Brian F. Mandell, MD, PhD

More than 15 million patients in the United States have prescriptions for proton pump inhibitors (PPIs), in most cases for “heartburn,” reflux, and swallowing problems, and many more are taking over-the-counter PPIs or histamine 2 receptor antagonists.

Gastroesophageal reflux disease (GERD) seems to be the initial reflexive diagnosis given to most patients who complain of chest or epigastric burning or seemingly nonspecific swallowing difficulties. The prevalence of diagnosed GERD is high; in addition to causing “heartburn,” in my clinic it seems to be the most commonly attributed cause of chronic cough with a normal chest radiograph or hoarseness, and a frequent contributing comorbidity warranting treatment in patients with bronchospasm—diagnosed by my otolaryngology and pulmonary colleagues.

GERD is so common that it is no surprise that patients are increasingly diagnosed with it on the basis of a superficial history, or that patients diagnose and treat it themselves based on information they find on the Internet. Objective diagnostic tests are suggested when PPIs do not produce the expected response.

But long-term, high-dose PPI therapy may not be totally benign. Omeprazole, commonly prescribed and also available over the counter, may in some patients interfere with clopidogrel and increase the risk of coronary events, although this increase may actually be due to the underlying medical condition for which the PPI is prescribed—“confounding by indication.” PPI use is associated with decreased absorption of iron and vitamin B₁₂, perhaps contributing to anemia. The estimated risks of vertebral and hip osteoporosis, interstitial nephritis, and dementia are slightly increased. Patients with severe liver disease seem to be at far higher risk of bacterial peritonitis. Clostridium difficile infection and some pneumonias may also be increased in chronic PPI users. Therefore, we should think twice when making a clinical diagnosis of GERD, a diagnosis that often leads us to prescribe antacid therapy (usually a PPI) for a long time, sometimes unnecessarily.¹

Kichler and Gabbard, in this issue of the Journal, work through a clinical management scenario focusing on the evaluation of a patient with dysphagia, a common symptom described in many ways by patients who may have previously been diagnosed with GERD. The authors remind us of the value of a careful, focused, and detailed medical history, and provide updated information on the performance and utility of motility and endoscopic studies in diagnosing esophageal disorders.

More than 15 million patients in the United States have prescriptions for proton pump inhibitors (PPIs), in most cases for “heartburn,” reflux, and swallowing problems, and many more are taking over-the-counter PPIs or histamine 2 receptor antagonists.

Gastroesophageal reflux disease (GERD) seems to be the initial reflexive diagnosis given to most patients who complain of chest or epigastric burning or seemingly nonspecific swallowing difficulties. The prevalence of diagnosed GERD is high; in addition to causing “heartburn,” in my clinic it seems to be the most commonly attributed cause of chronic cough with a normal chest radiograph or hoarseness, and a frequent contributing comorbidity warranting treatment in patients with bronchospasm—diagnosed by my otolaryngology and pulmonary colleagues.

GERD is so common that it is no surprise that patients are increasingly diagnosed with it on the basis of a superficial history, or that patients diagnose and treat it themselves based on information they find on the Internet. Objective diagnostic tests are suggested when PPIs do not produce the expected response.

But long-term, high-dose PPI therapy may not be totally benign. Omeprazole, commonly prescribed and also available over the counter, may in some patients interfere with clopidogrel and increase the risk of coronary events, although this increase may actually be due to the underlying medical condition for which the PPI is prescribed—“confounding by indication.” PPI use is associated with decreased absorption of iron and vitamin B₁₂, perhaps contributing to anemia. The estimated risks of vertebral and hip osteoporosis, interstitial nephritis, and dementia are slightly increased. Patients with severe liver disease seem to be at far higher risk of bacterial peritonitis. Clostridium difficile infection and some pneumonias may also be increased in chronic PPI users. Therefore, we should think twice when making a clinical diagnosis of GERD, a diagnosis that often leads us to prescribe antacid therapy (usually a PPI) for a long time, sometimes unnecessarily.¹

Kichler and Gabbard, in this issue of the Journal, work through a clinical management scenario focusing on the evaluation of a patient with dysphagia, a common symptom described in many ways by patients who may have previously been diagnosed with GERD. The authors remind us of the value of a careful, focused, and detailed medical history, and provide updated information on the performance and utility of motility and endoscopic studies in diagnosing esophageal disorders.

More than 15 million patients in the United States have prescriptions for proton pump inhibitors (PPIs), in most cases for “heartburn,” reflux, and swallowing problems, and many more are taking over-the-counter PPIs or histamine 2 receptor antagonists.

Gastroesophageal reflux disease (GERD) seems to be the initial reflexive diagnosis given to most patients who complain of chest or epigastric burning or seemingly nonspecific swallowing difficulties. The prevalence of diagnosed GERD is high; in addition to causing “heartburn,” in my clinic it seems to be the most commonly attributed cause of chronic cough with a normal chest radiograph or hoarseness, and a frequent contributing comorbidity warranting treatment in patients with bronchospasm—diagnosed by my otolaryngology and pulmonary colleagues.

GERD is so common that it is no surprise that patients are increasingly diagnosed with it on the basis of a superficial history, or that patients diagnose and treat it themselves based on information they find on the Internet. Objective diagnostic tests are suggested when PPIs do not produce the expected response.

But long-term, high-dose PPI therapy may not be totally benign. Omeprazole, commonly prescribed and also available over the counter, may in some patients interfere with clopidogrel and increase the risk of coronary events, although this increase may actually be due to the underlying medical condition for which the PPI is prescribed—“confounding by indication.” PPI use is associated with decreased absorption of iron and vitamin B₁₂, perhaps contributing to anemia. The estimated risks of vertebral and hip osteoporosis, interstitial nephritis, and dementia are slightly increased. Patients with severe liver disease seem to be at far higher risk of bacterial peritonitis. Clostridium difficile infection and some pneumonias may also be increased in chronic PPI users. Therefore, we should think twice when making a clinical diagnosis of GERD, a diagnosis that often leads us to prescribe antacid therapy (usually a PPI) for a long time, sometimes unnecessarily.¹

Kichler and Gabbard, in this issue of the Journal, work through a clinical management scenario focusing on the evaluation of a patient with dysphagia, a common symptom described in many ways by patients who may have previously been diagnosed with GERD. The authors remind us of the value of a careful, focused, and detailed medical history, and provide updated information on the performance and utility of motility and endoscopic studies in diagnosing esophageal disorders.

Few in mainstream medicine doubt the efficacy of vaccination and the net positive value of a thoughtful vaccination policy. We have witnessed within a professional lifetime the virtual eradication, at least regionally, of a number of previously devastating infectious diseases including polio, smallpox, pertussis, and measles. With growing understanding of disease mechanisms, the potential value of vaccination has expanded to include preventing sequelae of certain infections and malignancy—a holy grail in oncology, the true prevention of cancer. Sporadic local resistance to uniform vaccination against measles has resulted in geographic reappearance of the disease, providing further support for a uniform approach to vaccination against communicable diseases, with some potential to opt out, perhaps with associated societal repercussions for those who do so.

For most clinicians, certainly those of us dealing with chronically ill or immunosuppressed patients, the decision to recommend annual influenza vaccination and pneumococcal vaccinations per guidelines is an easy one. Vaccination against certain infections provides some protection for the individual patient and for the population, contributing to “herd immunity” and helping to protect against the occurrence of pandemics. But this is not the case for all vaccines. For some vaccines the issues of immunity and vaccination are more individual and complicated and warrant more education, reflection, and conversation.

The vaccine to protect against human papillomavirus is effective at reducing the incidence of cervical and anal cancers triggered by infection with certain strains of human papillomavirus. The viral infection itself is not immediately life-threatening. Thus, patients (and their parents) are asked to consider vaccination against a sexually transmitted virus (before sexual transmission of infection) to prevent a possible malignancy later in life. This decision can create social angst. Perhaps less socially challenging, but medically more complicated, is vaccination against the hepatitis B virus (HBV). HBV is also sexually transmissible, but the source in many patients infected with this virus is unclear. The HBV vaccine helps protect against clinically meaningful hepatitis and chronic liver disease from HBV and also will reduce the occurrence of HBV-associated hepatocellular carcinoma and progression of cirrhosis in patients coinfected with hepatitis C virus.

More complex yet is vaccination against the varicella-zoster virus (VZV) to reduce the likelihood of shingles and its possible consequence, postherpetic neuralgia. Le, Sabella, and Rothberg, in this issue of the Journal, review clinical and public health challenges affecting the use of this vaccine.

We are almost all exposed to this virus as children, through natural infection (chickenpox) or vaccination; many infections are seemingly subclinical. My older son had the distinct misfortune of getting chickenpox in a quite memorable way, developing a concentrated collection of the pruritic vesicles underneath a newly placed arm cast. Whether we remember the initial infection or not, VZV sets up housekeeping and lies dormant for decades within sensory neurons. Decades later, it may erupt as shingles along the distribution of the infected nerves with characteristic painful vesicles, sometimes with persistent, extremely painful, and debilitating residua within the same dermatomal distribution: postherpetic neuralgia. The triggers for this fairly common scenario are only generically understood and include waning cellular immunity attributed to aging, malignancy, immunosuppressive medications, human immunodeficiency virus, and perhaps stress and depression.

The zoster vaccine is unique in that it is given to bolster already present cellular immunity to prevent clinical recurrence of the earlier infection, decades after the virus has been dormant—not, as for the other vaccines noted above, to prevent primary infection. It doesn’t matter if the patient has already experienced an episode of shingles. The currently available vaccine is a live-attenuated strain (Oka) of VZV. Another vaccine in clinical testing uses isolated viral components with adjuvant and thus eliminates current concerns of giving the live-attenuated vaccine to immunosuppressed and elderly patients, those who may benefit the most from it.

Fortunately, it seems that even significantly immunosuppressed and elderly patients tolerate the current vaccine, but at present it is suggested that these groups not receive the vaccine, and vaccination rates in these patients is low. Hopefully, additional data will accumulate regarding the safety of the vaccine and will permit its more widespread use within these patient groups, or a replacement “dead” vaccine will become available.

As Le et al nicely discuss, the current vaccine efficacy wanes over about 10 years, and then a booster vaccine should be considered, but there are few data to provide safety and efficacy outcome measures from patients who received a booster vaccination. The potential need to receive a booster injection after about a decade, the demonstrated greater efficacy against zoster when the initial vaccination is provided to patients ages 60 through 69 than in those over 70, and the lower absolute impact when given to patients ages 50 through 59 (baseline zoster incidence increases with age) should enter into the conversation with patients as to when they should receive the vaccine.

Additionally, there are the extremely provocative and as yet unanswered questions surrounding the implications of vaccination if VZV infection is a trigger of inflammatory vascular diseases such as giant cell arteritis in the elderly, as was proposed by the late Dr. Don Gilden.¹

And yes, I did get the vaccine. I was 64 at the time.

Few in mainstream medicine doubt the efficacy of vaccination and the net positive value of a thoughtful vaccination policy. We have witnessed within a professional lifetime the virtual eradication, at least regionally, of a number of previously devastating infectious diseases including polio, smallpox, pertussis, and measles. With growing understanding of disease mechanisms, the potential value of vaccination has expanded to include preventing sequelae of certain infections and malignancy—a holy grail in oncology, the true prevention of cancer. Sporadic local resistance to uniform vaccination against measles has resulted in geographic reappearance of the disease, providing further support for a uniform approach to vaccination against communicable diseases, with some potential to opt out, perhaps with associated societal repercussions for those who do so.

For most clinicians, certainly those of us dealing with chronically ill or immunosuppressed patients, the decision to recommend annual influenza vaccination and pneumococcal vaccinations per guidelines is an easy one. Vaccination against certain infections provides some protection for the individual patient and for the population, contributing to “herd immunity” and helping to protect against the occurrence of pandemics. But this is not the case for all vaccines. For some vaccines the issues of immunity and vaccination are more individual and complicated and warrant more education, reflection, and conversation.

