Imaging

A 48-year-old Nicaraguan man underwent mag netic resonance imaging (MRI) 3 days after admission to a South Florida hospital for treatment of cellulitis of the right thigh with vancomycin. MRI had been ordered to evaluate for a possible drainable source of infection, as the clinical picture and duration of illness was worsening and longer than expected for typical uncomplicated cellulitis despite intravenous antibiotic therapy. The MRI showed multiple enlarged inguinal lymph nodes and cellulitis of the superficial soft tissues of the thigh without discrete drainable collections.

After the procedure, the patient was noted to have a bullous lesion on each thigh, each lesion roughly 1 cm in diameter and filled with clear serous fluid (Figure 1). He reported that his legs had been pressed together before entering the MRI machine and that he had felt a burning sensation in both thighs during the test. Examination confirmed that the lesions indeed aligned with each other when he pressed his thighs together.

Study of a biopsy of one of the lesions revealed subepidermal cell blisters with focal epidermal necrosis and coagulative changes in the superficial dermis, consistent with a thermal injury (Figure 2).

HOW BURNS CAN OCCUR DURING MRI

Thermal burns are a potential cause of injury during MRI. Most have been observed in patients connected to external metal-containing monitoring devices, such as electrocardiogram leads and pulse oximeters.^1,2 Thermal burns  in patients unconnected to external devices have occurred when the patient’s body was touching radiofrequency coils³ or, as with our patient, when skin touches skin.^2,4,5 Skin-to-skin contact during MRI can cause the scanner to emit high-power electromagnetic radiofrequency pulses that are conducted through the body, creating heat. Tissue loops are created at points of skin-to-skin contact, thus forming a closed conducting circuit. The current flowing through this circuit can produce second-degree burns.⁴

We believe that during placement in the scanner, our patient inadvertently moved his thighs together, forming a closed loop conduction circuit and resulting in a thermal burn.

This case illustrates the importance of correct positioning during MRI. The MRI technicians had taken standard precautions, placing a sheet over the patient and ensuring no direct contact with the radiofrequency transmitter receiver (MR unit). However, precautions against skin-to-skin contact were not taken, and the patient’s legs were not separated.

LESSONS LEARNED

Appropriate positioning prevents closed skin-to-skin loops, but this may be more challenging in a larger patient.⁶ While the patient is in the scanner, a “squeeze ball” alert system allows the patient to signal the technologist should unexpected distress or heating occur.^6,7 A patient’s inability to utilize the squeeze ball contributes to the risk of a severe injury. Further, in this instance, there may have been a language barrier. Also, proximity of the anatomic skin-to-skin loop to the imaged body part (and therefore the center of the MRI coil) may have conferred risk related to field strength in this patient.

The MRI technologist, under supervision of a radiologist, is primarily responsible for positioning the patient to decrease the risk of this complication and for following institutional MRI safety protocols and professional guidelines.^6–8 MRI technologist certification training highlights all aspects of safety, including skin-to-skin conducting loop prevention.^7,8

A 48-year-old Nicaraguan man underwent mag netic resonance imaging (MRI) 3 days after admission to a South Florida hospital for treatment of cellulitis of the right thigh with vancomycin. MRI had been ordered to evaluate for a possible drainable source of infection, as the clinical picture and duration of illness was worsening and longer than expected for typical uncomplicated cellulitis despite intravenous antibiotic therapy. The MRI showed multiple enlarged inguinal lymph nodes and cellulitis of the superficial soft tissues of the thigh without discrete drainable collections.

After the procedure, the patient was noted to have a bullous lesion on each thigh, each lesion roughly 1 cm in diameter and filled with clear serous fluid (Figure 1). He reported that his legs had been pressed together before entering the MRI machine and that he had felt a burning sensation in both thighs during the test. Examination confirmed that the lesions indeed aligned with each other when he pressed his thighs together.

Study of a biopsy of one of the lesions revealed subepidermal cell blisters with focal epidermal necrosis and coagulative changes in the superficial dermis, consistent with a thermal injury (Figure 2).

HOW BURNS CAN OCCUR DURING MRI

Thermal burns are a potential cause of injury during MRI. Most have been observed in patients connected to external metal-containing monitoring devices, such as electrocardiogram leads and pulse oximeters.^1,2 Thermal burns  in patients unconnected to external devices have occurred when the patient’s body was touching radiofrequency coils³ or, as with our patient, when skin touches skin.^2,4,5 Skin-to-skin contact during MRI can cause the scanner to emit high-power electromagnetic radiofrequency pulses that are conducted through the body, creating heat. Tissue loops are created at points of skin-to-skin contact, thus forming a closed conducting circuit. The current flowing through this circuit can produce second-degree burns.⁴

We believe that during placement in the scanner, our patient inadvertently moved his thighs together, forming a closed loop conduction circuit and resulting in a thermal burn.

This case illustrates the importance of correct positioning during MRI. The MRI technicians had taken standard precautions, placing a sheet over the patient and ensuring no direct contact with the radiofrequency transmitter receiver (MR unit). However, precautions against skin-to-skin contact were not taken, and the patient’s legs were not separated.

