaired metabolism affected by 2D6, which metabolizes nortriptyline and fluoxetine. "So pharmacogenomic testing is very useful in our practice," Dr. Patel said. "We really need to look at a patient’s 2D6 whenever it is possible."

"Sometimes when we cannot figure out why a patient is oversedated at a low dose, [genetic testing] is something that can answer that question," said Manju T. Beier, PharmD, who is a senior partner for Geriatric Consultant Resources and on the pharmacy faculty at the University of Michigan, Ann Arbor.

Dr. Beier explained that metabolism of prodrugs works counterintuitively. "You need an enzyme to metabolize it to active compound, so you will get higher adverse events if you are a rapid metabolizer and inefficacy if you are a poor metabolizer."

A 79-year-old woman hospitalized with pneumonia was treated with antibiotics and codeine for her cough, for example. She was found unresponsive on day 2 of admission. She was transferred to critical care, intubated, put on a respirator, and given supportive care.

She recovered fully, but genetic testing revealed that the patient "was an ultrarapid metabolizer ... and she converted that small amount of codeine [a prodrug] to large amounts of morphine rapidly," Dr. Beier said.

If a depressed patient also takes tamoxifen and is a poor metabolizer through 2D6, he or she will not convert as much tamoxifen to its active metabolite endoxifen, Dr. Patel said. When choosing an antidepressant for this type of patient, consider mirtazapine or venlafaxine (which do not strongly inhibit 2D6) vs. paroxetine or fluoxetine, she added.

The enzyme 2C9 metabolizes more than 90% of active S-warfarin, Dr. Beier said, and testing for variation in metabolism is clinically relevant with about 2 million patients started on warfarin each year. Testing for 2C9 and other genetic variations can explain up to 40% of the difference in current warfarin dosing, she added.

Another discovery of impaired metabolism led the Food and Drug Administration to require a black box warning for the anticlotting agent clopidogrel (Plavix) in 2010. The agency announced a reduced effectiveness of clopidogrel in patients who are poor metabolizers. Clopidogrel is another prodrug that has to be metabolized before it is biologically active, this time through the 2C19 enzyme pathway.

Available tests for such genetic differences in drug metabolism can cost $300-$700 and often are paid for out of pocket by patients, according to the panel. Dr. Beier recommended www.23andme.com for information on less expensive genetic testing. "I love this site. For $199, you can get a genome analysis. You can have your whole family spit in a cup, just not the same cup." (According to the Web site, the price is now $99.).

Full genome sequencing costs approximately $10,000. "When it comes down to a couple thousand dollars, it will be more affordable," Dr. Winner said, "but what are you going to do with the information?"

Dr. Winner is medical director for a genetic testing firm but had no other relevant disclosures. Dr. Patel and Dr. Beier disclosed no conflict of interest.

TAMPA – Why would two patients respond so differently the same medication? Although the reasons are several, recent advances support a prominent role for genetic differences in drug metabolism, according to a panel at the AMDA – Dedicated to Long Term Care Medicine annual meeting.

The good news is that this is not theoretical science. Some variations in patient response can be predicted using commercially available genetic assays, said the genetics and long-term care experts.

One strategy is to test patients for variations in genes for cytochrome P450 enzymes. Before prescribing an antidepressant, for example, you can test a patient for variations in their 2D6, 2C9, and 2C19 enzymes, which metabolize psychoactive medications and many others.

Depending on a patient’s genetics, in other words, he or she might be a poor, intermediate, or ultrarapid metabolizer of a particular medication, which can dramatically increase or decrease efficacy and side effects. Slow or poor metabolizers can experience a build-up of particular drug and extra side effects, whereas a rapid metabolizer might not get a full therapeutic benefit because of a drug’s quick clearance.

"If I have someone who is a 2D6-poor metabolizer, Paxil [paroxetine] is going to be at sky-high level, so instead I might try something like Luvox [fluvoxamine] or Celexa [citalopram]," said Dr. Joel Winner, medical director of Assure Rx Health, a laboratory service offering pharmacogenomics. "I am a clinician as well. I see patients and I use this technology," said Dr. Winner, who also is a private practice psychiatrist in Boulder, Colo.

He estimated that 60% of his patients undergo some form of genetic testing to help him make treatment decisions. "Fifty percent of depressed patients prescribed drugs are nonresponders," Dr. Winner said.

The ability to predict response versus waiting up to 8 weeks to judge a drug’s efficacy is an advantage, said Dr. Amita R. Patel, a geriatric psychiatrist at Wright State University, Dayton, Ohio.