The vaccine to protect against human papillomavirus is effective at reducing the incidence of cervical and anal cancers triggered by infection with certain strains of human papillomavirus. The viral infection itself is not immediately life-threatening. Thus, patients (and their parents) are asked to consider vaccination against a sexually transmitted virus (before sexual transmission of infection) to prevent a possible malignancy later in life. This decision can create social angst. Perhaps less socially challenging, but medically more complicated, is vaccination against the hepatitis B virus (HBV). HBV is also sexually transmissible, but the source in many patients infected with this virus is unclear. The HBV vaccine helps protect against clinically meaningful hepatitis and chronic liver disease from HBV and also will reduce the occurrence of HBV-associated hepatocellular carcinoma and progression of cirrhosis in patients coinfected with hepatitis C virus.

More complex yet is vaccination against the varicella-zoster virus (VZV) to reduce the likelihood of shingles and its possible consequence, postherpetic neuralgia. Le, Sabella, and Rothberg, in this issue of the Journal, review clinical and public health challenges affecting the use of this vaccine.

We are almost all exposed to this virus as children, through natural infection (chickenpox) or vaccination; many infections are seemingly subclinical. My older son had the distinct misfortune of getting chickenpox in a quite memorable way, developing a concentrated collection of the pruritic vesicles underneath a newly placed arm cast. Whether we remember the initial infection or not, VZV sets up housekeeping and lies dormant for decades within sensory neurons. Decades later, it may erupt as shingles along the distribution of the infected nerves with characteristic painful vesicles, sometimes with persistent, extremely painful, and debilitating residua within the same dermatomal distribution: postherpetic neuralgia. The triggers for this fairly common scenario are only generically understood and include waning cellular immunity attributed to aging, malignancy, immunosuppressive medications, human immunodeficiency virus, and perhaps stress and depression.

The zoster vaccine is unique in that it is given to bolster already present cellular immunity to prevent clinical recurrence of the earlier infection, decades after the virus has been dormant—not, as for the other vaccines noted above, to prevent primary infection. It doesn’t matter if the patient has already experienced an episode of shingles. The currently available vaccine is a live-attenuated strain (Oka) of VZV. Another vaccine in clinical testing uses isolated viral components with adjuvant and thus eliminates current concerns of giving the live-attenuated vaccine to immunosuppressed and elderly patients, those who may benefit the most from it.

Fortunately, it seems that even significantly immunosuppressed and elderly patients tolerate the current vaccine, but at present it is suggested that these groups not receive the vaccine, and vaccination rates in these patients is low. Hopefully, additional data will accumulate regarding the safety of the vaccine and will permit its more widespread use within these patient groups, or a replacement “dead” vaccine will become available.

As Le et al nicely discuss, the current vaccine efficacy wanes over about 10 years, and then a booster vaccine should be considered, but there are few data to provide safety and efficacy outcome measures from patients who received a booster vaccination. The potential need to receive a booster injection after about a decade, the demonstrated greater efficacy against zoster when the initial vaccination is provided to patients ages 60 through 69 than in those over 70, and the lower absolute impact when given to patients ages 50 through 59 (baseline zoster incidence increases with age) should enter into the conversation with patients as to when they should receive the vaccine.

Additionally, there are the extremely provocative and as yet unanswered questions surrounding the implications of vaccination if VZV infection is a trigger of inflammatory vascular diseases such as giant cell arteritis in the elderly, as was proposed by the late Dr. Don Gilden.¹

And yes, I did get the vaccine. I was 64 at the time.

Few in mainstream medicine doubt the efficacy of vaccination and the net positive value of a thoughtful vaccination policy. We have witnessed within a professional lifetime the virtual eradication, at least regionally, of a number of previously devastating infectious diseases including polio, smallpox, pertussis, and measles. With growing understanding of disease mechanisms, the potential value of vaccination has expanded to include preventing sequelae of certain infections and malignancy—a holy grail in oncology, the true prevention of cancer. Sporadic local resistance to uniform vaccination against measles has resulted in geographic reappearance of the disease, providing further support for a uniform approach to vaccination against communicable diseases, with some potential to opt out, perhaps with associated societal repercussions for those who do so.

For most clinicians, certainly those of us dealing with chronically ill or immunosuppressed patients, the decision to recommend annual influenza vaccination and pneumococcal vaccinations per guidelines is an easy one. Vaccination against certain infections provides some protection for the individual patient and for the population, contributing to “herd immunity” and helping to protect against the occurrence of pandemics. But this is not the case for all vaccines. For some vaccines the issues of immunity and vaccination are more individual and complicated and warrant more education, reflection, and conversation.

The vaccine to protect against human papillomavirus is effective at reducing the incidence of cervical and anal cancers triggered by infection with certain strains of human papillomavirus. The viral infection itself is not immediately life-threatening. Thus, patients (and their parents) are asked to consider vaccination against a sexually transmitted virus (before sexual transmission of infection) to prevent a possible malignancy later in life. This decision can create social angst. Perhaps less socially challenging, but medically more complicated, is vaccination against the hepatitis B virus (HBV). HBV is also sexually transmissible, but the source in many patients infected with this virus is unclear. The HBV vaccine helps protect against clinically meaningful hepatitis and chronic liver disease from HBV and also will reduce the occurrence of HBV-associated hepatocellular carcinoma and progression of cirrhosis in patients coinfected with hepatitis C virus.

More complex yet is vaccination against the varicella-zoster virus (VZV) to reduce the likelihood of shingles and its possible consequence, postherpetic neuralgia. Le, Sabella, and Rothberg, in this issue of the Journal, review clinical and public health challenges affecting the use of this vaccine.

We are almost all exposed to this virus as children, through natural infection (chickenpox) or vaccination; many infections are seemingly subclinical. My older son had the distinct misfortune of getting chickenpox in a quite memorable way, developing a concentrated collection of the pruritic vesicles underneath a newly placed arm cast. Whether we remember the initial infection or not, VZV sets up housekeeping and lies dormant for decades within sensory neurons. Decades later, it may erupt as shingles along the distribution of the infected nerves with characteristic painful vesicles, sometimes with persistent, extremely painful, and debilitating residua within the same dermatomal distribution: postherpetic neuralgia. The triggers for this fairly common scenario are only generically understood and include waning cellular immunity attributed to aging, malignancy, immunosuppressive medications, human immunodeficiency virus, and perhaps stress and depression.

The zoster vaccine is unique in that it is given to bolster already present cellular immunity to prevent clinical recurrence of the earlier infection, decades after the virus has been dormant—not, as for the other vaccines noted above, to prevent primary infection. It doesn’t matter if the patient has already experienced an episode of shingles. The currently available vaccine is a live-attenuated strain (Oka) of VZV. Another vaccine in clinical testing uses isolated viral components with adjuvant and thus eliminates current concerns of giving the live-attenuated vaccine to immunosuppressed and elderly patients, those who may benefit the most from it.

Fortunately, it seems that even significantly immunosuppressed and elderly patients tolerate the current vaccine, but at present it is suggested that these groups not receive the vaccine, and vaccination rates in these patients is low. Hopefully, additional data will accumulate regarding the safety of the vaccine and will permit its more widespread use within these patient groups, or a replacement “dead” vaccine will become available.

As Le et al nicely discuss, the current vaccine efficacy wanes over about 10 years, and then a booster vaccine should be considered, but there are few data to provide safety and efficacy outcome measures from patients who received a booster vaccination. The potential need to receive a booster injection after about a decade, the demonstrated greater efficacy against zoster when the initial vaccination is provided to patients ages 60 through 69 than in those over 70, and the lower absolute impact when given to patients ages 50 through 59 (baseline zoster incidence increases with age) should enter into the conversation with patients as to when they should receive the vaccine.

Additionally, there are the extremely provocative and as yet unanswered questions surrounding the implications of vaccination if VZV infection is a trigger of inflammatory vascular diseases such as giant cell arteritis in the elderly, as was proposed by the late Dr. Don Gilden.¹

And yes, I did get the vaccine. I was 64 at the time.

Now that we can order MRI studies on a break from rounds walking to Starbucks, utilize portable ultrasounds to direct IV line placement, and use dual-energy CT to detect a gout attack that has not yet occurred, it seems like a romantic anachronism to extol the ongoing virtues of the seemingly lost art of the physical examination. Back “in the day,” the giants of medicine roamed the halls with their natural instruments of palpation and percussion and their skills in observation and auscultation. They were giants because they stood out then, just as skilled diagnosticians stand out today using an upgraded set of tools. Some physicians a few decades ago were able to recognize, describe, and diagnose late-stage endocarditis with a stethoscope, a magnifying glass, and an ophthalmoscope. The giants of today recognize the patient with endocarditis and document its presence using transesophageal echocardiography before the peripheral eponymous stigmata of Janeway and Osler appear or the blood cultures turn positive. The physical examination, history, diagnostic reasoning, and clinical technology are all essential for a blend that provides efficient and effective medical care. The blending is the challenge.

Clinicians are not created equal. We learn and prioritize our skills in different ways. But if we are not taught to value and trust the physical examination, if we don’t have the opportunity to see it influence patient management in positive ways, we may eschew it and instead indiscriminately use easily available laboratory and imaging tests—a more expensive and often misleading strategic approach. Today while in clinic, I saw a 54-year-old woman for evaluation of possible lupus who had arthritis of the hands and a high positive antinuclear antibody titer, but negative or normal results on other, previously ordered tests, including anti-DNA, rheumatoid factor, anti-cyclic citrullinated peptide, hepatitis C studies, complement levels, and another half-dozen immune serologic tests. On examination, she had typical nodular osteoarthritis of the proximal and distal interphalangeal joints of her hand with squaring of her thumbs. The antinuclear antibody was most likely associated with her previously diagnosed autoimmune thyroid disease.

In an editorial in this issue of the Journal, Dr. Salvatore Mangione, the author of a book on physical diagnosis,¹ cites a recent study indicating that the most common recognized diagnostic error related to the physical examination is that the appropriate examination isn’t done.² I would add to that my concerns over the new common custom of cutting and pasting the findings from earlier physical examinations into later progress notes in the electronic record. So much for the value of being able to recognize “changing murmurs” when diagnosing infectious endocarditis.

The apparent efficiency (reflected in length of stay) and availability of technology, as well as a lack of physician skill and time, are often cited as reasons for the demise of the physical examination. Yet this does not need to be the case. If I had trained with portable ultrasonography readily available to confirm or refute my impressions, my skills at detecting low-grade synovitis would surely be better than they are. With a gold standard at hand, which may be technology or at times a skilled mentor, our examinations can be refined if we want them to be.

But the issue of limited physician time must be addressed. Efficiency is a critical concept in preserving how we practice and perform the physical examination. When we know what we are looking for, we are more likely to find it if it is present, or to have confidence that it is not present. I am far more likely to recognize a loud pulmonic second heart sound if I suspect that the dyspneic patient I am examining has pulmonary hypertension associated with her scleroderma than if I am doing a perfunctory cardiac auscultation in a patient admitted with cellulitis. Appropriate focus provides power to the directed physical examination. If I am looking for the cause of unexplained fevers, I will do a purposeful axillary and epitrochlear lymph node examination. I am not mindlessly probing the flesh.

Nishigori and colleagues have written of the “hypothesis-driven” physical examination.³ Busy clinicians, they say, don’t have time to perform a head-to-toe, by-the-book physical examination. Instead, we should, by a dynamic process, formulate a differential diagnosis from the history and other initial information, and then perform the directed physical examination in earnest, looking for evidence to support or refute our diagnostic hypothesis—and thus redirect it. Plus, in a nice break from electronic charting, we can actually explain our thought processes to the patient as we perform the examination.

This approach makes sense to me as both intellectually satisfying and clinically efficient. And then we can consider which lab tests and technologic gadgetry we should order, while walking to get the café latte we ordered with our cell phone app.

New technology can support and not necessarily replace old habits.

