A widely cited statistic in the national readmissions debate holds that one in five acute hospital discharges will lead to a readmission within 30 days.¹ Associated costs are estimated at $17.5 billion, although that figure encapsulates significant variation across diagnoses, regions, and hospital models.¹ Analyses by CMS and others suggest that average 30-day readmission rates have been falling, albeit slowly, to 17.8% during the fourth quarter of 2012 after averaging 19% over the previous five years, according to Congressional testimony by Medicare Director Jonathan Blum in February 2013.²

CMS calculates “excessive readmissions rates” for subsequent hospital admissions to the same or a different hospital for specific diagnoses within 30 days of discharge, risk-adjusted for planned and unrelated readmissions using methodology endorsed by the National Quality Forum. Based on the hospital’s rate of actual to expected readmissions, HRRP penalties are applied to all Medicare-based diagnosis-related group (DRG) payments to the hospital for the fiscal year in question, to a maximum of 3% of Medicare payments. The list of conditions now includes heart failure, acute myocardial infarction, pneumonia, acute exacerbation of COPD, other lung ailments such as chronic bronchitis, and admissions for elective total hip and total knee arthroplasty.

Aggregate average penalty in FY2015 for 2,610 hospitals paying penalties, or three-fourths of those subject to the program, will be 0.63% of total base hospital DRG reimbursement, or approximately $428 million in total readmissions penalties. Thirty-nine hospitals are paying the full 3% penalty, based on their posted readmissions between July 2010 and June 2013.³ If a hospital has fewer than 25 discharges for a given condition, then CMS does not calculate its excess readmissions penalty for that condition.

In its June 2013 report to Congress, the Medicare Payment Advisory Commission (MedPAC), which first proposed readmissions payment incentives in 2008, recommended steps to refine the computation of penalties, all with “the goal that any policy change should maintain a hospital’s incentive to reduce readmissions.”⁴ CMS has stated that it is continuing to revise its algorithms for excluding planned and unrelated readmissions from the penalty calculation.⁵

MedPAC found that the rate of “potentially preventable readmissions” (PPR) was 12.3% in 2011, according to the “3M Algorithm” developed by 3M Health Information Systems, which uses administrative data to identify hospital readmissions that may indicate problems with quality of care. The PPR logic determines whether the reason for readmission is clinically related to a prior admission and therefore potentially preventable.⁶

Others define preventable readmissions in terms of quality problems, medical errors through actions taken or omitted during the initial hospital stay that could lead to patient harm.

Larry Beresford is a freelance writer in Alameda, Calif.

References

1. Jencks SF, Williams MV, Coleman EA. Rehospitalizations among patients in the Medicare fee-for-service program. N Engl J Med. 2009;360(14):1418-1428.
2. Blum J. Statement of Jonathan Blum on delivery system reform: progress report from CMS before the U.S. Senate Finance Committee. February 28, 2013. Available at: http://www.finance.senate.gov/imo/media/doc/CMS%20Delivery%20System%20Reform%20Testimony%202.28.13%20(J.%20Blum).pdf. Accessed March 12, 2015.
3. Rau J. Medicare Fines 2,610 Hospitals in Third Round of Readmissions Penalties. Kaiser Health News. October 2, 2014. Available at: http://kaiserhealthnews.org/news/medicare-readmissions-penalties-2015/. Accessed March 12, 2015.
4. Medicare Payment Advisory Commission. Report to the Congress: Medicare and the health care delivery system. Chapter 4: refining the hospital readmissions reduction program. June 2013. Available at: http://www.medpac.gov/documents/reports/jun13_entirereport.pdf. Accessed March 12, 2015.
5. Rodak S. CMS responds to 6 major critiques of readmissions measures. Becker’s Infection Control and Clinical Quality. August 7, 2013. Available at: http://www.beckershospitalreview.com/quality/cms-responds-to-6-major-critiques-of-readmission-measure.html. Accessed March 12 2015.
6. Goldfield NI, McCullough EC, Hughes JS, et al. Identifying potentially preventable readmissions. Healthcare Financing Review. Available at: https://www.cms.gov/Research-Statistics-Data-and-Systems/Research/HealthCareFinancingReview/downloads/08Fallpg75.pdf. Accessed March 12, 2015.

A widely cited statistic in the national readmissions debate holds that one in five acute hospital discharges will lead to a readmission within 30 days.¹ Associated costs are estimated at $17.5 billion, although that figure encapsulates significant variation across diagnoses, regions, and hospital models.¹ Analyses by CMS and others suggest that average 30-day readmission rates have been falling, albeit slowly, to 17.8% during the fourth quarter of 2012 after averaging 19% over the previous five years, according to Congressional testimony by Medicare Director Jonathan Blum in February 2013.²

CMS calculates “excessive readmissions rates” for subsequent hospital admissions to the same or a different hospital for specific diagnoses within 30 days of discharge, risk-adjusted for planned and unrelated readmissions using methodology endorsed by the National Quality Forum. Based on the hospital’s rate of actual to expected readmissions, HRRP penalties are applied to all Medicare-based diagnosis-related group (DRG) payments to the hospital for the fiscal year in question, to a maximum of 3% of Medicare payments. The list of conditions now includes heart failure, acute myocardial infarction, pneumonia, acute exacerbation of COPD, other lung ailments such as chronic bronchitis, and admissions for elective total hip and total knee arthroplasty.

Aggregate average penalty in FY2015 for 2,610 hospitals paying penalties, or three-fourths of those subject to the program, will be 0.63% of total base hospital DRG reimbursement, or approximately $428 million in total readmissions penalties. Thirty-nine hospitals are paying the full 3% penalty, based on their posted readmissions between July 2010 and June 2013.³ If a hospital has fewer than 25 discharges for a given condition, then CMS does not calculate its excess readmissions penalty for that condition.

In its June 2013 report to Congress, the Medicare Payment Advisory Commission (MedPAC), which first proposed readmissions payment incentives in 2008, recommended steps to refine the computation of penalties, all with “the goal that any policy change should maintain a hospital’s incentive to reduce readmissions.”⁴ CMS has stated that it is continuing to revise its algorithms for excluding planned and unrelated readmissions from the penalty calculation.⁵

MedPAC found that the rate of “potentially preventable readmissions” (PPR) was 12.3% in 2011, according to the “3M Algorithm” developed by 3M Health Information Systems, which uses administrative data to identify hospital readmissions that may indicate problems with quality of care. The PPR logic determines whether the reason for readmission is clinically related to a prior admission and therefore potentially preventable.⁶

Others define preventable readmissions in terms of quality problems, medical errors through actions taken or omitted during the initial hospital stay that could lead to patient harm.

Larry Beresford is a freelance writer in Alameda, Calif.

References

1. Jencks SF, Williams MV, Coleman EA. Rehospitalizations among patients in the Medicare fee-for-service program. N Engl J Med. 2009;360(14):1418-1428.
2. Blum J. Statement of Jonathan Blum on delivery system reform: progress report from CMS before the U.S. Senate Finance Committee. February 28, 2013. Available at: http://www.finance.senate.gov/imo/media/doc/CMS%20Delivery%20System%20Reform%20Testimony%202.28.13%20(J.%20Blum).pdf. Accessed March 12, 2015.
3. Rau J. Medicare Fines 2,610 Hospitals in Third Round of Readmissions Penalties. Kaiser Health News. October 2, 2014. Available at: http://kaiserhealthnews.org/news/medicare-readmissions-penalties-2015/. Accessed March 12, 2015.
4. Medicare Payment Advisory Commission. Report to the Congress: Medicare and the health care delivery system. Chapter 4: refining the hospital readmissions reduction program. June 2013. Available at: http://www.medpac.gov/documents/reports/jun13_entirereport.pdf. Accessed March 12, 2015.
5. Rodak S. CMS responds to 6 major critiques of readmissions measures. Becker’s Infection Control and Clinical Quality. August 7, 2013. Available at: http://www.beckershospitalreview.com/quality/cms-responds-to-6-major-critiques-of-readmission-measure.html. Accessed March 12 2015.
6. Goldfield NI, McCullough EC, Hughes JS, et al. Identifying potentially preventable readmissions. Healthcare Financing Review. Available at: https://www.cms.gov/Research-Statistics-Data-and-Systems/Research/HealthCareFinancingReview/downloads/08Fallpg75.pdf. Accessed March 12, 2015.

A widely cited statistic in the national readmissions debate holds that one in five acute hospital discharges will lead to a readmission within 30 days.¹ Associated costs are estimated at $17.5 billion, although that figure encapsulates significant variation across diagnoses, regions, and hospital models.¹ Analyses by CMS and others suggest that average 30-day readmission rates have been falling, albeit slowly, to 17.8% during the fourth quarter of 2012 after averaging 19% over the previous five years, according to Congressional testimony by Medicare Director Jonathan Blum in February 2013.²

CMS calculates “excessive readmissions rates” for subsequent hospital admissions to the same or a different hospital for specific diagnoses within 30 days of discharge, risk-adjusted for planned and unrelated readmissions using methodology endorsed by the National Quality Forum. Based on the hospital’s rate of actual to expected readmissions, HRRP penalties are applied to all Medicare-based diagnosis-related group (DRG) payments to the hospital for the fiscal year in question, to a maximum of 3% of Medicare payments. The list of conditions now includes heart failure, acute myocardial infarction, pneumonia, acute exacerbation of COPD, other lung ailments such as chronic bronchitis, and admissions for elective total hip and total knee arthroplasty.

Aggregate average penalty in FY2015 for 2,610 hospitals paying penalties, or three-fourths of those subject to the program, will be 0.63% of total base hospital DRG reimbursement, or approximately $428 million in total readmissions penalties. Thirty-nine hospitals are paying the full 3% penalty, based on their posted readmissions between July 2010 and June 2013.³ If a hospital has fewer than 25 discharges for a given condition, then CMS does not calculate its excess readmissions penalty for that condition.

In its June 2013 report to Congress, the Medicare Payment Advisory Commission (MedPAC), which first proposed readmissions payment incentives in 2008, recommended steps to refine the computation of penalties, all with “the goal that any policy change should maintain a hospital’s incentive to reduce readmissions.”⁴ CMS has stated that it is continuing to revise its algorithms for excluding planned and unrelated readmissions from the penalty calculation.⁵

MedPAC found that the rate of “potentially preventable readmissions” (PPR) was 12.3% in 2011, according to the “3M Algorithm” developed by 3M Health Information Systems, which uses administrative data to identify hospital readmissions that may indicate problems with quality of care. The PPR logic determines whether the reason for readmission is clinically related to a prior admission and therefore potentially preventable.⁶

Others define preventable readmissions in terms of quality problems, medical errors through actions taken or omitted during the initial hospital stay that could lead to patient harm.

Larry Beresford is a freelance writer in Alameda, Calif.

References

1. Jencks SF, Williams MV, Coleman EA. Rehospitalizations among patients in the Medicare fee-for-service program. N Engl J Med. 2009;360(14):1418-1428.
2. Blum J. Statement of Jonathan Blum on delivery system reform: progress report from CMS before the U.S. Senate Finance Committee. February 28, 2013. Available at: http://www.finance.senate.gov/imo/media/doc/CMS%20Delivery%20System%20Reform%20Testimony%202.28.13%20(J.%20Blum).pdf. Accessed March 12, 2015.
3. Rau J. Medicare Fines 2,610 Hospitals in Third Round of Readmissions Penalties. Kaiser Health News. October 2, 2014. Available at: http://kaiserhealthnews.org/news/medicare-readmissions-penalties-2015/. Accessed March 12, 2015.
4. Medicare Payment Advisory Commission. Report to the Congress: Medicare and the health care delivery system. Chapter 4: refining the hospital readmissions reduction program. June 2013. Available at: http://www.medpac.gov/documents/reports/jun13_entirereport.pdf. Accessed March 12, 2015.
5. Rodak S. CMS responds to 6 major critiques of readmissions measures. Becker’s Infection Control and Clinical Quality. August 7, 2013. Available at: http://www.beckershospitalreview.com/quality/cms-responds-to-6-major-critiques-of-readmission-measure.html. Accessed March 12 2015.
6. Goldfield NI, McCullough EC, Hughes JS, et al. Identifying potentially preventable readmissions. Healthcare Financing Review. Available at: https://www.cms.gov/Research-Statistics-Data-and-Systems/Research/HealthCareFinancingReview/downloads/08Fallpg75.pdf. Accessed March 12, 2015.

Almost weekly, a white paper, report, journal article, or press release touts a new program, software, or technology system offering to help hospitals improve their readmissions avoidance processes and penalty exposure. Does this new readmissions cottage industry offer value to hospitals?

