Commentary

The unconscionable extended ED boarding of acutely ill psychiatric patients in need of inpatient care was the subject of one of the most requested recent EM editorials. Tragically, in the 2 years since “A Wintry Mix of Patients” first appeared (March 2013), little has changed.

An August 7, 2014 Washington State Supreme Court decision prohibiting the use of EDs to board acutely ill psychiatric patients may be one step in the right direction. But it offers no alternatives for actually providing the care. A week after the ruling, ACEP’s president expressed concern that EPs could be caught in the middle of conflicting federal and state mandates, and medical liability risks.

Throughout the United States this winter, admitted patients and their families waited hours to days in emergency departments for inpatient beds. Few waited longer or suffered more than those waiting for a psychiatric bed. The number of patients needing hospitalization for acute psychiatric conditions and behavioral disturbances frequently exceeds the capacity of psychiatric services to admit them and increasingly exceeds the capacity of psychiatric EDs to provide continued care until beds become available. When psychiatric patients are boarded in surrounding medical EDs that were never designed for this purpose, emergency physicians, nurses, and security officers must try to provide a safe and secure environment of care for both the displaced psychiatric patients and nearby medical and surgical patients.

In a January 22, 2013, article, Washington Post reporter Olga Khazan describes the plight of a 15-year-old girl with Asperger’s syndrome and an anxiety disorder who spent 2 days on stretchers in two EDs waiting for an inpatient bed. The article attributes the nationwide bed shortage to cutbacks after “28 states and the District [of Columbia] reduced their mental health funding by a total of $1.6 billion” between 2009 and 2012.

Similarly, in a July 2012 report, “No Room at the Inn: Trends and Consequences of Closing Public Psychiatric Hospitals,” the nonprofit Treatment Advocacy Center (TAC) points out that the total number of state psychiatric beds in this country decreased by 14% from 2005 to 2010, dropping the per-capita bed ratio to the same level it was in 1850, the year that our country began to provide more humane care by hospitalizing the most severely mentally ill patients. The TAC report also notes that, in the absence of needed psychiatric treatment and care, people in acute or chronic crises gravitate to hospital EDs, jails, prisons, or the streets, and are partly responsible for higher rates of violent crimes.

At the same time that state-supported psychiatric beds are disappearing at an alarming rate, a desperate need for more med/surg beds is leading many general hospitals to convert psychiatric beds to nonpsychiatric beds. But a lack of inpatient beds is not the only factor responsible for this crisis in care. Health insurance providers are much more selective with respect to which inpatient psychiatric services they will pay for, and often will not cover an available inpatient bed nearby. Why is there a difference between psychiatric and nonpsychiatric inpatient coverage, and why do states permit the difference? This practice adds to the misery and delays the care of all patients, as emergency psychiatrists and social workers must spend hours or days arranging for covered inpatient stays.

All inpatient care, including psychiatric care, can be expensive, but how much money does the elimination of psychiatric services really save if you add in the cost of extra prison capacity, the loss of income by family members waiting in the ED with an ill relative, or the loss of productivity by victims of violent crimes committed by nonhospitalized mentally ill patients? Psychiatrists utilizing potent modern medications have made incredible strides in treatment, but treating an illness is not the same as curing it, and patients who stop taking their medications after their prescriptions run out often end up back in the ED—sometimes repeatedly. Such episodic ED care also adds to the overall costs and, more important, hurts many people in the process.

For more than 150 years, states have assumed major responsibility for providing a safe therapeutic environment for those suffering from severe mental illness. Now is not the time to abandon this responsibility. As a nation, if we cannot recognize the seriousness of this problem and if we do nothing to fix it immediately, lack of beds is not the only lack of capacity from which we suffer.

The unconscionable extended ED boarding of acutely ill psychiatric patients in need of inpatient care was the subject of one of the most requested recent EM editorials. Tragically, in the 2 years since “A Wintry Mix of Patients” first appeared (March 2013), little has changed.

An August 7, 2014 Washington State Supreme Court decision prohibiting the use of EDs to board acutely ill psychiatric patients may be one step in the right direction. But it offers no alternatives for actually providing the care. A week after the ruling, ACEP’s president expressed concern that EPs could be caught in the middle of conflicting federal and state mandates, and medical liability risks.

Throughout the United States this winter, admitted patients and their families waited hours to days in emergency departments for inpatient beds. Few waited longer or suffered more than those waiting for a psychiatric bed. The number of patients needing hospitalization for acute psychiatric conditions and behavioral disturbances frequently exceeds the capacity of psychiatric services to admit them and increasingly exceeds the capacity of psychiatric EDs to provide continued care until beds become available. When psychiatric patients are boarded in surrounding medical EDs that were never designed for this purpose, emergency physicians, nurses, and security officers must try to provide a safe and secure environment of care for both the displaced psychiatric patients and nearby medical and surgical patients.

In a January 22, 2013, article, Washington Post reporter Olga Khazan describes the plight of a 15-year-old girl with Asperger’s syndrome and an anxiety disorder who spent 2 days on stretchers in two EDs waiting for an inpatient bed. The article attributes the nationwide bed shortage to cutbacks after “28 states and the District [of Columbia] reduced their mental health funding by a total of $1.6 billion” between 2009 and 2012.

Similarly, in a July 2012 report, “No Room at the Inn: Trends and Consequences of Closing Public Psychiatric Hospitals,” the nonprofit Treatment Advocacy Center (TAC) points out that the total number of state psychiatric beds in this country decreased by 14% from 2005 to 2010, dropping the per-capita bed ratio to the same level it was in 1850, the year that our country began to provide more humane care by hospitalizing the most severely mentally ill patients. The TAC report also notes that, in the absence of needed psychiatric treatment and care, people in acute or chronic crises gravitate to hospital EDs, jails, prisons, or the streets, and are partly responsible for higher rates of violent crimes.

At the same time that state-supported psychiatric beds are disappearing at an alarming rate, a desperate need for more med/surg beds is leading many general hospitals to convert psychiatric beds to nonpsychiatric beds. But a lack of inpatient beds is not the only factor responsible for this crisis in care. Health insurance providers are much more selective with respect to which inpatient psychiatric services they will pay for, and often will not cover an available inpatient bed nearby. Why is there a difference between psychiatric and nonpsychiatric inpatient coverage, and why do states permit the difference? This practice adds to the misery and delays the care of all patients, as emergency psychiatrists and social workers must spend hours or days arranging for covered inpatient stays.

All inpatient care, including psychiatric care, can be expensive, but how much money does the elimination of psychiatric services really save if you add in the cost of extra prison capacity, the loss of income by family members waiting in the ED with an ill relative, or the loss of productivity by victims of violent crimes committed by nonhospitalized mentally ill patients? Psychiatrists utilizing potent modern medications have made incredible strides in treatment, but treating an illness is not the same as curing it, and patients who stop taking their medications after their prescriptions run out often end up back in the ED—sometimes repeatedly. Such episodic ED care also adds to the overall costs and, more important, hurts many people in the process.

For more than 150 years, states have assumed major responsibility for providing a safe therapeutic environment for those suffering from severe mental illness. Now is not the time to abandon this responsibility. As a nation, if we cannot recognize the seriousness of this problem and if we do nothing to fix it immediately, lack of beds is not the only lack of capacity from which we suffer.

The unconscionable extended ED boarding of acutely ill psychiatric patients in need of inpatient care was the subject of one of the most requested recent EM editorials. Tragically, in the 2 years since “A Wintry Mix of Patients” first appeared (March 2013), little has changed.

An August 7, 2014 Washington State Supreme Court decision prohibiting the use of EDs to board acutely ill psychiatric patients may be one step in the right direction. But it offers no alternatives for actually providing the care. A week after the ruling, ACEP’s president expressed concern that EPs could be caught in the middle of conflicting federal and state mandates, and medical liability risks.

Throughout the United States this winter, admitted patients and their families waited hours to days in emergency departments for inpatient beds. Few waited longer or suffered more than those waiting for a psychiatric bed. The number of patients needing hospitalization for acute psychiatric conditions and behavioral disturbances frequently exceeds the capacity of psychiatric services to admit them and increasingly exceeds the capacity of psychiatric EDs to provide continued care until beds become available. When psychiatric patients are boarded in surrounding medical EDs that were never designed for this purpose, emergency physicians, nurses, and security officers must try to provide a safe and secure environment of care for both the displaced psychiatric patients and nearby medical and surgical patients.

In a January 22, 2013, article, Washington Post reporter Olga Khazan describes the plight of a 15-year-old girl with Asperger’s syndrome and an anxiety disorder who spent 2 days on stretchers in two EDs waiting for an inpatient bed. The article attributes the nationwide bed shortage to cutbacks after “28 states and the District [of Columbia] reduced their mental health funding by a total of $1.6 billion” between 2009 and 2012.

Similarly, in a July 2012 report, “No Room at the Inn: Trends and Consequences of Closing Public Psychiatric Hospitals,” the nonprofit Treatment Advocacy Center (TAC) points out that the total number of state psychiatric beds in this country decreased by 14% from 2005 to 2010, dropping the per-capita bed ratio to the same level it was in 1850, the year that our country began to provide more humane care by hospitalizing the most severely mentally ill patients. The TAC report also notes that, in the absence of needed psychiatric treatment and care, people in acute or chronic crises gravitate to hospital EDs, jails, prisons, or the streets, and are partly responsible for higher rates of violent crimes.

At the same time that state-supported psychiatric beds are disappearing at an alarming rate, a desperate need for more med/surg beds is leading many general hospitals to convert psychiatric beds to nonpsychiatric beds. But a lack of inpatient beds is not the only factor responsible for this crisis in care. Health insurance providers are much more selective with respect to which inpatient psychiatric services they will pay for, and often will not cover an available inpatient bed nearby. Why is there a difference between psychiatric and nonpsychiatric inpatient coverage, and why do states permit the difference? This practice adds to the misery and delays the care of all patients, as emergency psychiatrists and social workers must spend hours or days arranging for covered inpatient stays.

All inpatient care, including psychiatric care, can be expensive, but how much money does the elimination of psychiatric services really save if you add in the cost of extra prison capacity, the loss of income by family members waiting in the ED with an ill relative, or the loss of productivity by victims of violent crimes committed by nonhospitalized mentally ill patients? Psychiatrists utilizing potent modern medications have made incredible strides in treatment, but treating an illness is not the same as curing it, and patients who stop taking their medications after their prescriptions run out often end up back in the ED—sometimes repeatedly. Such episodic ED care also adds to the overall costs and, more important, hurts many people in the process.

For more than 150 years, states have assumed major responsibility for providing a safe therapeutic environment for those suffering from severe mental illness. Now is not the time to abandon this responsibility. As a nation, if we cannot recognize the seriousness of this problem and if we do nothing to fix it immediately, lack of beds is not the only lack of capacity from which we suffer.