Now that we can order MRI studies on a break from rounds walking to Starbucks, utilize portable ultrasounds to direct IV line placement, and use dual-energy CT to detect a gout attack that has not yet occurred, it seems like a romantic anachronism to extol the ongoing virtues of the seemingly lost art of the physical examination. Back “in the day,” the giants of medicine roamed the halls with their natural instruments of palpation and percussion and their skills in observation and auscultation. They were giants because they stood out then, just as skilled diagnosticians stand out today using an upgraded set of tools. Some physicians a few decades ago were able to recognize, describe, and diagnose late-stage endocarditis with a stethoscope, a magnifying glass, and an ophthalmoscope. The giants of today recognize the patient with endocarditis and document its presence using transesophageal echocardiography before the peripheral eponymous stigmata of Janeway and Osler appear or the blood cultures turn positive. The physical examination, history, diagnostic reasoning, and clinical technology are all essential for a blend that provides efficient and effective medical care. The blending is the challenge.

Clinicians are not created equal. We learn and prioritize our skills in different ways. But if we are not taught to value and trust the physical examination, if we don’t have the opportunity to see it influence patient management in positive ways, we may eschew it and instead indiscriminately use easily available laboratory and imaging tests—a more expensive and often misleading strategic approach. Today while in clinic, I saw a 54-year-old woman for evaluation of possible lupus who had arthritis of the hands and a high positive antinuclear antibody titer, but negative or normal results on other, previously ordered tests, including anti-DNA, rheumatoid factor, anti-cyclic citrullinated peptide, hepatitis C studies, complement levels, and another half-dozen immune serologic tests. On examination, she had typical nodular osteoarthritis of the proximal and distal interphalangeal joints of her hand with squaring of her thumbs. The antinuclear antibody was most likely associated with her previously diagnosed autoimmune thyroid disease.

In an editorial in this issue of the Journal, Dr. Salvatore Mangione, the author of a book on physical diagnosis,¹ cites a recent study indicating that the most common recognized diagnostic error related to the physical examination is that the appropriate examination isn’t done.² I would add to that my concerns over the new common custom of cutting and pasting the findings from earlier physical examinations into later progress notes in the electronic record. So much for the value of being able to recognize “changing murmurs” when diagnosing infectious endocarditis.

The apparent efficiency (reflected in length of stay) and availability of technology, as well as a lack of physician skill and time, are often cited as reasons for the demise of the physical examination. Yet this does not need to be the case. If I had trained with portable ultrasonography readily available to confirm or refute my impressions, my skills at detecting low-grade synovitis would surely be better than they are. With a gold standard at hand, which may be technology or at times a skilled mentor, our examinations can be refined if we want them to be.

But the issue of limited physician time must be addressed. Efficiency is a critical concept in preserving how we practice and perform the physical examination. When we know what we are looking for, we are more likely to find it if it is present, or to have confidence that it is not present. I am far more likely to recognize a loud pulmonic second heart sound if I suspect that the dyspneic patient I am examining has pulmonary hypertension associated with her scleroderma than if I am doing a perfunctory cardiac auscultation in a patient admitted with cellulitis. Appropriate focus provides power to the directed physical examination. If I am looking for the cause of unexplained fevers, I will do a purposeful axillary and epitrochlear lymph node examination. I am not mindlessly probing the flesh.

Nishigori and colleagues have written of the “hypothesis-driven” physical examination.³ Busy clinicians, they say, don’t have time to perform a head-to-toe, by-the-book physical examination. Instead, we should, by a dynamic process, formulate a differential diagnosis from the history and other initial information, and then perform the directed physical examination in earnest, looking for evidence to support or refute our diagnostic hypothesis—and thus redirect it. Plus, in a nice break from electronic charting, we can actually explain our thought processes to the patient as we perform the examination.

This approach makes sense to me as both intellectually satisfying and clinically efficient. And then we can consider which lab tests and technologic gadgetry we should order, while walking to get the café latte we ordered with our cell phone app.

New technology can support and not necessarily replace old habits.

Now that we can order MRI studies on a break from rounds walking to Starbucks, utilize portable ultrasounds to direct IV line placement, and use dual-energy CT to detect a gout attack that has not yet occurred, it seems like a romantic anachronism to extol the ongoing virtues of the seemingly lost art of the physical examination. Back “in the day,” the giants of medicine roamed the halls with their natural instruments of palpation and percussion and their skills in observation and auscultation. They were giants because they stood out then, just as skilled diagnosticians stand out today using an upgraded set of tools. Some physicians a few decades ago were able to recognize, describe, and diagnose late-stage endocarditis with a stethoscope, a magnifying glass, and an ophthalmoscope. The giants of today recognize the patient with endocarditis and document its presence using transesophageal echocardiography before the peripheral eponymous stigmata of Janeway and Osler appear or the blood cultures turn positive. The physical examination, history, diagnostic reasoning, and clinical technology are all essential for a blend that provides efficient and effective medical care. The blending is the challenge.

Clinicians are not created equal. We learn and prioritize our skills in different ways. But if we are not taught to value and trust the physical examination, if we don’t have the opportunity to see it influence patient management in positive ways, we may eschew it and instead indiscriminately use easily available laboratory and imaging tests—a more expensive and often misleading strategic approach. Today while in clinic, I saw a 54-year-old woman for evaluation of possible lupus who had arthritis of the hands and a high positive antinuclear antibody titer, but negative or normal results on other, previously ordered tests, including anti-DNA, rheumatoid factor, anti-cyclic citrullinated peptide, hepatitis C studies, complement levels, and another half-dozen immune serologic tests. On examination, she had typical nodular osteoarthritis of the proximal and distal interphalangeal joints of her hand with squaring of her thumbs. The antinuclear antibody was most likely associated with her previously diagnosed autoimmune thyroid disease.

In an editorial in this issue of the Journal, Dr. Salvatore Mangione, the author of a book on physical diagnosis,¹ cites a recent study indicating that the most common recognized diagnostic error related to the physical examination is that the appropriate examination isn’t done.² I would add to that my concerns over the new common custom of cutting and pasting the findings from earlier physical examinations into later progress notes in the electronic record. So much for the value of being able to recognize “changing murmurs” when diagnosing infectious endocarditis.

The apparent efficiency (reflected in length of stay) and availability of technology, as well as a lack of physician skill and time, are often cited as reasons for the demise of the physical examination. Yet this does not need to be the case. If I had trained with portable ultrasonography readily available to confirm or refute my impressions, my skills at detecting low-grade synovitis would surely be better than they are. With a gold standard at hand, which may be technology or at times a skilled mentor, our examinations can be refined if we want them to be.

But the issue of limited physician time must be addressed. Efficiency is a critical concept in preserving how we practice and perform the physical examination. When we know what we are looking for, we are more likely to find it if it is present, or to have confidence that it is not present. I am far more likely to recognize a loud pulmonic second heart sound if I suspect that the dyspneic patient I am examining has pulmonary hypertension associated with her scleroderma than if I am doing a perfunctory cardiac auscultation in a patient admitted with cellulitis. Appropriate focus provides power to the directed physical examination. If I am looking for the cause of unexplained fevers, I will do a purposeful axillary and epitrochlear lymph node examination. I am not mindlessly probing the flesh.

Nishigori and colleagues have written of the “hypothesis-driven” physical examination.³ Busy clinicians, they say, don’t have time to perform a head-to-toe, by-the-book physical examination. Instead, we should, by a dynamic process, formulate a differential diagnosis from the history and other initial information, and then perform the directed physical examination in earnest, looking for evidence to support or refute our diagnostic hypothesis—and thus redirect it. Plus, in a nice break from electronic charting, we can actually explain our thought processes to the patient as we perform the examination.

This approach makes sense to me as both intellectually satisfying and clinically efficient. And then we can consider which lab tests and technologic gadgetry we should order, while walking to get the café latte we ordered with our cell phone app.

New technology can support and not necessarily replace old habits.

New, changing technologies are being incorporated into every aspect of medical care and education, and the impact cannot be overstated. While the ultimate qualitative impact (beneficial, intrusive, efficient, obstructive, or neutral) of specific individual implementations remains to be seen, there is no doubt that the faces of patient care and the financial management of healthcare delivery have been forever altered.

The amount of information now literally at our fingertips is overwhelming. Some of my patients bring the latest from www.clinicaltrials.gov to their appointments. One patient recently brought downloaded online testimony from patients who were being given an oil supplement to treat disorders including gout, neuropathy, carpal tunnel, sinusitis, headache, and postop hip and knee pain and wanted to know why I hadn’t suggested it for her. Accessing the information pipeline is like drinking from a firehose, and there is no perfect valve that can adjust the flow to every thirst.

Lest we think that only patients use sites of variable reliability in getting their online medical information, in a recent survey by Kantar Media, when 508 physicians were asked which of 49 sites they looked at most often, Wikipedia came in at number 3 (UpToDate was number 1 and Cleveland Clinic Journal of Medicine was number 25). But when asked to rate the 49 sites for “quality clinical content,” responders listed Wikipedia as 47 (UpToDate was still number 1 and CCJM was number 6).

We healthcare providers can assess the accuracy and quality of clinical content. But it is not always easy, especially when trying to access, digest, and utilize information within the real-time constraints of an office visit or inpatient consultation. The now almost universal use of electronic medical records (EMRs) in major health systems provides access to true point-of-care information to assist in clinical decision-making, but how we filter and channel this information and apply it to the patient sitting in the exam room is not always straightforward. It is naïve to think that one source can fit all of our information needs.

A “smart” EMR can reflexively direct me to diagnosis-linked clinical guidelines or care paths. But without knowing the specifics of how the guidelines were written, I can’t know if they are ideally applicable to the patient in front of me. Guidelines based solely on clinical trial data may not be ideal for a given patient due to constraints of the clinical trial design and the tested clinical populations. There are times in areas outside my clinical field that I seek clinically nuanced expertise in interpreting clinical trials rather than the actual clinical trial data. Other times, when approaching problems within my own expertise, I want to see the raw data to reach a conclusion on its applicability and likely magnitude of effect in a specific patient. Using a trusted source of predigested, summarized data (as opposed to the raw data), knowing whether an author has a relationship with a specific company, and knowing that the clinical trials of a specific therapy are not intrinsically bad or good—all of these contribute to contextual decisions that lead to my clinical recommendations. I always want to know the nature of authors’ commercial relationships, as well as the track record of my information sources.

It is in this context that the paper by Andrews et al in this issue of the Journal addresses in a very practical way some of the nuances in using several popular point-of-care information resources. This is the second of 2 papers that these authors have contributed to the CCJM in an effort to inform and direct us how to quench our thirst for information without getting bloated.

New, changing technologies are being incorporated into every aspect of medical care and education, and the impact cannot be overstated. While the ultimate qualitative impact (beneficial, intrusive, efficient, obstructive, or neutral) of specific individual implementations remains to be seen, there is no doubt that the faces of patient care and the financial management of healthcare delivery have been forever altered.

The amount of information now literally at our fingertips is overwhelming. Some of my patients bring the latest from www.clinicaltrials.gov to their appointments. One patient recently brought downloaded online testimony from patients who were being given an oil supplement to treat disorders including gout, neuropathy, carpal tunnel, sinusitis, headache, and postop hip and knee pain and wanted to know why I hadn’t suggested it for her. Accessing the information pipeline is like drinking from a firehose, and there is no perfect valve that can adjust the flow to every thirst.

Lest we think that only patients use sites of variable reliability in getting their online medical information, in a recent survey by Kantar Media, when 508 physicians were asked which of 49 sites they looked at most often, Wikipedia came in at number 3 (UpToDate was number 1 and Cleveland Clinic Journal of Medicine was number 25). But when asked to rate the 49 sites for “quality clinical content,” responders listed Wikipedia as 47 (UpToDate was still number 1 and CCJM was number 6).

We healthcare providers can assess the accuracy and quality of clinical content. But it is not always easy, especially when trying to access, digest, and utilize information within the real-time constraints of an office visit or inpatient consultation. The now almost universal use of electronic medical records (EMRs) in major health systems provides access to true point-of-care information to assist in clinical decision-making, but how we filter and channel this information and apply it to the patient sitting in the exam room is not always straightforward. It is naïve to think that one source can fit all of our information needs.