LESSONS LEARNED

Appropriate positioning prevents closed skin-to-skin loops, but this may be more challenging in a larger patient.⁶ While the patient is in the scanner, a “squeeze ball” alert system allows the patient to signal the technologist should unexpected distress or heating occur.^6,7 A patient’s inability to utilize the squeeze ball contributes to the risk of a severe injury. Further, in this instance, there may have been a language barrier. Also, proximity of the anatomic skin-to-skin loop to the imaged body part (and therefore the center of the MRI coil) may have conferred risk related to field strength in this patient.

The MRI technologist, under supervision of a radiologist, is primarily responsible for positioning the patient to decrease the risk of this complication and for following institutional MRI safety protocols and professional guidelines.^6–8 MRI technologist certification training highlights all aspects of safety, including skin-to-skin conducting loop prevention.^7,8

A 48-year-old Nicaraguan man underwent mag netic resonance imaging (MRI) 3 days after admission to a South Florida hospital for treatment of cellulitis of the right thigh with vancomycin. MRI had been ordered to evaluate for a possible drainable source of infection, as the clinical picture and duration of illness was worsening and longer than expected for typical uncomplicated cellulitis despite intravenous antibiotic therapy. The MRI showed multiple enlarged inguinal lymph nodes and cellulitis of the superficial soft tissues of the thigh without discrete drainable collections.

After the procedure, the patient was noted to have a bullous lesion on each thigh, each lesion roughly 1 cm in diameter and filled with clear serous fluid (Figure 1). He reported that his legs had been pressed together before entering the MRI machine and that he had felt a burning sensation in both thighs during the test. Examination confirmed that the lesions indeed aligned with each other when he pressed his thighs together.

Study of a biopsy of one of the lesions revealed subepidermal cell blisters with focal epidermal necrosis and coagulative changes in the superficial dermis, consistent with a thermal injury (Figure 2).

HOW BURNS CAN OCCUR DURING MRI

Thermal burns are a potential cause of injury during MRI. Most have been observed in patients connected to external metal-containing monitoring devices, such as electrocardiogram leads and pulse oximeters.^1,2 Thermal burns  in patients unconnected to external devices have occurred when the patient’s body was touching radiofrequency coils³ or, as with our patient, when skin touches skin.^2,4,5 Skin-to-skin contact during MRI can cause the scanner to emit high-power electromagnetic radiofrequency pulses that are conducted through the body, creating heat. Tissue loops are created at points of skin-to-skin contact, thus forming a closed conducting circuit. The current flowing through this circuit can produce second-degree burns.⁴

We believe that during placement in the scanner, our patient inadvertently moved his thighs together, forming a closed loop conduction circuit and resulting in a thermal burn.

This case illustrates the importance of correct positioning during MRI. The MRI technicians had taken standard precautions, placing a sheet over the patient and ensuring no direct contact with the radiofrequency transmitter receiver (MR unit). However, precautions against skin-to-skin contact were not taken, and the patient’s legs were not separated.

LESSONS LEARNED

Appropriate positioning prevents closed skin-to-skin loops, but this may be more challenging in a larger patient.⁶ While the patient is in the scanner, a “squeeze ball” alert system allows the patient to signal the technologist should unexpected distress or heating occur.^6,7 A patient’s inability to utilize the squeeze ball contributes to the risk of a severe injury. Further, in this instance, there may have been a language barrier. Also, proximity of the anatomic skin-to-skin loop to the imaged body part (and therefore the center of the MRI coil) may have conferred risk related to field strength in this patient.

The MRI technologist, under supervision of a radiologist, is primarily responsible for positioning the patient to decrease the risk of this complication and for following institutional MRI safety protocols and professional guidelines.^6–8 MRI technologist certification training highlights all aspects of safety, including skin-to-skin conducting loop prevention.^7,8

SNOWMASS, COLO. – Mounting evidence attests to the value of noninvasive measurement of coronary flow reserve as a means of classifying cardiovascular risk in patients with stable coronary artery disease (CAD) more accurately than is possible via coronary angiography or measurement of fractional flow reserve, Marcelo F. Di Carli, MD, reported at the Annual Cardiovascular Conference at Snowmass.

“We use CFR [coronary flow reserve] as a way to exclude coronary disease. It’s a good practical measure of multivessel ischemic CAD. When the CFR is normal, you can with high confidence exclude the possibility of high-risk CAD,” according to Dr. Di Carli, executive director of the cardiovascular imaging program and chief of the division of nuclear medicine and molecular imaging at Brigham and Women’s Hospital, Boston.

Bruce Jancin/Frontline Medical News

[email protected]

SNOWMASS, COLO. – Mounting evidence attests to the value of noninvasive measurement of coronary flow reserve as a means of classifying cardiovascular risk in patients with stable coronary artery disease (CAD) more accurately than is possible via coronary angiography or measurement of fractional flow reserve, Marcelo F. Di Carli, MD, reported at the Annual Cardiovascular Conference at Snowmass.

“We use CFR [coronary flow reserve] as a way to exclude coronary disease. It’s a good practical measure of multivessel ischemic CAD. When the CFR is normal, you can with high confidence exclude the possibility of high-risk CAD,” according to Dr. Di Carli, executive director of the cardiovascular imaging program and chief of the division of nuclear medicine and molecular imaging at Brigham and Women’s Hospital, Boston.