Minimizing side effects is another goal of genetic testing, she added. "Drug-induced side effects, unfortunately, are very, very common and lead to noncompliance," Dr. Patel said. As an example, she described a woman not responding well to duloxetine [Cymbalta]. The patient felt sad, unmotivated, restless, anxious, and worried and reported sleep disturbances and daytime fatigue. Her Patient Health Questionnaire (PHQ-9) depression score was 15. Eight weeks after she switched to desvenlafaxine [Pristiq], her PHG-9 improved to a 5. (Desvenlafaxine and clonazepam are her current regimen.)

"She was not responding well to Cymbalta ... because her serum levels were too low. She was an ultrarapid metabolizer," Dr. Patel said. The patient also was taking insulin and omeprazole, two medications that were lowering her response to antidepressants.

"We are continuing to look at genes that predict weight gain, metabolic syndrome, or other issues relevant to psychiatry," Dr. Winner said.

A 60-year-old patient with treatment-resistant depression is another example. History revealed that the patient was unresponsive to escitalopram and budeprion XL. A switch to nortriptyline (Pamelor) did not significantly improve symptoms. When low-dose fluoxetine (Prozac) was added, the patient developed sedation and experienced a fall.

Subsequent genetic testing showed that the patient had impaired metabolism affected by 2D6, which metabolizes nortriptyline and fluoxetine. "So pharmacogenomic testing is very useful in our practice," Dr. Patel said. "We really need to look at a patient’s 2D6 whenever it is possible."

"Sometimes when we cannot figure out why a patient is oversedated at a low dose, [genetic testing] is something that can answer that question," said Manju T. Beier, PharmD, who is a senior partner for Geriatric Consultant Resources and on the pharmacy faculty at the University of Michigan, Ann Arbor.

Dr. Beier explained that metabolism of prodrugs works counterintuitively. "You need an enzyme to metabolize it to active compound, so you will get higher adverse events if you are a rapid metabolizer and inefficacy if you are a poor metabolizer."

A 79-year-old woman hospitalized with pneumonia was treated with antibiotics and codeine for her cough, for example. She was found unresponsive on day 2 of admission. She was transferred to critical care, intubated, put on a respirator, and given supportive care.

She recovered fully, but genetic testing revealed that the patient "was an ultrarapid metabolizer ... and she converted that small amount of codeine [a prodrug] to large amounts of morphine rapidly," Dr. Beier said.

If a depressed patient also takes tamoxifen and is a poor metabolizer through 2D6, he or she will not convert as much tamoxifen to its active metabolite endoxifen, Dr. Patel said. When choosing an antidepressant for this type of patient, consider mirtazapine or venlafaxine (which do not strongly inhibit 2D6) vs. paroxetine or fluoxetine, she added.

The enzyme 2C9 metabolizes more than 90% of active S-warfarin, Dr. Beier said, and testing for variation in metabolism is clinically relevant with about 2 million patients started on warfarin each year. Testing for 2C9 and other genetic variations can explain up to 40% of the difference in current warfarin dosing, she added.

Another discovery of impaired metabolism led the Food and Drug Administration to require a black box warning for the anticlotting agent clopidogrel (Plavix) in 2010. The agency announced a reduced effectiveness of clopidogrel in patients who are poor metabolizers. Clopidogrel is another prodrug that has to be metabolized before it is biologically active, this time through the 2C19 enzyme pathway.

Available tests for such genetic differences in drug metabolism can cost $300-$700 and often are paid for out of pocket by patients, according to the panel. Dr. Beier recommended www.23andme.com for information on less expensive genetic testing. "I love this site. For $199, you can get a genome analysis. You can have your whole family spit in a cup, just not the same cup." (According to the Web site, the price is now $99.).

Full genome sequencing costs approximately $10,000. "When it comes down to a couple thousand dollars, it will be more affordable," Dr. Winner said, "but what are you going to do with the information?"

Dr. Winner is medical director for a genetic testing firm but had no other relevant disclosures. Dr. Patel and Dr. Beier disclosed no conflict of interest.

TAMPA – Why would two patients respond so differently the same medication? Although the reasons are several, recent advances support a prominent role for genetic differences in drug metabolism, according to a panel at the AMDA – Dedicated to Long Term Care Medicine annual meeting.

The good news is that this is not theoretical science. Some variations in patient response can be predicted using commercially available genetic assays, said the genetics and long-term care experts.

One strategy is to test patients for variations in genes for cytochrome P450 enzymes. Before prescribing an antidepressant, for example, you can test a patient for variations in their 2D6, 2C9, and 2C19 enzymes, which metabolize psychoactive medications and many others.