A “smart” EMR can reflexively direct me to diagnosis-linked clinical guidelines or care paths. But without knowing the specifics of how the guidelines were written, I can’t know if they are ideally applicable to the patient in front of me. Guidelines based solely on clinical trial data may not be ideal for a given patient due to constraints of the clinical trial design and the tested clinical populations. There are times in areas outside my clinical field that I seek clinically nuanced expertise in interpreting clinical trials rather than the actual clinical trial data. Other times, when approaching problems within my own expertise, I want to see the raw data to reach a conclusion on its applicability and likely magnitude of effect in a specific patient. Using a trusted source of predigested, summarized data (as opposed to the raw data), knowing whether an author has a relationship with a specific company, and knowing that the clinical trials of a specific therapy are not intrinsically bad or good—all of these contribute to contextual decisions that lead to my clinical recommendations. I always want to know the nature of authors’ commercial relationships, as well as the track record of my information sources.

It is in this context that the paper by Andrews et al in this issue of the Journal addresses in a very practical way some of the nuances in using several popular point-of-care information resources. This is the second of 2 papers that these authors have contributed to the CCJM in an effort to inform and direct us how to quench our thirst for information without getting bloated.

New, changing technologies are being incorporated into every aspect of medical care and education, and the impact cannot be overstated. While the ultimate qualitative impact (beneficial, intrusive, efficient, obstructive, or neutral) of specific individual implementations remains to be seen, there is no doubt that the faces of patient care and the financial management of healthcare delivery have been forever altered.

The amount of information now literally at our fingertips is overwhelming. Some of my patients bring the latest from www.clinicaltrials.gov to their appointments. One patient recently brought downloaded online testimony from patients who were being given an oil supplement to treat disorders including gout, neuropathy, carpal tunnel, sinusitis, headache, and postop hip and knee pain and wanted to know why I hadn’t suggested it for her. Accessing the information pipeline is like drinking from a firehose, and there is no perfect valve that can adjust the flow to every thirst.

Lest we think that only patients use sites of variable reliability in getting their online medical information, in a recent survey by Kantar Media, when 508 physicians were asked which of 49 sites they looked at most often, Wikipedia came in at number 3 (UpToDate was number 1 and Cleveland Clinic Journal of Medicine was number 25). But when asked to rate the 49 sites for “quality clinical content,” responders listed Wikipedia as 47 (UpToDate was still number 1 and CCJM was number 6).

We healthcare providers can assess the accuracy and quality of clinical content. But it is not always easy, especially when trying to access, digest, and utilize information within the real-time constraints of an office visit or inpatient consultation. The now almost universal use of electronic medical records (EMRs) in major health systems provides access to true point-of-care information to assist in clinical decision-making, but how we filter and channel this information and apply it to the patient sitting in the exam room is not always straightforward. It is naïve to think that one source can fit all of our information needs.

A “smart” EMR can reflexively direct me to diagnosis-linked clinical guidelines or care paths. But without knowing the specifics of how the guidelines were written, I can’t know if they are ideally applicable to the patient in front of me. Guidelines based solely on clinical trial data may not be ideal for a given patient due to constraints of the clinical trial design and the tested clinical populations. There are times in areas outside my clinical field that I seek clinically nuanced expertise in interpreting clinical trials rather than the actual clinical trial data. Other times, when approaching problems within my own expertise, I want to see the raw data to reach a conclusion on its applicability and likely magnitude of effect in a specific patient. Using a trusted source of predigested, summarized data (as opposed to the raw data), knowing whether an author has a relationship with a specific company, and knowing that the clinical trials of a specific therapy are not intrinsically bad or good—all of these contribute to contextual decisions that lead to my clinical recommendations. I always want to know the nature of authors’ commercial relationships, as well as the track record of my information sources.

It is in this context that the paper by Andrews et al in this issue of the Journal addresses in a very practical way some of the nuances in using several popular point-of-care information resources. This is the second of 2 papers that these authors have contributed to the CCJM in an effort to inform and direct us how to quench our thirst for information without getting bloated.

Despite advances in therapy, more than 10% of patients with acute bacterial meningitis still die of it, and more suffer significant morbidity, including cognitive dysfunction and deafness. Well-defined protocols that include empiric antibiotics and systemic corticosteroids have improved the outcomes of patients with meningitis. But, as with other closed-space infections such as septic arthritis, any delay in providing appropriate antibiotic treatment is associated with a worse prognosis. In the case of bacterial meningitis, a retrospective analysis concluded that each hour of delay in delivering antibiotics and a corticosteroid can be associated with a relative (not absolute) increase in mortality of 13%.¹

The precise diagnosis of bacterial meningitis depends entirely on obtaining cerebrospinal fluid for analysis, including culture and antibiotic sensitivity testing. But that simple statement belies several current and historical complexities. From my experience, getting a prompt diagnostic lumbar puncture is not as simple as it once was.

Many hospitals have imposed patient safety initiatives, which overall have been beneficial but have had the effect that medical residents and probably even hospitalists in some medical centers are less frequently the ones doing interventional procedures. Some procedures, such as placement of pulmonary arterial catheters in the medical intensive care unit, have been shown to be less useful and to pose more risk than once believed. The tasks of placing other central lines and performing thoracenteses have been relegated to special procedure teams trained in using ultrasound guidance. Interventional radiologists now often do the visceral biopsies and lumbar punctures, and as a result, it is hoped that procedural complication rates will decline. On the other hand, these changes mean that medical residents and future staff are less experienced in performing these procedures, even though there are times that they are the only ones available to perform them. The result is a potential delay in performing a necessary lumbar puncture.

Another reason that a lumbar puncture may be delayed is concern over iatrogenic herniation if the procedure is done in a patient who has elevated intracranial pressure. We do not know precisely how often this occurs if there is an undiagnosed brain mass lesion such as an abscess, which can mimic bacterial meningitis, or a malignancy, and meningitis itself may be associated with herniation. Yet, for years physicians have hesitated to perform lumbar punctures in some patients without first ruling out a brain mass by computed tomography (CT), a diagnostic flow algorithm that often introduces at least an hour of delay in performing the procedure and in obtaining cultures before starting antibiotics.

When I was in training, we were perhaps more cavalier, appropriately or not. If the history and examination did not suggest a brain mass and the patient had retinal vein pulsations without papilledema, we did the lumbar puncture. It was a different time, and there was a different perspective on risks and benefits. More recently, the trend has been to obtain a CT scan before a lumbar puncture in several subsets of patients.

A 2015 analysis from Sweden¹ showed that we can probably do a lumbar puncture for suspected bacterial meningitis without first doing a CT scan in most patients, even in patients with moderately impaired mentation. Perhaps some other concerns can also be assuaged if evaluated, but we don’t have data. Mirrakhimov et al, in this issue of the Journal, review the current evidence on when to do CT before a lumbar puncture, even if it may significantly delay the procedure and the timely delivery of antibiotics. A perfect algorithm that balances the risks of delaying treatment, initiating less-than-ideal empiric antibiotics potentially without definitive culture, and inducing complications from a procedure done promptly may well be impossible to develop. Evidence helps us refine the diagnostic approach, but with limited data, some important decisions unfortunately remain within the “art” rather than the science of medicine.

Despite advances in therapy, more than 10% of patients with acute bacterial meningitis still die of it, and more suffer significant morbidity, including cognitive dysfunction and deafness. Well-defined protocols that include empiric antibiotics and systemic corticosteroids have improved the outcomes of patients with meningitis. But, as with other closed-space infections such as septic arthritis, any delay in providing appropriate antibiotic treatment is associated with a worse prognosis. In the case of bacterial meningitis, a retrospective analysis concluded that each hour of delay in delivering antibiotics and a corticosteroid can be associated with a relative (not absolute) increase in mortality of 13%.¹

The precise diagnosis of bacterial meningitis depends entirely on obtaining cerebrospinal fluid for analysis, including culture and antibiotic sensitivity testing. But that simple statement belies several current and historical complexities. From my experience, getting a prompt diagnostic lumbar puncture is not as simple as it once was.

Many hospitals have imposed patient safety initiatives, which overall have been beneficial but have had the effect that medical residents and probably even hospitalists in some medical centers are less frequently the ones doing interventional procedures. Some procedures, such as placement of pulmonary arterial catheters in the medical intensive care unit, have been shown to be less useful and to pose more risk than once believed. The tasks of placing other central lines and performing thoracenteses have been relegated to special procedure teams trained in using ultrasound guidance. Interventional radiologists now often do the visceral biopsies and lumbar punctures, and as a result, it is hoped that procedural complication rates will decline. On the other hand, these changes mean that medical residents and future staff are less experienced in performing these procedures, even though there are times that they are the only ones available to perform them. The result is a potential delay in performing a necessary lumbar puncture.

Another reason that a lumbar puncture may be delayed is concern over iatrogenic herniation if the procedure is done in a patient who has elevated intracranial pressure. We do not know precisely how often this occurs if there is an undiagnosed brain mass lesion such as an abscess, which can mimic bacterial meningitis, or a malignancy, and meningitis itself may be associated with herniation. Yet, for years physicians have hesitated to perform lumbar punctures in some patients without first ruling out a brain mass by computed tomography (CT), a diagnostic flow algorithm that often introduces at least an hour of delay in performing the procedure and in obtaining cultures before starting antibiotics.

When I was in training, we were perhaps more cavalier, appropriately or not. If the history and examination did not suggest a brain mass and the patient had retinal vein pulsations without papilledema, we did the lumbar puncture. It was a different time, and there was a different perspective on risks and benefits. More recently, the trend has been to obtain a CT scan before a lumbar puncture in several subsets of patients.

A 2015 analysis from Sweden¹ showed that we can probably do a lumbar puncture for suspected bacterial meningitis without first doing a CT scan in most patients, even in patients with moderately impaired mentation. Perhaps some other concerns can also be assuaged if evaluated, but we don’t have data. Mirrakhimov et al, in this issue of the Journal, review the current evidence on when to do CT before a lumbar puncture, even if it may significantly delay the procedure and the timely delivery of antibiotics. A perfect algorithm that balances the risks of delaying treatment, initiating less-than-ideal empiric antibiotics potentially without definitive culture, and inducing complications from a procedure done promptly may well be impossible to develop. Evidence helps us refine the diagnostic approach, but with limited data, some important decisions unfortunately remain within the “art” rather than the science of medicine.

Despite advances in therapy, more than 10% of patients with acute bacterial meningitis still die of it, and more suffer significant morbidity, including cognitive dysfunction and deafness. Well-defined protocols that include empiric antibiotics and systemic corticosteroids have improved the outcomes of patients with meningitis. But, as with other closed-space infections such as septic arthritis, any delay in providing appropriate antibiotic treatment is associated with a worse prognosis. In the case of bacterial meningitis, a retrospective analysis concluded that each hour of delay in delivering antibiotics and a corticosteroid can be associated with a relative (not absolute) increase in mortality of 13%.¹

The precise diagnosis of bacterial meningitis depends entirely on obtaining cerebrospinal fluid for analysis, including culture and antibiotic sensitivity testing. But that simple statement belies several current and historical complexities. From my experience, getting a prompt diagnostic lumbar puncture is not as simple as it once was.

Many hospitals have imposed patient safety initiatives, which overall have been beneficial but have had the effect that medical residents and probably even hospitalists in some medical centers are less frequently the ones doing interventional procedures. Some procedures, such as placement of pulmonary arterial catheters in the medical intensive care unit, have been shown to be less useful and to pose more risk than once believed. The tasks of placing other central lines and performing thoracenteses have been relegated to special procedure teams trained in using ultrasound guidance. Interventional radiologists now often do the visceral biopsies and lumbar punctures, and as a result, it is hoped that procedural complication rates will decline. On the other hand, these changes mean that medical residents and future staff are less experienced in performing these procedures, even though there are times that they are the only ones available to perform them. The result is a potential delay in performing a necessary lumbar puncture.

Another reason that a lumbar puncture may be delayed is concern over iatrogenic herniation if the procedure is done in a patient who has elevated intracranial pressure. We do not know precisely how often this occurs if there is an undiagnosed brain mass lesion such as an abscess, which can mimic bacterial meningitis, or a malignancy, and meningitis itself may be associated with herniation. Yet, for years physicians have hesitated to perform lumbar punctures in some patients without first ruling out a brain mass by computed tomography (CT), a diagnostic flow algorithm that often introduces at least an hour of delay in performing the procedure and in obtaining cultures before starting antibiotics.