Some technologies focus on interdisciplinary team communication, with electronic repositories or virtual rounding, automated communications to the PCP, personalized patient instructions booklets, or telecommunications or mobile applications. Others aim to help coordinate patients’ care transitions and providers’ post-discharge outreach, empower patients, increase compliance with discharge instructions, or schedule and coordinate follow-up activities.

An August 16, 2013, blog post at HISTalk identified other technologies and services being employed by advisory panelists’ hospitals to reduce their readmissions, including electronic health record (EHR) vendors, predictive modeling vendors, home-grown analytics reports, decision support, niche software vendors focused on supporting case management, telemonitoring programs, and use of the LACE (length of stay, acuity of admission, co-morbidities, and number of previous ED visits in the last six months) index to identify patients at risk.

“I view these as tools and, like any tool, they can be helpful if they are the right tool for the job, applied correctly,” says Gregory Maynard, MD, MSc, SFHM, clinical professor and chief quality officer at the University of California Davis Medical Center in Sacramento. “In many cases, these tech tools are trying to reproduce virtually what ideally would be done in person—interdisciplinary bedside rounds with the active engagement of the patient.”

Mark V. Williams, MD, FACP, MHM, director of the Center for Health Services Research and vice chair of the department of internal medicine at the University of Kentucky in Lexington, says he’s stunned by the sheer number of entrepreneurial readmissions management programs and systems on the market.

“Obviously, people see a need. But I’m not that sanguine about this new tech stuff,” says Dr. Williams, Project BOOST’s principal investigator.

There has to be some kind of integration with the hospital’s EHR, he says; otherwise, it just makes extra work.

“I wish our existing EHRs had the capacity to develop their own readmissions applications,” he says.

Larry Beresford is a freelance writer in Alameda, Calif.

Almost weekly, a white paper, report, journal article, or press release touts a new program, software, or technology system offering to help hospitals improve their readmissions avoidance processes and penalty exposure. Does this new readmissions cottage industry offer value to hospitals?

Some technologies focus on interdisciplinary team communication, with electronic repositories or virtual rounding, automated communications to the PCP, personalized patient instructions booklets, or telecommunications or mobile applications. Others aim to help coordinate patients’ care transitions and providers’ post-discharge outreach, empower patients, increase compliance with discharge instructions, or schedule and coordinate follow-up activities.

An August 16, 2013, blog post at HISTalk identified other technologies and services being employed by advisory panelists’ hospitals to reduce their readmissions, including electronic health record (EHR) vendors, predictive modeling vendors, home-grown analytics reports, decision support, niche software vendors focused on supporting case management, telemonitoring programs, and use of the LACE (length of stay, acuity of admission, co-morbidities, and number of previous ED visits in the last six months) index to identify patients at risk.

“I view these as tools and, like any tool, they can be helpful if they are the right tool for the job, applied correctly,” says Gregory Maynard, MD, MSc, SFHM, clinical professor and chief quality officer at the University of California Davis Medical Center in Sacramento. “In many cases, these tech tools are trying to reproduce virtually what ideally would be done in person—interdisciplinary bedside rounds with the active engagement of the patient.”

Mark V. Williams, MD, FACP, MHM, director of the Center for Health Services Research and vice chair of the department of internal medicine at the University of Kentucky in Lexington, says he’s stunned by the sheer number of entrepreneurial readmissions management programs and systems on the market.

“Obviously, people see a need. But I’m not that sanguine about this new tech stuff,” says Dr. Williams, Project BOOST’s principal investigator.

There has to be some kind of integration with the hospital’s EHR, he says; otherwise, it just makes extra work.

“I wish our existing EHRs had the capacity to develop their own readmissions applications,” he says.

Larry Beresford is a freelance writer in Alameda, Calif.

Almost weekly, a white paper, report, journal article, or press release touts a new program, software, or technology system offering to help hospitals improve their readmissions avoidance processes and penalty exposure. Does this new readmissions cottage industry offer value to hospitals?

Some technologies focus on interdisciplinary team communication, with electronic repositories or virtual rounding, automated communications to the PCP, personalized patient instructions booklets, or telecommunications or mobile applications. Others aim to help coordinate patients’ care transitions and providers’ post-discharge outreach, empower patients, increase compliance with discharge instructions, or schedule and coordinate follow-up activities.

An August 16, 2013, blog post at HISTalk identified other technologies and services being employed by advisory panelists’ hospitals to reduce their readmissions, including electronic health record (EHR) vendors, predictive modeling vendors, home-grown analytics reports, decision support, niche software vendors focused on supporting case management, telemonitoring programs, and use of the LACE (length of stay, acuity of admission, co-morbidities, and number of previous ED visits in the last six months) index to identify patients at risk.

“I view these as tools and, like any tool, they can be helpful if they are the right tool for the job, applied correctly,” says Gregory Maynard, MD, MSc, SFHM, clinical professor and chief quality officer at the University of California Davis Medical Center in Sacramento. “In many cases, these tech tools are trying to reproduce virtually what ideally would be done in person—interdisciplinary bedside rounds with the active engagement of the patient.”

Mark V. Williams, MD, FACP, MHM, director of the Center for Health Services Research and vice chair of the department of internal medicine at the University of Kentucky in Lexington, says he’s stunned by the sheer number of entrepreneurial readmissions management programs and systems on the market.

“Obviously, people see a need. But I’m not that sanguine about this new tech stuff,” says Dr. Williams, Project BOOST’s principal investigator.

There has to be some kind of integration with the hospital’s EHR, he says; otherwise, it just makes extra work.

“I wish our existing EHRs had the capacity to develop their own readmissions applications,” he says.

Larry Beresford is a freelance writer in Alameda, Calif.

This month, our cover story focuses on how hospitalists fit into the readmission prevention framework. Hospitalist Dr. Eric Howell discusses the ongoing problem of hospital discharges and sees preventing readmissions as a way to fix it. Also on our cover, endocrinologists share 10 things hospitalists need to know about treating endocrine disease. In addition this month, hospital medicine leader Dr. Bob Wachter shares insights on his new book, “The Digital Doctor.”

[audio mp3="http://www.the-hospitalist.org/wp-content/uploads/2015/03/The-Hospitalist-Highlights-April-2015.mp3"][/audio]

This month, our cover story focuses on how hospitalists fit into the readmission prevention framework. Hospitalist Dr. Eric Howell discusses the ongoing problem of hospital discharges and sees preventing readmissions as a way to fix it. Also on our cover, endocrinologists share 10 things hospitalists need to know about treating endocrine disease. In addition this month, hospital medicine leader Dr. Bob Wachter shares insights on his new book, “The Digital Doctor.”

[audio mp3="http://www.the-hospitalist.org/wp-content/uploads/2015/03/The-Hospitalist-Highlights-April-2015.mp3"][/audio]

This month, our cover story focuses on how hospitalists fit into the readmission prevention framework. Hospitalist Dr. Eric Howell discusses the ongoing problem of hospital discharges and sees preventing readmissions as a way to fix it. Also on our cover, endocrinologists share 10 things hospitalists need to know about treating endocrine disease. In addition this month, hospital medicine leader Dr. Bob Wachter shares insights on his new book, “The Digital Doctor.”

[audio mp3="http://www.the-hospitalist.org/wp-content/uploads/2015/03/The-Hospitalist-Highlights-April-2015.mp3"][/audio]

Diabetes is as prevalent in hospitals today as lab coats and heart monitors. More than 8% of the population—almost 26 million people—and nearly 27% (11 million) of Americans 65 or older have diabetes, according to American Diabetes Association (ADA) statistics. That makes diabetes one of the most common conditions hospitalists face day in and day out.

Other endocrine disorders also pose a challenge to hospitalists because they may be relatively uncommon, endocrinologists say.

The Hospitalist spoke to several endocrinologists and veteran hospitalists, mining their backgrounds and observations for tips on caring for hospitalized patients with endocrine disorders. Here are nine things they think hospitalists need to know:

1. Realize the far-reaching impact of good care for diabetic patients.

Part of the reason this is important is the numbers of patients with the disease who will be hospitalized and come under the care of a hospitalist.

“They’re coming in for a host of medical conditions, not the least of which is that diabetes is a comorbid factor that goes along with it,” says John Anderson, MD, the ADA’s immediate past president of medicine and science and an internist and diabetician at The Frist Clinic in Nashville, Tenn. “For those who are critically ill—those having bypass, those having stroke—diabetes is overrepresented even more once they get inside the hospital and in the intensive care unit.”

Job No. 1, controlling blood sugar, can have broad implications, he says.

“We know that control of their glucose through the hospital stay actually makes a difference in long-term outcomes, particularly things like surgery, coronary bypass grafting, that type of thing,” he says, noting that the standard of care is to try to keep glucose under 200. “A lot of studies have been done that demonstrate that really poor control of glucose in the hospital, regardless of the disease entity they’re in with, can lead to worsening long-term outcomes. It’s really imperative that you control the blood sugar.^1,2

“A lot of studies have been done that demonstrate that really poor control of glucose in the hospital, regardless of the disease entity they’re in with, can lead to worsening long-term outcomes. It’s really imperative that you control the blood sugar.^1,2 However, if you control it so tightly that these patients are dropping their blood sugar and having significant hypoglycemia problems in the hospital, that’s not good either.”

—John Anderson, MD, past president, American Diabetes Association, internist and diabetician, The Frist Clinic, Nashville, Tenn.

“However, the other part of this is…that if you control it so tightly that these patients are dropping their blood sugar and having significant hypoglycemia problems in the hospital, that’s not good either.”

2. You probably shouldn’t be testing for thyroid-stimulating hormone (TSH) level by itself in an acutely ill inpatient.

Simply put, the results probably won’t be useful, says Tamara Wexler, MD, PhD, an endocrinologist attending at Massachusetts General Hospital in Boston.

“TSH alone, for some reason, seems to be often measured,” she says, but “it’s extremely rarely indicated during acute hospitalization.”

TSH is “notoriously spurious” in inpatients, she adds, because the stress of an illness can make the test difficult to interpret.

“Many endocrine hormone levels are affected by stress, for example, and thus are better measured in an outpatient setting than in an acute hospitalized illness because of the impact of the illness on interpreting the test results,” she says.

Euthyroid sick syndrome—or “sick euthyroid”—is a term used for abnormalities in thyroid tests in patients with systemic illnesses that are nonthyroidal.

In cases in which thyroid dysfunction is strongly suspected, TSH should be measured in conjunction with other levels, such as a free thyroxine (free T4) level, Dr. Wexler says.

3. Don’t forget to watch potassium in patients with diabetic ketoacidosis (DKA).

A patient with a normal level of potassium, or even a high one, at baseline can encounter a problem with plummeting levels, says Bruce Mitchell, MD, director of hospital medicine services at Emory Hospital Midtown and assistant professor of hospital medicine at Emory University in Atlanta.

“Once you start insulin and correcting the hyperosmolality, the potassium shifts,” says Dr. Mitchell, who has a particular interest in endocrinology, “so it can become abnormally low fairly quickly.

“You start the insulin and fluids; then all of a sudden that person’s potassium is drastically abnormal and they’re coding,” he says. “It’s important to make sure your hospital’s diabetic ketoacidosis protocol includes frequent potassium checks.”

4. Be sure to wait long enough before rechecking TSH after a medication change.

It takes several weeks before thyroid medication dose changes start to show their effects, says Jeffrey Greenwald, MD, a hospitalist at Massachusetts General with expertise in endocrinology. Guidelines published in 2012 by the American Association of Clinical Endocrinologists and the American Thyroid Association recommend rechecking TSH within four to eight weeks.³

“It bears reminding that [for] patients who have recently changed their thyroid medication dose, you need to wait several weeks before you recheck their TSH. That’s another reason why the TSH can be somewhat difficult to interpret. There’s a tendency that I have seen, too, if the TSH is high and they’re on thyroid replacement, to want to adjust the dose while they’re in the hospital, which is probably not the time to do it.”—Jeffrey Greenwald, MD, hospitalist, Massachusetts General, Boston

“It bears reminding that [for] patients who have recently changed their thyroid medication dose, you need to wait several weeks before you recheck their TSH,” he says. “That’s another reason why the TSH can be somewhat difficult to interpret.

“There’s a tendency that I have seen, too, if the TSH is high and they’re on thyroid replacement, to want to adjust the dose while they’re in the hospital, which is probably not the time to do it.”

5. When administering insulin, factor in soon-to-arrive meals and give prandial insulin as needed.

If patients with diabetes are receiving insulin in the hospital, even if their glucose is in the normal range, they will need insulin if they’re about to have a carb-loaded breakfast, says Jose Florez, MD, PhD, an endocrinologist at Massachusetts General and associate professor of medicine at Harvard Medical School in Boston.

“A person with a glucose of 98 who is about to eat pancakes needs standing short-acting insulin regardless of the fingerstick,” Dr. Florez says. “A person with a glucose of 250 who is about to eat needs both the correction insulin and the amount needed to handle the impending carbohydrate load.”