“STOP USING THE HCG DISCRIMINATORY ZONE OF 1,500 TO
2,000 mIU/mL TO GUIDE INTERVENTION DURING EARLY PREGNANCY”
ROBERT L. BARBIERI, MD (EDITORIAL; JANUARY 2015)

Defining “abnormal rise” is the elephant in the room
It was refreshing to read Dr. Barbieri’srecent editorial on the management of ectopic pregnancies based on human chorionic gonadotropin (hCG) levels. However, I feel there’s an elephant in the room. The phrase “abnormal rise” is not clearly defined, even though countless texts and review articles continue to use the phrase. In fact, many authors include a flow chart in which an abnormal rise usually is followed by a recommendation to empty the uterus in an attempt to find chorionic villi.^1,2 The most recent versions of several widely used textbooks advocate this practice,^3–5 and a current UpToDate article includes a flow chart suggesting that a “suboptimal rise” is sufficient for diagnosis of an abnormal pregnancy requiring treatment.⁶  

Kadar and colleagues originally suggested that 85% of viable intrauterine pregnancies (IUPs) will have a rise in hCG levels of at least 66% every 48 hours, leading to what is commonly called the “doub­ling rule.”⁷ Barnhart and colleagues showed that the slowest recorded hCG rise for a viable pregnancy in 48 hours was 53%, demonstrating that the hCG level does not double in 48 to 72 hours as traditionally expected.⁸ In their final model, the authors calculated that 99% percent of normal IUPs should have an increase of at least 53% in 2 days, moving the bar for a “normal” hCG rise even lower. This also implies that 1% of viable IUPs may have a rise of less than 53% over 2 days. I have to wonder how many viable, wanted pregnancies have been interrupted by the misguided use of discriminatory zones or abnormal rises resulting in the emptying of the pregnant uterus?

Clinical assessment and ultrasonography should continue to be the mainstay of management of ectopic pregnancy. When surgical diagnosis is needed, laparoscopy should be considered. In this day and age, when we are being more cautious about emptying a uterus based on ultrasound measurements of the fetus or gestational sac, why are we still so eager to base that decision on laboratory values? Are we really willing to accept that 1% of the time we will be terminating a viable pregnancy? We should stop the continued propagation of flow charts and strategies that use hCG discriminatory zones or abnormal rises to determine viability and when to evacuate the uterus. A contemporary update to address the issue is needed.
Devin Namaky, MD
Cincinnati, Ohio

References
1. Seeber B, Barnhart K. Suspected ectopic pregnancy. Obstet Gynecol. 2006;107(2):399–413.

2. Mukul LV, Teal SB. Current management of ectopic pregnancy. Obstet Gynecol Clin North Am. 2007;34(3):403–419.

3. Ectopic pregnancy. In: Hoffman BL, Schorge JP, Schaffer JI, et al, eds. Williams Gynecology. 2nd ed. New York, NY: McGraw-Hill Professional; 2012:198–218.

4. Lobo RA. Ectopic pregnancy. In: Lentz GM, ed. Comprehensive Gynecology. 6th ed. Philadelphia, PA: Elsevier Mosby; 2012:361–382 .

5. Damario MA, Rock JA. Ectopic pregnancy. In: Rock JA, Jones HW III, eds. Te Linde’s Operative Gynecology. 10th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008:798–824.

6. Tulandi T. Ectopic pregnancy: clinical manifestations and diagnosis. UpToDate Web site. http://www.uptodate.com/contents/ectopic-pregnancy-clinical-manifestations-and-diag nosis. Updated October 22, 2014. Accessed February 18, 2015. 

7. Kadar N, Caldwell BV, Romera R. A method of screening for ectopic pregnancy and its indications. Obstet Gynecol. 1981;58(2):162–166.

8. Barnhart KT, Sammel MD, Rinaudo PF, Zhou L, Hummel AC, Guo W. Symptomatic patients with an early viable intrauterine pregnancy: hCG curves redefined. Obstet Gynecol. 2004;104(1):50–55.

Why not use serum progesterone to determine early pregnancy viability?

I read with attention Dr. Barbieri’s recent editorial about evaluation of early pregnancy. My question is: Why is serum progesterone not recommended or used to assess the health of an early pregnancy?

In my practice, I always use a serum progesterone test along with hCG measurements to ascertain if an early pregnancy is healthy. I have observed, as biased as this observation can be, as I have not done any study about it, that a serum progesterone level above 12 ng/dL correlates quite well with a healthy pregnancy. I only follow more intensively with serial ultrasonography and hCG measurements in a patient whose progesterone level is below 11 ng/dL.

When a patient’s only symptom is bleeding, if the serum progesterone level is below 11 ng/dL, and her serum quantitative hCG level does not double as appropriate, I consider the pregnancy not normal and counsel the patient about continuing observation or terminating the pregnancy.

In the same laboratory scenario but with a patient who has bleeding and pain, and even moreso if the progesterone level is below 8 ng/dL, I strongly consider an ectopic pregnancy until it is proven otherwise. In this case, I offer treatment with methotrexate, as it’s my experience that the vast majority of these patients are carrying an abnormal pregnancy— either a spontaneous abortion or an ectopic pregnancy. Methotrexate therapy will prevent further complications without causing the loss of normal pregnancies.

For me, progesterone levels add one more piece to the puzzle. A patient with pain, vaginal bleeding, a quantitative hCG value of
500 mIU/mL, and a serum progesterone level of 20 ng/dL will have a normal pregnancy and is not a candidate for any intervention besides a follow-up hCG measurement to ascertain “doubling” of the analyte as expected in a normal pregnancy.

An asymptomatic patient whose quantitative hCG measurement is 1,000 mIU/mL and progesterone level is 4 ng/dL is carrying an abnormal pregnancy. If this quantitative hCG does not double appropriately in the follow-up, I counsel the patient about the greater chance of a spontaneous abortion or ectopic pregnancy.

Is this approach faulty?
Tomas Hernandez, MD
Pasco, Washington

Know the sensitivity of the HCG test

I found Dr. Barbieri’s editorial very timely. It brings some clarity to the use of the hCG discriminatory zone in symptomatic pregnant patients.

An additional important point is that it is the clinician’s obligation to know the sensitivity of the test the laboratory uses. Serum tests use the threshold for a negative result of either less than 1 mIU/mL or less than 5 mIU/mL. If possible, serial hCG measurements should be performed in the same laboratory, because the result may not represent a true change in the hCG concentration if the second test is performed at a different laboratory.¹ This is especially important when the clinician is considering the use of methotrexate to treat a suspected ectopic pregnancy.
Magdalen E. Hull, MD, MPH
Great River, New York

Reference
1. Meriko Mori K, Lurain, JR. Human chorionic gonadotropin: testing in pregnancy and gestational trophoblastic disease and causes of low persistent levels. UpToDate. http://www.uptodate.com/contents/human-chorionic-gonadotropin-testing-in-pregnancy-and-gesta tional-trophoblastic-disease-and-causes-of-low-persistent-levels. Published October 23, 2013. Accessed January 29, 2015.

Further thoughts on HCG, ultrasound, and early pregnancy diagnosis

I want to thank Dr. Barbieri for his important, timely message about suspected nonviable pregnancy. I agree with virtually all of his excellent suggestions. In fact, I was part of the consensus panel that developed the findings diagnostic of and suggestive of IUP failure.1 There are a few points, however, that I believe the readership of OBG Management should know.

The endothelial heart tube, the first organ system to form, folds in on itself and begins to beat at 21 days postconception. Thus, it is present and beating prior to our ability to image it on transvaginal ultrasound. Yet new guidelines¹ now say not to call an IUP failed until there is a crown-rump length of 7 mm or greater with no cardiac activity. In the past, many clinicians used 4 or 5 mm. In fact, one of the most recent studies utilizing an 8-mHz transducer found all cardiac activity was visualized by 3.1 mm embryonic size!²

So why has the number been increased to 7 mm? I’ve given this a lot of thought. Most clinical trials, from which guidelines were derived in the past, were well-designed, tightly controlled, and performed by better-trained clinicians, often with state-of-the-art equipment. In contrast, well-meaning health-care providers practicing in the field are often without the same level of quality control, equipment, or expertise but are still expected to duplicate the data from the trials used to create the guidelines. The reason this is relevant pertains to the statement that 94% of 291 cases of ectopic pregnancy had an adnexal mass.³ This is an excellent study, done at one of the nation’s most outstanding academic institutions by world-class sonologists. I do not believe that well-meaning clinicians in the field will be able to achieve this level of detection.

Dr. Barbieri also discusses an inability to see an IUP even when hCG levels are greater than 1,500 or 2,000 mIU/mL or above. He mentions obesity, fibroids, and adenomyosis as increasing the risk of an ultrasound failing to detect an early IUP. This point needs to be expanded upon. Twenty-seven years ago, we claimed a discriminatory level of 1,025 mIU/mL of hCG if the gestational sac was normal and the uterus was normal with normal echo patterns. We had three cases with markedly greater hCG levels (one, in fact, as high as 5,544 mIU/mL)with coexisting fibroids.⁴

I would also submit that it is the axial uterus that is a very important source of potential error. The closer the beam of sound coming off of the footprint is to a right angle with the endometrium (as it will be in a markedly anteverted or retroverted uterus), the better the resulting image. With an axial uterus, the endometrium is in the same plane as the beam of sound, and this diminishes imaging capability. Furthermore, twin pregnancies are a potential confounder in attempting to correlate hCG levels in transvaginal ultrasound findings.

I wholeheartedly agree with Dr. Barbieri: There is virtually no role to administer methotrexate based on a single hCG determination in a hemodynamically stable patient.
Steven R. Goldstein, MD
New York, New York

References
1. Doubilet PM, Benson CB, Bourne T, Blaivas M; Society of Radiologists in Ultrasound Multispecialty Panel on Early First Trimester Diagnosis of Miscarriage and Exclusion of a Viable Intrauterine Pregnancy. Diagnostic criteria for nonviable pregnancy early in the first trimester. N Engl J Med. 2013;369(15):1443–1451.

2. Abaid LN, As-Sanie S, Wolfe HM. Relationship between crown-rump length and early detection of cardiac activity. J Reprod Med. 2007;52(5):375–378.

3. Frates MC, Doubilet PM, Peters HE, Benson CR. Adnexal sonographic findings in ectopic pregnancy and their correlation with tubal rupture and human chorionic gonadotropin levels. J Ultrasound Med. 2014;33(4):697–703.

4. Goldstein SR, Snyder JR, Watson C, Danon M. Very early pregnancy detection with endovaginal ultrasound. Obstet Gynecol. 1988;72(2):200–204.

‡‡Dr. Barbieri responds
Dr. Namaky, Dr. Hernandez, Dr. Hull, and Dr. Goldstein provide great clinical advice for readers. I agree with Dr. Namaky that the mainstays of managing a pregnancy of unknown location in a stable patient are clinical assessment and ultrasonography. Dr. Hernandez recommends using the serum progesterone measurement to help guide clinical decisions in a pregnancy of unknown location. I also use serum progesterone in my practice because a very low progesterone level helps the patient to understand that she has a failed pregnancy, and facilitates her acceptance of timely intervention. Many of my colleagues do not use progesterone measurement because they prefer to rely on clinical assessment, serial hCG measurement, and ultrasound results to guide their treatment. I agree with Dr. Hull that serial hCG measurements are most useful when the same laboratory performs all the tests. Dr. Goldstein, a world class expert in the evaluation and management of early pregnancy problems, provides great advice for all readers on how to best integrate ultrasonography in their practices to optimize patient care.

Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

“STOP USING THE HCG DISCRIMINATORY ZONE OF 1,500 TO
2,000 mIU/mL TO GUIDE INTERVENTION DURING EARLY PREGNANCY”
ROBERT L. BARBIERI, MD (EDITORIAL; JANUARY 2015)

Defining “abnormal rise” is the elephant in the room
It was refreshing to read Dr. Barbieri’srecent editorial on the management of ectopic pregnancies based on human chorionic gonadotropin (hCG) levels. However, I feel there’s an elephant in the room. The phrase “abnormal rise” is not clearly defined, even though countless texts and review articles continue to use the phrase. In fact, many authors include a flow chart in which an abnormal rise usually is followed by a recommendation to empty the uterus in an attempt to find chorionic villi.^1,2 The most recent versions of several widely used textbooks advocate this practice,^3–5 and a current UpToDate article includes a flow chart suggesting that a “suboptimal rise” is sufficient for diagnosis of an abnormal pregnancy requiring treatment.⁶  

Kadar and colleagues originally suggested that 85% of viable intrauterine pregnancies (IUPs) will have a rise in hCG levels of at least 66% every 48 hours, leading to what is commonly called the “doub­ling rule.”⁷ Barnhart and colleagues showed that the slowest recorded hCG rise for a viable pregnancy in 48 hours was 53%, demonstrating that the hCG level does not double in 48 to 72 hours as traditionally expected.⁸ In their final model, the authors calculated that 99% percent of normal IUPs should have an increase of at least 53% in 2 days, moving the bar for a “normal” hCG rise even lower. This also implies that 1% of viable IUPs may have a rise of less than 53% over 2 days. I have to wonder how many viable, wanted pregnancies have been interrupted by the misguided use of discriminatory zones or abnormal rises resulting in the emptying of the pregnant uterus?

Clinical assessment and ultrasonography should continue to be the mainstay of management of ectopic pregnancy. When surgical diagnosis is needed, laparoscopy should be considered. In this day and age, when we are being more cautious about emptying a uterus based on ultrasound measurements of the fetus or gestational sac, why are we still so eager to base that decision on laboratory values? Are we really willing to accept that 1% of the time we will be terminating a viable pregnancy? We should stop the continued propagation of flow charts and strategies that use hCG discriminatory zones or abnormal rises to determine viability and when to evacuate the uterus. A contemporary update to address the issue is needed.
Devin Namaky, MD
Cincinnati, Ohio

References
1. Seeber B, Barnhart K. Suspected ectopic pregnancy. Obstet Gynecol. 2006;107(2):399–413.

2. Mukul LV, Teal SB. Current management of ectopic pregnancy. Obstet Gynecol Clin North Am. 2007;34(3):403–419.

3. Ectopic pregnancy. In: Hoffman BL, Schorge JP, Schaffer JI, et al, eds. Williams Gynecology. 2nd ed. New York, NY: McGraw-Hill Professional; 2012:198–218.

4. Lobo RA. Ectopic pregnancy. In: Lentz GM, ed. Comprehensive Gynecology. 6th ed. Philadelphia, PA: Elsevier Mosby; 2012:361–382 .

5. Damario MA, Rock JA. Ectopic pregnancy. In: Rock JA, Jones HW III, eds. Te Linde’s Operative Gynecology. 10th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008:798–824.

6. Tulandi T. Ectopic pregnancy: clinical manifestations and diagnosis. UpToDate Web site. http://www.uptodate.com/contents/ectopic-pregnancy-clinical-manifestations-and-diag nosis. Updated October 22, 2014. Accessed February 18, 2015. 

7. Kadar N, Caldwell BV, Romera R. A method of screening for ectopic pregnancy and its indications. Obstet Gynecol. 1981;58(2):162–166.

8. Barnhart KT, Sammel MD, Rinaudo PF, Zhou L, Hummel AC, Guo W. Symptomatic patients with an early viable intrauterine pregnancy: hCG curves redefined. Obstet Gynecol. 2004;104(1):50–55.

Why not use serum progesterone to determine early pregnancy viability?

I read with attention Dr. Barbieri’s recent editorial about evaluation of early pregnancy. My question is: Why is serum progesterone not recommended or used to assess the health of an early pregnancy?

In my practice, I always use a serum progesterone test along with hCG measurements to ascertain if an early pregnancy is healthy. I have observed, as biased as this observation can be, as I have not done any study about it, that a serum progesterone level above 12 ng/dL correlates quite well with a healthy pregnancy. I only follow more intensively with serial ultrasonography and hCG measurements in a patient whose progesterone level is below 11 ng/dL.

When a patient’s only symptom is bleeding, if the serum progesterone level is below 11 ng/dL, and her serum quantitative hCG level does not double as appropriate, I consider the pregnancy not normal and counsel the patient about continuing observation or terminating the pregnancy.

In the same laboratory scenario but with a patient who has bleeding and pain, and even moreso if the progesterone level is below 8 ng/dL, I strongly consider an ectopic pregnancy until it is proven otherwise. In this case, I offer treatment with methotrexate, as it’s my experience that the vast majority of these patients are carrying an abnormal pregnancy— either a spontaneous abortion or an ectopic pregnancy. Methotrexate therapy will prevent further complications without causing the loss of normal pregnancies.

For me, progesterone levels add one more piece to the puzzle. A patient with pain, vaginal bleeding, a quantitative hCG value of
500 mIU/mL, and a serum progesterone level of 20 ng/dL will have a normal pregnancy and is not a candidate for any intervention besides a follow-up hCG measurement to ascertain “doubling” of the analyte as expected in a normal pregnancy.

An asymptomatic patient whose quantitative hCG measurement is 1,000 mIU/mL and progesterone level is 4 ng/dL is carrying an abnormal pregnancy. If this quantitative hCG does not double appropriately in the follow-up, I counsel the patient about the greater chance of a spontaneous abortion or ectopic pregnancy.

Is this approach faulty?
Tomas Hernandez, MD
Pasco, Washington

Know the sensitivity of the HCG test

I found Dr. Barbieri’s editorial very timely. It brings some clarity to the use of the hCG discriminatory zone in symptomatic pregnant patients.

An additional important point is that it is the clinician’s obligation to know the sensitivity of the test the laboratory uses. Serum tests use the threshold for a negative result of either less than 1 mIU/mL or less than 5 mIU/mL. If possible, serial hCG measurements should be performed in the same laboratory, because the result may not represent a true change in the hCG concentration if the second test is performed at a different laboratory.¹ This is especially important when the clinician is considering the use of methotrexate to treat a suspected ectopic pregnancy.
Magdalen E. Hull, MD, MPH
Great River, New York

Reference
1. Meriko Mori K, Lurain, JR. Human chorionic gonadotropin: testing in pregnancy and gestational trophoblastic disease and causes of low persistent levels. UpToDate. http://www.uptodate.com/contents/human-chorionic-gonadotropin-testing-in-pregnancy-and-gesta tional-trophoblastic-disease-and-causes-of-low-persistent-levels. Published October 23, 2013. Accessed January 29, 2015.

Further thoughts on HCG, ultrasound, and early pregnancy diagnosis

I want to thank Dr. Barbieri for his important, timely message about suspected nonviable pregnancy. I agree with virtually all of his excellent suggestions. In fact, I was part of the consensus panel that developed the findings diagnostic of and suggestive of IUP failure.1 There are a few points, however, that I believe the readership of OBG Management should know.

The endothelial heart tube, the first organ system to form, folds in on itself and begins to beat at 21 days postconception. Thus, it is present and beating prior to our ability to image it on transvaginal ultrasound. Yet new guidelines¹ now say not to call an IUP failed until there is a crown-rump length of 7 mm or greater with no cardiac activity. In the past, many clinicians used 4 or 5 mm. In fact, one of the most recent studies utilizing an 8-mHz transducer found all cardiac activity was visualized by 3.1 mm embryonic size!²

So why has the number been increased to 7 mm? I’ve given this a lot of thought. Most clinical trials, from which guidelines were derived in the past, were well-designed, tightly controlled, and performed by better-trained clinicians, often with state-of-the-art equipment. In contrast, well-meaning health-care providers practicing in the field are often without the same level of quality control, equipment, or expertise but are still expected to duplicate the data from the trials used to create the guidelines. The reason this is relevant pertains to the statement that 94% of 291 cases of ectopic pregnancy had an adnexal mass.³ This is an excellent study, done at one of the nation’s most outstanding academic institutions by world-class sonologists. I do not believe that well-meaning clinicians in the field will be able to achieve this level of detection.

Dr. Barbieri also discusses an inability to see an IUP even when hCG levels are greater than 1,500 or 2,000 mIU/mL or above. He mentions obesity, fibroids, and adenomyosis as increasing the risk of an ultrasound failing to detect an early IUP. This point needs to be expanded upon. Twenty-seven years ago, we claimed a discriminatory level of 1,025 mIU/mL of hCG if the gestational sac was normal and the uterus was normal with normal echo patterns. We had three cases with markedly greater hCG levels (one, in fact, as high as 5,544 mIU/mL)with coexisting fibroids.⁴

I would also submit that it is the axial uterus that is a very important source of potential error. The closer the beam of sound coming off of the footprint is to a right angle with the endometrium (as it will be in a markedly anteverted or retroverted uterus), the better the resulting image. With an axial uterus, the endometrium is in the same plane as the beam of sound, and this diminishes imaging capability. Furthermore, twin pregnancies are a potential confounder in attempting to correlate hCG levels in transvaginal ultrasound findings.

I wholeheartedly agree with Dr. Barbieri: There is virtually no role to administer methotrexate based on a single hCG determination in a hemodynamically stable patient.
Steven R. Goldstein, MD
New York, New York

References
1. Doubilet PM, Benson CB, Bourne T, Blaivas M; Society of Radiologists in Ultrasound Multispecialty Panel on Early First Trimester Diagnosis of Miscarriage and Exclusion of a Viable Intrauterine Pregnancy. Diagnostic criteria for nonviable pregnancy early in the first trimester. N Engl J Med. 2013;369(15):1443–1451.

2. Abaid LN, As-Sanie S, Wolfe HM. Relationship between crown-rump length and early detection of cardiac activity. J Reprod Med. 2007;52(5):375–378.

3. Frates MC, Doubilet PM, Peters HE, Benson CR. Adnexal sonographic findings in ectopic pregnancy and their correlation with tubal rupture and human chorionic gonadotropin levels. J Ultrasound Med. 2014;33(4):697–703.

4. Goldstein SR, Snyder JR, Watson C, Danon M. Very early pregnancy detection with endovaginal ultrasound. Obstet Gynecol. 1988;72(2):200–204.

‡‡Dr. Barbieri responds
Dr. Namaky, Dr. Hernandez, Dr. Hull, and Dr. Goldstein provide great clinical advice for readers. I agree with Dr. Namaky that the mainstays of managing a pregnancy of unknown location in a stable patient are clinical assessment and ultrasonography. Dr. Hernandez recommends using the serum progesterone measurement to help guide clinical decisions in a pregnancy of unknown location. I also use serum progesterone in my practice because a very low progesterone level helps the patient to understand that she has a failed pregnancy, and facilitates her acceptance of timely intervention. Many of my colleagues do not use progesterone measurement because they prefer to rely on clinical assessment, serial hCG measurement, and ultrasound results to guide their treatment. I agree with Dr. Hull that serial hCG measurements are most useful when the same laboratory performs all the tests. Dr. Goldstein, a world class expert in the evaluation and management of early pregnancy problems, provides great advice for all readers on how to best integrate ultrasonography in their practices to optimize patient care.

Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

“STOP USING THE HCG DISCRIMINATORY ZONE OF 1,500 TO
2,000 mIU/mL TO GUIDE INTERVENTION DURING EARLY PREGNANCY”
ROBERT L. BARBIERI, MD (EDITORIAL; JANUARY 2015)

Defining “abnormal rise” is the elephant in the room
It was refreshing to read Dr. Barbieri’srecent editorial on the management of ectopic pregnancies based on human chorionic gonadotropin (hCG) levels. However, I feel there’s an elephant in the room. The phrase “abnormal rise” is not clearly defined, even though countless texts and review articles continue to use the phrase. In fact, many authors include a flow chart in which an abnormal rise usually is followed by a recommendation to empty the uterus in an attempt to find chorionic villi.^1,2 The most recent versions of several widely used textbooks advocate this practice,^3–5 and a current UpToDate article includes a flow chart suggesting that a “suboptimal rise” is sufficient for diagnosis of an abnormal pregnancy requiring treatment.⁶  

Kadar and colleagues originally suggested that 85% of viable intrauterine pregnancies (IUPs) will have a rise in hCG levels of at least 66% every 48 hours, leading to what is commonly called the “doub­ling rule.”⁷ Barnhart and colleagues showed that the slowest recorded hCG rise for a viable pregnancy in 48 hours was 53%, demonstrating that the hCG level does not double in 48 to 72 hours as traditionally expected.⁸ In their final model, the authors calculated that 99% percent of normal IUPs should have an increase of at least 53% in 2 days, moving the bar for a “normal” hCG rise even lower. This also implies that 1% of viable IUPs may have a rise of less than 53% over 2 days. I have to wonder how many viable, wanted pregnancies have been interrupted by the misguided use of discriminatory zones or abnormal rises resulting in the emptying of the pregnant uterus?

Clinical assessment and ultrasonography should continue to be the mainstay of management of ectopic pregnancy. When surgical diagnosis is needed, laparoscopy should be considered. In this day and age, when we are being more cautious about emptying a uterus based on ultrasound measurements of the fetus or gestational sac, why are we still so eager to base that decision on laboratory values? Are we really willing to accept that 1% of the time we will be terminating a viable pregnancy? We should stop the continued propagation of flow charts and strategies that use hCG discriminatory zones or abnormal rises to determine viability and when to evacuate the uterus. A contemporary update to address the issue is needed.
Devin Namaky, MD
Cincinnati, Ohio

References
1. Seeber B, Barnhart K. Suspected ectopic pregnancy. Obstet Gynecol. 2006;107(2):399–413.

2. Mukul LV, Teal SB. Current management of ectopic pregnancy. Obstet Gynecol Clin North Am. 2007;34(3):403–419.

3. Ectopic pregnancy. In: Hoffman BL, Schorge JP, Schaffer JI, et al, eds. Williams Gynecology. 2nd ed. New York, NY: McGraw-Hill Professional; 2012:198–218.

4. Lobo RA. Ectopic pregnancy. In: Lentz GM, ed. Comprehensive Gynecology. 6th ed. Philadelphia, PA: Elsevier Mosby; 2012:361–382 .

5. Damario MA, Rock JA. Ectopic pregnancy. In: Rock JA, Jones HW III, eds. Te Linde’s Operative Gynecology. 10th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008:798–824.

6. Tulandi T. Ectopic pregnancy: clinical manifestations and diagnosis. UpToDate Web site. http://www.uptodate.com/contents/ectopic-pregnancy-clinical-manifestations-and-diag nosis. Updated October 22, 2014. Accessed February 18, 2015. 

7. Kadar N, Caldwell BV, Romera R. A method of screening for ectopic pregnancy and its indications. Obstet Gynecol. 1981;58(2):162–166.

8. Barnhart KT, Sammel MD, Rinaudo PF, Zhou L, Hummel AC, Guo W. Symptomatic patients with an early viable intrauterine pregnancy: hCG curves redefined. Obstet Gynecol. 2004;104(1):50–55.

Why not use serum progesterone to determine early pregnancy viability?

I read with attention Dr. Barbieri’s recent editorial about evaluation of early pregnancy. My question is: Why is serum progesterone not recommended or used to assess the health of an early pregnancy?

In my practice, I always use a serum progesterone test along with hCG measurements to ascertain if an early pregnancy is healthy. I have observed, as biased as this observation can be, as I have not done any study about it, that a serum progesterone level above 12 ng/dL correlates quite well with a healthy pregnancy. I only follow more intensively with serial ultrasonography and hCG measurements in a patient whose progesterone level is below 11 ng/dL.

When a patient’s only symptom is bleeding, if the serum progesterone level is below 11 ng/dL, and her serum quantitative hCG level does not double as appropriate, I consider the pregnancy not normal and counsel the patient about continuing observation or terminating the pregnancy.

In the same laboratory scenario but with a patient who has bleeding and pain, and even moreso if the progesterone level is below 8 ng/dL, I strongly consider an ectopic pregnancy until it is proven otherwise. In this case, I offer treatment with methotrexate, as it’s my experience that the vast majority of these patients are carrying an abnormal pregnancy— either a spontaneous abortion or an ectopic pregnancy. Methotrexate therapy will prevent further complications without causing the loss of normal pregnancies.

For me, progesterone levels add one more piece to the puzzle. A patient with pain, vaginal bleeding, a quantitative hCG value of
500 mIU/mL, and a serum progesterone level of 20 ng/dL will have a normal pregnancy and is not a candidate for any intervention besides a follow-up hCG measurement to ascertain “doubling” of the analyte as expected in a normal pregnancy.

An asymptomatic patient whose quantitative hCG measurement is 1,000 mIU/mL and progesterone level is 4 ng/dL is carrying an abnormal pregnancy. If this quantitative hCG does not double appropriately in the follow-up, I counsel the patient about the greater chance of a spontaneous abortion or ectopic pregnancy.

Is this approach faulty?
Tomas Hernandez, MD
Pasco, Washington

Know the sensitivity of the HCG test

I found Dr. Barbieri’s editorial very timely. It brings some clarity to the use of the hCG discriminatory zone in symptomatic pregnant patients.

An additional important point is that it is the clinician’s obligation to know the sensitivity of the test the laboratory uses. Serum tests use the threshold for a negative result of either less than 1 mIU/mL or less than 5 mIU/mL. If possible, serial hCG measurements should be performed in the same laboratory, because the result may not represent a true change in the hCG concentration if the second test is performed at a different laboratory.¹ This is especially important when the clinician is considering the use of methotrexate to treat a suspected ectopic pregnancy.
Magdalen E. Hull, MD, MPH
Great River, New York

Reference
1. Meriko Mori K, Lurain, JR. Human chorionic gonadotropin: testing in pregnancy and gestational trophoblastic disease and causes of low persistent levels. UpToDate. http://www.uptodate.com/contents/human-chorionic-gonadotropin-testing-in-pregnancy-and-gesta tional-trophoblastic-disease-and-causes-of-low-persistent-levels. Published October 23, 2013. Accessed January 29, 2015.

Further thoughts on HCG, ultrasound, and early pregnancy diagnosis

I want to thank Dr. Barbieri for his important, timely message about suspected nonviable pregnancy. I agree with virtually all of his excellent suggestions. In fact, I was part of the consensus panel that developed the findings diagnostic of and suggestive of IUP failure.1 There are a few points, however, that I believe the readership of OBG Management should know.

The endothelial heart tube, the first organ system to form, folds in on itself and begins to beat at 21 days postconception. Thus, it is present and beating prior to our ability to image it on transvaginal ultrasound. Yet new guidelines¹ now say not to call an IUP failed until there is a crown-rump length of 7 mm or greater with no cardiac activity. In the past, many clinicians used 4 or 5 mm. In fact, one of the most recent studies utilizing an 8-mHz transducer found all cardiac activity was visualized by 3.1 mm embryonic size!²

So why has the number been increased to 7 mm? I’ve given this a lot of thought. Most clinical trials, from which guidelines were derived in the past, were well-designed, tightly controlled, and performed by better-trained clinicians, often with state-of-the-art equipment. In contrast, well-meaning health-care providers practicing in the field are often without the same level of quality control, equipment, or expertise but are still expected to duplicate the data from the trials used to create the guidelines. The reason this is relevant pertains to the statement that 94% of 291 cases of ectopic pregnancy had an adnexal mass.³ This is an excellent study, done at one of the nation’s most outstanding academic institutions by world-class sonologists. I do not believe that well-meaning clinicians in the field will be able to achieve this level of detection.

Dr. Barbieri also discusses an inability to see an IUP even when hCG levels are greater than 1,500 or 2,000 mIU/mL or above. He mentions obesity, fibroids, and adenomyosis as increasing the risk of an ultrasound failing to detect an early IUP. This point needs to be expanded upon. Twenty-seven years ago, we claimed a discriminatory level of 1,025 mIU/mL of hCG if the gestational sac was normal and the uterus was normal with normal echo patterns. We had three cases with markedly greater hCG levels (one, in fact, as high as 5,544 mIU/mL)with coexisting fibroids.⁴

I would also submit that it is the axial uterus that is a very important source of potential error. The closer the beam of sound coming off of the footprint is to a right angle with the endometrium (as it will be in a markedly anteverted or retroverted uterus), the better the resulting image. With an axial uterus, the endometrium is in the same plane as the beam of sound, and this diminishes imaging capability. Furthermore, twin pregnancies are a potential confounder in attempting to correlate hCG levels in transvaginal ultrasound findings.

I wholeheartedly agree with Dr. Barbieri: There is virtually no role to administer methotrexate based on a single hCG determination in a hemodynamically stable patient.
Steven R. Goldstein, MD
New York, New York

References
1. Doubilet PM, Benson CB, Bourne T, Blaivas M; Society of Radiologists in Ultrasound Multispecialty Panel on Early First Trimester Diagnosis of Miscarriage and Exclusion of a Viable Intrauterine Pregnancy. Diagnostic criteria for nonviable pregnancy early in the first trimester. N Engl J Med. 2013;369(15):1443–1451.

2. Abaid LN, As-Sanie S, Wolfe HM. Relationship between crown-rump length and early detection of cardiac activity. J Reprod Med. 2007;52(5):375–378.

3. Frates MC, Doubilet PM, Peters HE, Benson CR. Adnexal sonographic findings in ectopic pregnancy and their correlation with tubal rupture and human chorionic gonadotropin levels. J Ultrasound Med. 2014;33(4):697–703.

4. Goldstein SR, Snyder JR, Watson C, Danon M. Very early pregnancy detection with endovaginal ultrasound. Obstet Gynecol. 1988;72(2):200–204.

‡‡Dr. Barbieri responds
Dr. Namaky, Dr. Hernandez, Dr. Hull, and Dr. Goldstein provide great clinical advice for readers. I agree with Dr. Namaky that the mainstays of managing a pregnancy of unknown location in a stable patient are clinical assessment and ultrasonography. Dr. Hernandez recommends using the serum progesterone measurement to help guide clinical decisions in a pregnancy of unknown location. I also use serum progesterone in my practice because a very low progesterone level helps the patient to understand that she has a failed pregnancy, and facilitates her acceptance of timely intervention. Many of my colleagues do not use progesterone measurement because they prefer to rely on clinical assessment, serial hCG measurement, and ultrasound results to guide their treatment. I agree with Dr. Hull that serial hCG measurements are most useful when the same laboratory performs all the tests. Dr. Goldstein, a world class expert in the evaluation and management of early pregnancy problems, provides great advice for all readers on how to best integrate ultrasonography in their practices to optimize patient care.

Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Letter to the Editor

Is Hemolysis a Clinical Marker of Propionibacterium acnes Orthopedic Infection or a Phylogenetic Marker?

We read with great interest the study by Nodzo and colleagues in the May 2014 issue of The American Journal of Orthopedics on hemolysis as a clinical marker for Propionibacterium acnes orthopedic infection.¹ We agree with the authors that determining if a P acnes culture is a true infection or a contaminant remains a challenge. Although P acnes is described as a commensal bacterium with a low pathogenicity, its involvement has been reported in many clinical entities, especially device-related infections.²P acnes is usually the cause of delayed infections occurring 3 to 24 months or more after prosthesis placement. The rate of P acnes involvement, probably underestimated, is about 10%.³ Although this bacterium was considered to be a contaminant, several virulence factors have been recently identified: putative hemolysins or cytotoxins (CAMP factors, hemolysin III) and enzymes putatively involved in degrading host tissue or molecules (GehA lipase, lysophospholipase, hyaluronate lyase, endoglycoceramidase, etc).⁴

Interestingly, Nodzo and colleagues revealed that 13 out of 22 P acnes strains were hemolytic and, among them, 10 were considered as definite infections, including 3 with only 1 positive sample. The authors could not identify a statistically significant trend, probably because their study was underpowered due to the size of this case series, as discussed by the authors. Nevertheless, the hemolytic activity of the strains was investigated in the 1980s by adding different concentrations of blood obtained from rabbits, sheep, or humans.⁵ The hemolytic activity was recorded as positive when a clear, colorless zone around the colonies appeared or weak when slight and incomplete hemolysis under the colonies was found.⁵ Depending on the erythrocyte origin, differences in the lytic action of hemolysin or cytotoxin may indicate the existence of various enzymes. These enzymes could have different levels of production and provide a distinct hemolytic profile. This hemolytic activity observation could also be correlated to the genetic background of the isolates.

In fact, from a genetic and epidemiological point of view, the sequence analysis of recA gene distinguished 2 distinct lineages of P acnes: types I and II.⁴ The association of some strains with specific clinical presentations was also demonstrated. Later, McDowell and colleagues⁶ reported 5 main phylogenetically distinct groups: IA, IB, IC, II, and III. It would have been interesting to know the phylogenetic groups of the strains tested in the study by Nodzo and coauthors, especially as Sampedro and colleagues⁷ recently reported more phylogenetic groups IA and IB among P acnes strains involved in bone and joint infections. Both of these phylotypes are hemolytic, unlike phylotypes II and III, less often encountered in this clinical entity as reported recently.⁸ We agree with the authors that hemolytic behavior may be one of the key factors in the variability in the pathogenicity of P acnes strains, suggesting that some strains could be more aggressive than others during deep infection. Another feature is likely the biofilm-production ability of the strains.^9,10

According to our experience, the hemolysis behavior was slightly different depending on which blood agar plates were used to detect hemolytic properties. We have selected 8 isolates or reference ATCC strains from different phylotypes. Each isolate was seeded on 5 different blood agar plates with erythrocyte from various origins (Table). We can confirm that only strains belonging to IA and IB phylotypes were hemolytic, with different behavior as previously reported (Figure).⁸ Similarly, within IA phylotype strains, the hemolytic property could be different suggesting a difference in the genetic background. However, as the genes encoding all 5 CAMP factors are present in all P acnes groups studied by Valanne and colleagues¹¹ (IA, IB, and II), observed differences reflected different levels of expression rather than missing genes. Moreover, when camp2 or camp4 genes were deleted, the ∆camp2 but not the ∆camp4 mutant exhibited reduced hemolytic activity with sheep erythrocytes, indicating that CAMP factor 2 seems to be the major active cohemolytic factor, but in an IA phylotype P acnes genetic background.¹²

To conclude, the link between hemolysis and P acnes deep infection remains controversial and complex. The phenotypic differences observed between strains from various types reflect deeper differences in their phylogeny. The hemolytic ability raises the possibility that strains may also display a specific behavior according to their type and variation in their expression of putative virulence factors, including hemolysin, cytotoxin, or lipase. Further studies are clearly needed to better understand the virulence and phylogeny of P acnes strains in order to distinguish contamination from bone infection.

Stéphane Corvec, PharmD, PhD, Jérémy Luchetta, MSc, and Guillaume Ghislain Aubin, PharmD

Nantes University Hospital, Microbiology Laboratory, Nantes, France

Authors’ Response

Corvec and colleagues wrote an interesting summary and make excellent points about the role of hemolysis in Propionibacterium acnes. P acnes upper extremity infection has become an increasingly recognized problem, and determining whether a P acnes culture represents a true infection or a contaminant is still a challenge. We performed this study in hopes of finding an easily usable characteristic of P acnes that would assist the clinician in identifying P acnes strains as true infections rather than contaminants.

Certain pathogenic characteristics of P acnes have been identified, but the clinical implications of this bacterium are still being evaluated. We recognize that the hemolysis phenotype is a characteristic, and may not be the main pathogenic feature, of certain phylotypes of P acnes. It is possible the hemolytic strains in our study were from the IA and IB phylotypes, but, unfortunately, we did not specifically evaluate for phylogeny in our study. This would have correlated well with the work of Sampedro and colleagues,¹ which suggested most deep bone and joint infections occur with type IA and IB P acnes phylotypes. Although less common in orthopedic infections, the type II and III phylotypes of P acnes are also capable of causing deep infection, and may not cause a hemolytic reaction on blood agar, which may be why we had some patients classified as a definite infection that did not have a hemolytic strain of P acnes. It is also possible a hemolytic strain may truly be a contaminant, but we did not observe this in our small case series. A larger series may help elucidate this finding, but the majority of truly infected patients in our case series had a hemolytic P acnes phenotype.

The type of blood agar used could have also influenced our results, as noted in the Table in Corvec and colleagues’ letter. We observed the most robust hemolysis on brucella blood agar, and limited hemolysis on CDC (Centers for Disease Control and Prevention) anaerobe blood agar; however, we did not evaluate multiple different blood agar preparations, which could have identified more hemolytic strains.

In our study, the presence of hemolysis was helpful in determining whether or not a true infection existed, but the absence of the hemolytic phenotype did not offer much additional information. The hemolytic phenotype may be a potential marker for those strains that are more aggressive and possibly represent the IA and IB phylotypes, which, as previously stated, are more commonly found in deep bone and joint infections.¹ Hemolysis may serve as a surrogate marker for determining these phylotypes since determining phylogeny in a hospital laboratory is burdensome and not possible in most institutions. 

In summary, we agree the hemolytic phenotype is commonly observed in certain P acnes phylotypes, and that not all upper extremity orthopedic P acnes infections will have a hemolytic finding. The genetic differences in P acnes strains are complex, and finding a marker of truly pathogenic strains has yet to be established. Larger studies evaluating the clinical outcomes and laboratory findings of patients with and without hemolytic strains of P acnes and evaluating which blood agar is the best at identifying the hemolytic phenotype may be beneficial. Identifying or combining multiple clinical and microbe-specific characteristics may also help guide treatment recommendations when a positive P acnes culture is identified.

Scott R. Nodzo, MD
John K. Crane, MD, PhD
Thomas R. Duquin, MD
Department of Orthopedics
University at Buffalo
Buffalo, NY

Letter to the Editor

Is Hemolysis a Clinical Marker of Propionibacterium acnes Orthopedic Infection or a Phylogenetic Marker?

We read with great interest the study by Nodzo and colleagues in the May 2014 issue of The American Journal of Orthopedics on hemolysis as a clinical marker for Propionibacterium acnes orthopedic infection.¹ We agree with the authors that determining if a P acnes culture is a true infection or a contaminant remains a challenge. Although P acnes is described as a commensal bacterium with a low pathogenicity, its involvement has been reported in many clinical entities, especially device-related infections.²P acnes is usually the cause of delayed infections occurring 3 to 24 months or more after prosthesis placement. The rate of P acnes involvement, probably underestimated, is about 10%.³ Although this bacterium was considered to be a contaminant, several virulence factors have been recently identified: putative hemolysins or cytotoxins (CAMP factors, hemolysin III) and enzymes putatively involved in degrading host tissue or molecules (GehA lipase, lysophospholipase, hyaluronate lyase, endoglycoceramidase, etc).⁴

Interestingly, Nodzo and colleagues revealed that 13 out of 22 P acnes strains were hemolytic and, among them, 10 were considered as definite infections, including 3 with only 1 positive sample. The authors could not identify a statistically significant trend, probably because their study was underpowered due to the size of this case series, as discussed by the authors. Nevertheless, the hemolytic activity of the strains was investigated in the 1980s by adding different concentrations of blood obtained from rabbits, sheep, or humans.⁵ The hemolytic activity was recorded as positive when a clear, colorless zone around the colonies appeared or weak when slight and incomplete hemolysis under the colonies was found.⁵ Depending on the erythrocyte origin, differences in the lytic action of hemolysin or cytotoxin may indicate the existence of various enzymes. These enzymes could have different levels of production and provide a distinct hemolytic profile. This hemolytic activity observation could also be correlated to the genetic background of the isolates.

In fact, from a genetic and epidemiological point of view, the sequence analysis of recA gene distinguished 2 distinct lineages of P acnes: types I and II.⁴ The association of some strains with specific clinical presentations was also demonstrated. Later, McDowell and colleagues⁶ reported 5 main phylogenetically distinct groups: IA, IB, IC, II, and III. It would have been interesting to know the phylogenetic groups of the strains tested in the study by Nodzo and coauthors, especially as Sampedro and colleagues⁷ recently reported more phylogenetic groups IA and IB among P acnes strains involved in bone and joint infections. Both of these phylotypes are hemolytic, unlike phylotypes II and III, less often encountered in this clinical entity as reported recently.⁸ We agree with the authors that hemolytic behavior may be one of the key factors in the variability in the pathogenicity of P acnes strains, suggesting that some strains could be more aggressive than others during deep infection. Another feature is likely the biofilm-production ability of the strains.^9,10

According to our experience, the hemolysis behavior was slightly different depending on which blood agar plates were used to detect hemolytic properties. We have selected 8 isolates or reference ATCC strains from different phylotypes. Each isolate was seeded on 5 different blood agar plates with erythrocyte from various origins (Table). We can confirm that only strains belonging to IA and IB phylotypes were hemolytic, with different behavior as previously reported (Figure).⁸ Similarly, within IA phylotype strains, the hemolytic property could be different suggesting a difference in the genetic background. However, as the genes encoding all 5 CAMP factors are present in all P acnes groups studied by Valanne and colleagues¹¹ (IA, IB, and II), observed differences reflected different levels of expression rather than missing genes. Moreover, when camp2 or camp4 genes were deleted, the ∆camp2 but not the ∆camp4 mutant exhibited reduced hemolytic activity with sheep erythrocytes, indicating that CAMP factor 2 seems to be the major active cohemolytic factor, but in an IA phylotype P acnes genetic background.¹²

To conclude, the link between hemolysis and P acnes deep infection remains controversial and complex. The phenotypic differences observed between strains from various types reflect deeper differences in their phylogeny. The hemolytic ability raises the possibility that strains may also display a specific behavior according to their type and variation in their expression of putative virulence factors, including hemolysin, cytotoxin, or lipase. Further studies are clearly needed to better understand the virulence and phylogeny of P acnes strains in order to distinguish contamination from bone infection.