Bruce Jancin/Frontline Medical News

[email protected]

SNOWMASS, COLO. – Mounting evidence attests to the value of noninvasive measurement of coronary flow reserve as a means of classifying cardiovascular risk in patients with stable coronary artery disease (CAD) more accurately than is possible via coronary angiography or measurement of fractional flow reserve, Marcelo F. Di Carli, MD, reported at the Annual Cardiovascular Conference at Snowmass.

“We use CFR [coronary flow reserve] as a way to exclude coronary disease. It’s a good practical measure of multivessel ischemic CAD. When the CFR is normal, you can with high confidence exclude the possibility of high-risk CAD,” according to Dr. Di Carli, executive director of the cardiovascular imaging program and chief of the division of nuclear medicine and molecular imaging at Brigham and Women’s Hospital, Boston.

Bruce Jancin/Frontline Medical News

[email protected]

“... with the rapid extension of laboratory tests of greater accuracy, there is a tendency for some clinicians and hence for some students in reaching a diagnosis to rely more on laboratory reports and less on the history of the illness, the examination and behavior of the patient and clinical judgment. While in many cases laboratory findings are invaluable for reaching correct conclusions, the student should never be allowed to forget that it takes a man, not a machine, to understand a man.”

—Raymond B. Allen, MD, PhD, 1946¹

From Hippocrates onward, accurate diagnosis has always been the prerequisite for prognosis and treatment. Physicians typically diagnosed through astute interviewing, deductive reasoning, and skillful use of observation and touch. Then, in the past 250 years they added 2 more tools to their diagnostic skill set: percussion and auscultation, the dual foundation of bedside assessment. Intriguingly, both these skills were first envisioned by multifaceted minds: percussion by Leopold Auenbrugger, an Austrian music-lover who even wrote librettos for operas; and stethoscopy by René Laennec, a Breton flutist, poet, and dancer—not exactly the kind of doctors we tend to produce today.

See related article

Still, the point of this preamble is not to say that eclecticism may help creativity (it does), but to remind ourselves that it has only been for a century or so that physicians have been able to rely on laboratory and radiologic studies. In fact, the now ubiquitous and almost obligatory imaging tests (computed tomography, magnetic resonance imaging, positron-emission tomography, and ultrasonography) have been available to practitioners for only threescore years or less. Yet tests have become so dominant in our culture that it is hard to imagine a time when physicians could count only on their wit and senses.

CLINICAL SKILLS ARE STILL RELEVANT

Ironically, many studies tell us that history and bedside examination can still deliver most diagnoses.^2,3 In fact, clinical skills can solve even the most perplexing dilemmas. In an automated analysis of the clinicopathologic conference cases presented in the New England Journal of Medicine,⁴ history and physical examination still yielded a correct diagnosis in 64% of those very challenging patients.

Bedside examination may be especially important in the hospital. In a study of inpatients,⁵ physical examination detected crucial findings in one-fourth of the cases and prompted management changes in many others. As the authors concluded, sick patients need careful examination, the more skilled the better.

Unfortunately, errors in physical examination are common. In a recent review of 208 cases, 63% of oversights were due to failure to perform an examination, while 25% were either missed or misinterpreted findings.⁶ These errors interfered with diagnosis in three-fourths of the cases, and with treatment in half.

Which brings us to the interesting observation by Kondo et al,⁷ who in this issue of the Journal report how the lowly physical examination proved more helpful than expensive magnetic resonance imaging in evaluating a perplexing case of refractory shoulder pain.

This is not an isolated instance. To get back to Laennec, whose stethoscope just turned 200, auscultation too can help the 21st-century physician. For example, posturally induced crackles, a recently discovered phenomenon, are the third-best predictor of outcome following myocardial infarction, immediately after the number of diseased vessels and pulmonary capillary wedge pressure.⁸

The time-honored art of observation can also yield new and important clues. From the earlobe crease of Dr. Frank, to the elfin face of Dr. Williams, there are lots of diseases out there waiting for our name—if only we could see them. As William Osler put it, “The whole art of medicine is in observation.”⁹

 

 

TECHNOLOGY: MASTER OR SERVANT?

But how can residents truly “observe” when they have to spend 40% of their time looking at computer screens and only 12% looking at people?¹⁰ To quote Osler again, “To educate the eye to see, the ear to hear, and the finger to feel takes time.”⁹ Yet time in medicine is at a premium. In a large national survey, the average ambulatory care visit to a general practitioner lasted 16 minutes,¹¹ which makes it difficult to use inexpensive but time-consuming maneuvers. Detection of posturally induced crackles, for example, may require as much as 9 minutes, and a thorough breast examination up to 10.¹² On the other hand, ordering tests costs little time to the physician but a huge sum to patients and society. Paradoxically, “tests” may be quite profitable for the medical-industrial complex. Hence the erosion of clinical skills.

Overreliance on diagnostic technology is particularly concerning when the cost of medicine has skyrocketed. The United States now spends $3.2 trillion a year for healthcare, and much of this money goes into technology.