“The person not only needs to correct what the glucose is at the moment, but they also need to account for the impending carbohydrate intake,” he says.

Dr. Anderson says he always cautions those caring for hospitalized diabetic patients against using the “sliding-scale philosophy”—marked by set amounts of long-acting insulin and set amounts of carbohydrate intake—because it’s overly formulaic for that setting.

“It leads to really variable glucoses,” he says, “and usually not good control.”

6. Giving isotonic fluids to someone who has fixed water retention or hypertonic urine can worsen the problem.

This can stem from an incomplete or incorrect evaluation of hyponatremia, which is a common problem in hospitalized patients. When hyponatremia is present, the first order of business should be to exclude pseudohyponatremia and confirm that it’s hypotonic hyponatremia.

After confirmation, the volume status should be assessed. One useful way to do this is to measure urine creatinine, urine sodium, and urine osmolality (osm), Dr. Florez says. If a patient has water retention or hypertonic urine from syndrome of inappropriate diuretic hormone secretion (SIADH), hypothyroidism, or glucocorticoid deficiency, the hospitalist needs to act accordingly.

“If the urine osm is high, higher than the serum osm, and is fixed at that level for some reason…giving that person isotonic fluids will lead to additional water retention and make the situation worse,” he says. “It’s very important to assess the volume status and establish the cause. And then, if you’re going to give fluids, be mindful of what the urine might look like. Do not give fluids that are hypotonic with respect to what the urine is making, unless you are completely convinced that the person is dry and therefore needs volume.”

“Once you start insulin and correcting the hyperosmolality, the potassium shifts, so it can become abnormally low fairly quickly. You start the insulin and fluids; then all of a sudden that person’s potassium is drastically abnormal and they’re coding. It’s important to make sure your hospital’s diabetic ketoacidosis protocol includes frequent potassium checks.”—Bruce Mitchell, MD, director of hospital medicine services, Emory Hospital Midtown, assistant professor of hospital medicine, Emory University, Atlanta.

7. Encourage patients to check their own glucose and administer their own insulin while still in the hospital.

“We often deal with patients who start insulin treatment for diabetes during an admission or who seem not to be doing very well giving insulin at home,” Dr. Wexler says. “Many patients can benefit from supervised insulin injections and glucose testing.”

Going through the process while in the hospital with supervision can be a good refresher, she says.

“You don’t have to necessarily order specific diabetic teaching,” she adds, noting that not all hospitals have diabetic educators available at all times.

A patient might be waiting for diabetic teaching before discharge, but this might be one way to speed the process, Dr. Wexler says. She suggests teaching by example.

8. Patients on steroids every day are at risk for adrenal insufficiency.

Even if they aren’t on corticosteroids when they present, hospitalists should think of these patients as “at risk for adrenal insufficiency and potentially immunocompromised,” Dr. Greenwald says. “The bigger issue in most cases is the adrenal insufficiency.”

That means their bodies can’t mount an appropriate response to stress.

“And without that appropriate response of additional stress hormone the body would normally make, they may not be able, for example, to maintain their blood pressure,” he says. “This can be extremely dangerous.”

Inhaled steroids, and topical steroids if they are applied to broken skin, can have a kind of stealth effect.

“That’s something to keep in mind,” Dr. Wexler says, noting the connection between blood pressure management and endocrine conditions.

9. Thyroid hormone might not be as well absorbed under certain conditions.

With calcium or iron supplementation, thyroid hormones might present a problem, Dr. Wexler says. For patients at home taking thyroid hormone appropriately (an hour or two separated from calcium or iron supplementation), there “should be no issue,” she says. “But if they are administered at the same time at the hospital, patients may not absorb the full dose.”

Tom Collins is a freelance writer in South Florida.

Misinterpreting Thyroid Function Tests Can Lead You Down the Wrong Path, Expert Warns

Thyroid function tests in hospitalized patients can sometimes be a case of a mistake begetting a mistake.⁴ Don’t fall into the trap, endocrinologists say.³

Consider a patient presenting with new atrial fibrillation. One of the triggers for the condition is hyperthyroidism, so it’s common to do a thyroid function test.

“Say the TSH [thyroid-stimulating hormone] is up because the patient is recovering from an acute illness,”

Dr. Florez says. “All of a sudden you were looking for hyperthyroidism, but now you have a high TSH, so that initiates a workup for hypothyroidism.” But that is not the proper course, because a high TSH is not uncommon in a person getting over an illness.

Once the TSH comes back high, you’ve ruled out hyperthyroidism as the reason for the atrial fibrillation.

The matter should be considered settled, he said. “No reason to get all excited about pursuing a hypothyroidism diagnosis,” Dr. Florez says. If thereis any concern, the thyroid function tests could be repeated in the outpatient setting when the patient is no longer acutely ill.

Misdirected concerns about hypothyroidism should also be avoided.

For example, a patient presents with altered mental status, which can be brought about by myxedema coma, or profound hypothyroidism.

If the TSH comes back low—eliminating hypothyroidism as a problem—a hospitalist should not embark on a hyperthyroidism diagnosis, Dr. Florez says. It’s probably just sick euthyroid causing the abnormal TSH level.

“What you need to do is work on the reasons for altered mental status,” he says. “You’ve already exonerated myxedema coma. Move on, and then have the thyroid test pursued as an outpatient to ensure it normalizes.”

—Thomas R. Collins

Slow Down

Because diabetes is such a common disease among hospitalized patients, it might be easy to gloss over, but it’s important to regard each inpatient as an individual and not go on auto-pilot, diabetes experts say.

“Not every type 2 or type 1 patient is alike. They all have different insulin requirements. Some patients are on oral meds with type 2 diabetes, some are on one insulin shot a day, [and] some are on several insulin injections a day,” Dr. Anderson says. “It’s managing that glucose in that individual and trying to optimize their therapy.”

Plenty of factors in the hospital might get in the way of that optimal care, he adds. Is a patient NPO (nothing by mouth) before a surgery? Feeling too nauseous to follow the appropriate eating schedule? Has a meal been delivered late by the meal service?

“The hospital introduces an incredible layer of complexity to the care of the patient with type 2 diabetes,” Dr. Anderson says. “That’s why it’s really important for everybody who takes care of people with diabetes in the hospital to be pretty savvy about this.”

Hospitalists shouldn’t be lulled into complacency just because diabetes is usually non-life-threatening. Often, patients with diabetes are admitted for a completely different condition.

“And by the time [providers] get to diabetes as an issue, they may just say ‘diabetes, sliding scale, check A1C as a reflex,’ and then not take the time to think about what is this person’s regimen,” Dr. Florez says.

All the details about that person’s eating status and insulin requirements should be tended to carefully.

“I don’t think diabetes is rocket science,” Dr. Florez says. “But it does require attention.

I think it’s not so much [hospitalists’] level of expertise as it is the time and the pressures and the stresses. They have to actually slow down and give the diabetes some thought.”

—Thomas R. Collins

References

1. Omar AS, Salama A, Allam M, et al. Association of time in blood glucose range with outcomes following cardiac surgery. BMC Anesthesiol. 2015;15(1):14.
2. Han HS, Kang SB. Relations between long-term glycemic control and postoperative wound and infectious complications after total knee arthroplasty in type 2 diabetics. Clin Orthop Surg. 2013;5(2):118–123.
3. Garber JR, Cobin RH, Gharib H, et al. Clinical practice guidelines for hypothyroidism in adults: cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Endocr Pract. 2012;18(6):988-1028.
4. Supit EJ, Peiris AN. Interpretation of laboratory thyroid function tests for the primary care physician. South Med J. 2002;95(5):481-485.

Diabetes is as prevalent in hospitals today as lab coats and heart monitors. More than 8% of the population—almost 26 million people—and nearly 27% (11 million) of Americans 65 or older have diabetes, according to American Diabetes Association (ADA) statistics. That makes diabetes one of the most common conditions hospitalists face day in and day out.

Other endocrine disorders also pose a challenge to hospitalists because they may be relatively uncommon, endocrinologists say.

The Hospitalist spoke to several endocrinologists and veteran hospitalists, mining their backgrounds and observations for tips on caring for hospitalized patients with endocrine disorders. Here are nine things they think hospitalists need to know:

1. Realize the far-reaching impact of good care for diabetic patients.

Part of the reason this is important is the numbers of patients with the disease who will be hospitalized and come under the care of a hospitalist.

“They’re coming in for a host of medical conditions, not the least of which is that diabetes is a comorbid factor that goes along with it,” says John Anderson, MD, the ADA’s immediate past president of medicine and science and an internist and diabetician at The Frist Clinic in Nashville, Tenn. “For those who are critically ill—those having bypass, those having stroke—diabetes is overrepresented even more once they get inside the hospital and in the intensive care unit.”

Job No. 1, controlling blood sugar, can have broad implications, he says.

“We know that control of their glucose through the hospital stay actually makes a difference in long-term outcomes, particularly things like surgery, coronary bypass grafting, that type of thing,” he says, noting that the standard of care is to try to keep glucose under 200. “A lot of studies have been done that demonstrate that really poor control of glucose in the hospital, regardless of the disease entity they’re in with, can lead to worsening long-term outcomes. It’s really imperative that you control the blood sugar.^1,2

“A lot of studies have been done that demonstrate that really poor control of glucose in the hospital, regardless of the disease entity they’re in with, can lead to worsening long-term outcomes. It’s really imperative that you control the blood sugar.^1,2 However, if you control it so tightly that these patients are dropping their blood sugar and having significant hypoglycemia problems in the hospital, that’s not good either.”

—John Anderson, MD, past president, American Diabetes Association, internist and diabetician, The Frist Clinic, Nashville, Tenn.

“However, the other part of this is…that if you control it so tightly that these patients are dropping their blood sugar and having significant hypoglycemia problems in the hospital, that’s not good either.”

2. You probably shouldn’t be testing for thyroid-stimulating hormone (TSH) level by itself in an acutely ill inpatient.

Simply put, the results probably won’t be useful, says Tamara Wexler, MD, PhD, an endocrinologist attending at Massachusetts General Hospital in Boston.

“TSH alone, for some reason, seems to be often measured,” she says, but “it’s extremely rarely indicated during acute hospitalization.”

TSH is “notoriously spurious” in inpatients, she adds, because the stress of an illness can make the test difficult to interpret.

“Many endocrine hormone levels are affected by stress, for example, and thus are better measured in an outpatient setting than in an acute hospitalized illness because of the impact of the illness on interpreting the test results,” she says.

Euthyroid sick syndrome—or “sick euthyroid”—is a term used for abnormalities in thyroid tests in patients with systemic illnesses that are nonthyroidal.

In cases in which thyroid dysfunction is strongly suspected, TSH should be measured in conjunction with other levels, such as a free thyroxine (free T4) level, Dr. Wexler says.

3. Don’t forget to watch potassium in patients with diabetic ketoacidosis (DKA).

A patient with a normal level of potassium, or even a high one, at baseline can encounter a problem with plummeting levels, says Bruce Mitchell, MD, director of hospital medicine services at Emory Hospital Midtown and assistant professor of hospital medicine at Emory University in Atlanta.

“Once you start insulin and correcting the hyperosmolality, the potassium shifts,” says Dr. Mitchell, who has a particular interest in endocrinology, “so it can become abnormally low fairly quickly.

“You start the insulin and fluids; then all of a sudden that person’s potassium is drastically abnormal and they’re coding,” he says. “It’s important to make sure your hospital’s diabetic ketoacidosis protocol includes frequent potassium checks.”

4. Be sure to wait long enough before rechecking TSH after a medication change.

It takes several weeks before thyroid medication dose changes start to show their effects, says Jeffrey Greenwald, MD, a hospitalist at Massachusetts General with expertise in endocrinology. Guidelines published in 2012 by the American Association of Clinical Endocrinologists and the American Thyroid Association recommend rechecking TSH within four to eight weeks.³

“It bears reminding that [for] patients who have recently changed their thyroid medication dose, you need to wait several weeks before you recheck their TSH. That’s another reason why the TSH can be somewhat difficult to interpret. There’s a tendency that I have seen, too, if the TSH is high and they’re on thyroid replacement, to want to adjust the dose while they’re in the hospital, which is probably not the time to do it.”—Jeffrey Greenwald, MD, hospitalist, Massachusetts General, Boston

“It bears reminding that [for] patients who have recently changed their thyroid medication dose, you need to wait several weeks before you recheck their TSH,” he says. “That’s another reason why the TSH can be somewhat difficult to interpret.

“There’s a tendency that I have seen, too, if the TSH is high and they’re on thyroid replacement, to want to adjust the dose while they’re in the hospital, which is probably not the time to do it.”