Depending on a patient’s genetics, in other words, he or she might be a poor, intermediate, or ultrarapid metabolizer of a particular medication, which can dramatically increase or decrease efficacy and side effects. Slow or poor metabolizers can experience a build-up of particular drug and extra side effects, whereas a rapid metabolizer might not get a full therapeutic benefit because of a drug’s quick clearance.

"If I have someone who is a 2D6-poor metabolizer, Paxil [paroxetine] is going to be at sky-high level, so instead I might try something like Luvox [fluvoxamine] or Celexa [citalopram]," said Dr. Joel Winner, medical director of Assure Rx Health, a laboratory service offering pharmacogenomics. "I am a clinician as well. I see patients and I use this technology," said Dr. Winner, who also is a private practice psychiatrist in Boulder, Colo.

He estimated that 60% of his patients undergo some form of genetic testing to help him make treatment decisions. "Fifty percent of depressed patients prescribed drugs are nonresponders," Dr. Winner said.

The ability to predict response versus waiting up to 8 weeks to judge a drug’s efficacy is an advantage, said Dr. Amita R. Patel, a geriatric psychiatrist at Wright State University, Dayton, Ohio.

Minimizing side effects is another goal of genetic testing, she added. "Drug-induced side effects, unfortunately, are very, very common and lead to noncompliance," Dr. Patel said. As an example, she described a woman not responding well to duloxetine [Cymbalta]. The patient felt sad, unmotivated, restless, anxious, and worried and reported sleep disturbances and daytime fatigue. Her Patient Health Questionnaire (PHQ-9) depression score was 15. Eight weeks after she switched to desvenlafaxine [Pristiq], her PHG-9 improved to a 5. (Desvenlafaxine and clonazepam are her current regimen.)

"She was not responding well to Cymbalta ... because her serum levels were too low. She was an ultrarapid metabolizer," Dr. Patel said. The patient also was taking insulin and omeprazole, two medications that were lowering her response to antidepressants.

"We are continuing to look at genes that predict weight gain, metabolic syndrome, or other issues relevant to psychiatry," Dr. Winner said.

A 60-year-old patient with treatment-resistant depression is another example. History revealed that the patient was unresponsive to escitalopram and budeprion XL. A switch to nortriptyline (Pamelor) did not significantly improve symptoms. When low-dose fluoxetine (Prozac) was added, the patient developed sedation and experienced a fall.

Subsequent genetic testing showed that the patient had impaired metabolism affected by 2D6, which metabolizes nortriptyline and fluoxetine. "So pharmacogenomic testing is very useful in our practice," Dr. Patel said. "We really need to look at a patient’s 2D6 whenever it is possible."

"Sometimes when we cannot figure out why a patient is oversedated at a low dose, [genetic testing] is something that can answer that question," said Manju T. Beier, PharmD, who is a senior partner for Geriatric Consultant Resources and on the pharmacy faculty at the University of Michigan, Ann Arbor.

Dr. Beier explained that metabolism of prodrugs works counterintuitively. "You need an enzyme to metabolize it to active compound, so you will get higher adverse events if you are a rapid metabolizer and inefficacy if you are a poor metabolizer."

A 79-year-old woman hospitalized with pneumonia was treated with antibiotics and codeine for her cough, for example. She was found unresponsive on day 2 of admission. She was transferred to critical care, intubated, put on a respirator, and given supportive care.

She recovered fully, but genetic testing revealed that the patient "was an ultrarapid metabolizer ... and she converted that small amount of codeine [a prodrug] to large amounts of morphine rapidly," Dr. Beier said.

If a depressed patient also takes tamoxifen and is a poor metabolizer through 2D6, he or she will not convert as much tamoxifen to its active metabolite endoxifen, Dr. Patel said. When choosing an antidepressant for this type of patient, consider mirtazapine or venlafaxine (which do not strongly inhibit 2D6) vs. paroxetine or fluoxetine, she added.

The enzyme 2C9 metabolizes more than 90% of active S-warfarin, Dr. Beier said, and testing for variation in metabolism is clinically relevant with about 2 million patients started on warfarin each year. Testing for 2C9 and other genetic variations can explain up to 40% of the difference in current warfarin dosing, she added.

Another discovery of impaired metabolism led the Food and Drug Administration to require a black box warning for the anticlotting agent clopidogrel (Plavix) in 2010. The agency announced a reduced effectiveness of clopidogrel in patients who are poor metabolizers. Clopidogrel is another prodrug that has to be metabolized before it is biologically active, this time through the 2C19 enzyme pathway.