In fact, high-tech might hurt us even more than in the pocket. It is a sad fact of modern medicine that when unguided by clinical skills, technology can take us down a rabbit hole, wherein tests beget tests, and where at the end there is usually a surgeon, often a lawyer, and sometimes even an undertaker. The literature is full of such cases, to the point that the risk of unnecessary tests has spawned a charming new acronym: VOMIT (victims of modern imaging technology).¹³

I’m not suggesting that we discard appropriate laboratory and radiologic testing. To the contrary. Yet contributions like those of Kondo et al remind us that even in today’s medicine, the bedside remains not only the royal road to diagnosis, but also the best filter for a more judicious and cost-effective use of technology.

That filter starts with history-taking (“Listen to the patient” said Osler, “he is telling you the diagnosis.”),⁹ and continues with the physical examination. In fact, the history typically guides the physical examination. Hence, when the patient’s symptoms point away from a particular organ, the examination of that organ may be reduced to a minimum. For instance, in neurologic patients whose history made certain findings unlikely, a Canadian group was able to cut in half the number of core items of their neurologic examination.¹⁴

Yet when the history flags a system, the clinician needs to go deeper into the examination. It’s very much what we do with laboratory tests, moving from screening tests to more advanced inquiries as we tailor our diagnostic studies to the patient’s presentation. For that we need validated maneuvers. Recent efforts in this direction have turned the art of physical examination into a science.¹⁵

Lastly, patients expect to be examined, and in fact they resent when this doesn’t happen.¹⁶ Lewis Thomas called touching our “real professional secret” and “the oldest and most effective art of doctors.”¹⁷ It may even have therapeutic value.

TEACHING BEDSIDE DIAGNOSIS

So, if bedside diagnosis is important, what can we do to rekindle it? Probably anything but continue in the old ways. Studies have consistently shown that auscultation does not improve with years of training, and that in fact attending physicians may be no more proficient than third-year medical students.¹⁸ Other areas of the examination have shown similarly depressing trends,¹⁹ thus suggesting that the traditional apprenticeship mode of learning from both faculty and senior trainees may not be helpful. In fact, it may be akin to Bruegel the Elder’s painting of the blind leading the blind, and all ending up in a ditch.

Advanced physical diagnosis courses have thus been advocated, and indeed implemented at many institutions, but usually as electives. Faculty development programs have also been recommended. Still, these interventions may not suffice.

Cutting the cord to technology by serving in a developing country

My hunch is that the rekindling of physical diagnosis may require extreme measures, like putting ourselves in a zero-tech, zero-tests environment. Years ago, I had that kind of cold-turkey experience when I spent a month in a remote Nepali clinic with neither electricity nor running water—and, of course, no cell phone and no Internet. In fact, my only tools were a translator, a stethoscope, and my brain and senses. It was both terrifying and instructive, very much like the time my uncle tried to teach me how to swim by suddenly throwing me into the Mediterranean.

Maybe we should offer that kind of “immersion” to our students. A senior rotation in a technology-depleted country might do a lot of good for a young medical mind. For one, it could remind students that physicians are not only the “natural attorneys of the poor,” as Virchow famously put it,²⁰ but also the ultimate citizens of the world. To quote Dr. Osler again, “Distinctions of race, nationality, color, and creed are unknown within the portals of the temple of Æsculapius.”²¹ Such an experience might also foster empathy and tolerance for ambiguity, 2 other traits whose absence we lament in today’s medicine. More importantly, if preceded by an advanced physical diagnosis course, a rotation in a developing country could work miracles for honing bedside skills, especially if the students are accompanied by a faculty member who can be both inspiring and gifted in the art and science of bedside diagnosis.

Ultimately, this experience could remind our young that the art of medicine is much harder to acquire than the science, and that medicine is indeed a calling and not a trade. Osler said it too, and these are indeed provocative thoughts, but short of provocations and out-of-the-box ideas, the tail will continue to wag the dog. And in the end it will cost us more than money. It will cost us the art of medicine.

“... with the rapid extension of laboratory tests of greater accuracy, there is a tendency for some clinicians and hence for some students in reaching a diagnosis to rely more on laboratory reports and less on the history of the illness, the examination and behavior of the patient and clinical judgment. While in many cases laboratory findings are invaluable for reaching correct conclusions, the student should never be allowed to forget that it takes a man, not a machine, to understand a man.”

—Raymond B. Allen, MD, PhD, 1946¹

From Hippocrates onward, accurate diagnosis has always been the prerequisite for prognosis and treatment. Physicians typically diagnosed through astute interviewing, deductive reasoning, and skillful use of observation and touch. Then, in the past 250 years they added 2 more tools to their diagnostic skill set: percussion and auscultation, the dual foundation of bedside assessment. Intriguingly, both these skills were first envisioned by multifaceted minds: percussion by Leopold Auenbrugger, an Austrian music-lover who even wrote librettos for operas; and stethoscopy by René Laennec, a Breton flutist, poet, and dancer—not exactly the kind of doctors we tend to produce today.

See related article

Still, the point of this preamble is not to say that eclecticism may help creativity (it does), but to remind ourselves that it has only been for a century or so that physicians have been able to rely on laboratory and radiologic studies. In fact, the now ubiquitous and almost obligatory imaging tests (computed tomography, magnetic resonance imaging, positron-emission tomography, and ultrasonography) have been available to practitioners for only threescore years or less. Yet tests have become so dominant in our culture that it is hard to imagine a time when physicians could count only on their wit and senses.