5. When administering insulin, factor in soon-to-arrive meals and give prandial insulin as needed.

If patients with diabetes are receiving insulin in the hospital, even if their glucose is in the normal range, they will need insulin if they’re about to have a carb-loaded breakfast, says Jose Florez, MD, PhD, an endocrinologist at Massachusetts General and associate professor of medicine at Harvard Medical School in Boston.

“A person with a glucose of 98 who is about to eat pancakes needs standing short-acting insulin regardless of the fingerstick,” Dr. Florez says. “A person with a glucose of 250 who is about to eat needs both the correction insulin and the amount needed to handle the impending carbohydrate load.”

“The person not only needs to correct what the glucose is at the moment, but they also need to account for the impending carbohydrate intake,” he says.

Dr. Anderson says he always cautions those caring for hospitalized diabetic patients against using the “sliding-scale philosophy”—marked by set amounts of long-acting insulin and set amounts of carbohydrate intake—because it’s overly formulaic for that setting.

“It leads to really variable glucoses,” he says, “and usually not good control.”

6. Giving isotonic fluids to someone who has fixed water retention or hypertonic urine can worsen the problem.

This can stem from an incomplete or incorrect evaluation of hyponatremia, which is a common problem in hospitalized patients. When hyponatremia is present, the first order of business should be to exclude pseudohyponatremia and confirm that it’s hypotonic hyponatremia.

After confirmation, the volume status should be assessed. One useful way to do this is to measure urine creatinine, urine sodium, and urine osmolality (osm), Dr. Florez says. If a patient has water retention or hypertonic urine from syndrome of inappropriate diuretic hormone secretion (SIADH), hypothyroidism, or glucocorticoid deficiency, the hospitalist needs to act accordingly.

“If the urine osm is high, higher than the serum osm, and is fixed at that level for some reason…giving that person isotonic fluids will lead to additional water retention and make the situation worse,” he says. “It’s very important to assess the volume status and establish the cause. And then, if you’re going to give fluids, be mindful of what the urine might look like. Do not give fluids that are hypotonic with respect to what the urine is making, unless you are completely convinced that the person is dry and therefore needs volume.”

“Once you start insulin and correcting the hyperosmolality, the potassium shifts, so it can become abnormally low fairly quickly. You start the insulin and fluids; then all of a sudden that person’s potassium is drastically abnormal and they’re coding. It’s important to make sure your hospital’s diabetic ketoacidosis protocol includes frequent potassium checks.”—Bruce Mitchell, MD, director of hospital medicine services, Emory Hospital Midtown, assistant professor of hospital medicine, Emory University, Atlanta.

7. Encourage patients to check their own glucose and administer their own insulin while still in the hospital.

“We often deal with patients who start insulin treatment for diabetes during an admission or who seem not to be doing very well giving insulin at home,” Dr. Wexler says. “Many patients can benefit from supervised insulin injections and glucose testing.”

Going through the process while in the hospital with supervision can be a good refresher, she says.

“You don’t have to necessarily order specific diabetic teaching,” she adds, noting that not all hospitals have diabetic educators available at all times.

A patient might be waiting for diabetic teaching before discharge, but this might be one way to speed the process, Dr. Wexler says. She suggests teaching by example.

8. Patients on steroids every day are at risk for adrenal insufficiency.

Even if they aren’t on corticosteroids when they present, hospitalists should think of these patients as “at risk for adrenal insufficiency and potentially immunocompromised,” Dr. Greenwald says. “The bigger issue in most cases is the adrenal insufficiency.”

That means their bodies can’t mount an appropriate response to stress.

“And without that appropriate response of additional stress hormone the body would normally make, they may not be able, for example, to maintain their blood pressure,” he says. “This can be extremely dangerous.”

Inhaled steroids, and topical steroids if they are applied to broken skin, can have a kind of stealth effect.

“That’s something to keep in mind,” Dr. Wexler says, noting the connection between blood pressure management and endocrine conditions.

9. Thyroid hormone might not be as well absorbed under certain conditions.

With calcium or iron supplementation, thyroid hormones might present a problem, Dr. Wexler says. For patients at home taking thyroid hormone appropriately (an hour or two separated from calcium or iron supplementation), there “should be no issue,” she says. “But if they are administered at the same time at the hospital, patients may not absorb the full dose.”

Tom Collins is a freelance writer in South Florida.

Misinterpreting Thyroid Function Tests Can Lead You Down the Wrong Path, Expert Warns

Thyroid function tests in hospitalized patients can sometimes be a case of a mistake begetting a mistake.⁴ Don’t fall into the trap, endocrinologists say.³

Consider a patient presenting with new atrial fibrillation. One of the triggers for the condition is hyperthyroidism, so it’s common to do a thyroid function test.

“Say the TSH [thyroid-stimulating hormone] is up because the patient is recovering from an acute illness,”

Dr. Florez says. “All of a sudden you were looking for hyperthyroidism, but now you have a high TSH, so that initiates a workup for hypothyroidism.” But that is not the proper course, because a high TSH is not uncommon in a person getting over an illness.

Once the TSH comes back high, you’ve ruled out hyperthyroidism as the reason for the atrial fibrillation.

The matter should be considered settled, he said. “No reason to get all excited about pursuing a hypothyroidism diagnosis,” Dr. Florez says. If thereis any concern, the thyroid function tests could be repeated in the outpatient setting when the patient is no longer acutely ill.

Misdirected concerns about hypothyroidism should also be avoided.

For example, a patient presents with altered mental status, which can be brought about by myxedema coma, or profound hypothyroidism.

If the TSH comes back low—eliminating hypothyroidism as a problem—a hospitalist should not embark on a hyperthyroidism diagnosis, Dr. Florez says. It’s probably just sick euthyroid causing the abnormal TSH level.

“What you need to do is work on the reasons for altered mental status,” he says. “You’ve already exonerated myxedema coma. Move on, and then have the thyroid test pursued as an outpatient to ensure it normalizes.”

—Thomas R. Collins

Slow Down

Because diabetes is such a common disease among hospitalized patients, it might be easy to gloss over, but it’s important to regard each inpatient as an individual and not go on auto-pilot, diabetes experts say.

“Not every type 2 or type 1 patient is alike. They all have different insulin requirements. Some patients are on oral meds with type 2 diabetes, some are on one insulin shot a day, [and] some are on several insulin injections a day,” Dr. Anderson says. “It’s managing that glucose in that individual and trying to optimize their therapy.”

Plenty of factors in the hospital might get in the way of that optimal care, he adds. Is a patient NPO (nothing by mouth) before a surgery? Feeling too nauseous to follow the appropriate eating schedule? Has a meal been delivered late by the meal service?

“The hospital introduces an incredible layer of complexity to the care of the patient with type 2 diabetes,” Dr. Anderson says. “That’s why it’s really important for everybody who takes care of people with diabetes in the hospital to be pretty savvy about this.”

Hospitalists shouldn’t be lulled into complacency just because diabetes is usually non-life-threatening. Often, patients with diabetes are admitted for a completely different condition.

“And by the time [providers] get to diabetes as an issue, they may just say ‘diabetes, sliding scale, check A1C as a reflex,’ and then not take the time to think about what is this person’s regimen,” Dr. Florez says.

All the details about that person’s eating status and insulin requirements should be tended to carefully.

“I don’t think diabetes is rocket science,” Dr. Florez says. “But it does require attention.

I think it’s not so much [hospitalists’] level of expertise as it is the time and the pressures and the stresses. They have to actually slow down and give the diabetes some thought.”

—Thomas R. Collins

References

1. Omar AS, Salama A, Allam M, et al. Association of time in blood glucose range with outcomes following cardiac surgery. BMC Anesthesiol. 2015;15(1):14.
2. Han HS, Kang SB. Relations between long-term glycemic control and postoperative wound and infectious complications after total knee arthroplasty in type 2 diabetics. Clin Orthop Surg. 2013;5(2):118–123.
3. Garber JR, Cobin RH, Gharib H, et al. Clinical practice guidelines for hypothyroidism in adults: cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Endocr Pract. 2012;18(6):988-1028.
4. Supit EJ, Peiris AN. Interpretation of laboratory thyroid function tests for the primary care physician. South Med J. 2002;95(5):481-485.

Diabetes is as prevalent in hospitals today as lab coats and heart monitors. More than 8% of the population—almost 26 million people—and nearly 27% (11 million) of Americans 65 or older have diabetes, according to American Diabetes Association (ADA) statistics. That makes diabetes one of the most common conditions hospitalists face day in and day out.

Other endocrine disorders also pose a challenge to hospitalists because they may be relatively uncommon, endocrinologists say.

The Hospitalist spoke to several endocrinologists and veteran hospitalists, mining their backgrounds and observations for tips on caring for hospitalized patients with endocrine disorders. Here are nine things they think hospitalists need to know:

1. Realize the far-reaching impact of good care for diabetic patients.

Part of the reason this is important is the numbers of patients with the disease who will be hospitalized and come under the care of a hospitalist.

“They’re coming in for a host of medical conditions, not the least of which is that diabetes is a comorbid factor that goes along with it,” says John Anderson, MD, the ADA’s immediate past president of medicine and science and an internist and diabetician at The Frist Clinic in Nashville, Tenn. “For those who are critically ill—those having bypass, those having stroke—diabetes is overrepresented even more once they get inside the hospital and in the intensive care unit.”

Job No. 1, controlling blood sugar, can have broad implications, he says.

“We know that control of their glucose through the hospital stay actually makes a difference in long-term outcomes, particularly things like surgery, coronary bypass grafting, that type of thing,” he says, noting that the standard of care is to try to keep glucose under 200. “A lot of studies have been done that demonstrate that really poor control of glucose in the hospital, regardless of the disease entity they’re in with, can lead to worsening long-term outcomes. It’s really imperative that you control the blood sugar.^1,2

“A lot of studies have been done that demonstrate that really poor control of glucose in the hospital, regardless of the disease entity they’re in with, can lead to worsening long-term outcomes. It’s really imperative that you control the blood sugar.^1,2 However, if you control it so tightly that these patients are dropping their blood sugar and having significant hypoglycemia problems in the hospital, that’s not good either.”

—John Anderson, MD, past president, American Diabetes Association, internist and diabetician, The Frist Clinic, Nashville, Tenn.

“However, the other part of this is…that if you control it so tightly that these patients are dropping their blood sugar and having significant hypoglycemia problems in the hospital, that’s not good either.”

2. You probably shouldn’t be testing for thyroid-stimulating hormone (TSH) level by itself in an acutely ill inpatient.

Simply put, the results probably won’t be useful, says Tamara Wexler, MD, PhD, an endocrinologist attending at Massachusetts General Hospital in Boston.

“TSH alone, for some reason, seems to be often measured,” she says, but “it’s extremely rarely indicated during acute hospitalization.”

TSH is “notoriously spurious” in inpatients, she adds, because the stress of an illness can make the test difficult to interpret.

“Many endocrine hormone levels are affected by stress, for example, and thus are better measured in an outpatient setting than in an acute hospitalized illness because of the impact of the illness on interpreting the test results,” she says.

Euthyroid sick syndrome—or “sick euthyroid”—is a term used for abnormalities in thyroid tests in patients with systemic illnesses that are nonthyroidal.

In cases in which thyroid dysfunction is strongly suspected, TSH should be measured in conjunction with other levels, such as a free thyroxine (free T4) level, Dr. Wexler says.

3. Don’t forget to watch potassium in patients with diabetic ketoacidosis (DKA).

A patient with a normal level of potassium, or even a high one, at baseline can encounter a problem with plummeting levels, says Bruce Mitchell, MD, director of hospital medicine services at Emory Hospital Midtown and assistant professor of hospital medicine at Emory University in Atlanta.

“Once you start insulin and correcting the hyperosmolality, the potassium shifts,” says Dr. Mitchell, who has a particular interest in endocrinology, “so it can become abnormally low fairly quickly.

“You start the insulin and fluids; then all of a sudden that person’s potassium is drastically abnormal and they’re coding,” he says. “It’s important to make sure your hospital’s diabetic ketoacidosis protocol includes frequent potassium checks.”

4. Be sure to wait long enough before rechecking TSH after a medication change.

It takes several weeks before thyroid medication dose changes start to show their effects, says Jeffrey Greenwald, MD, a hospitalist at Massachusetts General with expertise in endocrinology. Guidelines published in 2012 by the American Association of Clinical Endocrinologists and the American Thyroid Association recommend rechecking TSH within four to eight weeks.³

“It bears reminding that [for] patients who have recently changed their thyroid medication dose, you need to wait several weeks before you recheck their TSH. That’s another reason why the TSH can be somewhat difficult to interpret. There’s a tendency that I have seen, too, if the TSH is high and they’re on thyroid replacement, to want to adjust the dose while they’re in the hospital, which is probably not the time to do it.”—Jeffrey Greenwald, MD, hospitalist, Massachusetts General, Boston

“It bears reminding that [for] patients who have recently changed their thyroid medication dose, you need to wait several weeks before you recheck their TSH,” he says. “That’s another reason why the TSH can be somewhat difficult to interpret.