When I was in training, we were perhaps more cavalier, appropriately or not. If the history and examination did not suggest a brain mass and the patient had retinal vein pulsations without papilledema, we did the lumbar puncture. It was a different time, and there was a different perspective on risks and benefits. More recently, the trend has been to obtain a CT scan before a lumbar puncture in several subsets of patients.

A 2015 analysis from Sweden¹ showed that we can probably do a lumbar puncture for suspected bacterial meningitis without first doing a CT scan in most patients, even in patients with moderately impaired mentation. Perhaps some other concerns can also be assuaged if evaluated, but we don’t have data. Mirrakhimov et al, in this issue of the Journal, review the current evidence on when to do CT before a lumbar puncture, even if it may significantly delay the procedure and the timely delivery of antibiotics. A perfect algorithm that balances the risks of delaying treatment, initiating less-than-ideal empiric antibiotics potentially without definitive culture, and inducing complications from a procedure done promptly may well be impossible to develop. Evidence helps us refine the diagnostic approach, but with limited data, some important decisions unfortunately remain within the “art” rather than the science of medicine.

Christopher Columbus, age 41, returned to Europe from his first voyage to the New World suffering from what would turn out to be a chronic illness that included recurrent febrile bouts of severe lower-extremity arthritis. For many years he was thought to have had gout, but careful reanalysis led Allison¹ and then Arnett et al² to propose an alternative diagnosis. Based on the pattern of Columbus’s arthritis and the accompanying symptoms, which these clinicians linked to the arthritis, they proposed the diagnosis of reactive arthritis—actually a subset of reactive arthritis, which at the time of their publications was called Reiter’s syndrome. Arnett discussed this extensively at a historic clinicopathologic conference, noting that the bouts of arthritis were prolonged (too long for typical gout) and that the historically described recurrent episodes of red (“bleeding”) eyes with intermittent “blindness” and ultimate immobility due to spine pain (arthritis) would not be typical of gout. Arnett et al recognized the pattern of this arthritis—lower-extremity-predominant with prolonged episodes, associated inflammatory eye disease, spine involvement, and the protracted course of nearly a decade—as far more typical of a reactive arthritis than gout (or ongoing bacterial infection), occurring in a likely HLA-B27-positive individual. They proposed that the probable trigger for the arthritis was an episode of food-borne bacterial infection acquired during the extensive transatlantic journey.

Fast forward about 470 years to an epidemic aboard a US Navy ship of Shigella-associated dysentery that was accompanied by readily diagnosed reactive arthritis.³ Several diarrheal epidemics with associated reactive arthritis aboard cruise ships have been described, and the association is well documented following Shigella, Salmonella, Campylobacter, and nondiarrheal chlamydial infections.

In this issue of the Journal, Gómez-Moyano et al present images of a patient with dermatologic features of reactive arthritis. I have two points to make in introducing this historical background. First, I want to highlight some features of this syndrome that are distinctive enough as a clinical pattern to enable a diagnosis by appearance alone or, as in the case of Columbus, by historical description alone. But second and more important, I wonder, as perhaps you do, why similar inflammatory features occur in patients of seemingly diverse backgrounds, triggered by different organisms that may have infected different mucosal areas. Why does this rose look like a rose and not a gardenia?

Reactive arthritis is classically thought of as self-limited, lasting less than 6 months. But a significant minority of patients may have chronic disease, particularly with spondylitis, which may be more common in patients who have the HLA-B27 haplotype. The peripheral arthritis generally affects relatively few joints, with the larger lower-extremity joints a common target. Enthesitis, especially at the Achilles tendon heel insertion, is common, and dactylitis or “sausage digits” can occur. These features may also be seen in patients with psoriatic or enteropathic arthritis. Inflammation of the skin (as shown by Gómez-Moyano et al), the eye (conjunctivitis, uveitis, episcleritis), oral mucosa, and the genitourinary tract (urethritis, prostatitis) can also occur. Urethritis can occur in patients with enteric diarrhea as the trigger; thus, it is not just associated with genitourinary infections like chlamydia. What all these sites have in common to be targeted following an infection is not known with certainty; relevant bacterial antigens cannot always be detected in the involved tissues. It is intriguing that transgenic rats engineered to contain many copies of the human HLA-B27 gene develop arthritis along with mucosal, eye, and skin inflammation, which can be avoided if the animals are raised in a germ-free environment. But probably fewer than 50% of patients with reactive arthritis have the B27 gene, so other factors must contribute to this uncommon syndrome. B27 is thus not a generally useful diagnostic test.

When a patient presents with acute inflammatory asymmetric oligoarthritis (affecting < 4 joints), infectious arthritis and crystal-induced arthritis need to be excluded. But looking for and finding other features more typical of reactive arthritis may spare the patient a more extensive and expensive inpatient evaluation.

Recognizing a rose can provide an aesthetic moment, even if we can’t define exactly what makes it a rose. Pattern recognition matters in clinical practice, even without full understanding of the molecular backdrop.

Christopher Columbus, age 41, returned to Europe from his first voyage to the New World suffering from what would turn out to be a chronic illness that included recurrent febrile bouts of severe lower-extremity arthritis. For many years he was thought to have had gout, but careful reanalysis led Allison¹ and then Arnett et al² to propose an alternative diagnosis. Based on the pattern of Columbus’s arthritis and the accompanying symptoms, which these clinicians linked to the arthritis, they proposed the diagnosis of reactive arthritis—actually a subset of reactive arthritis, which at the time of their publications was called Reiter’s syndrome. Arnett discussed this extensively at a historic clinicopathologic conference, noting that the bouts of arthritis were prolonged (too long for typical gout) and that the historically described recurrent episodes of red (“bleeding”) eyes with intermittent “blindness” and ultimate immobility due to spine pain (arthritis) would not be typical of gout. Arnett et al recognized the pattern of this arthritis—lower-extremity-predominant with prolonged episodes, associated inflammatory eye disease, spine involvement, and the protracted course of nearly a decade—as far more typical of a reactive arthritis than gout (or ongoing bacterial infection), occurring in a likely HLA-B27-positive individual. They proposed that the probable trigger for the arthritis was an episode of food-borne bacterial infection acquired during the extensive transatlantic journey.

Fast forward about 470 years to an epidemic aboard a US Navy ship of Shigella-associated dysentery that was accompanied by readily diagnosed reactive arthritis.³ Several diarrheal epidemics with associated reactive arthritis aboard cruise ships have been described, and the association is well documented following Shigella, Salmonella, Campylobacter, and nondiarrheal chlamydial infections.

In this issue of the Journal, Gómez-Moyano et al present images of a patient with dermatologic features of reactive arthritis. I have two points to make in introducing this historical background. First, I want to highlight some features of this syndrome that are distinctive enough as a clinical pattern to enable a diagnosis by appearance alone or, as in the case of Columbus, by historical description alone. But second and more important, I wonder, as perhaps you do, why similar inflammatory features occur in patients of seemingly diverse backgrounds, triggered by different organisms that may have infected different mucosal areas. Why does this rose look like a rose and not a gardenia?

Reactive arthritis is classically thought of as self-limited, lasting less than 6 months. But a significant minority of patients may have chronic disease, particularly with spondylitis, which may be more common in patients who have the HLA-B27 haplotype. The peripheral arthritis generally affects relatively few joints, with the larger lower-extremity joints a common target. Enthesitis, especially at the Achilles tendon heel insertion, is common, and dactylitis or “sausage digits” can occur. These features may also be seen in patients with psoriatic or enteropathic arthritis. Inflammation of the skin (as shown by Gómez-Moyano et al), the eye (conjunctivitis, uveitis, episcleritis), oral mucosa, and the genitourinary tract (urethritis, prostatitis) can also occur. Urethritis can occur in patients with enteric diarrhea as the trigger; thus, it is not just associated with genitourinary infections like chlamydia. What all these sites have in common to be targeted following an infection is not known with certainty; relevant bacterial antigens cannot always be detected in the involved tissues. It is intriguing that transgenic rats engineered to contain many copies of the human HLA-B27 gene develop arthritis along with mucosal, eye, and skin inflammation, which can be avoided if the animals are raised in a germ-free environment. But probably fewer than 50% of patients with reactive arthritis have the B27 gene, so other factors must contribute to this uncommon syndrome. B27 is thus not a generally useful diagnostic test.

When a patient presents with acute inflammatory asymmetric oligoarthritis (affecting < 4 joints), infectious arthritis and crystal-induced arthritis need to be excluded. But looking for and finding other features more typical of reactive arthritis may spare the patient a more extensive and expensive inpatient evaluation.

Recognizing a rose can provide an aesthetic moment, even if we can’t define exactly what makes it a rose. Pattern recognition matters in clinical practice, even without full understanding of the molecular backdrop.

Christopher Columbus, age 41, returned to Europe from his first voyage to the New World suffering from what would turn out to be a chronic illness that included recurrent febrile bouts of severe lower-extremity arthritis. For many years he was thought to have had gout, but careful reanalysis led Allison¹ and then Arnett et al² to propose an alternative diagnosis. Based on the pattern of Columbus’s arthritis and the accompanying symptoms, which these clinicians linked to the arthritis, they proposed the diagnosis of reactive arthritis—actually a subset of reactive arthritis, which at the time of their publications was called Reiter’s syndrome. Arnett discussed this extensively at a historic clinicopathologic conference, noting that the bouts of arthritis were prolonged (too long for typical gout) and that the historically described recurrent episodes of red (“bleeding”) eyes with intermittent “blindness” and ultimate immobility due to spine pain (arthritis) would not be typical of gout. Arnett et al recognized the pattern of this arthritis—lower-extremity-predominant with prolonged episodes, associated inflammatory eye disease, spine involvement, and the protracted course of nearly a decade—as far more typical of a reactive arthritis than gout (or ongoing bacterial infection), occurring in a likely HLA-B27-positive individual. They proposed that the probable trigger for the arthritis was an episode of food-borne bacterial infection acquired during the extensive transatlantic journey.

Fast forward about 470 years to an epidemic aboard a US Navy ship of Shigella-associated dysentery that was accompanied by readily diagnosed reactive arthritis.³ Several diarrheal epidemics with associated reactive arthritis aboard cruise ships have been described, and the association is well documented following Shigella, Salmonella, Campylobacter, and nondiarrheal chlamydial infections.

In this issue of the Journal, Gómez-Moyano et al present images of a patient with dermatologic features of reactive arthritis. I have two points to make in introducing this historical background. First, I want to highlight some features of this syndrome that are distinctive enough as a clinical pattern to enable a diagnosis by appearance alone or, as in the case of Columbus, by historical description alone. But second and more important, I wonder, as perhaps you do, why similar inflammatory features occur in patients of seemingly diverse backgrounds, triggered by different organisms that may have infected different mucosal areas. Why does this rose look like a rose and not a gardenia?

Reactive arthritis is classically thought of as self-limited, lasting less than 6 months. But a significant minority of patients may have chronic disease, particularly with spondylitis, which may be more common in patients who have the HLA-B27 haplotype. The peripheral arthritis generally affects relatively few joints, with the larger lower-extremity joints a common target. Enthesitis, especially at the Achilles tendon heel insertion, is common, and dactylitis or “sausage digits” can occur. These features may also be seen in patients with psoriatic or enteropathic arthritis. Inflammation of the skin (as shown by Gómez-Moyano et al), the eye (conjunctivitis, uveitis, episcleritis), oral mucosa, and the genitourinary tract (urethritis, prostatitis) can also occur. Urethritis can occur in patients with enteric diarrhea as the trigger; thus, it is not just associated with genitourinary infections like chlamydia. What all these sites have in common to be targeted following an infection is not known with certainty; relevant bacterial antigens cannot always be detected in the involved tissues. It is intriguing that transgenic rats engineered to contain many copies of the human HLA-B27 gene develop arthritis along with mucosal, eye, and skin inflammation, which can be avoided if the animals are raised in a germ-free environment. But probably fewer than 50% of patients with reactive arthritis have the B27 gene, so other factors must contribute to this uncommon syndrome. B27 is thus not a generally useful diagnostic test.