Stéphane Corvec, PharmD, PhD, Jérémy Luchetta, MSc, and Guillaume Ghislain Aubin, PharmD

Nantes University Hospital, Microbiology Laboratory, Nantes, France

Authors’ Response

Corvec and colleagues wrote an interesting summary and make excellent points about the role of hemolysis in Propionibacterium acnes. P acnes upper extremity infection has become an increasingly recognized problem, and determining whether a P acnes culture represents a true infection or a contaminant is still a challenge. We performed this study in hopes of finding an easily usable characteristic of P acnes that would assist the clinician in identifying P acnes strains as true infections rather than contaminants.

Certain pathogenic characteristics of P acnes have been identified, but the clinical implications of this bacterium are still being evaluated. We recognize that the hemolysis phenotype is a characteristic, and may not be the main pathogenic feature, of certain phylotypes of P acnes. It is possible the hemolytic strains in our study were from the IA and IB phylotypes, but, unfortunately, we did not specifically evaluate for phylogeny in our study. This would have correlated well with the work of Sampedro and colleagues,¹ which suggested most deep bone and joint infections occur with type IA and IB P acnes phylotypes. Although less common in orthopedic infections, the type II and III phylotypes of P acnes are also capable of causing deep infection, and may not cause a hemolytic reaction on blood agar, which may be why we had some patients classified as a definite infection that did not have a hemolytic strain of P acnes. It is also possible a hemolytic strain may truly be a contaminant, but we did not observe this in our small case series. A larger series may help elucidate this finding, but the majority of truly infected patients in our case series had a hemolytic P acnes phenotype.

The type of blood agar used could have also influenced our results, as noted in the Table in Corvec and colleagues’ letter. We observed the most robust hemolysis on brucella blood agar, and limited hemolysis on CDC (Centers for Disease Control and Prevention) anaerobe blood agar; however, we did not evaluate multiple different blood agar preparations, which could have identified more hemolytic strains.

In our study, the presence of hemolysis was helpful in determining whether or not a true infection existed, but the absence of the hemolytic phenotype did not offer much additional information. The hemolytic phenotype may be a potential marker for those strains that are more aggressive and possibly represent the IA and IB phylotypes, which, as previously stated, are more commonly found in deep bone and joint infections.¹ Hemolysis may serve as a surrogate marker for determining these phylotypes since determining phylogeny in a hospital laboratory is burdensome and not possible in most institutions. 

In summary, we agree the hemolytic phenotype is commonly observed in certain P acnes phylotypes, and that not all upper extremity orthopedic P acnes infections will have a hemolytic finding. The genetic differences in P acnes strains are complex, and finding a marker of truly pathogenic strains has yet to be established. Larger studies evaluating the clinical outcomes and laboratory findings of patients with and without hemolytic strains of P acnes and evaluating which blood agar is the best at identifying the hemolytic phenotype may be beneficial. Identifying or combining multiple clinical and microbe-specific characteristics may also help guide treatment recommendations when a positive P acnes culture is identified.

Scott R. Nodzo, MD
John K. Crane, MD, PhD
Thomas R. Duquin, MD
Department of Orthopedics
University at Buffalo
Buffalo, NY

Letter to the Editor

Is Hemolysis a Clinical Marker of Propionibacterium acnes Orthopedic Infection or a Phylogenetic Marker?

We read with great interest the study by Nodzo and colleagues in the May 2014 issue of The American Journal of Orthopedics on hemolysis as a clinical marker for Propionibacterium acnes orthopedic infection.¹ We agree with the authors that determining if a P acnes culture is a true infection or a contaminant remains a challenge. Although P acnes is described as a commensal bacterium with a low pathogenicity, its involvement has been reported in many clinical entities, especially device-related infections.²P acnes is usually the cause of delayed infections occurring 3 to 24 months or more after prosthesis placement. The rate of P acnes involvement, probably underestimated, is about 10%.³ Although this bacterium was considered to be a contaminant, several virulence factors have been recently identified: putative hemolysins or cytotoxins (CAMP factors, hemolysin III) and enzymes putatively involved in degrading host tissue or molecules (GehA lipase, lysophospholipase, hyaluronate lyase, endoglycoceramidase, etc).⁴

Interestingly, Nodzo and colleagues revealed that 13 out of 22 P acnes strains were hemolytic and, among them, 10 were considered as definite infections, including 3 with only 1 positive sample. The authors could not identify a statistically significant trend, probably because their study was underpowered due to the size of this case series, as discussed by the authors. Nevertheless, the hemolytic activity of the strains was investigated in the 1980s by adding different concentrations of blood obtained from rabbits, sheep, or humans.⁵ The hemolytic activity was recorded as positive when a clear, colorless zone around the colonies appeared or weak when slight and incomplete hemolysis under the colonies was found.⁵ Depending on the erythrocyte origin, differences in the lytic action of hemolysin or cytotoxin may indicate the existence of various enzymes. These enzymes could have different levels of production and provide a distinct hemolytic profile. This hemolytic activity observation could also be correlated to the genetic background of the isolates.

In fact, from a genetic and epidemiological point of view, the sequence analysis of recA gene distinguished 2 distinct lineages of P acnes: types I and II.⁴ The association of some strains with specific clinical presentations was also demonstrated. Later, McDowell and colleagues⁶ reported 5 main phylogenetically distinct groups: IA, IB, IC, II, and III. It would have been interesting to know the phylogenetic groups of the strains tested in the study by Nodzo and coauthors, especially as Sampedro and colleagues⁷ recently reported more phylogenetic groups IA and IB among P acnes strains involved in bone and joint infections. Both of these phylotypes are hemolytic, unlike phylotypes II and III, less often encountered in this clinical entity as reported recently.⁸ We agree with the authors that hemolytic behavior may be one of the key factors in the variability in the pathogenicity of P acnes strains, suggesting that some strains could be more aggressive than others during deep infection. Another feature is likely the biofilm-production ability of the strains.^9,10

According to our experience, the hemolysis behavior was slightly different depending on which blood agar plates were used to detect hemolytic properties. We have selected 8 isolates or reference ATCC strains from different phylotypes. Each isolate was seeded on 5 different blood agar plates with erythrocyte from various origins (Table). We can confirm that only strains belonging to IA and IB phylotypes were hemolytic, with different behavior as previously reported (Figure).⁸ Similarly, within IA phylotype strains, the hemolytic property could be different suggesting a difference in the genetic background. However, as the genes encoding all 5 CAMP factors are present in all P acnes groups studied by Valanne and colleagues¹¹ (IA, IB, and II), observed differences reflected different levels of expression rather than missing genes. Moreover, when camp2 or camp4 genes were deleted, the ∆camp2 but not the ∆camp4 mutant exhibited reduced hemolytic activity with sheep erythrocytes, indicating that CAMP factor 2 seems to be the major active cohemolytic factor, but in an IA phylotype P acnes genetic background.¹²

To conclude, the link between hemolysis and P acnes deep infection remains controversial and complex. The phenotypic differences observed between strains from various types reflect deeper differences in their phylogeny. The hemolytic ability raises the possibility that strains may also display a specific behavior according to their type and variation in their expression of putative virulence factors, including hemolysin, cytotoxin, or lipase. Further studies are clearly needed to better understand the virulence and phylogeny of P acnes strains in order to distinguish contamination from bone infection.

Stéphane Corvec, PharmD, PhD, Jérémy Luchetta, MSc, and Guillaume Ghislain Aubin, PharmD

Nantes University Hospital, Microbiology Laboratory, Nantes, France

Authors’ Response

Corvec and colleagues wrote an interesting summary and make excellent points about the role of hemolysis in Propionibacterium acnes. P acnes upper extremity infection has become an increasingly recognized problem, and determining whether a P acnes culture represents a true infection or a contaminant is still a challenge. We performed this study in hopes of finding an easily usable characteristic of P acnes that would assist the clinician in identifying P acnes strains as true infections rather than contaminants.

Certain pathogenic characteristics of P acnes have been identified, but the clinical implications of this bacterium are still being evaluated. We recognize that the hemolysis phenotype is a characteristic, and may not be the main pathogenic feature, of certain phylotypes of P acnes. It is possible the hemolytic strains in our study were from the IA and IB phylotypes, but, unfortunately, we did not specifically evaluate for phylogeny in our study. This would have correlated well with the work of Sampedro and colleagues,¹ which suggested most deep bone and joint infections occur with type IA and IB P acnes phylotypes. Although less common in orthopedic infections, the type II and III phylotypes of P acnes are also capable of causing deep infection, and may not cause a hemolytic reaction on blood agar, which may be why we had some patients classified as a definite infection that did not have a hemolytic strain of P acnes. It is also possible a hemolytic strain may truly be a contaminant, but we did not observe this in our small case series. A larger series may help elucidate this finding, but the majority of truly infected patients in our case series had a hemolytic P acnes phenotype.

The type of blood agar used could have also influenced our results, as noted in the Table in Corvec and colleagues’ letter. We observed the most robust hemolysis on brucella blood agar, and limited hemolysis on CDC (Centers for Disease Control and Prevention) anaerobe blood agar; however, we did not evaluate multiple different blood agar preparations, which could have identified more hemolytic strains.

In our study, the presence of hemolysis was helpful in determining whether or not a true infection existed, but the absence of the hemolytic phenotype did not offer much additional information. The hemolytic phenotype may be a potential marker for those strains that are more aggressive and possibly represent the IA and IB phylotypes, which, as previously stated, are more commonly found in deep bone and joint infections.¹ Hemolysis may serve as a surrogate marker for determining these phylotypes since determining phylogeny in a hospital laboratory is burdensome and not possible in most institutions. 

In summary, we agree the hemolytic phenotype is commonly observed in certain P acnes phylotypes, and that not all upper extremity orthopedic P acnes infections will have a hemolytic finding. The genetic differences in P acnes strains are complex, and finding a marker of truly pathogenic strains has yet to be established. Larger studies evaluating the clinical outcomes and laboratory findings of patients with and without hemolytic strains of P acnes and evaluating which blood agar is the best at identifying the hemolytic phenotype may be beneficial. Identifying or combining multiple clinical and microbe-specific characteristics may also help guide treatment recommendations when a positive P acnes culture is identified.

Scott R. Nodzo, MD
John K. Crane, MD, PhD
Thomas R. Duquin, MD
Department of Orthopedics
University at Buffalo
Buffalo, NY

As orthopedic surgeons, we typically equate a quality outcome with the patient’s end result—resolved or diminished functional disability, fracture union, and/or pain relief, to name a few metrics. Although research has not identified a clear link between quality outcomes and patient satisfaction scores, patient satisfaction is increasingly used as a proxy for quality of care. It’s speculated that more personal care may result in better communication, more reasonable expectations, and more patient involvement, all of which may result in better quality of care. Regardless, it’s unclear whether satisfaction is an attribute of quality care or an indicator.