“There’s a tendency that I have seen, too, if the TSH is high and they’re on thyroid replacement, to want to adjust the dose while they’re in the hospital, which is probably not the time to do it.”

5. When administering insulin, factor in soon-to-arrive meals and give prandial insulin as needed.

If patients with diabetes are receiving insulin in the hospital, even if their glucose is in the normal range, they will need insulin if they’re about to have a carb-loaded breakfast, says Jose Florez, MD, PhD, an endocrinologist at Massachusetts General and associate professor of medicine at Harvard Medical School in Boston.

“A person with a glucose of 98 who is about to eat pancakes needs standing short-acting insulin regardless of the fingerstick,” Dr. Florez says. “A person with a glucose of 250 who is about to eat needs both the correction insulin and the amount needed to handle the impending carbohydrate load.”

“The person not only needs to correct what the glucose is at the moment, but they also need to account for the impending carbohydrate intake,” he says.

Dr. Anderson says he always cautions those caring for hospitalized diabetic patients against using the “sliding-scale philosophy”—marked by set amounts of long-acting insulin and set amounts of carbohydrate intake—because it’s overly formulaic for that setting.

“It leads to really variable glucoses,” he says, “and usually not good control.”

6. Giving isotonic fluids to someone who has fixed water retention or hypertonic urine can worsen the problem.

This can stem from an incomplete or incorrect evaluation of hyponatremia, which is a common problem in hospitalized patients. When hyponatremia is present, the first order of business should be to exclude pseudohyponatremia and confirm that it’s hypotonic hyponatremia.

After confirmation, the volume status should be assessed. One useful way to do this is to measure urine creatinine, urine sodium, and urine osmolality (osm), Dr. Florez says. If a patient has water retention or hypertonic urine from syndrome of inappropriate diuretic hormone secretion (SIADH), hypothyroidism, or glucocorticoid deficiency, the hospitalist needs to act accordingly.

“If the urine osm is high, higher than the serum osm, and is fixed at that level for some reason…giving that person isotonic fluids will lead to additional water retention and make the situation worse,” he says. “It’s very important to assess the volume status and establish the cause. And then, if you’re going to give fluids, be mindful of what the urine might look like. Do not give fluids that are hypotonic with respect to what the urine is making, unless you are completely convinced that the person is dry and therefore needs volume.”

“Once you start insulin and correcting the hyperosmolality, the potassium shifts, so it can become abnormally low fairly quickly. You start the insulin and fluids; then all of a sudden that person’s potassium is drastically abnormal and they’re coding. It’s important to make sure your hospital’s diabetic ketoacidosis protocol includes frequent potassium checks.”—Bruce Mitchell, MD, director of hospital medicine services, Emory Hospital Midtown, assistant professor of hospital medicine, Emory University, Atlanta.

7. Encourage patients to check their own glucose and administer their own insulin while still in the hospital.

“We often deal with patients who start insulin treatment for diabetes during an admission or who seem not to be doing very well giving insulin at home,” Dr. Wexler says. “Many patients can benefit from supervised insulin injections and glucose testing.”

Going through the process while in the hospital with supervision can be a good refresher, she says.

“You don’t have to necessarily order specific diabetic teaching,” she adds, noting that not all hospitals have diabetic educators available at all times.

A patient might be waiting for diabetic teaching before discharge, but this might be one way to speed the process, Dr. Wexler says. She suggests teaching by example.

8. Patients on steroids every day are at risk for adrenal insufficiency.

Even if they aren’t on corticosteroids when they present, hospitalists should think of these patients as “at risk for adrenal insufficiency and potentially immunocompromised,” Dr. Greenwald says. “The bigger issue in most cases is the adrenal insufficiency.”

That means their bodies can’t mount an appropriate response to stress.

“And without that appropriate response of additional stress hormone the body would normally make, they may not be able, for example, to maintain their blood pressure,” he says. “This can be extremely dangerous.”

Inhaled steroids, and topical steroids if they are applied to broken skin, can have a kind of stealth effect.

“That’s something to keep in mind,” Dr. Wexler says, noting the connection between blood pressure management and endocrine conditions.

9. Thyroid hormone might not be as well absorbed under certain conditions.

With calcium or iron supplementation, thyroid hormones might present a problem, Dr. Wexler says. For patients at home taking thyroid hormone appropriately (an hour or two separated from calcium or iron supplementation), there “should be no issue,” she says. “But if they are administered at the same time at the hospital, patients may not absorb the full dose.”

Tom Collins is a freelance writer in South Florida.

Misinterpreting Thyroid Function Tests Can Lead You Down the Wrong Path, Expert Warns

Thyroid function tests in hospitalized patients can sometimes be a case of a mistake begetting a mistake.⁴ Don’t fall into the trap, endocrinologists say.³

Consider a patient presenting with new atrial fibrillation. One of the triggers for the condition is hyperthyroidism, so it’s common to do a thyroid function test.

“Say the TSH [thyroid-stimulating hormone] is up because the patient is recovering from an acute illness,”

Dr. Florez says. “All of a sudden you were looking for hyperthyroidism, but now you have a high TSH, so that initiates a workup for hypothyroidism.” But that is not the proper course, because a high TSH is not uncommon in a person getting over an illness.

Once the TSH comes back high, you’ve ruled out hyperthyroidism as the reason for the atrial fibrillation.

The matter should be considered settled, he said. “No reason to get all excited about pursuing a hypothyroidism diagnosis,” Dr. Florez says. If thereis any concern, the thyroid function tests could be repeated in the outpatient setting when the patient is no longer acutely ill.

Misdirected concerns about hypothyroidism should also be avoided.

For example, a patient presents with altered mental status, which can be brought about by myxedema coma, or profound hypothyroidism.

If the TSH comes back low—eliminating hypothyroidism as a problem—a hospitalist should not embark on a hyperthyroidism diagnosis, Dr. Florez says. It’s probably just sick euthyroid causing the abnormal TSH level.

“What you need to do is work on the reasons for altered mental status,” he says. “You’ve already exonerated myxedema coma. Move on, and then have the thyroid test pursued as an outpatient to ensure it normalizes.”

—Thomas R. Collins

Slow Down

Because diabetes is such a common disease among hospitalized patients, it might be easy to gloss over, but it’s important to regard each inpatient as an individual and not go on auto-pilot, diabetes experts say.

“Not every type 2 or type 1 patient is alike. They all have different insulin requirements. Some patients are on oral meds with type 2 diabetes, some are on one insulin shot a day, [and] some are on several insulin injections a day,” Dr. Anderson says. “It’s managing that glucose in that individual and trying to optimize their therapy.”

Plenty of factors in the hospital might get in the way of that optimal care, he adds. Is a patient NPO (nothing by mouth) before a surgery? Feeling too nauseous to follow the appropriate eating schedule? Has a meal been delivered late by the meal service?

“The hospital introduces an incredible layer of complexity to the care of the patient with type 2 diabetes,” Dr. Anderson says. “That’s why it’s really important for everybody who takes care of people with diabetes in the hospital to be pretty savvy about this.”

Hospitalists shouldn’t be lulled into complacency just because diabetes is usually non-life-threatening. Often, patients with diabetes are admitted for a completely different condition.

“And by the time [providers] get to diabetes as an issue, they may just say ‘diabetes, sliding scale, check A1C as a reflex,’ and then not take the time to think about what is this person’s regimen,” Dr. Florez says.

All the details about that person’s eating status and insulin requirements should be tended to carefully.

“I don’t think diabetes is rocket science,” Dr. Florez says. “But it does require attention.

I think it’s not so much [hospitalists’] level of expertise as it is the time and the pressures and the stresses. They have to actually slow down and give the diabetes some thought.”

—Thomas R. Collins

References

1. Omar AS, Salama A, Allam M, et al. Association of time in blood glucose range with outcomes following cardiac surgery. BMC Anesthesiol. 2015;15(1):14.
2. Han HS, Kang SB. Relations between long-term glycemic control and postoperative wound and infectious complications after total knee arthroplasty in type 2 diabetics. Clin Orthop Surg. 2013;5(2):118–123.
3. Garber JR, Cobin RH, Gharib H, et al. Clinical practice guidelines for hypothyroidism in adults: cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Endocr Pract. 2012;18(6):988-1028.
4. Supit EJ, Peiris AN. Interpretation of laboratory thyroid function tests for the primary care physician. South Med J. 2002;95(5):481-485.

A new guide on the use of medications to treat patients with alcohol use disorder has been released by the Substance Abuse and Mental Health Services Administration in conjunction with National Alcohol Awareness Month.

The guide provides an overview of four Food and Drug Administration–approved drugs developed to treat alcohol use disorder: disulfiram, oral naltrexone, extended-release injectable naltrexone, and acamprosate. It also discusses how to screen, treat, and monitor patients based on their individual needs.

“Current evidence shows that medications are underused in the treatment of alcohol use disorder,” the agency said in a statement announcing the new guidance. “As the Patient Protection and Affordable Care Act (ACA) continues to be implemented, there is considerable potential for expanding use of medication-assisted treatment to treat alcohol use disorder,” they concluded.

The guide can be found online at http://store.samhsa.gov.

A new guide on the use of medications to treat patients with alcohol use disorder has been released by the Substance Abuse and Mental Health Services Administration in conjunction with National Alcohol Awareness Month.

The guide provides an overview of four Food and Drug Administration–approved drugs developed to treat alcohol use disorder: disulfiram, oral naltrexone, extended-release injectable naltrexone, and acamprosate. It also discusses how to screen, treat, and monitor patients based on their individual needs.

“Current evidence shows that medications are underused in the treatment of alcohol use disorder,” the agency said in a statement announcing the new guidance. “As the Patient Protection and Affordable Care Act (ACA) continues to be implemented, there is considerable potential for expanding use of medication-assisted treatment to treat alcohol use disorder,” they concluded.

The guide can be found online at http://store.samhsa.gov.

A new guide on the use of medications to treat patients with alcohol use disorder has been released by the Substance Abuse and Mental Health Services Administration in conjunction with National Alcohol Awareness Month.

The guide provides an overview of four Food and Drug Administration–approved drugs developed to treat alcohol use disorder: disulfiram, oral naltrexone, extended-release injectable naltrexone, and acamprosate. It also discusses how to screen, treat, and monitor patients based on their individual needs.

“Current evidence shows that medications are underused in the treatment of alcohol use disorder,” the agency said in a statement announcing the new guidance. “As the Patient Protection and Affordable Care Act (ACA) continues to be implemented, there is considerable potential for expanding use of medication-assisted treatment to treat alcohol use disorder,” they concluded.

The guide can be found online at http://store.samhsa.gov.

It’s not uncommon to read about neurologists of yore and be stunned, if not horrified, to think of what they had to work with.

Going back perhaps 100 years, it wasn’t uncommon for anyone with a head injury and hemiparesis to have one (or more) burr holes placed in hope of draining a subdural hematoma causing the symptoms.

In more recent memory was the dreaded ventriculogram, or pneumoencephalogram: A painful procedure in which a lumbar puncture was done in order to blow air bubbles into the spinal fluid, then use skull X-rays to watch them outline the ventricles and other structures to look for midline shift.

I remember one of my old teachers (RIP, Al) recalling that imaging in his younger era consisted of a cerebral angiogram to look for displaced vessels and an EEG for focal slowing.

The CT scan obviously changed all that, with its excellent noninvasive imaging of the brain, and the MRI made things even better by several orders of magnitude.

But where are we now? As frightening as the practices of 50-100 years ago may seem now, we have to keep in mind that, to the doctors using them, they were at the cutting edge of medical technology. They weren’t saying “this would be so much easier if the MRI had been invented.”

None of us can clearly see what the next big advances will be. We use what we have, knowing it’s the best we can do. As the leading philosopher of our era (Yogi Berra) said, “It’s tough to make predictions, especially about the future.”

So what will future doctors think of us? What tests will they look at and shudder, asking, “They actually DID that to people?”

I’m sure the CT-myelogram will be one of them. It is perhaps the last descendant of the pneumoencephalogram still in use; it’s done uncommonly, but still has value. For those who can’t have an MRI or where confirmation of an MRI is needed, it’s quite accurate.

What other tests will be considered archaic? The EMG/NCV [electromyogram and nerve conduction studies]? Lumbar puncture? Cerebral angiogram?

Of course, these are just in neurology. Every field is going to have a past test that today is looked upon with horror, and the knowledge that someday another generation will look at us the same way.