CLINICAL SKILLS ARE STILL RELEVANT

Ironically, many studies tell us that history and bedside examination can still deliver most diagnoses.^2,3 In fact, clinical skills can solve even the most perplexing dilemmas. In an automated analysis of the clinicopathologic conference cases presented in the New England Journal of Medicine,⁴ history and physical examination still yielded a correct diagnosis in 64% of those very challenging patients.

Bedside examination may be especially important in the hospital. In a study of inpatients,⁵ physical examination detected crucial findings in one-fourth of the cases and prompted management changes in many others. As the authors concluded, sick patients need careful examination, the more skilled the better.

Unfortunately, errors in physical examination are common. In a recent review of 208 cases, 63% of oversights were due to failure to perform an examination, while 25% were either missed or misinterpreted findings.⁶ These errors interfered with diagnosis in three-fourths of the cases, and with treatment in half.

Which brings us to the interesting observation by Kondo et al,⁷ who in this issue of the Journal report how the lowly physical examination proved more helpful than expensive magnetic resonance imaging in evaluating a perplexing case of refractory shoulder pain.

This is not an isolated instance. To get back to Laennec, whose stethoscope just turned 200, auscultation too can help the 21st-century physician. For example, posturally induced crackles, a recently discovered phenomenon, are the third-best predictor of outcome following myocardial infarction, immediately after the number of diseased vessels and pulmonary capillary wedge pressure.⁸

The time-honored art of observation can also yield new and important clues. From the earlobe crease of Dr. Frank, to the elfin face of Dr. Williams, there are lots of diseases out there waiting for our name—if only we could see them. As William Osler put it, “The whole art of medicine is in observation.”⁹

 

 

TECHNOLOGY: MASTER OR SERVANT?

But how can residents truly “observe” when they have to spend 40% of their time looking at computer screens and only 12% looking at people?¹⁰ To quote Osler again, “To educate the eye to see, the ear to hear, and the finger to feel takes time.”⁹ Yet time in medicine is at a premium. In a large national survey, the average ambulatory care visit to a general practitioner lasted 16 minutes,¹¹ which makes it difficult to use inexpensive but time-consuming maneuvers. Detection of posturally induced crackles, for example, may require as much as 9 minutes, and a thorough breast examination up to 10.¹² On the other hand, ordering tests costs little time to the physician but a huge sum to patients and society. Paradoxically, “tests” may be quite profitable for the medical-industrial complex. Hence the erosion of clinical skills.

Overreliance on diagnostic technology is particularly concerning when the cost of medicine has skyrocketed. The United States now spends $3.2 trillion a year for healthcare, and much of this money goes into technology.

In fact, high-tech might hurt us even more than in the pocket. It is a sad fact of modern medicine that when unguided by clinical skills, technology can take us down a rabbit hole, wherein tests beget tests, and where at the end there is usually a surgeon, often a lawyer, and sometimes even an undertaker. The literature is full of such cases, to the point that the risk of unnecessary tests has spawned a charming new acronym: VOMIT (victims of modern imaging technology).¹³

I’m not suggesting that we discard appropriate laboratory and radiologic testing. To the contrary. Yet contributions like those of Kondo et al remind us that even in today’s medicine, the bedside remains not only the royal road to diagnosis, but also the best filter for a more judicious and cost-effective use of technology.

That filter starts with history-taking (“Listen to the patient” said Osler, “he is telling you the diagnosis.”),⁹ and continues with the physical examination. In fact, the history typically guides the physical examination. Hence, when the patient’s symptoms point away from a particular organ, the examination of that organ may be reduced to a minimum. For instance, in neurologic patients whose history made certain findings unlikely, a Canadian group was able to cut in half the number of core items of their neurologic examination.¹⁴

Yet when the history flags a system, the clinician needs to go deeper into the examination. It’s very much what we do with laboratory tests, moving from screening tests to more advanced inquiries as we tailor our diagnostic studies to the patient’s presentation. For that we need validated maneuvers. Recent efforts in this direction have turned the art of physical examination into a science.¹⁵

Lastly, patients expect to be examined, and in fact they resent when this doesn’t happen.¹⁶ Lewis Thomas called touching our “real professional secret” and “the oldest and most effective art of doctors.”¹⁷ It may even have therapeutic value.

TEACHING BEDSIDE DIAGNOSIS

So, if bedside diagnosis is important, what can we do to rekindle it? Probably anything but continue in the old ways. Studies have consistently shown that auscultation does not improve with years of training, and that in fact attending physicians may be no more proficient than third-year medical students.¹⁸ Other areas of the examination have shown similarly depressing trends,¹⁹ thus suggesting that the traditional apprenticeship mode of learning from both faculty and senior trainees may not be helpful. In fact, it may be akin to Bruegel the Elder’s painting of the blind leading the blind, and all ending up in a ditch.

Advanced physical diagnosis courses have thus been advocated, and indeed implemented at many institutions, but usually as electives. Faculty development programs have also been recommended. Still, these interventions may not suffice.