Available tests for such genetic differences in drug metabolism can cost $300-$700 and often are paid for out of pocket by patients, according to the panel. Dr. Beier recommended www.23andme.com for information on less expensive genetic testing. "I love this site. For $199, you can get a genome analysis. You can have your whole family spit in a cup, just not the same cup." (According to the Web site, the price is now $99.).

Full genome sequencing costs approximately $10,000. "When it comes down to a couple thousand dollars, it will be more affordable," Dr. Winner said, "but what are you going to do with the information?"

Dr. Winner is medical director for a genetic testing firm but had no other relevant disclosures. Dr. Patel and Dr. Beier disclosed no conflict of interest.

TAMPA – Why would two patients respond so differently the same medication? Although the reasons are several, recent advances support a prominent role for genetic differences in drug metabolism, according to a panel at the AMDA – Dedicated to Long Term Care Medicine annual meeting.

The good news is that this is not theoretical science. Some variations in patient response can be predicted using commercially available genetic assays, said the genetics and long-term care experts.

One strategy is to test patients for variations in genes for cytochrome P450 enzymes. Before prescribing an antidepressant, for example, you can test a patient for variations in their 2D6, 2C9, and 2C19 enzymes, which metabolize psychoactive medications and many others.

Depending on a patient’s genetics, in other words, he or she might be a poor, intermediate, or ultrarapid metabolizer of a particular medication, which can dramatically increase or decrease efficacy and side effects. Slow or poor metabolizers can experience a build-up of particular drug and extra side effects, whereas a rapid metabolizer might not get a full therapeutic benefit because of a drug’s quick clearance.

"If I have someone who is a 2D6-poor metabolizer, Paxil [paroxetine] is going to be at sky-high level, so instead I might try something like Luvox [fluvoxamine] or Celexa [citalopram]," said Dr. Joel Winner, medical director of Assure Rx Health, a laboratory service offering pharmacogenomics. "I am a clinician as well. I see patients and I use this technology," said Dr. Winner, who also is a private practice psychiatrist in Boulder, Colo.

He estimated that 60% of his patients undergo some form of genetic testing to help him make treatment decisions. "Fifty percent of depressed patients prescribed drugs are nonresponders," Dr. Winner said.

The ability to predict response versus waiting up to 8 weeks to judge a drug’s efficacy is an advantage, said Dr. Amita R. Patel, a geriatric psychiatrist at Wright State University, Dayton, Ohio.

Minimizing side effects is another goal of genetic testing, she added. "Drug-induced side effects, unfortunately, are very, very common and lead to noncompliance," Dr. Patel said. As an example, she described a woman not responding well to duloxetine [Cymbalta]. The patient felt sad, unmotivated, restless, anxious, and worried and reported sleep disturbances and daytime fatigue. Her Patient Health Questionnaire (PHQ-9) depression score was 15. Eight weeks after she switched to desvenlafaxine [Pristiq], her PHG-9 improved to a 5. (Desvenlafaxine and clonazepam are her current regimen.)

"She was not responding well to Cymbalta ... because her serum levels were too low. She was an ultrarapid metabolizer," Dr. Patel said. The patient also was taking insulin and omeprazole, two medications that were lowering her response to antidepressants.

"We are continuing to look at genes that predict weight gain, metabolic syndrome, or other issues relevant to psychiatry," Dr. Winner said.

A 60-year-old patient with treatment-resistant depression is another example. History revealed that the patient was unresponsive to escitalopram and budeprion XL. A switch to nortriptyline (Pamelor) did not significantly improve symptoms. When low-dose fluoxetine (Prozac) was added, the patient developed sedation and experienced a fall.

Subsequent genetic testing showed that the patient had impaired metabolism affected by 2D6, which metabolizes nortriptyline and fluoxetine. "So pharmacogenomic testing is very useful in our practice," Dr. Patel said. "We really need to look at a patient’s 2D6 whenever it is possible."

"Sometimes when we cannot figure out why a patient is oversedated at a low dose, [genetic testing] is something that can answer that question," said Manju T. Beier, PharmD, who is a senior partner for Geriatric Consultant Resources and on the pharmacy faculty at the University of Michigan, Ann Arbor.

Dr. Beier explained that metabolism of prodrugs works counterintuitively. "You need an enzyme to metabolize it to active compound, so you will get higher adverse events if you are a rapid metabolizer and inefficacy if you are a poor metabolizer."

A 79-year-old woman hospitalized with pneumonia was treated with antibiotics and codeine for her cough, for example. She was found unresponsive on day 2 of admission. She was transferred to critical care, intubated, put on a respirator, and given supportive care.