Like all scientific disciplines, what we do is based on the foundation laid by those before us, and it’s up to the next generation to push the horizon further back.

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

It’s not uncommon to read about neurologists of yore and be stunned, if not horrified, to think of what they had to work with.

Going back perhaps 100 years, it wasn’t uncommon for anyone with a head injury and hemiparesis to have one (or more) burr holes placed in hope of draining a subdural hematoma causing the symptoms.

In more recent memory was the dreaded ventriculogram, or pneumoencephalogram: A painful procedure in which a lumbar puncture was done in order to blow air bubbles into the spinal fluid, then use skull X-rays to watch them outline the ventricles and other structures to look for midline shift.

I remember one of my old teachers (RIP, Al) recalling that imaging in his younger era consisted of a cerebral angiogram to look for displaced vessels and an EEG for focal slowing.

The CT scan obviously changed all that, with its excellent noninvasive imaging of the brain, and the MRI made things even better by several orders of magnitude.

But where are we now? As frightening as the practices of 50-100 years ago may seem now, we have to keep in mind that, to the doctors using them, they were at the cutting edge of medical technology. They weren’t saying “this would be so much easier if the MRI had been invented.”

None of us can clearly see what the next big advances will be. We use what we have, knowing it’s the best we can do. As the leading philosopher of our era (Yogi Berra) said, “It’s tough to make predictions, especially about the future.”

So what will future doctors think of us? What tests will they look at and shudder, asking, “They actually DID that to people?”

I’m sure the CT-myelogram will be one of them. It is perhaps the last descendant of the pneumoencephalogram still in use; it’s done uncommonly, but still has value. For those who can’t have an MRI or where confirmation of an MRI is needed, it’s quite accurate.

What other tests will be considered archaic? The EMG/NCV [electromyogram and nerve conduction studies]? Lumbar puncture? Cerebral angiogram?

Of course, these are just in neurology. Every field is going to have a past test that today is looked upon with horror, and the knowledge that someday another generation will look at us the same way.

Like all scientific disciplines, what we do is based on the foundation laid by those before us, and it’s up to the next generation to push the horizon further back.

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

It’s not uncommon to read about neurologists of yore and be stunned, if not horrified, to think of what they had to work with.

Going back perhaps 100 years, it wasn’t uncommon for anyone with a head injury and hemiparesis to have one (or more) burr holes placed in hope of draining a subdural hematoma causing the symptoms.

In more recent memory was the dreaded ventriculogram, or pneumoencephalogram: A painful procedure in which a lumbar puncture was done in order to blow air bubbles into the spinal fluid, then use skull X-rays to watch them outline the ventricles and other structures to look for midline shift.

I remember one of my old teachers (RIP, Al) recalling that imaging in his younger era consisted of a cerebral angiogram to look for displaced vessels and an EEG for focal slowing.

The CT scan obviously changed all that, with its excellent noninvasive imaging of the brain, and the MRI made things even better by several orders of magnitude.

But where are we now? As frightening as the practices of 50-100 years ago may seem now, we have to keep in mind that, to the doctors using them, they were at the cutting edge of medical technology. They weren’t saying “this would be so much easier if the MRI had been invented.”

None of us can clearly see what the next big advances will be. We use what we have, knowing it’s the best we can do. As the leading philosopher of our era (Yogi Berra) said, “It’s tough to make predictions, especially about the future.”

So what will future doctors think of us? What tests will they look at and shudder, asking, “They actually DID that to people?”

I’m sure the CT-myelogram will be one of them. It is perhaps the last descendant of the pneumoencephalogram still in use; it’s done uncommonly, but still has value. For those who can’t have an MRI or where confirmation of an MRI is needed, it’s quite accurate.

What other tests will be considered archaic? The EMG/NCV [electromyogram and nerve conduction studies]? Lumbar puncture? Cerebral angiogram?

Of course, these are just in neurology. Every field is going to have a past test that today is looked upon with horror, and the knowledge that someday another generation will look at us the same way.

Like all scientific disciplines, what we do is based on the foundation laid by those before us, and it’s up to the next generation to push the horizon further back.

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

Summary: Delirium is a common problem in hospitalized patients, and all too often delirium is iatrogenic. Delirium is associated with poor outcomes such as prolonged hospitalization and functional decline, and it increases the risk of nursing home admission. The most common tool to assess the presence of delirium is the Confusion Assessment Method (CAM). Dr. Cumbler educated the audience on a more refined tool, the 3D CAM [PDF], and provided the algorithm for diagnosis and evaluation of hospital-onset delirium.

Where delirium is concerned (as with most conditions), “an ounce of prevention is worth a pound of cure.” Namely, avoid prescribing problem medications such as anticholinergics, sedative/hypnotics (except benzodiazepines for treatment of alcohol withdrawal), and antihistamines; and minimize narcotics, but don’t undertreat pain as uncontrolled pain is a more potent delirium trigger than narcotics.

Avoid sleep deprivation. Do we really require vital signs and phlebotomy between midnight and 6 a.m.? Make sure patients have their glasses and hearing aids, and keep them up and moving during daylight hours. Sleep and sensory deprivation are effective forms of human torture and are known to be rather disorienting.

Finally, antipsychotics are associated with increased mortality in dementia. Patients with agitated delirium may benefit from a low dose of haloperidol. When prescribing haloperidol, remember IV administration requires EKG monitoring (FDA black box warning), and a reasonable starting dose is 0.5 mg, NOT 5 mg.

HM takeaways:

• Use CAM, 3D CAM to diagnose delirium;
• Avoid anticholinergic medications (promethazine, cyclobenzaprine, oxybutynin, amitriptyline, prednisolone, theophylline, dixogin, furosemide);
• Minimize, but do not avoid, narcotics in patients with both pain and delirium;
• Use low-dose antipsychotics, not benzodiazepines, for agitated delirium; and
• STOP antipsychotics ASAP, ideally prior to discharge; if not prior to discharge, then include discontinuation date on discharge medication list. TH

Summary: Delirium is a common problem in hospitalized patients, and all too often delirium is iatrogenic. Delirium is associated with poor outcomes such as prolonged hospitalization and functional decline, and it increases the risk of nursing home admission. The most common tool to assess the presence of delirium is the Confusion Assessment Method (CAM). Dr. Cumbler educated the audience on a more refined tool, the 3D CAM [PDF], and provided the algorithm for diagnosis and evaluation of hospital-onset delirium.

Where delirium is concerned (as with most conditions), “an ounce of prevention is worth a pound of cure.” Namely, avoid prescribing problem medications such as anticholinergics, sedative/hypnotics (except benzodiazepines for treatment of alcohol withdrawal), and antihistamines; and minimize narcotics, but don’t undertreat pain as uncontrolled pain is a more potent delirium trigger than narcotics.

Avoid sleep deprivation. Do we really require vital signs and phlebotomy between midnight and 6 a.m.? Make sure patients have their glasses and hearing aids, and keep them up and moving during daylight hours. Sleep and sensory deprivation are effective forms of human torture and are known to be rather disorienting.

Finally, antipsychotics are associated with increased mortality in dementia. Patients with agitated delirium may benefit from a low dose of haloperidol. When prescribing haloperidol, remember IV administration requires EKG monitoring (FDA black box warning), and a reasonable starting dose is 0.5 mg, NOT 5 mg.

HM takeaways:

• Use CAM, 3D CAM to diagnose delirium;
• Avoid anticholinergic medications (promethazine, cyclobenzaprine, oxybutynin, amitriptyline, prednisolone, theophylline, dixogin, furosemide);
• Minimize, but do not avoid, narcotics in patients with both pain and delirium;
• Use low-dose antipsychotics, not benzodiazepines, for agitated delirium; and
• STOP antipsychotics ASAP, ideally prior to discharge; if not prior to discharge, then include discontinuation date on discharge medication list. TH

Summary: Delirium is a common problem in hospitalized patients, and all too often delirium is iatrogenic. Delirium is associated with poor outcomes such as prolonged hospitalization and functional decline, and it increases the risk of nursing home admission. The most common tool to assess the presence of delirium is the Confusion Assessment Method (CAM). Dr. Cumbler educated the audience on a more refined tool, the 3D CAM [PDF], and provided the algorithm for diagnosis and evaluation of hospital-onset delirium.

Where delirium is concerned (as with most conditions), “an ounce of prevention is worth a pound of cure.” Namely, avoid prescribing problem medications such as anticholinergics, sedative/hypnotics (except benzodiazepines for treatment of alcohol withdrawal), and antihistamines; and minimize narcotics, but don’t undertreat pain as uncontrolled pain is a more potent delirium trigger than narcotics.

Avoid sleep deprivation. Do we really require vital signs and phlebotomy between midnight and 6 a.m.? Make sure patients have their glasses and hearing aids, and keep them up and moving during daylight hours. Sleep and sensory deprivation are effective forms of human torture and are known to be rather disorienting.

Finally, antipsychotics are associated with increased mortality in dementia. Patients with agitated delirium may benefit from a low dose of haloperidol. When prescribing haloperidol, remember IV administration requires EKG monitoring (FDA black box warning), and a reasonable starting dose is 0.5 mg, NOT 5 mg.

HM takeaways:

• Use CAM, 3D CAM to diagnose delirium;
• Avoid anticholinergic medications (promethazine, cyclobenzaprine, oxybutynin, amitriptyline, prednisolone, theophylline, dixogin, furosemide);
• Minimize, but do not avoid, narcotics in patients with both pain and delirium;
• Use low-dose antipsychotics, not benzodiazepines, for agitated delirium; and
• STOP antipsychotics ASAP, ideally prior to discharge; if not prior to discharge, then include discontinuation date on discharge medication list. TH

Summary: The panel of high-tech doctors helped a standing-room-only crowd navigate numerous apps to be used at point-of-care [PDF, 458 kb]. Groups worked through case studies utilizing applicable mobile apps. Examples and most useful apps, including occasional user reviews, follow:

Provider-to-Provider Communication, HIPAA secure

• Doximity.
• HIPAA-chat.
• Pros: HIPAA-secure, real-time communication.
• Cons: Both parties must be on app to securely communicate.

Provider-to-Patient Communication, Language Translators

• Google Translate: multiple platforms, free, 90 languages.
• MediBabble: iOS only, free, seven languages, dedicated medical application.

Diagnostic Apps for Providers

• Calculate by QxM.
• PreOpEval14: iOS only.
• PreopRisk Assessment: Android only.
• ASCVD Risk Estimator.
• MDCalc.com in addition to usual formulas, great abg-analyzer (online version only).
• AnticoagEvaluator.
• epocrates: calculators.

Click here for a PDF of useful apps and resource links  [PDF, 177 kb]

Resources for Evidence-Based Practice

• ACP Clinical Guidelines.
• ACP Smart Medicine.
• Read by QxMD.
• UpToDate.
• AHRQ ePPS: identifies clinical preventive services.
• epocrates.

Patient Engagement Apps

• Medication reminders: MediSafe, CareZone.
• Pharmaceutical costs: Walmart, Target Healthful, GoodRx.
• Proper inhaler usage: User Inhalers App.
• Smoking cessation: QuitSTART.

HM15 takeaways

• Apps are available to providers and patients to enhance quality, value, and compliance;
• Before “prescribing” any app to patients, vet the application yourself; and
• Use apps to supplement your clinical practice, but be wary of becoming over-reliant upon them, to the detriment of long-term memory. In order to utilize information in critical-thinking processes, it must be stored in long-term memory. TH

Summary: The panel of high-tech doctors helped a standing-room-only crowd navigate numerous apps to be used at point-of-care [PDF, 458 kb]. Groups worked through case studies utilizing applicable mobile apps. Examples and most useful apps, including occasional user reviews, follow:

Provider-to-Provider Communication, HIPAA secure

• Doximity.
• HIPAA-chat.
• Pros: HIPAA-secure, real-time communication.
• Cons: Both parties must be on app to securely communicate.

Provider-to-Patient Communication, Language Translators

• Google Translate: multiple platforms, free, 90 languages.
• MediBabble: iOS only, free, seven languages, dedicated medical application.

Diagnostic Apps for Providers

• Calculate by QxM.
• PreOpEval14: iOS only.
• PreopRisk Assessment: Android only.
• ASCVD Risk Estimator.
• MDCalc.com in addition to usual formulas, great abg-analyzer (online version only).
• AnticoagEvaluator.
• epocrates: calculators.

Click here for a PDF of useful apps and resource links  [PDF, 177 kb]

Resources for Evidence-Based Practice

• ACP Clinical Guidelines.
• ACP Smart Medicine.
• Read by QxMD.
• UpToDate.
• AHRQ ePPS: identifies clinical preventive services.
• epocrates.

Patient Engagement Apps

• Medication reminders: MediSafe, CareZone.
• Pharmaceutical costs: Walmart, Target Healthful, GoodRx.
• Proper inhaler usage: User Inhalers App.
• Smoking cessation: QuitSTART.