Cutting the cord to technology by serving in a developing country

My hunch is that the rekindling of physical diagnosis may require extreme measures, like putting ourselves in a zero-tech, zero-tests environment. Years ago, I had that kind of cold-turkey experience when I spent a month in a remote Nepali clinic with neither electricity nor running water—and, of course, no cell phone and no Internet. In fact, my only tools were a translator, a stethoscope, and my brain and senses. It was both terrifying and instructive, very much like the time my uncle tried to teach me how to swim by suddenly throwing me into the Mediterranean.

Maybe we should offer that kind of “immersion” to our students. A senior rotation in a technology-depleted country might do a lot of good for a young medical mind. For one, it could remind students that physicians are not only the “natural attorneys of the poor,” as Virchow famously put it,²⁰ but also the ultimate citizens of the world. To quote Dr. Osler again, “Distinctions of race, nationality, color, and creed are unknown within the portals of the temple of Æsculapius.”²¹ Such an experience might also foster empathy and tolerance for ambiguity, 2 other traits whose absence we lament in today’s medicine. More importantly, if preceded by an advanced physical diagnosis course, a rotation in a developing country could work miracles for honing bedside skills, especially if the students are accompanied by a faculty member who can be both inspiring and gifted in the art and science of bedside diagnosis.

Ultimately, this experience could remind our young that the art of medicine is much harder to acquire than the science, and that medicine is indeed a calling and not a trade. Osler said it too, and these are indeed provocative thoughts, but short of provocations and out-of-the-box ideas, the tail will continue to wag the dog. And in the end it will cost us more than money. It will cost us the art of medicine.

“... with the rapid extension of laboratory tests of greater accuracy, there is a tendency for some clinicians and hence for some students in reaching a diagnosis to rely more on laboratory reports and less on the history of the illness, the examination and behavior of the patient and clinical judgment. While in many cases laboratory findings are invaluable for reaching correct conclusions, the student should never be allowed to forget that it takes a man, not a machine, to understand a man.”

—Raymond B. Allen, MD, PhD, 1946¹

From Hippocrates onward, accurate diagnosis has always been the prerequisite for prognosis and treatment. Physicians typically diagnosed through astute interviewing, deductive reasoning, and skillful use of observation and touch. Then, in the past 250 years they added 2 more tools to their diagnostic skill set: percussion and auscultation, the dual foundation of bedside assessment. Intriguingly, both these skills were first envisioned by multifaceted minds: percussion by Leopold Auenbrugger, an Austrian music-lover who even wrote librettos for operas; and stethoscopy by René Laennec, a Breton flutist, poet, and dancer—not exactly the kind of doctors we tend to produce today.

See related article

Still, the point of this preamble is not to say that eclecticism may help creativity (it does), but to remind ourselves that it has only been for a century or so that physicians have been able to rely on laboratory and radiologic studies. In fact, the now ubiquitous and almost obligatory imaging tests (computed tomography, magnetic resonance imaging, positron-emission tomography, and ultrasonography) have been available to practitioners for only threescore years or less. Yet tests have become so dominant in our culture that it is hard to imagine a time when physicians could count only on their wit and senses.

CLINICAL SKILLS ARE STILL RELEVANT

Ironically, many studies tell us that history and bedside examination can still deliver most diagnoses.^2,3 In fact, clinical skills can solve even the most perplexing dilemmas. In an automated analysis of the clinicopathologic conference cases presented in the New England Journal of Medicine,⁴ history and physical examination still yielded a correct diagnosis in 64% of those very challenging patients.

Bedside examination may be especially important in the hospital. In a study of inpatients,⁵ physical examination detected crucial findings in one-fourth of the cases and prompted management changes in many others. As the authors concluded, sick patients need careful examination, the more skilled the better.

Unfortunately, errors in physical examination are common. In a recent review of 208 cases, 63% of oversights were due to failure to perform an examination, while 25% were either missed or misinterpreted findings.⁶ These errors interfered with diagnosis in three-fourths of the cases, and with treatment in half.

Which brings us to the interesting observation by Kondo et al,⁷ who in this issue of the Journal report how the lowly physical examination proved more helpful than expensive magnetic resonance imaging in evaluating a perplexing case of refractory shoulder pain.

This is not an isolated instance. To get back to Laennec, whose stethoscope just turned 200, auscultation too can help the 21st-century physician. For example, posturally induced crackles, a recently discovered phenomenon, are the third-best predictor of outcome following myocardial infarction, immediately after the number of diseased vessels and pulmonary capillary wedge pressure.⁸

The time-honored art of observation can also yield new and important clues. From the earlobe crease of Dr. Frank, to the elfin face of Dr. Williams, there are lots of diseases out there waiting for our name—if only we could see them. As William Osler put it, “The whole art of medicine is in observation.”⁹

 

 

TECHNOLOGY: MASTER OR SERVANT?

But how can residents truly “observe” when they have to spend 40% of their time looking at computer screens and only 12% looking at people?¹⁰ To quote Osler again, “To educate the eye to see, the ear to hear, and the finger to feel takes time.”⁹ Yet time in medicine is at a premium. In a large national survey, the average ambulatory care visit to a general practitioner lasted 16 minutes,¹¹ which makes it difficult to use inexpensive but time-consuming maneuvers. Detection of posturally induced crackles, for example, may require as much as 9 minutes, and a thorough breast examination up to 10.¹² On the other hand, ordering tests costs little time to the physician but a huge sum to patients and society. Paradoxically, “tests” may be quite profitable for the medical-industrial complex. Hence the erosion of clinical skills.