When a patient presents with acute inflammatory asymmetric oligoarthritis (affecting < 4 joints), infectious arthritis and crystal-induced arthritis need to be excluded. But looking for and finding other features more typical of reactive arthritis may spare the patient a more extensive and expensive inpatient evaluation.

Recognizing a rose can provide an aesthetic moment, even if we can’t define exactly what makes it a rose. Pattern recognition matters in clinical practice, even without full understanding of the molecular backdrop.

In this issue of the Journal, Ota et al provide a clinical image and vignette of a woman with emphysematous cystitis and a psoas abscess. Genitourinary infections with Escherichia coli are well known to occasionally produce gas—especially, it seems, in people with diabetes. But I thought it valuable to publish these images to provide a reminder of this infectious complication, as well as to highlight the cloaking effect of pharmacologic immunosuppression.

The patient they describe was receiving corticosteroids for brain metastases and was thus likely receiving a high dose. She had experienced abdominal pain for 3 days before seeking medical attention, but the infectious process undoubtedly predated that. Despite receiving appropriate antibiotics for more than 3 weeks, she harbored an expanding psoas abscess that was heralded by fever after the antibiotics were discontinued. This scenario is of little surprise in an ill 69-year-old diabetic woman with metastatic cancer who was receiving high-dose corticosteroids. We have all been taught about and likely have witnessed the devastating effect of delayed diagnosis of abdominal infections in patients on high-dose steroids.

With the current explosion of new targeted therapies for systemic and organ-specific inflammatory diseases, it is hard to keep up with their names, not to mention their mechanisms of action and potential complications. Much attention has been given, highlighted by the requisite warnings in direct-to-consumer advertising, to the reactivation of tuberculosis, the occurrence of fungal infections, and the risk of malignancy in patients taking many of these drugs. The risk of cancer seems to have been overstated, at least for the anti-tumor necrosis factor (anti-TNF) agents, but there is no question that some new biologics carry a real risk of reactivating latent tuberculosis and even some viral infections. But I have seen a more common problem, one that is inadequately emphasized: the delayed diagnosis of deep-tissue infection due to a blunting of the signs of inflammation that would normally accompany the infection.

Anti-TNF therapies (eg, infliximab, etanercept, adalimumab) are being increasingly prescribed for the gamut of systemic and organ-specific inflammatory diseases, from sarcoidosis and rheumatoid arthritis to uveitis. I have no doubt that these agents suppress the inflammatory response in ways that can delay diagnosis. I have seen it happen in patients with diverticular abscess, bacterial pneumonia, epidural abscess, and bacterial septic arthritis, and I believe it is a more concerning clinical issue than any actual increase in the number of opportunistic infections.

The anti-interleukin 6 biologic agent tocilizumab, like the anti-TNF agents, not only blunts the inflammatory response and masks infection, but also seems to contribute to an increased occurrence of lower intestinal perforation.¹ This is potentially important, as it seems likely that indications for this agent will be expanded to diseases other than rheumatoid arthritis.

Equal concern is likely warranted at the present time in patients receiving newer drugs such as Janus kinase (JAK) inhibitors and blockers of the interleukin 17 and 23 pathways, at least until more “real-life” patient experience is accumulated. Not all anti-inflammatory and immunosuppressive drugs have this dramatic blunting effect on findings of infection-associated inflammation (methotrexate seems not to), but we need to be wary and should perform extra-fastidious physical examinations followed by imaging studies when our patients complain of any localizing symptoms that are not readily and completely explained.

At the end of a tumultuous and divisive year, we at the Journal send to you, our readers, our heartfelt wishes for personal tranquility and for a universally peaceful and harmonious 2017.

In this issue of the Journal, Ota et al provide a clinical image and vignette of a woman with emphysematous cystitis and a psoas abscess. Genitourinary infections with Escherichia coli are well known to occasionally produce gas—especially, it seems, in people with diabetes. But I thought it valuable to publish these images to provide a reminder of this infectious complication, as well as to highlight the cloaking effect of pharmacologic immunosuppression.

The patient they describe was receiving corticosteroids for brain metastases and was thus likely receiving a high dose. She had experienced abdominal pain for 3 days before seeking medical attention, but the infectious process undoubtedly predated that. Despite receiving appropriate antibiotics for more than 3 weeks, she harbored an expanding psoas abscess that was heralded by fever after the antibiotics were discontinued. This scenario is of little surprise in an ill 69-year-old diabetic woman with metastatic cancer who was receiving high-dose corticosteroids. We have all been taught about and likely have witnessed the devastating effect of delayed diagnosis of abdominal infections in patients on high-dose steroids.

With the current explosion of new targeted therapies for systemic and organ-specific inflammatory diseases, it is hard to keep up with their names, not to mention their mechanisms of action and potential complications. Much attention has been given, highlighted by the requisite warnings in direct-to-consumer advertising, to the reactivation of tuberculosis, the occurrence of fungal infections, and the risk of malignancy in patients taking many of these drugs. The risk of cancer seems to have been overstated, at least for the anti-tumor necrosis factor (anti-TNF) agents, but there is no question that some new biologics carry a real risk of reactivating latent tuberculosis and even some viral infections. But I have seen a more common problem, one that is inadequately emphasized: the delayed diagnosis of deep-tissue infection due to a blunting of the signs of inflammation that would normally accompany the infection.

Anti-TNF therapies (eg, infliximab, etanercept, adalimumab) are being increasingly prescribed for the gamut of systemic and organ-specific inflammatory diseases, from sarcoidosis and rheumatoid arthritis to uveitis. I have no doubt that these agents suppress the inflammatory response in ways that can delay diagnosis. I have seen it happen in patients with diverticular abscess, bacterial pneumonia, epidural abscess, and bacterial septic arthritis, and I believe it is a more concerning clinical issue than any actual increase in the number of opportunistic infections.

The anti-interleukin 6 biologic agent tocilizumab, like the anti-TNF agents, not only blunts the inflammatory response and masks infection, but also seems to contribute to an increased occurrence of lower intestinal perforation.¹ This is potentially important, as it seems likely that indications for this agent will be expanded to diseases other than rheumatoid arthritis.

Equal concern is likely warranted at the present time in patients receiving newer drugs such as Janus kinase (JAK) inhibitors and blockers of the interleukin 17 and 23 pathways, at least until more “real-life” patient experience is accumulated. Not all anti-inflammatory and immunosuppressive drugs have this dramatic blunting effect on findings of infection-associated inflammation (methotrexate seems not to), but we need to be wary and should perform extra-fastidious physical examinations followed by imaging studies when our patients complain of any localizing symptoms that are not readily and completely explained.

At the end of a tumultuous and divisive year, we at the Journal send to you, our readers, our heartfelt wishes for personal tranquility and for a universally peaceful and harmonious 2017.

In this issue of the Journal, Ota et al provide a clinical image and vignette of a woman with emphysematous cystitis and a psoas abscess. Genitourinary infections with Escherichia coli are well known to occasionally produce gas—especially, it seems, in people with diabetes. But I thought it valuable to publish these images to provide a reminder of this infectious complication, as well as to highlight the cloaking effect of pharmacologic immunosuppression.

The patient they describe was receiving corticosteroids for brain metastases and was thus likely receiving a high dose. She had experienced abdominal pain for 3 days before seeking medical attention, but the infectious process undoubtedly predated that. Despite receiving appropriate antibiotics for more than 3 weeks, she harbored an expanding psoas abscess that was heralded by fever after the antibiotics were discontinued. This scenario is of little surprise in an ill 69-year-old diabetic woman with metastatic cancer who was receiving high-dose corticosteroids. We have all been taught about and likely have witnessed the devastating effect of delayed diagnosis of abdominal infections in patients on high-dose steroids.

With the current explosion of new targeted therapies for systemic and organ-specific inflammatory diseases, it is hard to keep up with their names, not to mention their mechanisms of action and potential complications. Much attention has been given, highlighted by the requisite warnings in direct-to-consumer advertising, to the reactivation of tuberculosis, the occurrence of fungal infections, and the risk of malignancy in patients taking many of these drugs. The risk of cancer seems to have been overstated, at least for the anti-tumor necrosis factor (anti-TNF) agents, but there is no question that some new biologics carry a real risk of reactivating latent tuberculosis and even some viral infections. But I have seen a more common problem, one that is inadequately emphasized: the delayed diagnosis of deep-tissue infection due to a blunting of the signs of inflammation that would normally accompany the infection.

Anti-TNF therapies (eg, infliximab, etanercept, adalimumab) are being increasingly prescribed for the gamut of systemic and organ-specific inflammatory diseases, from sarcoidosis and rheumatoid arthritis to uveitis. I have no doubt that these agents suppress the inflammatory response in ways that can delay diagnosis. I have seen it happen in patients with diverticular abscess, bacterial pneumonia, epidural abscess, and bacterial septic arthritis, and I believe it is a more concerning clinical issue than any actual increase in the number of opportunistic infections.

The anti-interleukin 6 biologic agent tocilizumab, like the anti-TNF agents, not only blunts the inflammatory response and masks infection, but also seems to contribute to an increased occurrence of lower intestinal perforation.¹ This is potentially important, as it seems likely that indications for this agent will be expanded to diseases other than rheumatoid arthritis.

Equal concern is likely warranted at the present time in patients receiving newer drugs such as Janus kinase (JAK) inhibitors and blockers of the interleukin 17 and 23 pathways, at least until more “real-life” patient experience is accumulated. Not all anti-inflammatory and immunosuppressive drugs have this dramatic blunting effect on findings of infection-associated inflammation (methotrexate seems not to), but we need to be wary and should perform extra-fastidious physical examinations followed by imaging studies when our patients complain of any localizing symptoms that are not readily and completely explained.

At the end of a tumultuous and divisive year, we at the Journal send to you, our readers, our heartfelt wishes for personal tranquility and for a universally peaceful and harmonious 2017.

Of the seven deadly sins, the worst is said to be pride, often represented in allegorical form as a peacock. In this month’s Journal, Kelly A. Cawcutt, MD and John W. Wilson, MD, and Nizar N. Zein, MD, note the rewards and challenges of caring for international patients. Pride, it seems to me, can get in the way of a successful relationship with these patients.

In the United States, we encounter a wide range of international patients, but there are two distinct categories: medical tourists, who come here by choice and often have significant financial means, and immigrants, who come here by choice or necessity and run the gamut of economic status.

The former group generally seeks care at major academic medical centers such as Cleveland Clinic and Mayo Clinic, which have built infrastructures to accommodate them, including paying special attention to the social aspects of the visit. For the medical center, there are immediate financial gains as well as potential long-term benefits, including international networking and philanthropy.

On the other hand, new immigrants, including refugees, generally seek care as needed where they have settled, mostly hoping that medical issues will not arise in the midst of the challenges of resettlement. They deserve and should expect to be able to establish a comfortable therapeutic relationship with a physician in a local medical practice, although one likely dissimilar from what they previously encountered.

For all of these patients, the focal point of interaction is us, the physician next to the examination table. Dr. Zein emphasizes the power of empathy and how our demeanor and choice of words are critical in building the therapeutic relationship. But pride can slip in, and the peacock subtly fans his tail.

While medical practice in the United States is technologically advanced in terms of tests and procedures, we are not the world leaders in outcomes or cost-effective care. We most certainly do not have a monopoly on delivering compassionate and empathic care or forging one-on-one doctor-patient relationships. We must be careful not to express a demeaning or dismissive attitude about the care our patients’ physicians provided in their home countries. That the laboratory and imaging reports are written in a different language, and perhaps reported in different units, should not imply any lower standard. We should also recognize that many of our physical examination skills have atrophied as we have come to over-rely on imaging studies. The apparent omission of an echocardiogram may in fact be an act of commission—a careful and confident physical examination may have resulted in a thoughtful decision to save the patient money. Careless words or a casually chauvinistic attitude can be disruptive to building a comfortable ongoing doctor-patient relationship.

At the same time, international patients come to see us with significant expectations (they may even have read our hospital’s marketing materials). But they may not be accustomed to their physician openly expressing a lack of certainty about a diagnosis. They may never have heard their at-home doctor say, “I don’t know.” The concept of patient involvement in the treatment plan may be totally foreign and discomforting to some, while others will expect that the entire family entourage (filling the exam room) will have an active role in decision-making.