HM15 takeaways

• Apps are available to providers and patients to enhance quality, value, and compliance;
• Before “prescribing” any app to patients, vet the application yourself; and
• Use apps to supplement your clinical practice, but be wary of becoming over-reliant upon them, to the detriment of long-term memory. In order to utilize information in critical-thinking processes, it must be stored in long-term memory. TH

Summary: The panel of high-tech doctors helped a standing-room-only crowd navigate numerous apps to be used at point-of-care [PDF, 458 kb]. Groups worked through case studies utilizing applicable mobile apps. Examples and most useful apps, including occasional user reviews, follow:

Provider-to-Provider Communication, HIPAA secure

• Doximity.
• HIPAA-chat.
• Pros: HIPAA-secure, real-time communication.
• Cons: Both parties must be on app to securely communicate.

Provider-to-Patient Communication, Language Translators

• Google Translate: multiple platforms, free, 90 languages.
• MediBabble: iOS only, free, seven languages, dedicated medical application.

Diagnostic Apps for Providers

• Calculate by QxM.
• PreOpEval14: iOS only.
• PreopRisk Assessment: Android only.
• ASCVD Risk Estimator.
• MDCalc.com in addition to usual formulas, great abg-analyzer (online version only).
• AnticoagEvaluator.
• epocrates: calculators.

Click here for a PDF of useful apps and resource links  [PDF, 177 kb]

Resources for Evidence-Based Practice

• ACP Clinical Guidelines.
• ACP Smart Medicine.
• Read by QxMD.
• UpToDate.
• AHRQ ePPS: identifies clinical preventive services.
• epocrates.

Patient Engagement Apps

• Medication reminders: MediSafe, CareZone.
• Pharmaceutical costs: Walmart, Target Healthful, GoodRx.
• Proper inhaler usage: User Inhalers App.
• Smoking cessation: QuitSTART.

HM15 takeaways

• Apps are available to providers and patients to enhance quality, value, and compliance;
• Before “prescribing” any app to patients, vet the application yourself; and
• Use apps to supplement your clinical practice, but be wary of becoming over-reliant upon them, to the detriment of long-term memory. In order to utilize information in critical-thinking processes, it must be stored in long-term memory. TH

The Diagnosis: Levamisole-Contaminated Cocaine

Physical examination revealed scattered palpable purpura including the nasal tip and large necrotizing skin lesions with bullae (Figure 1). Retiform purpura was noted on the patient’s trunk and legs. Purpuric plaques in various stages of necrosis were identified on the arms, trunk, breasts, and thighs, with an early lesion involving the left ear (Figure 2). Vitals revealed a blood pressure of 151/79 mm Hg and a temperature of 37.3°C. Although the patient initially denied illicit drug use, she later admitted to smoking crack cocaine prior to the skin eruption.

Figure 1. Scattered palpable purpura including the nasal tip (A). Large necrotizing skin lesions with bullae on the arm (B).

Levamisole, an agent used in the veterinary setting to deworm cattle and pigs, is a common additive found in nearly 77% of the seized cocaine supplies in the United States.¹ Because of its immunomodulator effects, the agent was once used in humans to treat conditions such as colon cancer, rheumatoid arthritis, and nephritic syndrome. Therapeutic levamisole use has been associated with purpura on the external ears, cheeks, and nasal tip. The predilection for purpura on the ears was first described in children using levam-isole as treatment of nephritic syndrome.² Antinuclear cytoplasmic antibodies (ANCA) and antiphospholipid antibodies also were associated with therapeutic use.³ Reported effects of levamisole in cocaine users include fever, agranulocytosis, and infection. The mechanism is currently unknown but is thought to be an immunological process as evidenced by the presence of positive autoantibodies.⁴ Characteristic purpura in a cocaine abuser should alert the physician to consider levamisole as the culprit.

The diagnosis is largely a clinical one and other serious etiologies must be ruled out. The differential should include purpura fulminans, a rare hemorrhagic condition caused by severe infection, such as meningococcemia or deficiency of the vitamin K–dependent anticoagulants protein C and protein S. Given our patient’s history of hepatitis, purpura fulminans could have been likely. Purpura fulminans is rapidly progressive and is usually accompanied by disseminated intravascular coagulation. Coagulation studies and evidence of a consumptive coagulopathy such as thrombocytopenia, prolonged partial thromboplastin time, and activated partial thromboplastin time would favor this diagnosis. These studies as well as protein C and protein S were normal in our patient. Mixed cryoglobulinemia also should be suspected in a patient with hepatitis C virus who presents with vasculitis and arthralgia. An undetectable viral load in addition to a negative assay for cryoglobulins and normal complement (C3 and C4) levels make this diagnosis unlikely. Further, the purpura in cryoglobulinemia is typically confined to the lower extremities.⁵ Warfarin-induced skin necrosis also should be considered in patients who are taking warfarin.

Laboratory tests can be used to confirm the presence of infection, agranulocytosis, and coagulopathy. Although urine drug screen can confirm exposure to cocaine, levamisole is not detected in routine toxicology screening. Its half-life is between 5 and 6 hours; therefore, detection in blood or urine should be done within 48 hours of exposure.^3,4 Unfortunately, our patient presented 2 weeks after cocaine use, making detection of levamisole unfeasible. Rheumatologic screening also is appropriate in cases of suspected vasculitis. Our patient had a negative antinuclear antibody but tested positive for lupus anticoagulant and perinuclear ANCA. IgA and IgG anticardiolipin were negative with an indeterminate IgM anticardiolipin level. The literature supports these findings, as ANCA antibodies occurred in more than 90% of reported cases.³ Further, IgM anticardiolipin antibodies and lupus anticoagulant were positive in 65% and 51% of cases, respectively.³ Leukocyte and neutrophil count were normal in our patient.

Figure 2. An early purpuric plaque on the left ear.

Management of these patients is mainly supportive. Complete avoidance of the offending agent is absolutely essential for resolution and avoidance of recurrence. Provided that the patient abstains from cocaine, the skin findings typically resolve in 2 to 3 weeks.^3,6 The antibodies, however, may be present for up to 14 months.^2,3,6 Treatment with steroids and other immunosuppressants has been reported, but evidence is lacking on their role in the resolution of the lesions.³ In patients who develop a temporary antiphospholipid syndrome, aspirin may be recommended as a preventative measure.⁶ Pain management, treatment of secondary infection especially in situations with agranulocytosis, and surgical debridement of wounds are all potential problems that can arise.

Our patient had complete resolution of the purpura involving the nose and ear over the course of 3 weeks. She did, however, have to undergo surgical debridement of the nonhealing full-thickness necrotic lesions on her legs and arms.

The 2013 National Survey on Drug Use and Health estimates 1.5 million individuals aged 12 years or older were current (within the last month) users of cocaine.⁷ With levamisole becoming more prevalent in cocaine supplies, clinicians should be aware of this emerging condition. Rapid recognition can spare the patient unnecessary testing and inappropriate treatment regimens. Because testing for levamisole is difficult and not routinely performed, this case highlights the importance of clinical clues and an accurate social history in clinching the diagnosis.

The Diagnosis: Levamisole-Contaminated Cocaine

Physical examination revealed scattered palpable purpura including the nasal tip and large necrotizing skin lesions with bullae (Figure 1). Retiform purpura was noted on the patient’s trunk and legs. Purpuric plaques in various stages of necrosis were identified on the arms, trunk, breasts, and thighs, with an early lesion involving the left ear (Figure 2). Vitals revealed a blood pressure of 151/79 mm Hg and a temperature of 37.3°C. Although the patient initially denied illicit drug use, she later admitted to smoking crack cocaine prior to the skin eruption.

Figure 1. Scattered palpable purpura including the nasal tip (A). Large necrotizing skin lesions with bullae on the arm (B).

Levamisole, an agent used in the veterinary setting to deworm cattle and pigs, is a common additive found in nearly 77% of the seized cocaine supplies in the United States.¹ Because of its immunomodulator effects, the agent was once used in humans to treat conditions such as colon cancer, rheumatoid arthritis, and nephritic syndrome. Therapeutic levamisole use has been associated with purpura on the external ears, cheeks, and nasal tip. The predilection for purpura on the ears was first described in children using levam-isole as treatment of nephritic syndrome.² Antinuclear cytoplasmic antibodies (ANCA) and antiphospholipid antibodies also were associated with therapeutic use.³ Reported effects of levamisole in cocaine users include fever, agranulocytosis, and infection. The mechanism is currently unknown but is thought to be an immunological process as evidenced by the presence of positive autoantibodies.⁴ Characteristic purpura in a cocaine abuser should alert the physician to consider levamisole as the culprit.

The diagnosis is largely a clinical one and other serious etiologies must be ruled out. The differential should include purpura fulminans, a rare hemorrhagic condition caused by severe infection, such as meningococcemia or deficiency of the vitamin K–dependent anticoagulants protein C and protein S. Given our patient’s history of hepatitis, purpura fulminans could have been likely. Purpura fulminans is rapidly progressive and is usually accompanied by disseminated intravascular coagulation. Coagulation studies and evidence of a consumptive coagulopathy such as thrombocytopenia, prolonged partial thromboplastin time, and activated partial thromboplastin time would favor this diagnosis. These studies as well as protein C and protein S were normal in our patient. Mixed cryoglobulinemia also should be suspected in a patient with hepatitis C virus who presents with vasculitis and arthralgia. An undetectable viral load in addition to a negative assay for cryoglobulins and normal complement (C3 and C4) levels make this diagnosis unlikely. Further, the purpura in cryoglobulinemia is typically confined to the lower extremities.⁵ Warfarin-induced skin necrosis also should be considered in patients who are taking warfarin.

Laboratory tests can be used to confirm the presence of infection, agranulocytosis, and coagulopathy. Although urine drug screen can confirm exposure to cocaine, levamisole is not detected in routine toxicology screening. Its half-life is between 5 and 6 hours; therefore, detection in blood or urine should be done within 48 hours of exposure.^3,4 Unfortunately, our patient presented 2 weeks after cocaine use, making detection of levamisole unfeasible. Rheumatologic screening also is appropriate in cases of suspected vasculitis. Our patient had a negative antinuclear antibody but tested positive for lupus anticoagulant and perinuclear ANCA. IgA and IgG anticardiolipin were negative with an indeterminate IgM anticardiolipin level. The literature supports these findings, as ANCA antibodies occurred in more than 90% of reported cases.³ Further, IgM anticardiolipin antibodies and lupus anticoagulant were positive in 65% and 51% of cases, respectively.³ Leukocyte and neutrophil count were normal in our patient.

Figure 2. An early purpuric plaque on the left ear.

Management of these patients is mainly supportive. Complete avoidance of the offending agent is absolutely essential for resolution and avoidance of recurrence. Provided that the patient abstains from cocaine, the skin findings typically resolve in 2 to 3 weeks.^3,6 The antibodies, however, may be present for up to 14 months.^2,3,6 Treatment with steroids and other immunosuppressants has been reported, but evidence is lacking on their role in the resolution of the lesions.³ In patients who develop a temporary antiphospholipid syndrome, aspirin may be recommended as a preventative measure.⁶ Pain management, treatment of secondary infection especially in situations with agranulocytosis, and surgical debridement of wounds are all potential problems that can arise.

Our patient had complete resolution of the purpura involving the nose and ear over the course of 3 weeks. She did, however, have to undergo surgical debridement of the nonhealing full-thickness necrotic lesions on her legs and arms.

The 2013 National Survey on Drug Use and Health estimates 1.5 million individuals aged 12 years or older were current (within the last month) users of cocaine.⁷ With levamisole becoming more prevalent in cocaine supplies, clinicians should be aware of this emerging condition. Rapid recognition can spare the patient unnecessary testing and inappropriate treatment regimens. Because testing for levamisole is difficult and not routinely performed, this case highlights the importance of clinical clues and an accurate social history in clinching the diagnosis.

The Diagnosis: Levamisole-Contaminated Cocaine

Physical examination revealed scattered palpable purpura including the nasal tip and large necrotizing skin lesions with bullae (Figure 1). Retiform purpura was noted on the patient’s trunk and legs. Purpuric plaques in various stages of necrosis were identified on the arms, trunk, breasts, and thighs, with an early lesion involving the left ear (Figure 2). Vitals revealed a blood pressure of 151/79 mm Hg and a temperature of 37.3°C. Although the patient initially denied illicit drug use, she later admitted to smoking crack cocaine prior to the skin eruption.

Figure 1. Scattered palpable purpura including the nasal tip (A). Large necrotizing skin lesions with bullae on the arm (B).