Overreliance on diagnostic technology is particularly concerning when the cost of medicine has skyrocketed. The United States now spends $3.2 trillion a year for healthcare, and much of this money goes into technology.

In fact, high-tech might hurt us even more than in the pocket. It is a sad fact of modern medicine that when unguided by clinical skills, technology can take us down a rabbit hole, wherein tests beget tests, and where at the end there is usually a surgeon, often a lawyer, and sometimes even an undertaker. The literature is full of such cases, to the point that the risk of unnecessary tests has spawned a charming new acronym: VOMIT (victims of modern imaging technology).¹³

I’m not suggesting that we discard appropriate laboratory and radiologic testing. To the contrary. Yet contributions like those of Kondo et al remind us that even in today’s medicine, the bedside remains not only the royal road to diagnosis, but also the best filter for a more judicious and cost-effective use of technology.

That filter starts with history-taking (“Listen to the patient” said Osler, “he is telling you the diagnosis.”),⁹ and continues with the physical examination. In fact, the history typically guides the physical examination. Hence, when the patient’s symptoms point away from a particular organ, the examination of that organ may be reduced to a minimum. For instance, in neurologic patients whose history made certain findings unlikely, a Canadian group was able to cut in half the number of core items of their neurologic examination.¹⁴

Yet when the history flags a system, the clinician needs to go deeper into the examination. It’s very much what we do with laboratory tests, moving from screening tests to more advanced inquiries as we tailor our diagnostic studies to the patient’s presentation. For that we need validated maneuvers. Recent efforts in this direction have turned the art of physical examination into a science.¹⁵

Lastly, patients expect to be examined, and in fact they resent when this doesn’t happen.¹⁶ Lewis Thomas called touching our “real professional secret” and “the oldest and most effective art of doctors.”¹⁷ It may even have therapeutic value.

TEACHING BEDSIDE DIAGNOSIS

So, if bedside diagnosis is important, what can we do to rekindle it? Probably anything but continue in the old ways. Studies have consistently shown that auscultation does not improve with years of training, and that in fact attending physicians may be no more proficient than third-year medical students.¹⁸ Other areas of the examination have shown similarly depressing trends,¹⁹ thus suggesting that the traditional apprenticeship mode of learning from both faculty and senior trainees may not be helpful. In fact, it may be akin to Bruegel the Elder’s painting of the blind leading the blind, and all ending up in a ditch.

Advanced physical diagnosis courses have thus been advocated, and indeed implemented at many institutions, but usually as electives. Faculty development programs have also been recommended. Still, these interventions may not suffice.

Cutting the cord to technology by serving in a developing country

My hunch is that the rekindling of physical diagnosis may require extreme measures, like putting ourselves in a zero-tech, zero-tests environment. Years ago, I had that kind of cold-turkey experience when I spent a month in a remote Nepali clinic with neither electricity nor running water—and, of course, no cell phone and no Internet. In fact, my only tools were a translator, a stethoscope, and my brain and senses. It was both terrifying and instructive, very much like the time my uncle tried to teach me how to swim by suddenly throwing me into the Mediterranean.

Maybe we should offer that kind of “immersion” to our students. A senior rotation in a technology-depleted country might do a lot of good for a young medical mind. For one, it could remind students that physicians are not only the “natural attorneys of the poor,” as Virchow famously put it,²⁰ but also the ultimate citizens of the world. To quote Dr. Osler again, “Distinctions of race, nationality, color, and creed are unknown within the portals of the temple of Æsculapius.”²¹ Such an experience might also foster empathy and tolerance for ambiguity, 2 other traits whose absence we lament in today’s medicine. More importantly, if preceded by an advanced physical diagnosis course, a rotation in a developing country could work miracles for honing bedside skills, especially if the students are accompanied by a faculty member who can be both inspiring and gifted in the art and science of bedside diagnosis.

Ultimately, this experience could remind our young that the art of medicine is much harder to acquire than the science, and that medicine is indeed a calling and not a trade. Osler said it too, and these are indeed provocative thoughts, but short of provocations and out-of-the-box ideas, the tail will continue to wag the dog. And in the end it will cost us more than money. It will cost us the art of medicine.

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.

A   43-year-old woman presented to the  clinic complaining of bilateral ankle joint pain for 2 months. She denied a history of fever, weight loss, addictions, cough, or trauma. On physical examinatio, she had swelling of the ankle and wrist joints and digital clubbing (Figure 1). Active movement of the ankles and wrists was restricted due to pain. The examination was otherwise unremarkable.

Radiography of both ankles showed a lamellar type periosteal reaction suggestive of periostitis (Figure 2). Computed tomography of the chest revealed a spiculated mass over the right lower lobe. Biopsy study of the mass was positive for squamous cell carcinoma. She was referred to the oncology center for further management.

FEATURES OF HYPERTROPHIC OSTEOARTHROPATHY

Digital clubbing is one of the oldest signs in clinical medicine. It is characterized by bulbous enlargement of the terminal segments of the fingers and toes due to proliferation of subungual connective tissue. It usually appears as a painless finger deformity and is clinically appreciated as a loss of the normal angle between the nail bed and proximal nail fold.