She recovered fully, but genetic testing revealed that the patient "was an ultrarapid metabolizer ... and she converted that small amount of codeine [a prodrug] to large amounts of morphine rapidly," Dr. Beier said.

If a depressed patient also takes tamoxifen and is a poor metabolizer through 2D6, he or she will not convert as much tamoxifen to its active metabolite endoxifen, Dr. Patel said. When choosing an antidepressant for this type of patient, consider mirtazapine or venlafaxine (which do not strongly inhibit 2D6) vs. paroxetine or fluoxetine, she added.

The enzyme 2C9 metabolizes more than 90% of active S-warfarin, Dr. Beier said, and testing for variation in metabolism is clinically relevant with about 2 million patients started on warfarin each year. Testing for 2C9 and other genetic variations can explain up to 40% of the difference in current warfarin dosing, she added.

Another discovery of impaired metabolism led the Food and Drug Administration to require a black box warning for the anticlotting agent clopidogrel (Plavix) in 2010. The agency announced a reduced effectiveness of clopidogrel in patients who are poor metabolizers. Clopidogrel is another prodrug that has to be metabolized before it is biologically active, this time through the 2C19 enzyme pathway.

Available tests for such genetic differences in drug metabolism can cost $300-$700 and often are paid for out of pocket by patients, according to the panel. Dr. Beier recommended www.23andme.com for information on less expensive genetic testing. "I love this site. For $199, you can get a genome analysis. You can have your whole family spit in a cup, just not the same cup." (According to the Web site, the price is now $99.).

Full genome sequencing costs approximately $10,000. "When it comes down to a couple thousand dollars, it will be more affordable," Dr. Winner said, "but what are you going to do with the information?"

Dr. Winner is medical director for a genetic testing firm but had no other relevant disclosures. Dr. Patel and Dr. Beier disclosed no conflict of interest.

TAMPA – Consistently safe and effective transfers of patients from hospitals to nursing homes take effort and planning that health care facilities and professionals typically do not focused on, according to two medical directors with more than 2 decades of hospital and nursing home experience in South Dakota.

"The hospital’s job until now, and the job of the hospitalist as well, is to treat the acute illness, keep patients safe during hospitalization, and discharge patients as soon as possible," Dr. David Sandvik said at the annual meeting of AMDA – Dedicated to Long Term Care Medicine. "There have been no incentives so far regarding safe transfers."

Moving patients safely means overcoming numerous physician and institutional barriers, said Dr. Sandvik, professor of internal and family medicine at the University of South Dakota, Sioux Falls. "Hospital discharge is viewed as the least important part of the stay."

"In the hospital, you should start working on discharge planning on day 1," Dr. Priscilla Bade said. Where she practices, the sole tertiary care hospital, Rapid City (South Dakota) Regional Hospital, and eight community nursing homes have created standardized discharge checklists that facilitate safe transfers, said Dr. Bade, who is an attending physician at the hospital and director of hospice care and a member of the internal medicine faculty at the University. Regular, ongoing meetings of a work group on transfers have been instrumental as well, she said.

Dr. Bade advised others to assemble groups of people with common interests in improving patient transfers, including clinicians at the hospital and the skilled nursing facilities. "This will help hospital administrators see we all need to work together or we will hang separately."

Dr. Sandvik said that administration participation is a natural. "It’s not hard to get [because] you end up with messes if you don’t have a good transfer system." Others important to include in meetings on better transfers are members of hospital and nursing home departments of nursing, social services, information systems, medical records, and pharmacy, he said, "and this is just in the planning."

Designate a meeting coordinator and find appropriate space to meet, Dr. Bade advised. Involve everyone present and "get input from those people on what to change" about the current transfer procedures, she said. "At each meeting, set practical goals for the next meeting and assign people to work on them."

Several talking points can start the conversation, Dr. Bade said. They include: Optimal transfers maintain patient safety, improve patient satisfaction, improve facility and physician workflow, reduce delays and the number of transfers, and lower readmission rates.

Transitions are not only logistically challenging but also one of the most cognitively challenging tasks for a physician, Dr. Sandvik said. For an effective transfer, doctors on both ends need to know, for example, events that occurred during hospitalization; the capabilities and needs of the receiving facility; the patient’s medication list at discharge and possible drug interactions; the need for rehabilitation; the potential for reimbursements through Medicare, Medicaid, private insurance, and private payments; and what appropriate physician follow-up can be arranged.

"This is a daunting list," Dr. Sandvik said, and payment for all that work can be challenging. "The more complex the patient or transfer, the lower physician reimbursement per time unit," Dr. Sandvik said. "Current charges for extended time require patient face-to-face time ... which is often the least productive time to spend arranging a transfer with a confused, older patient."