In a recent article in Modern Healthcare, Irwin Press,¹ cofounder of Press Ganey, challenges any campaign to cast doubt on satisfaction as a relevant indicator of quality care: “It can be argued that diagnostic procedures, surgeries and therapies constitute treatment, but not care. Treatment alone isn’t care…. One is objective, involving highly standardized technical, mechanical or chemical interventions. The other is subjective, composed of behaviors, decisions and interactions of humans with idiosyncratic personalities, stresses, agendas and sensitivities.”

As surgeons, we understandably focus on objective treatment and outcome and may underappreciate the importance of the process—the experience of care. Wellness probably requires mastery of both. Indeed, just as a patient’s poor coping skills, depression, anxiety, and proclivity to catastrophize may compromise their recovery and self-reported assessments of outcome,^2-5 so too do the qualitative components of our interaction with patients undoubtedly impact, not only their experience, but also their recovery. Patient self-efficacy (the feeling that they can do it), engagement (“activation”), compliance, and expectations all derive in part from the “Art” of our practice. Our “Heart” is as important to that Art, if not more so, than our “Head” (our intellect and knowledge). Whether we buy into this or not is a matter of personal opinion and experience, I suppose, but the reality is that the important singular metric of patient satisfaction is here to stay—patient satisfaction has become an important component of pay-for-performance metrics which expressly intend to reward quality over volume.

What does this mean for us? First, we need to adapt to the reality that the patient’s perception of their interaction with us impacts their experience and their level of satisfaction, and accept our role in their overall perception of quality. Being rewarded with a high satisfaction score is within our sphere of influence and requires more than just providing a good objective outcome. We might not revisit a restaurant with great food but lousy service and an underwhelming environment. We might also never eat at a place that was really nice inside and had great service, but which provided horrible food. So we must aspire to provide both objective quality outcomes and stellar patient care. As third-party payers increasingly follow the lead of the Centers for Medicare and Medicaid Services (CMS), the patient will not be at our table unless we both ask for feedback and respond to it. We all aspire to be great technicians and have a command of the knowledge base in our respective areas of practice. Some of us are privileged to have earned regional, national, or international reputations among our peers, but we all will be increasingly judged based on patient satisfaction with our care. This means that we must care about their experience and how they perceive our care: Do we spend enough time, listen attentively, answer questions, and explain the diagnosis and plan?

Just as we may hold our breath unknowingly during stressful situations when we are not mindful, so too might our “Heart” not be clearly evident in the complex health care environment today—too little time, too much paperwork, increasing patient demands. But practicing with heightened self-awareness, empathy, and unambiguous intention, and modeling our values during our interaction with our patients—“mindful practice”—is increasingly advocated as a necessary component to “best practice.” For truly rewarding practice, during which we can attain not only great results but also satisfied patients, we need to revisit why we do what we do, and rebalance our emphasis on what we do and how we do it. Mindful practice is both an objective and a strategy. It may require making structural adjustments to our practice, such as seeing fewer patients per hour, for, perhaps, an hour or two more in a day, completing some of our electronic medical record notes at day’s end, and maybe adding an extra clinic day every other week. We must also deliberately solicit feedback from our patients so that we can respond to any perceived room for improvement.

Thirteen years ago when I received my Master of Business Administration (MBA) degree, I felt that improving operational efficiency would enable me to do more in a day—and it did. But when patient satisfaction becomes the proxy for quality, sound business practice may not translate into sound clinical practice. After 21 years of practice, and deliberate attentiveness to patient feedback, I am increasingly aware that the Art of practice is as important as the Science—our Heart is as important as our Head. In this light, patient satisfaction is a very sound metric for quality.

As orthopedic surgeons, we typically equate a quality outcome with the patient’s end result—resolved or diminished functional disability, fracture union, and/or pain relief, to name a few metrics. Although research has not identified a clear link between quality outcomes and patient satisfaction scores, patient satisfaction is increasingly used as a proxy for quality of care. It’s speculated that more personal care may result in better communication, more reasonable expectations, and more patient involvement, all of which may result in better quality of care. Regardless, it’s unclear whether satisfaction is an attribute of quality care or an indicator.

In a recent article in Modern Healthcare, Irwin Press,¹ cofounder of Press Ganey, challenges any campaign to cast doubt on satisfaction as a relevant indicator of quality care: “It can be argued that diagnostic procedures, surgeries and therapies constitute treatment, but not care. Treatment alone isn’t care…. One is objective, involving highly standardized technical, mechanical or chemical interventions. The other is subjective, composed of behaviors, decisions and interactions of humans with idiosyncratic personalities, stresses, agendas and sensitivities.”

As surgeons, we understandably focus on objective treatment and outcome and may underappreciate the importance of the process—the experience of care. Wellness probably requires mastery of both. Indeed, just as a patient’s poor coping skills, depression, anxiety, and proclivity to catastrophize may compromise their recovery and self-reported assessments of outcome,^2-5 so too do the qualitative components of our interaction with patients undoubtedly impact, not only their experience, but also their recovery. Patient self-efficacy (the feeling that they can do it), engagement (“activation”), compliance, and expectations all derive in part from the “Art” of our practice. Our “Heart” is as important to that Art, if not more so, than our “Head” (our intellect and knowledge). Whether we buy into this or not is a matter of personal opinion and experience, I suppose, but the reality is that the important singular metric of patient satisfaction is here to stay—patient satisfaction has become an important component of pay-for-performance metrics which expressly intend to reward quality over volume.

What does this mean for us? First, we need to adapt to the reality that the patient’s perception of their interaction with us impacts their experience and their level of satisfaction, and accept our role in their overall perception of quality. Being rewarded with a high satisfaction score is within our sphere of influence and requires more than just providing a good objective outcome. We might not revisit a restaurant with great food but lousy service and an underwhelming environment. We might also never eat at a place that was really nice inside and had great service, but which provided horrible food. So we must aspire to provide both objective quality outcomes and stellar patient care. As third-party payers increasingly follow the lead of the Centers for Medicare and Medicaid Services (CMS), the patient will not be at our table unless we both ask for feedback and respond to it. We all aspire to be great technicians and have a command of the knowledge base in our respective areas of practice. Some of us are privileged to have earned regional, national, or international reputations among our peers, but we all will be increasingly judged based on patient satisfaction with our care. This means that we must care about their experience and how they perceive our care: Do we spend enough time, listen attentively, answer questions, and explain the diagnosis and plan?

Just as we may hold our breath unknowingly during stressful situations when we are not mindful, so too might our “Heart” not be clearly evident in the complex health care environment today—too little time, too much paperwork, increasing patient demands. But practicing with heightened self-awareness, empathy, and unambiguous intention, and modeling our values during our interaction with our patients—“mindful practice”—is increasingly advocated as a necessary component to “best practice.” For truly rewarding practice, during which we can attain not only great results but also satisfied patients, we need to revisit why we do what we do, and rebalance our emphasis on what we do and how we do it. Mindful practice is both an objective and a strategy. It may require making structural adjustments to our practice, such as seeing fewer patients per hour, for, perhaps, an hour or two more in a day, completing some of our electronic medical record notes at day’s end, and maybe adding an extra clinic day every other week. We must also deliberately solicit feedback from our patients so that we can respond to any perceived room for improvement.

Thirteen years ago when I received my Master of Business Administration (MBA) degree, I felt that improving operational efficiency would enable me to do more in a day—and it did. But when patient satisfaction becomes the proxy for quality, sound business practice may not translate into sound clinical practice. After 21 years of practice, and deliberate attentiveness to patient feedback, I am increasingly aware that the Art of practice is as important as the Science—our Heart is as important as our Head. In this light, patient satisfaction is a very sound metric for quality.

As orthopedic surgeons, we typically equate a quality outcome with the patient’s end result—resolved or diminished functional disability, fracture union, and/or pain relief, to name a few metrics. Although research has not identified a clear link between quality outcomes and patient satisfaction scores, patient satisfaction is increasingly used as a proxy for quality of care. It’s speculated that more personal care may result in better communication, more reasonable expectations, and more patient involvement, all of which may result in better quality of care. Regardless, it’s unclear whether satisfaction is an attribute of quality care or an indicator.

In a recent article in Modern Healthcare, Irwin Press,¹ cofounder of Press Ganey, challenges any campaign to cast doubt on satisfaction as a relevant indicator of quality care: “It can be argued that diagnostic procedures, surgeries and therapies constitute treatment, but not care. Treatment alone isn’t care…. One is objective, involving highly standardized technical, mechanical or chemical interventions. The other is subjective, composed of behaviors, decisions and interactions of humans with idiosyncratic personalities, stresses, agendas and sensitivities.”

As surgeons, we understandably focus on objective treatment and outcome and may underappreciate the importance of the process—the experience of care. Wellness probably requires mastery of both. Indeed, just as a patient’s poor coping skills, depression, anxiety, and proclivity to catastrophize may compromise their recovery and self-reported assessments of outcome,^2-5 so too do the qualitative components of our interaction with patients undoubtedly impact, not only their experience, but also their recovery. Patient self-efficacy (the feeling that they can do it), engagement (“activation”), compliance, and expectations all derive in part from the “Art” of our practice. Our “Heart” is as important to that Art, if not more so, than our “Head” (our intellect and knowledge). Whether we buy into this or not is a matter of personal opinion and experience, I suppose, but the reality is that the important singular metric of patient satisfaction is here to stay—patient satisfaction has become an important component of pay-for-performance metrics which expressly intend to reward quality over volume.

What does this mean for us? First, we need to adapt to the reality that the patient’s perception of their interaction with us impacts their experience and their level of satisfaction, and accept our role in their overall perception of quality. Being rewarded with a high satisfaction score is within our sphere of influence and requires more than just providing a good objective outcome. We might not revisit a restaurant with great food but lousy service and an underwhelming environment. We might also never eat at a place that was really nice inside and had great service, but which provided horrible food. So we must aspire to provide both objective quality outcomes and stellar patient care. As third-party payers increasingly follow the lead of the Centers for Medicare and Medicaid Services (CMS), the patient will not be at our table unless we both ask for feedback and respond to it. We all aspire to be great technicians and have a command of the knowledge base in our respective areas of practice. Some of us are privileged to have earned regional, national, or international reputations among our peers, but we all will be increasingly judged based on patient satisfaction with our care. This means that we must care about their experience and how they perceive our care: Do we spend enough time, listen attentively, answer questions, and explain the diagnosis and plan?

Just as we may hold our breath unknowingly during stressful situations when we are not mindful, so too might our “Heart” not be clearly evident in the complex health care environment today—too little time, too much paperwork, increasing patient demands. But practicing with heightened self-awareness, empathy, and unambiguous intention, and modeling our values during our interaction with our patients—“mindful practice”—is increasingly advocated as a necessary component to “best practice.” For truly rewarding practice, during which we can attain not only great results but also satisfied patients, we need to revisit why we do what we do, and rebalance our emphasis on what we do and how we do it. Mindful practice is both an objective and a strategy. It may require making structural adjustments to our practice, such as seeing fewer patients per hour, for, perhaps, an hour or two more in a day, completing some of our electronic medical record notes at day’s end, and maybe adding an extra clinic day every other week. We must also deliberately solicit feedback from our patients so that we can respond to any perceived room for improvement.