Levamisole, an agent used in the veterinary setting to deworm cattle and pigs, is a common additive found in nearly 77% of the seized cocaine supplies in the United States.¹ Because of its immunomodulator effects, the agent was once used in humans to treat conditions such as colon cancer, rheumatoid arthritis, and nephritic syndrome. Therapeutic levamisole use has been associated with purpura on the external ears, cheeks, and nasal tip. The predilection for purpura on the ears was first described in children using levam-isole as treatment of nephritic syndrome.² Antinuclear cytoplasmic antibodies (ANCA) and antiphospholipid antibodies also were associated with therapeutic use.³ Reported effects of levamisole in cocaine users include fever, agranulocytosis, and infection. The mechanism is currently unknown but is thought to be an immunological process as evidenced by the presence of positive autoantibodies.⁴ Characteristic purpura in a cocaine abuser should alert the physician to consider levamisole as the culprit.

The diagnosis is largely a clinical one and other serious etiologies must be ruled out. The differential should include purpura fulminans, a rare hemorrhagic condition caused by severe infection, such as meningococcemia or deficiency of the vitamin K–dependent anticoagulants protein C and protein S. Given our patient’s history of hepatitis, purpura fulminans could have been likely. Purpura fulminans is rapidly progressive and is usually accompanied by disseminated intravascular coagulation. Coagulation studies and evidence of a consumptive coagulopathy such as thrombocytopenia, prolonged partial thromboplastin time, and activated partial thromboplastin time would favor this diagnosis. These studies as well as protein C and protein S were normal in our patient. Mixed cryoglobulinemia also should be suspected in a patient with hepatitis C virus who presents with vasculitis and arthralgia. An undetectable viral load in addition to a negative assay for cryoglobulins and normal complement (C3 and C4) levels make this diagnosis unlikely. Further, the purpura in cryoglobulinemia is typically confined to the lower extremities.⁵ Warfarin-induced skin necrosis also should be considered in patients who are taking warfarin.

Laboratory tests can be used to confirm the presence of infection, agranulocytosis, and coagulopathy. Although urine drug screen can confirm exposure to cocaine, levamisole is not detected in routine toxicology screening. Its half-life is between 5 and 6 hours; therefore, detection in blood or urine should be done within 48 hours of exposure.^3,4 Unfortunately, our patient presented 2 weeks after cocaine use, making detection of levamisole unfeasible. Rheumatologic screening also is appropriate in cases of suspected vasculitis. Our patient had a negative antinuclear antibody but tested positive for lupus anticoagulant and perinuclear ANCA. IgA and IgG anticardiolipin were negative with an indeterminate IgM anticardiolipin level. The literature supports these findings, as ANCA antibodies occurred in more than 90% of reported cases.³ Further, IgM anticardiolipin antibodies and lupus anticoagulant were positive in 65% and 51% of cases, respectively.³ Leukocyte and neutrophil count were normal in our patient.

Figure 2. An early purpuric plaque on the left ear.

Management of these patients is mainly supportive. Complete avoidance of the offending agent is absolutely essential for resolution and avoidance of recurrence. Provided that the patient abstains from cocaine, the skin findings typically resolve in 2 to 3 weeks.^3,6 The antibodies, however, may be present for up to 14 months.^2,3,6 Treatment with steroids and other immunosuppressants has been reported, but evidence is lacking on their role in the resolution of the lesions.³ In patients who develop a temporary antiphospholipid syndrome, aspirin may be recommended as a preventative measure.⁶ Pain management, treatment of secondary infection especially in situations with agranulocytosis, and surgical debridement of wounds are all potential problems that can arise.

Our patient had complete resolution of the purpura involving the nose and ear over the course of 3 weeks. She did, however, have to undergo surgical debridement of the nonhealing full-thickness necrotic lesions on her legs and arms.

The 2013 National Survey on Drug Use and Health estimates 1.5 million individuals aged 12 years or older were current (within the last month) users of cocaine.⁷ With levamisole becoming more prevalent in cocaine supplies, clinicians should be aware of this emerging condition. Rapid recognition can spare the patient unnecessary testing and inappropriate treatment regimens. Because testing for levamisole is difficult and not routinely performed, this case highlights the importance of clinical clues and an accurate social history in clinching the diagnosis.

AML cells in the bone marrow

Results of single-cell genotyping suggest the evolution of acute myeloid leukemia (AML) is more complex than we thought.

In screening for mutations in 2 genes, researchers identified at least 9 distinct clonal populations, each harboring unique mutational patterns.

Some mutations seemed to arise not sequentially, but independently and at different points in time.

These results suggest single-cell analysis may be more effective than bulk-tumor analysis for assessing cancer evolution.

Carlo Maley, PhD, of Arizona State University in Tempe, and his colleagues recounted the results in Science Translational Medicine.

The researchers set out to provide a more accurate picture of what takes place at the genetic level when an AML patient experiences relapse or metastasis. So they examined individual cells, screening them for  mutations in FLT3 and NPM1.

The results suggested the same mutation was occurring multiple times within an AML patient. The team examined individual cells from 6 AML patients, and the results showed all combinations of homozygous and heterozygous mutations of FLT3 and NPM1.

“There’s no way to explain that with each mutation only happening once,” Dr Maley said. “That’s scary because it means that these cancers have access to many mutations and can find the same mutation over and over.”

Dr Maley noted that the process of convergent evolution, in which separate lineages develop similar features, appears to account for some of the observed diversity. And influences from the environment may drive convergent evolution, but identical mutations can also arise through pure coincidence, simply by virtue of the enormous numbers involved.

For example, a 1 cm³ AML tumor may contain a billion cells, each containing some 3 billion base pairs in its genome. Mutations are estimated to occur at a rate of 1 mutation in every billion base pairs.

“That means every time the population of cells in a 1 cm³ tumor undergoes 1 generation, which we think takes just a couple days, every possible mutation of the genome is happening somewhere in that tumor,” Dr Maley said.

This alone would lead to the same mutation likely occurring independently multiple times.

Curbing cancer’s lethality

Given AML’s near-limitless capacity for creating novel variants, what can clinicians do to halt the disease’s advance? According to Dr Maley, one approach would be to use cancer’s ability to evolve to our advantage, rather than attempt to fight it head on.

This paradigm draws on a branch of ecology known as life history theory. The idea is to carefully study the environmental factors that may lead organisms to favor either a fast or slow reproducing strategy to maximize their ability to survive.

According to the theory, fast reproduction tends to occur in environments with high extrinsic mortality. Aggressive cancer treatment creates just such an environment, favoring those cells able to reproduce quickly, producing large numbers of daughter cells, with a few evading extrinsic mortality to repopulate the tumor.

On the other hand, a very stable environment often favors slow reproduction, because organisms reach a carrying capacity of their surrounding environment. In this case, the limiting factor becomes competition between like organisms. Here, a slow reproducing strategy favoring greater investment in maintenance and survivability wins the competition.

“This approach would say, ‘Let’s keep tumors as stable as possible and keep their resources limited,’” Dr Maley said. “If we are able to keep the tumor cells contained and let them fight it out, we would expect to see more competitively fit cells that are growing very slowly.”

AML cells in the bone marrow

Results of single-cell genotyping suggest the evolution of acute myeloid leukemia (AML) is more complex than we thought.

In screening for mutations in 2 genes, researchers identified at least 9 distinct clonal populations, each harboring unique mutational patterns.

Some mutations seemed to arise not sequentially, but independently and at different points in time.

These results suggest single-cell analysis may be more effective than bulk-tumor analysis for assessing cancer evolution.

Carlo Maley, PhD, of Arizona State University in Tempe, and his colleagues recounted the results in Science Translational Medicine.

The researchers set out to provide a more accurate picture of what takes place at the genetic level when an AML patient experiences relapse or metastasis. So they examined individual cells, screening them for  mutations in FLT3 and NPM1.

The results suggested the same mutation was occurring multiple times within an AML patient. The team examined individual cells from 6 AML patients, and the results showed all combinations of homozygous and heterozygous mutations of FLT3 and NPM1.

“There’s no way to explain that with each mutation only happening once,” Dr Maley said. “That’s scary because it means that these cancers have access to many mutations and can find the same mutation over and over.”

Dr Maley noted that the process of convergent evolution, in which separate lineages develop similar features, appears to account for some of the observed diversity. And influences from the environment may drive convergent evolution, but identical mutations can also arise through pure coincidence, simply by virtue of the enormous numbers involved.

For example, a 1 cm³ AML tumor may contain a billion cells, each containing some 3 billion base pairs in its genome. Mutations are estimated to occur at a rate of 1 mutation in every billion base pairs.

“That means every time the population of cells in a 1 cm³ tumor undergoes 1 generation, which we think takes just a couple days, every possible mutation of the genome is happening somewhere in that tumor,” Dr Maley said.

This alone would lead to the same mutation likely occurring independently multiple times.

Curbing cancer’s lethality

Given AML’s near-limitless capacity for creating novel variants, what can clinicians do to halt the disease’s advance? According to Dr Maley, one approach would be to use cancer’s ability to evolve to our advantage, rather than attempt to fight it head on.

This paradigm draws on a branch of ecology known as life history theory. The idea is to carefully study the environmental factors that may lead organisms to favor either a fast or slow reproducing strategy to maximize their ability to survive.

According to the theory, fast reproduction tends to occur in environments with high extrinsic mortality. Aggressive cancer treatment creates just such an environment, favoring those cells able to reproduce quickly, producing large numbers of daughter cells, with a few evading extrinsic mortality to repopulate the tumor.

On the other hand, a very stable environment often favors slow reproduction, because organisms reach a carrying capacity of their surrounding environment. In this case, the limiting factor becomes competition between like organisms. Here, a slow reproducing strategy favoring greater investment in maintenance and survivability wins the competition.

“This approach would say, ‘Let’s keep tumors as stable as possible and keep their resources limited,’” Dr Maley said. “If we are able to keep the tumor cells contained and let them fight it out, we would expect to see more competitively fit cells that are growing very slowly.”

AML cells in the bone marrow

Results of single-cell genotyping suggest the evolution of acute myeloid leukemia (AML) is more complex than we thought.

In screening for mutations in 2 genes, researchers identified at least 9 distinct clonal populations, each harboring unique mutational patterns.

Some mutations seemed to arise not sequentially, but independently and at different points in time.

These results suggest single-cell analysis may be more effective than bulk-tumor analysis for assessing cancer evolution.

Carlo Maley, PhD, of Arizona State University in Tempe, and his colleagues recounted the results in Science Translational Medicine.

The researchers set out to provide a more accurate picture of what takes place at the genetic level when an AML patient experiences relapse or metastasis. So they examined individual cells, screening them for  mutations in FLT3 and NPM1.

The results suggested the same mutation was occurring multiple times within an AML patient. The team examined individual cells from 6 AML patients, and the results showed all combinations of homozygous and heterozygous mutations of FLT3 and NPM1.

“There’s no way to explain that with each mutation only happening once,” Dr Maley said. “That’s scary because it means that these cancers have access to many mutations and can find the same mutation over and over.”

Dr Maley noted that the process of convergent evolution, in which separate lineages develop similar features, appears to account for some of the observed diversity. And influences from the environment may drive convergent evolution, but identical mutations can also arise through pure coincidence, simply by virtue of the enormous numbers involved.

For example, a 1 cm³ AML tumor may contain a billion cells, each containing some 3 billion base pairs in its genome. Mutations are estimated to occur at a rate of 1 mutation in every billion base pairs.

“That means every time the population of cells in a 1 cm³ tumor undergoes 1 generation, which we think takes just a couple days, every possible mutation of the genome is happening somewhere in that tumor,” Dr Maley said.

This alone would lead to the same mutation likely occurring independently multiple times.

Curbing cancer’s lethality

Given AML’s near-limitless capacity for creating novel variants, what can clinicians do to halt the disease’s advance? According to Dr Maley, one approach would be to use cancer’s ability to evolve to our advantage, rather than attempt to fight it head on.

This paradigm draws on a branch of ecology known as life history theory. The idea is to carefully study the environmental factors that may lead organisms to favor either a fast or slow reproducing strategy to maximize their ability to survive.

According to the theory, fast reproduction tends to occur in environments with high extrinsic mortality. Aggressive cancer treatment creates just such an environment, favoring those cells able to reproduce quickly, producing large numbers of daughter cells, with a few evading extrinsic mortality to repopulate the tumor.

On the other hand, a very stable environment often favors slow reproduction, because organisms reach a carrying capacity of their surrounding environment. In this case, the limiting factor becomes competition between like organisms. Here, a slow reproducing strategy favoring greater investment in maintenance and survivability wins the competition.

“This approach would say, ‘Let’s keep tumors as stable as possible and keep their resources limited,’” Dr Maley said. “If we are able to keep the tumor cells contained and let them fight it out, we would expect to see more competitively fit cells that are growing very slowly.”