Many transfer problems result from poor communication, Dr. Sandvik said, so improving information exchange is crucial. He said he has witnessed the transfer of a hospital patient on a day other than what a nursing home had been told and the transfer of a hypoxic patient without any oxygen.

"The reality is we all have to migrate to a technologic solution," Dr. Sandvik said. Electronic medical records and other technologies could end cases of incomplete information accompanying a transferred patient. "I can’t get a fishing license unless all the required fields are filled in," yet patients often come to nursing homes without important information, Dr. Sandvik said.

"Hospitalists do not start out to do a bad job," he added. "We have to figure out why those forms are not getting filled out." "Sometimes, we spend days in the nursing home trying to figure out why an order was given or not given." In some cases, that’s made harder when the hospitalist who took care of a patient and wrote the discharge orders is off-duty at the time of the transfer.

Dr. Bade suggested that one way to improve transfers is to give a limited number of staff at the nursing home password-protected, remote access to the hospital’s electronic medical record system. Allowing such access to Rapid City Regional Hospital records has improved transfer accuracy and completeness, she said. The arrangement requires much interfacility cooperation, said Dr. Bade.

Until technology comes to the rescue at more nursing homes, Dr. Sandvik and Dr. Bade recommended relying on standardized, paper-based forms. The universal transfer form they use at works for transfers of patients not only from the hospital to nursing home but also from surgery to a bed within the hospital, from the intensive care unit to another hospital floor, and from one hospital to another, Dr. Sandvik said.

Some forms, however, "are specific for transfers to specific types of institutions, including skilled nursing facilities, assisted living facilities, home health care agencies," said Dr. Bade. One is specific to patients leaving a nursing home for the hospital emergency department. "These are basically checklists," she said. The forms include medications, other treatments, specific orders, and appointment information and are not valid in South Dakota until signed by a physician.

The nurses also have a separate transfer sheet. "It’s self explanatory, but if it’s not listed, it doesn’t get done," Dr. Sandvik said. "There has to be a reason for each medication given in the nursing home."

An audience member asked if Dr. Bade or Dr. Sandvik experience any pushback on the forms. "Yes, you get pushback," Dr. Sandvik said. "There is more work involved."

"The nursing home transfer forms serve as the discharge orders," Dr. Bade said. "We do have a challenge with them filling out the diagnoses, and we need [to do] more education on that."

Another challenge is adapting to changes in key personnel or facility policies over time. "We are dealing with a moving target," Dr. Sandvik said. Improving the system is an ongoing effort. "Once you have created the perfect transfer process, you will have a perfect transfer process for a very short time."

Dr. Sandvik and Dr. Bade said that they had no relevant disclosures.

TAMPA – Consistently safe and effective transfers of patients from hospitals to nursing homes take effort and planning that health care facilities and professionals typically do not focused on, according to two medical directors with more than 2 decades of hospital and nursing home experience in South Dakota.

"The hospital’s job until now, and the job of the hospitalist as well, is to treat the acute illness, keep patients safe during hospitalization, and discharge patients as soon as possible," Dr. David Sandvik said at the annual meeting of AMDA – Dedicated to Long Term Care Medicine. "There have been no incentives so far regarding safe transfers."

Moving patients safely means overcoming numerous physician and institutional barriers, said Dr. Sandvik, professor of internal and family medicine at the University of South Dakota, Sioux Falls. "Hospital discharge is viewed as the least important part of the stay."

"In the hospital, you should start working on discharge planning on day 1," Dr. Priscilla Bade said. Where she practices, the sole tertiary care hospital, Rapid City (South Dakota) Regional Hospital, and eight community nursing homes have created standardized discharge checklists that facilitate safe transfers, said Dr. Bade, who is an attending physician at the hospital and director of hospice care and a member of the internal medicine faculty at the University. Regular, ongoing meetings of a work group on transfers have been instrumental as well, she said.

Dr. Bade advised others to assemble groups of people with common interests in improving patient transfers, including clinicians at the hospital and the skilled nursing facilities. "This will help hospital administrators see we all need to work together or we will hang separately."

Dr. Sandvik said that administration participation is a natural. "It’s not hard to get [because] you end up with messes if you don’t have a good transfer system." Others important to include in meetings on better transfers are members of hospital and nursing home departments of nursing, social services, information systems, medical records, and pharmacy, he said, "and this is just in the planning."

Designate a meeting coordinator and find appropriate space to meet, Dr. Bade advised. Involve everyone present and "get input from those people on what to change" about the current transfer procedures, she said. "At each meeting, set practical goals for the next meeting and assign people to work on them."