Thirteen years ago when I received my Master of Business Administration (MBA) degree, I felt that improving operational efficiency would enable me to do more in a day—and it did. But when patient satisfaction becomes the proxy for quality, sound business practice may not translate into sound clinical practice. After 21 years of practice, and deliberate attentiveness to patient feedback, I am increasingly aware that the Art of practice is as important as the Science—our Heart is as important as our Head. In this light, patient satisfaction is a very sound metric for quality.

Hoping to learn a bit more about the apparently healthy 8-year-old who has been deposited in your exam room for his biannual checkup, you take the opportunity to ask him a few questions with his mother in the waiting room. “So, Jason, what do you like to do for fun?”

“Well, yesterday I started a fire with my buddy Rudy, and we burned a whole bunch of sticks and stuff.”

“Does your mother know about this?”

“She wasn’t around, but I think so. We’ve done it a bunch of times before.”

Okay, here you are with an 8-year-old pyromaniac whose parents are clearly under-supervising him. Who do you call first? The folks at Child Protective Services or the State Fire Marshall’s Office? Clearly, he and your community are at significant risk.

If you were practicing in Wrexham, a town in North Wales, you would continue your questioning with, “So you like to go to The Land after school? I’ve heard it’s a fun place?”

The Land is 3-year-old adventure playground that I learned about in a thought-provoking article in The Atlantic (The Overprotected Kid, by Hanna Rosin, April 2014). The nearly acre-sized site would look like a junkyard to any adult whose imagination has atrophied with age. Strewn with used tires, wooden palettes, dirty old mattresses, and decrepit lawn furniture, it provides endless opportunities for children to create their own places for play and adventure. By stacking, rolling, hammering together, and rearranging the loose detritus of society, children can transform the junk into an ever-changing landscape for fun. A fire pit and an old oil drum – among the most popular items – are often smoldering with fires the children have started. The filthy mattresses become trampolines. The children are observed by professionally trained “playworkers” who are continually updating the risk assessments of the activities that were begun prior to the opening of the facility. The observers seldom have to intervene. Other than a few scraped knees, no children have been injured.

Although adventure playgrounds were relatively common in the U.K. during the 1940’s, their popularity faded until the last few years when they have enjoyed a modest resurgence. In the article in The Atlantic, author Hanna Rosin chronicles the de-riskification of playgrounds in America that began in the 1970’s. The process was fueled by an unfortunate incident in which a toddler supervised by his mother fell off a 12-foot playground slide in a Chicago playground. The child sustained a significant and permanent brain injury and received a multimillion dollar award in the suit that followed.

A commentary in Pediatrics entitled “X-rated playgrounds?” (Pediatrics 1979;64:961) and a crusade by its author, Theodora Briggs Sweeney culminated in the release of the Handbook for Public Playground Safety (U.S. Consumer Product Safety Commission, 1981) which listed in minute detail guidelines for dimensions and materials for playground equipment and play surfaces. Although these were only “guidelines,” only the most foolish manufacturer would ignore them. Little thought was given to the validity of the alarming statistics that had prompted these changes. What were the denominators? Can you compare 1970’s hospital data with those from the 1950’s when injured children were managed at home or in their doctors’ offices?

Regardless of the validity of the data, the result was that these redesigned playgrounds offered so little sense of risk that they were abandoned by all but the youngest children. Numerous studies suggest that by eliminating risk or at least the appearance of risk, we are robbing children of important learning experiences on which they can build fuller, more creative, successful, and less anxiety-dominated lives. I urge you to look at that Atlantic article for a more robust description of the evidence.

I suspect that you may be a bit uncomfortable with 8-year-old boys playing with fire, but do you agree that we need to seriously rethink our attempts to protect children from the ordinary risks of an active life? Or do you think those of us who believe children will benefit from more perceived risk are just a bunch of fogys who begin every other sentence, “When I was your age ... .”

Do you encourage parents to allow their children to walk to school unattended? Do you caution parents about being overprotective? Have I ignited a spark of concern in you, or am I just playing with fire?

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “Coping with a Picky Eater.” E-mail him at [email protected].

Hoping to learn a bit more about the apparently healthy 8-year-old who has been deposited in your exam room for his biannual checkup, you take the opportunity to ask him a few questions with his mother in the waiting room. “So, Jason, what do you like to do for fun?”

“Well, yesterday I started a fire with my buddy Rudy, and we burned a whole bunch of sticks and stuff.”

“Does your mother know about this?”

“She wasn’t around, but I think so. We’ve done it a bunch of times before.”

Okay, here you are with an 8-year-old pyromaniac whose parents are clearly under-supervising him. Who do you call first? The folks at Child Protective Services or the State Fire Marshall’s Office? Clearly, he and your community are at significant risk.

If you were practicing in Wrexham, a town in North Wales, you would continue your questioning with, “So you like to go to The Land after school? I’ve heard it’s a fun place?”

The Land is 3-year-old adventure playground that I learned about in a thought-provoking article in The Atlantic (The Overprotected Kid, by Hanna Rosin, April 2014). The nearly acre-sized site would look like a junkyard to any adult whose imagination has atrophied with age. Strewn with used tires, wooden palettes, dirty old mattresses, and decrepit lawn furniture, it provides endless opportunities for children to create their own places for play and adventure. By stacking, rolling, hammering together, and rearranging the loose detritus of society, children can transform the junk into an ever-changing landscape for fun. A fire pit and an old oil drum – among the most popular items – are often smoldering with fires the children have started. The filthy mattresses become trampolines. The children are observed by professionally trained “playworkers” who are continually updating the risk assessments of the activities that were begun prior to the opening of the facility. The observers seldom have to intervene. Other than a few scraped knees, no children have been injured.

Although adventure playgrounds were relatively common in the U.K. during the 1940’s, their popularity faded until the last few years when they have enjoyed a modest resurgence. In the article in The Atlantic, author Hanna Rosin chronicles the de-riskification of playgrounds in America that began in the 1970’s. The process was fueled by an unfortunate incident in which a toddler supervised by his mother fell off a 12-foot playground slide in a Chicago playground. The child sustained a significant and permanent brain injury and received a multimillion dollar award in the suit that followed.

A commentary in Pediatrics entitled “X-rated playgrounds?” (Pediatrics 1979;64:961) and a crusade by its author, Theodora Briggs Sweeney culminated in the release of the Handbook for Public Playground Safety (U.S. Consumer Product Safety Commission, 1981) which listed in minute detail guidelines for dimensions and materials for playground equipment and play surfaces. Although these were only “guidelines,” only the most foolish manufacturer would ignore them. Little thought was given to the validity of the alarming statistics that had prompted these changes. What were the denominators? Can you compare 1970’s hospital data with those from the 1950’s when injured children were managed at home or in their doctors’ offices?

Regardless of the validity of the data, the result was that these redesigned playgrounds offered so little sense of risk that they were abandoned by all but the youngest children. Numerous studies suggest that by eliminating risk or at least the appearance of risk, we are robbing children of important learning experiences on which they can build fuller, more creative, successful, and less anxiety-dominated lives. I urge you to look at that Atlantic article for a more robust description of the evidence.

I suspect that you may be a bit uncomfortable with 8-year-old boys playing with fire, but do you agree that we need to seriously rethink our attempts to protect children from the ordinary risks of an active life? Or do you think those of us who believe children will benefit from more perceived risk are just a bunch of fogys who begin every other sentence, “When I was your age ... .”

Do you encourage parents to allow their children to walk to school unattended? Do you caution parents about being overprotective? Have I ignited a spark of concern in you, or am I just playing with fire?

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “Coping with a Picky Eater.” E-mail him at [email protected].

Hoping to learn a bit more about the apparently healthy 8-year-old who has been deposited in your exam room for his biannual checkup, you take the opportunity to ask him a few questions with his mother in the waiting room. “So, Jason, what do you like to do for fun?”

“Well, yesterday I started a fire with my buddy Rudy, and we burned a whole bunch of sticks and stuff.”

“Does your mother know about this?”

“She wasn’t around, but I think so. We’ve done it a bunch of times before.”

Okay, here you are with an 8-year-old pyromaniac whose parents are clearly under-supervising him. Who do you call first? The folks at Child Protective Services or the State Fire Marshall’s Office? Clearly, he and your community are at significant risk.

If you were practicing in Wrexham, a town in North Wales, you would continue your questioning with, “So you like to go to The Land after school? I’ve heard it’s a fun place?”

The Land is 3-year-old adventure playground that I learned about in a thought-provoking article in The Atlantic (The Overprotected Kid, by Hanna Rosin, April 2014). The nearly acre-sized site would look like a junkyard to any adult whose imagination has atrophied with age. Strewn with used tires, wooden palettes, dirty old mattresses, and decrepit lawn furniture, it provides endless opportunities for children to create their own places for play and adventure. By stacking, rolling, hammering together, and rearranging the loose detritus of society, children can transform the junk into an ever-changing landscape for fun. A fire pit and an old oil drum – among the most popular items – are often smoldering with fires the children have started. The filthy mattresses become trampolines. The children are observed by professionally trained “playworkers” who are continually updating the risk assessments of the activities that were begun prior to the opening of the facility. The observers seldom have to intervene. Other than a few scraped knees, no children have been injured.

Although adventure playgrounds were relatively common in the U.K. during the 1940’s, their popularity faded until the last few years when they have enjoyed a modest resurgence. In the article in The Atlantic, author Hanna Rosin chronicles the de-riskification of playgrounds in America that began in the 1970’s. The process was fueled by an unfortunate incident in which a toddler supervised by his mother fell off a 12-foot playground slide in a Chicago playground. The child sustained a significant and permanent brain injury and received a multimillion dollar award in the suit that followed.

A commentary in Pediatrics entitled “X-rated playgrounds?” (Pediatrics 1979;64:961) and a crusade by its author, Theodora Briggs Sweeney culminated in the release of the Handbook for Public Playground Safety (U.S. Consumer Product Safety Commission, 1981) which listed in minute detail guidelines for dimensions and materials for playground equipment and play surfaces. Although these were only “guidelines,” only the most foolish manufacturer would ignore them. Little thought was given to the validity of the alarming statistics that had prompted these changes. What were the denominators? Can you compare 1970’s hospital data with those from the 1950’s when injured children were managed at home or in their doctors’ offices?

Regardless of the validity of the data, the result was that these redesigned playgrounds offered so little sense of risk that they were abandoned by all but the youngest children. Numerous studies suggest that by eliminating risk or at least the appearance of risk, we are robbing children of important learning experiences on which they can build fuller, more creative, successful, and less anxiety-dominated lives. I urge you to look at that Atlantic article for a more robust description of the evidence.

I suspect that you may be a bit uncomfortable with 8-year-old boys playing with fire, but do you agree that we need to seriously rethink our attempts to protect children from the ordinary risks of an active life? Or do you think those of us who believe children will benefit from more perceived risk are just a bunch of fogys who begin every other sentence, “When I was your age ... .”

Do you encourage parents to allow their children to walk to school unattended? Do you caution parents about being overprotective? Have I ignited a spark of concern in you, or am I just playing with fire?

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “Coping with a Picky Eater.” E-mail him at [email protected].