Cultural awareness is critical as we sort these issues out so they do not stand in the way of successfully caring for the patient in front of us. We should avoid being too self-confident in our entrenched approach to healthcare delivery in the exam room (as well as in the redesign of our healthcare system). The peacock can be an attractive impediment.

Of the seven deadly sins, the worst is said to be pride, often represented in allegorical form as a peacock. In this month’s Journal, Kelly A. Cawcutt, MD and John W. Wilson, MD, and Nizar N. Zein, MD, note the rewards and challenges of caring for international patients. Pride, it seems to me, can get in the way of a successful relationship with these patients.

In the United States, we encounter a wide range of international patients, but there are two distinct categories: medical tourists, who come here by choice and often have significant financial means, and immigrants, who come here by choice or necessity and run the gamut of economic status.

The former group generally seeks care at major academic medical centers such as Cleveland Clinic and Mayo Clinic, which have built infrastructures to accommodate them, including paying special attention to the social aspects of the visit. For the medical center, there are immediate financial gains as well as potential long-term benefits, including international networking and philanthropy.

On the other hand, new immigrants, including refugees, generally seek care as needed where they have settled, mostly hoping that medical issues will not arise in the midst of the challenges of resettlement. They deserve and should expect to be able to establish a comfortable therapeutic relationship with a physician in a local medical practice, although one likely dissimilar from what they previously encountered.

For all of these patients, the focal point of interaction is us, the physician next to the examination table. Dr. Zein emphasizes the power of empathy and how our demeanor and choice of words are critical in building the therapeutic relationship. But pride can slip in, and the peacock subtly fans his tail.

While medical practice in the United States is technologically advanced in terms of tests and procedures, we are not the world leaders in outcomes or cost-effective care. We most certainly do not have a monopoly on delivering compassionate and empathic care or forging one-on-one doctor-patient relationships. We must be careful not to express a demeaning or dismissive attitude about the care our patients’ physicians provided in their home countries. That the laboratory and imaging reports are written in a different language, and perhaps reported in different units, should not imply any lower standard. We should also recognize that many of our physical examination skills have atrophied as we have come to over-rely on imaging studies. The apparent omission of an echocardiogram may in fact be an act of commission—a careful and confident physical examination may have resulted in a thoughtful decision to save the patient money. Careless words or a casually chauvinistic attitude can be disruptive to building a comfortable ongoing doctor-patient relationship.

At the same time, international patients come to see us with significant expectations (they may even have read our hospital’s marketing materials). But they may not be accustomed to their physician openly expressing a lack of certainty about a diagnosis. They may never have heard their at-home doctor say, “I don’t know.” The concept of patient involvement in the treatment plan may be totally foreign and discomforting to some, while others will expect that the entire family entourage (filling the exam room) will have an active role in decision-making.

Cultural awareness is critical as we sort these issues out so they do not stand in the way of successfully caring for the patient in front of us. We should avoid being too self-confident in our entrenched approach to healthcare delivery in the exam room (as well as in the redesign of our healthcare system). The peacock can be an attractive impediment.

Of the seven deadly sins, the worst is said to be pride, often represented in allegorical form as a peacock. In this month’s Journal, Kelly A. Cawcutt, MD and John W. Wilson, MD, and Nizar N. Zein, MD, note the rewards and challenges of caring for international patients. Pride, it seems to me, can get in the way of a successful relationship with these patients.

In the United States, we encounter a wide range of international patients, but there are two distinct categories: medical tourists, who come here by choice and often have significant financial means, and immigrants, who come here by choice or necessity and run the gamut of economic status.

The former group generally seeks care at major academic medical centers such as Cleveland Clinic and Mayo Clinic, which have built infrastructures to accommodate them, including paying special attention to the social aspects of the visit. For the medical center, there are immediate financial gains as well as potential long-term benefits, including international networking and philanthropy.

On the other hand, new immigrants, including refugees, generally seek care as needed where they have settled, mostly hoping that medical issues will not arise in the midst of the challenges of resettlement. They deserve and should expect to be able to establish a comfortable therapeutic relationship with a physician in a local medical practice, although one likely dissimilar from what they previously encountered.

For all of these patients, the focal point of interaction is us, the physician next to the examination table. Dr. Zein emphasizes the power of empathy and how our demeanor and choice of words are critical in building the therapeutic relationship. But pride can slip in, and the peacock subtly fans his tail.

While medical practice in the United States is technologically advanced in terms of tests and procedures, we are not the world leaders in outcomes or cost-effective care. We most certainly do not have a monopoly on delivering compassionate and empathic care or forging one-on-one doctor-patient relationships. We must be careful not to express a demeaning or dismissive attitude about the care our patients’ physicians provided in their home countries. That the laboratory and imaging reports are written in a different language, and perhaps reported in different units, should not imply any lower standard. We should also recognize that many of our physical examination skills have atrophied as we have come to over-rely on imaging studies. The apparent omission of an echocardiogram may in fact be an act of commission—a careful and confident physical examination may have resulted in a thoughtful decision to save the patient money. Careless words or a casually chauvinistic attitude can be disruptive to building a comfortable ongoing doctor-patient relationship.

At the same time, international patients come to see us with significant expectations (they may even have read our hospital’s marketing materials). But they may not be accustomed to their physician openly expressing a lack of certainty about a diagnosis. They may never have heard their at-home doctor say, “I don’t know.” The concept of patient involvement in the treatment plan may be totally foreign and discomforting to some, while others will expect that the entire family entourage (filling the exam room) will have an active role in decision-making.

Cultural awareness is critical as we sort these issues out so they do not stand in the way of successfully caring for the patient in front of us. We should avoid being too self-confident in our entrenched approach to healthcare delivery in the exam room (as well as in the redesign of our healthcare system). The peacock can be an attractive impediment.

Over the summer, I lectured in an internal medicine maintenance-of-certification course. Using a case-based discussion format, I presented real patients to review the breadth of rheumatic diseases that the course participants might encounter in their practices and on board examinations. At a break, one of the participants, obviously frustrated, approached me to say that he thought that I had mentioned too many uncommon situations, that he didn’t need to know secondary treatment options and disease mimics—I should just have reviewed the common aspects of the common diseases he would encounter in practice (and on the exam).

I was a bit taken aback. I try hard to avoid emphasizing the arcane details that only a subspecialist needs to know. I reconsidered my approach: should I only review the common and the expected? But without knowing something about the clinical permutations and the mimics of the common diseases we encounter, I don’t know how we can avoid making incorrect diagnoses due to the cognitive bias of familiarity. Common diseases are indeed common, but that doesn’t mean patients with less-common ones don’t find their way into our practices. As internists, we need to constantly humble ourselves with the knowledge that there is much in medicine, in every specialty, that we can’t remember, do not recognize, or just don’t know enough about. It is not just about “what will be on the test.” When a patient exhibits atypical features of the common disease that they have been diagnosed with, or doesn’t respond as expected to therapy, we need to remember that less-common mimics of that disease exist, even if we can’t remember the specific names or the pathophysiology.

Peripheral vascular disease is common, is rarely diagnosed early, and is usually related to atherosclerosis. Significant disease is generally manifested by symptoms of exertional limb ischemia or even pain at rest and stigmata of distal tissue hypoxia and necrosis from the decreased supply of oxygen and nutrients. But there are nonatherosclerotic causes of limb claudication, distal ischemia, and livedo reticularis. In my clinic, patients with those symptoms and findings are quite likely to have a form of large vessel arteritis, Raynaud phenomenon, or both. In a patient with Takayasu or giant cell arteritis, pain with repetitive arm use is more likely from subclavian occlusion than rotator cuff disease, whereas the latter is the far more common cause of arm pain with repetitive motion when patients see a physician for “arm pain” before the diagnosis of arteritis is considered. We need to entertain alternative diagnoses in order to perform the appropriate physical examination, obtain appropriate diagnostic studies, and initiate the correct therapy.

Eun et al, in this issue of the Journal, highlight and briefly discuss nine nonatherosclerotic entities that cause limb ischemia. The diagnostic assessment of these can be invasive and expensive, yet may be warranted to provide the appropriate therapy. The diagnosis not pursued will rarely be made in a timely manner, and the diagnosis not considered will not be pursued at all. And with these diseases, the patient’s history and examination usually provide the clues that the horse has stripes.

Eun et al highlight clinical features that may distinguish these entities from typical atherosclerotic peripheral vascular disease. Recognizing the features that are atypical for atherosclerosis implies that we know the more typical features of the disease. Knowing something about the uncommon as well as the common helps prepare us for the real test—the patient in front of us. And that patient doesn’t usually know that he or she is a zebra and not a horse.

Last month, I highlighted some staff changes in our editorial staff. I want to take this opportunity to introduce Craig Nielsen, MD, as our new deputy editor. Craig is a superb internist in both inpatient and outpatient arenas, a medical educator, and former director of our internal medicine residency program.

Over the summer, I lectured in an internal medicine maintenance-of-certification course. Using a case-based discussion format, I presented real patients to review the breadth of rheumatic diseases that the course participants might encounter in their practices and on board examinations. At a break, one of the participants, obviously frustrated, approached me to say that he thought that I had mentioned too many uncommon situations, that he didn’t need to know secondary treatment options and disease mimics—I should just have reviewed the common aspects of the common diseases he would encounter in practice (and on the exam).

I was a bit taken aback. I try hard to avoid emphasizing the arcane details that only a subspecialist needs to know. I reconsidered my approach: should I only review the common and the expected? But without knowing something about the clinical permutations and the mimics of the common diseases we encounter, I don’t know how we can avoid making incorrect diagnoses due to the cognitive bias of familiarity. Common diseases are indeed common, but that doesn’t mean patients with less-common ones don’t find their way into our practices. As internists, we need to constantly humble ourselves with the knowledge that there is much in medicine, in every specialty, that we can’t remember, do not recognize, or just don’t know enough about. It is not just about “what will be on the test.” When a patient exhibits atypical features of the common disease that they have been diagnosed with, or doesn’t respond as expected to therapy, we need to remember that less-common mimics of that disease exist, even if we can’t remember the specific names or the pathophysiology.

Peripheral vascular disease is common, is rarely diagnosed early, and is usually related to atherosclerosis. Significant disease is generally manifested by symptoms of exertional limb ischemia or even pain at rest and stigmata of distal tissue hypoxia and necrosis from the decreased supply of oxygen and nutrients. But there are nonatherosclerotic causes of limb claudication, distal ischemia, and livedo reticularis. In my clinic, patients with those symptoms and findings are quite likely to have a form of large vessel arteritis, Raynaud phenomenon, or both. In a patient with Takayasu or giant cell arteritis, pain with repetitive arm use is more likely from subclavian occlusion than rotator cuff disease, whereas the latter is the far more common cause of arm pain with repetitive motion when patients see a physician for “arm pain” before the diagnosis of arteritis is considered. We need to entertain alternative diagnoses in order to perform the appropriate physical examination, obtain appropriate diagnostic studies, and initiate the correct therapy.

Eun et al, in this issue of the Journal, highlight and briefly discuss nine nonatherosclerotic entities that cause limb ischemia. The diagnostic assessment of these can be invasive and expensive, yet may be warranted to provide the appropriate therapy. The diagnosis not pursued will rarely be made in a timely manner, and the diagnosis not considered will not be pursued at all. And with these diseases, the patient’s history and examination usually provide the clues that the horse has stripes.

Eun et al highlight clinical features that may distinguish these entities from typical atherosclerotic peripheral vascular disease. Recognizing the features that are atypical for atherosclerosis implies that we know the more typical features of the disease. Knowing something about the uncommon as well as the common helps prepare us for the real test—the patient in front of us. And that patient doesn’t usually know that he or she is a zebra and not a horse.

Last month, I highlighted some staff changes in our editorial staff. I want to take this opportunity to introduce Craig Nielsen, MD, as our new deputy editor. Craig is a superb internist in both inpatient and outpatient arenas, a medical educator, and former director of our internal medicine residency program.