Several talking points can start the conversation, Dr. Bade said. They include: Optimal transfers maintain patient safety, improve patient satisfaction, improve facility and physician workflow, reduce delays and the number of transfers, and lower readmission rates.

Transitions are not only logistically challenging but also one of the most cognitively challenging tasks for a physician, Dr. Sandvik said. For an effective transfer, doctors on both ends need to know, for example, events that occurred during hospitalization; the capabilities and needs of the receiving facility; the patient’s medication list at discharge and possible drug interactions; the need for rehabilitation; the potential for reimbursements through Medicare, Medicaid, private insurance, and private payments; and what appropriate physician follow-up can be arranged.

"This is a daunting list," Dr. Sandvik said, and payment for all that work can be challenging. "The more complex the patient or transfer, the lower physician reimbursement per time unit," Dr. Sandvik said. "Current charges for extended time require patient face-to-face time ... which is often the least productive time to spend arranging a transfer with a confused, older patient."

Many transfer problems result from poor communication, Dr. Sandvik said, so improving information exchange is crucial. He said he has witnessed the transfer of a hospital patient on a day other than what a nursing home had been told and the transfer of a hypoxic patient without any oxygen.

"The reality is we all have to migrate to a technologic solution," Dr. Sandvik said. Electronic medical records and other technologies could end cases of incomplete information accompanying a transferred patient. "I can’t get a fishing license unless all the required fields are filled in," yet patients often come to nursing homes without important information, Dr. Sandvik said.

"Hospitalists do not start out to do a bad job," he added. "We have to figure out why those forms are not getting filled out." "Sometimes, we spend days in the nursing home trying to figure out why an order was given or not given." In some cases, that’s made harder when the hospitalist who took care of a patient and wrote the discharge orders is off-duty at the time of the transfer.

Dr. Bade suggested that one way to improve transfers is to give a limited number of staff at the nursing home password-protected, remote access to the hospital’s electronic medical record system. Allowing such access to Rapid City Regional Hospital records has improved transfer accuracy and completeness, she said. The arrangement requires much interfacility cooperation, said Dr. Bade.

Until technology comes to the rescue at more nursing homes, Dr. Sandvik and Dr. Bade recommended relying on standardized, paper-based forms. The universal transfer form they use at works for transfers of patients not only from the hospital to nursing home but also from surgery to a bed within the hospital, from the intensive care unit to another hospital floor, and from one hospital to another, Dr. Sandvik said.

Some forms, however, "are specific for transfers to specific types of institutions, including skilled nursing facilities, assisted living facilities, home health care agencies," said Dr. Bade. One is specific to patients leaving a nursing home for the hospital emergency department. "These are basically checklists," she said. The forms include medications, other treatments, specific orders, and appointment information and are not valid in South Dakota until signed by a physician.

The nurses also have a separate transfer sheet. "It’s self explanatory, but if it’s not listed, it doesn’t get done," Dr. Sandvik said. "There has to be a reason for each medication given in the nursing home."

An audience member asked if Dr. Bade or Dr. Sandvik experience any pushback on the forms. "Yes, you get pushback," Dr. Sandvik said. "There is more work involved."

"The nursing home transfer forms serve as the discharge orders," Dr. Bade said. "We do have a challenge with them filling out the diagnoses, and we need [to do] more education on that."

Another challenge is adapting to changes in key personnel or facility policies over time. "We are dealing with a moving target," Dr. Sandvik said. Improving the system is an ongoing effort. "Once you have created the perfect transfer process, you will have a perfect transfer process for a very short time."

Dr. Sandvik and Dr. Bade said that they had no relevant disclosures.

TAMPA – Consistently safe and effective transfers of patients from hospitals to nursing homes take effort and planning that health care facilities and professionals typically do not focused on, according to two medical directors with more than 2 decades of hospital and nursing home experience in South Dakota.

"The hospital’s job until now, and the job of the hospitalist as well, is to treat the acute illness, keep patients safe during hospitalization, and discharge patients as soon as possible," Dr. David Sandvik said at the annual meeting of AMDA – Dedicated to Long Term Care Medicine. "There have been no incentives so far regarding safe transfers."

Moving patients safely means overcoming numerous physician and institutional barriers, said Dr. Sandvik, professor of internal and family medicine at the University of South Dakota, Sioux Falls. "Hospital discharge is viewed as the least important part of the stay."

"In the hospital, you should start working on discharge planning on day 1," Dr. Priscilla Bade said. Where she practices, the sole tertiary care hospital, Rapid City (South Dakota) Regional Hospital, and eight community nursing homes have created standardized discharge checklists that facilitate safe transfers, said Dr. Bade, who is an attending physician at the hospital and director of hospice care and a member of the internal medicine faculty at the University. Regular, ongoing meetings of a work group on transfers have been instrumental as well, she said.

Dr. Bade advised others to assemble groups of people with common interests in improving patient transfers, including clinicians at the hospital and the skilled nursing facilities. "This will help hospital administrators see we all need to work together or we will hang separately."

Dr. Sandvik said that administration participation is a natural. "It’s not hard to get [because] you end up with messes if you don’t have a good transfer system." Others important to include in meetings on better transfers are members of hospital and nursing home departments of nursing, social services, information systems, medical records, and pharmacy, he said, "and this is just in the planning."

Designate a meeting coordinator and find appropriate space to meet, Dr. Bade advised. Involve everyone present and "get input from those people on what to change" about the current transfer procedures, she said. "At each meeting, set practical goals for the next meeting and assign people to work on them."

Several talking points can start the conversation, Dr. Bade said. They include: Optimal transfers maintain patient safety, improve patient satisfaction, improve facility and physician workflow, reduce delays and the number of transfers, and lower readmission rates.

Transitions are not only logistically challenging but also one of the most cognitively challenging tasks for a physician, Dr. Sandvik said. For an effective transfer, doctors on both ends need to know, for example, events that occurred during hospitalization; the capabilities and needs of the receiving facility; the patient’s medication list at discharge and possible drug interactions; the need for rehabilitation; the potential for reimbursements through Medicare, Medicaid, private insurance, and private payments; and what appropriate physician follow-up can be arranged.

"This is a daunting list," Dr. Sandvik said, and payment for all that work can be challenging. "The more complex the patient or transfer, the lower physician reimbursement per time unit," Dr. Sandvik said. "Current charges for extended time require patient face-to-face time ... which is often the least productive time to spend arranging a transfer with a confused, older patient."

Many transfer problems result from poor communication, Dr. Sandvik said, so improving information exchange is crucial. He said he has witnessed the transfer of a hospital patient on a day other than what a nursing home had been told and the transfer of a hypoxic patient without any oxygen.

"The reality is we all have to migrate to a technologic solution," Dr. Sandvik said. Electronic medical records and other technologies could end cases of incomplete information accompanying a transferred patient. "I can’t get a fishing license unless all the required fields are filled in," yet patients often come to nursing homes without important information, Dr. Sandvik said.

"Hospitalists do not start out to do a bad job," he added. "We have to figure out why those forms are not getting filled out." "Sometimes, we spend days in the nursing home trying to figure out why an order was given or not given." In some cases, that’s made harder when the hospitalist who took care of a patient and wrote the discharge orders is off-duty at the time of the transfer.

Dr. Bade suggested that one way to improve transfers is to give a limited number of staff at the nursing home password-protected, remote access to the hospital’s electronic medical record system. Allowing such access to Rapid City Regional Hospital records has improved transfer accuracy and completeness, she said. The arrangement requires much interfacility cooperation, said Dr. Bade.

Until technology comes to the rescue at more nursing homes, Dr. Sandvik and Dr. Bade recommended relying on standardized, paper-based forms. The universal transfer form they use at works for transfers of patients not only from the hospital to nursing home but also from surgery to a bed within the hospital, from the intensive care unit to another hospital floor, and from one hospital to another, Dr. Sandvik said.

Some forms, however, "are specific for transfers to specific types of institutions, including skilled nursing facilities, assisted living facilities, home health care agencies," said Dr. Bade. One is specific to patients leaving a nursing home for the hospital emergency department. "These are basically checklists," she said. The forms include medications, other treatments, specific orders, and appointment information and are not valid in South Dakota until signed by a physician.

The nurses also have a separate transfer sheet. "It’s self explanatory, but if it’s not listed, it doesn’t get done," Dr. Sandvik said. "There has to be a reason for each medication given in the nursing home."

An audience member asked if Dr. Bade or Dr. Sandvik experience any pushback on the forms. "Yes, you get pushback," Dr. Sandvik said. "There is more work involved."

"The nursing home transfer forms serve as the discharge orders," Dr. Bade said. "We do have a challenge with them filling out the diagnoses, and we need [to do] more education on that."

Another challenge is adapting to changes in key personnel or facility policies over time. "We are dealing with a moving target," Dr. Sandvik said. Improving the system is an ongoing effort. "Once you have created the perfect transfer process, you will have a perfect transfer process for a very short time."

Dr. Sandvik and Dr. Bade said that they had no relevant disclosures.