Over the summer, I lectured in an internal medicine maintenance-of-certification course. Using a case-based discussion format, I presented real patients to review the breadth of rheumatic diseases that the course participants might encounter in their practices and on board examinations. At a break, one of the participants, obviously frustrated, approached me to say that he thought that I had mentioned too many uncommon situations, that he didn’t need to know secondary treatment options and disease mimics—I should just have reviewed the common aspects of the common diseases he would encounter in practice (and on the exam).

I was a bit taken aback. I try hard to avoid emphasizing the arcane details that only a subspecialist needs to know. I reconsidered my approach: should I only review the common and the expected? But without knowing something about the clinical permutations and the mimics of the common diseases we encounter, I don’t know how we can avoid making incorrect diagnoses due to the cognitive bias of familiarity. Common diseases are indeed common, but that doesn’t mean patients with less-common ones don’t find their way into our practices. As internists, we need to constantly humble ourselves with the knowledge that there is much in medicine, in every specialty, that we can’t remember, do not recognize, or just don’t know enough about. It is not just about “what will be on the test.” When a patient exhibits atypical features of the common disease that they have been diagnosed with, or doesn’t respond as expected to therapy, we need to remember that less-common mimics of that disease exist, even if we can’t remember the specific names or the pathophysiology.

Peripheral vascular disease is common, is rarely diagnosed early, and is usually related to atherosclerosis. Significant disease is generally manifested by symptoms of exertional limb ischemia or even pain at rest and stigmata of distal tissue hypoxia and necrosis from the decreased supply of oxygen and nutrients. But there are nonatherosclerotic causes of limb claudication, distal ischemia, and livedo reticularis. In my clinic, patients with those symptoms and findings are quite likely to have a form of large vessel arteritis, Raynaud phenomenon, or both. In a patient with Takayasu or giant cell arteritis, pain with repetitive arm use is more likely from subclavian occlusion than rotator cuff disease, whereas the latter is the far more common cause of arm pain with repetitive motion when patients see a physician for “arm pain” before the diagnosis of arteritis is considered. We need to entertain alternative diagnoses in order to perform the appropriate physical examination, obtain appropriate diagnostic studies, and initiate the correct therapy.

Eun et al, in this issue of the Journal, highlight and briefly discuss nine nonatherosclerotic entities that cause limb ischemia. The diagnostic assessment of these can be invasive and expensive, yet may be warranted to provide the appropriate therapy. The diagnosis not pursued will rarely be made in a timely manner, and the diagnosis not considered will not be pursued at all. And with these diseases, the patient’s history and examination usually provide the clues that the horse has stripes.

Eun et al highlight clinical features that may distinguish these entities from typical atherosclerotic peripheral vascular disease. Recognizing the features that are atypical for atherosclerosis implies that we know the more typical features of the disease. Knowing something about the uncommon as well as the common helps prepare us for the real test—the patient in front of us. And that patient doesn’t usually know that he or she is a zebra and not a horse.

Last month, I highlighted some staff changes in our editorial staff. I want to take this opportunity to introduce Craig Nielsen, MD, as our new deputy editor. Craig is a superb internist in both inpatient and outpatient arenas, a medical educator, and former director of our internal medicine residency program.

Our goal at the Cleveland Clinic Journal of Medicine is to provide timely, readily digestible, and useful clinical information to our readers. To do so, we need authors who buy into our educational mission, but we also need conscientious peer reviewers and an editorial staff capable of turning “doctorese” into readily understood English.

Our physician deputy editors Pelin Batur and James Pile solicit articles, guide authors, draft and revise CME questions, and assist greatly in the peer review process. Our nonphysician editors edit manuscripts to achieve a consistent editorial style in all of our published papers, but they serve many other key functions. They  manage the business of publishing a monthly journal at a time of drastically shrinking advertising revenue, they ensure that Journal content complies with rules for CME material published in print and online, and they keep up with continuous changes in online publishing. The Journal receives significant funding from Cleveland Clinic’s Education Institute, funding we need to pursue our role as an independent, peer-reviewed conveyer of clinical information.

I write this to emphasize that real people manage all of these tasks, and to gratefully acknowledge two people who are leaving the Journal: Mr. Joseph Dennehy and Dr. James Pile.

Long-time sales and marketing director Joe Dennehy played a key role in the Journal’s rise from relative obscurity about 20 years ago. This period was marked by many hospital-based journals closing up shop. Published since 1931, the Journal was relaunched in 1995 as a resource for postgraduate medical education with a national and international reach. Joe was brought in to guide and implement the marketing of the Journal as an independent, high-quality, clinical educational journal to increase its attractiveness as an advertising medium for the pharmaceutical industry so we could at least partly defray the significant expenses of publishing.

Joe is well known to medical publishers and media buyers, and over the past 20 years he became the face of the Journal in sales and marketing circles. In 2010, the Association of Medical Media recognized Joe’s achievements at its 18th Annual Nexus Representatives of the Year Awards, which acknowledge outstanding sales and marketing directors for their superior service, professionalism, and communication of ideas. Joe exemplifies these qualities and has been an inspiration to those of us who know and work with him. He has fully understood the sincerity of our mission and has never asked us to stray from it. Although Joe and his wife Holly live in New York, they are part of the Cleveland-based Journal family, and we will miss them. We wish them happiness and good health.

Dr. James Pile is an internal medicine hospitalist, an infectious disease specialist, and a superior medical educator. His work with us for the past several years has enhanced the Journal’s educational value for practicing hospitalists. His working familiarity with clinical leaders in the Society of Hospital Medicine has provided us with willing and skilled peer reviewers. Jim is now transitioning to a role as director of the internal medicine residency program at MetroHealth Medical Center, also here in Cleveland. He will continue to be a clinical resource for us as author and reviewer, but his ever-calm demeanor and clinical common sense will be hard to replace.

The Journal continues to evolve with the publishing times. We are assuming a greater presence in the digital world and adjusting to an environment of ever-diminishing advertising revenue. But with the work of our editorial team (I invite you to periodically glance at our masthead to note our team of writers, managers, and production staff), we intend to stay true to our educational mission. Our personal thanks to Joe and Jim for their contributions of the past, and to our current team in Scientific Publications for their ongoing and very personal commitment to providing the highest quality medical education that we can.

Our goal at the Cleveland Clinic Journal of Medicine is to provide timely, readily digestible, and useful clinical information to our readers. To do so, we need authors who buy into our educational mission, but we also need conscientious peer reviewers and an editorial staff capable of turning “doctorese” into readily understood English.

Our physician deputy editors Pelin Batur and James Pile solicit articles, guide authors, draft and revise CME questions, and assist greatly in the peer review process. Our nonphysician editors edit manuscripts to achieve a consistent editorial style in all of our published papers, but they serve many other key functions. They  manage the business of publishing a monthly journal at a time of drastically shrinking advertising revenue, they ensure that Journal content complies with rules for CME material published in print and online, and they keep up with continuous changes in online publishing. The Journal receives significant funding from Cleveland Clinic’s Education Institute, funding we need to pursue our role as an independent, peer-reviewed conveyer of clinical information.

I write this to emphasize that real people manage all of these tasks, and to gratefully acknowledge two people who are leaving the Journal: Mr. Joseph Dennehy and Dr. James Pile.

Long-time sales and marketing director Joe Dennehy played a key role in the Journal’s rise from relative obscurity about 20 years ago. This period was marked by many hospital-based journals closing up shop. Published since 1931, the Journal was relaunched in 1995 as a resource for postgraduate medical education with a national and international reach. Joe was brought in to guide and implement the marketing of the Journal as an independent, high-quality, clinical educational journal to increase its attractiveness as an advertising medium for the pharmaceutical industry so we could at least partly defray the significant expenses of publishing.

Joe is well known to medical publishers and media buyers, and over the past 20 years he became the face of the Journal in sales and marketing circles. In 2010, the Association of Medical Media recognized Joe’s achievements at its 18th Annual Nexus Representatives of the Year Awards, which acknowledge outstanding sales and marketing directors for their superior service, professionalism, and communication of ideas. Joe exemplifies these qualities and has been an inspiration to those of us who know and work with him. He has fully understood the sincerity of our mission and has never asked us to stray from it. Although Joe and his wife Holly live in New York, they are part of the Cleveland-based Journal family, and we will miss them. We wish them happiness and good health.

Dr. James Pile is an internal medicine hospitalist, an infectious disease specialist, and a superior medical educator. His work with us for the past several years has enhanced the Journal’s educational value for practicing hospitalists. His working familiarity with clinical leaders in the Society of Hospital Medicine has provided us with willing and skilled peer reviewers. Jim is now transitioning to a role as director of the internal medicine residency program at MetroHealth Medical Center, also here in Cleveland. He will continue to be a clinical resource for us as author and reviewer, but his ever-calm demeanor and clinical common sense will be hard to replace.

The Journal continues to evolve with the publishing times. We are assuming a greater presence in the digital world and adjusting to an environment of ever-diminishing advertising revenue. But with the work of our editorial team (I invite you to periodically glance at our masthead to note our team of writers, managers, and production staff), we intend to stay true to our educational mission. Our personal thanks to Joe and Jim for their contributions of the past, and to our current team in Scientific Publications for their ongoing and very personal commitment to providing the highest quality medical education that we can.

Our goal at the Cleveland Clinic Journal of Medicine is to provide timely, readily digestible, and useful clinical information to our readers. To do so, we need authors who buy into our educational mission, but we also need conscientious peer reviewers and an editorial staff capable of turning “doctorese” into readily understood English.

Our physician deputy editors Pelin Batur and James Pile solicit articles, guide authors, draft and revise CME questions, and assist greatly in the peer review process. Our nonphysician editors edit manuscripts to achieve a consistent editorial style in all of our published papers, but they serve many other key functions. They  manage the business of publishing a monthly journal at a time of drastically shrinking advertising revenue, they ensure that Journal content complies with rules for CME material published in print and online, and they keep up with continuous changes in online publishing. The Journal receives significant funding from Cleveland Clinic’s Education Institute, funding we need to pursue our role as an independent, peer-reviewed conveyer of clinical information.

I write this to emphasize that real people manage all of these tasks, and to gratefully acknowledge two people who are leaving the Journal: Mr. Joseph Dennehy and Dr. James Pile.

Long-time sales and marketing director Joe Dennehy played a key role in the Journal’s rise from relative obscurity about 20 years ago. This period was marked by many hospital-based journals closing up shop. Published since 1931, the Journal was relaunched in 1995 as a resource for postgraduate medical education with a national and international reach. Joe was brought in to guide and implement the marketing of the Journal as an independent, high-quality, clinical educational journal to increase its attractiveness as an advertising medium for the pharmaceutical industry so we could at least partly defray the significant expenses of publishing.

Joe is well known to medical publishers and media buyers, and over the past 20 years he became the face of the Journal in sales and marketing circles. In 2010, the Association of Medical Media recognized Joe’s achievements at its 18th Annual Nexus Representatives of the Year Awards, which acknowledge outstanding sales and marketing directors for their superior service, professionalism, and communication of ideas. Joe exemplifies these qualities and has been an inspiration to those of us who know and work with him. He has fully understood the sincerity of our mission and has never asked us to stray from it. Although Joe and his wife Holly live in New York, they are part of the Cleveland-based Journal family, and we will miss them. We wish them happiness and good health.

Dr. James Pile is an internal medicine hospitalist, an infectious disease specialist, and a superior medical educator. His work with us for the past several years has enhanced the Journal’s educational value for practicing hospitalists. His working familiarity with clinical leaders in the Society of Hospital Medicine has provided us with willing and skilled peer reviewers. Jim is now transitioning to a role as director of the internal medicine residency program at MetroHealth Medical Center, also here in Cleveland. He will continue to be a clinical resource for us as author and reviewer, but his ever-calm demeanor and clinical common sense will be hard to replace.

The Journal continues to evolve with the publishing times. We are assuming a greater presence in the digital world and adjusting to an environment of ever-diminishing advertising revenue. But with the work of our editorial team (I invite you to periodically glance at our masthead to note our team of writers, managers, and production staff), we intend to stay true to our educational mission. Our personal thanks to Joe and Jim for their contributions of the past, and to our current team in Scientific Publications for their ongoing and very personal commitment to providing the highest quality medical education that we can.