Hypertrophic osteoarthropathy is a symptomatic form of clubbing associated with proliferative periostosis of the distal end of long tubular bones, commonly those adjacent to the wrist and ankle joints.¹ The laminated appearance of these bones on radiography is due to the excess connective tissue secondary to new osteoid material deposited under the periosteum.

There is evidence to suggest that clubbing and hypertrophic osteoarthropathy represent different stages of the same disease process.² In most cases, finger deformity is the first manifestation; as the disease progresses, periostosis becomes evident.

Hypertrophic osteoarthropathy can be classified as primary or secondary. The primary form, also known as primary pachydermoperiostosis, is rare and constitutes only 3% of all cases.³ The exact cause is not yet known; it occurs as a hereditary disease with autosomal dominant inheritance with variable penetrance. Congenital clubbing without periostosis is of no clinical significance.⁴

CONDITIONS ASSOCIATED WITH CLUBBING

Primary bronchogenic carcinoma is the most common cause of clubbing and hypertrophic osteoarthropathy. In one retrospective series, 4.5% of patients with lung cancer had radiologic evidence of hypertrophic osteoarthropathy.⁵ Other malignancies associated with this condition are mesothelioma, hepatocellular carcinoma, and certain types of gastrointestinal adenocarcinoma.

Other conditions associated with clubbing include:

• Cardiovascular disease such as congenital cyanotic heart disease and infective endocarditis
• Gastrointestinal conditions such as cirrhosis, primary sclerosing cholangitis, Crohn disease, and ulcerative colitis
• Infections such as lung abscess and empyema.

Clubbing is generally bilaterally symmetrical. Asymmetric clubbing is rare and usually indicates impaired regional blood flow due to vascular disease. Unilateral clubbing or hypertrophic osteoarthropathy restricted to 1 upper limb can result from an anomaly of the aortic arch or from a subclavian or brachial artery aneurysm. Clubbing affecting predominantly the lower limbs has been reported in coarctation of aorta and patent ductus arteriosus.⁶ Rare cases of unidigital clubbing are reported in sarcoidosis.⁷

The importance of recognizing hypertrophic osteoarthropathy cannot be overemphasized. If any of the manifestations of the syndrome become evident in a previously healthy person, a thorough evaluation for an underlying disease should be done.

Clubbing should be differentiated from pseudoclubbing, which is seen in conditions such as hyperparathyroidism and scleroderma. The central mechanism for nail deformity in pseudoclubbing is acro-osteolysis with the resulting collapse of the subungual soft tissues. The important features differentiating it from true clubbing are preservation of the angle between the nail bed and proximal nail fold and asymmetric finger involvement.⁸

MANAGEMENT

The management of primary hypertrophic osteoarthropathy focuses on relieving the symptoms of periosteitis. Secondary forms require a detailed evaluation to rule out the underlying disease. In refractory cases, a bone-modifying agent (eg, zoledronic acid),⁹ octreotide,¹⁰ nonsteroidal anti-inflammatory drugs, or vagotomy¹¹ may help.

A   43-year-old woman presented to the  clinic complaining of bilateral ankle joint pain for 2 months. She denied a history of fever, weight loss, addictions, cough, or trauma. On physical examinatio, she had swelling of the ankle and wrist joints and digital clubbing (Figure 1). Active movement of the ankles and wrists was restricted due to pain. The examination was otherwise unremarkable.

Radiography of both ankles showed a lamellar type periosteal reaction suggestive of periostitis (Figure 2). Computed tomography of the chest revealed a spiculated mass over the right lower lobe. Biopsy study of the mass was positive for squamous cell carcinoma. She was referred to the oncology center for further management.

FEATURES OF HYPERTROPHIC OSTEOARTHROPATHY

Digital clubbing is one of the oldest signs in clinical medicine. It is characterized by bulbous enlargement of the terminal segments of the fingers and toes due to proliferation of subungual connective tissue. It usually appears as a painless finger deformity and is clinically appreciated as a loss of the normal angle between the nail bed and proximal nail fold.

Hypertrophic osteoarthropathy is a symptomatic form of clubbing associated with proliferative periostosis of the distal end of long tubular bones, commonly those adjacent to the wrist and ankle joints.¹ The laminated appearance of these bones on radiography is due to the excess connective tissue secondary to new osteoid material deposited under the periosteum.

There is evidence to suggest that clubbing and hypertrophic osteoarthropathy represent different stages of the same disease process.² In most cases, finger deformity is the first manifestation; as the disease progresses, periostosis becomes evident.

Hypertrophic osteoarthropathy can be classified as primary or secondary. The primary form, also known as primary pachydermoperiostosis, is rare and constitutes only 3% of all cases.³ The exact cause is not yet known; it occurs as a hereditary disease with autosomal dominant inheritance with variable penetrance. Congenital clubbing without periostosis is of no clinical significance.⁴

CONDITIONS ASSOCIATED WITH CLUBBING

Primary bronchogenic carcinoma is the most common cause of clubbing and hypertrophic osteoarthropathy. In one retrospective series, 4.5% of patients with lung cancer had radiologic evidence of hypertrophic osteoarthropathy.⁵ Other malignancies associated with this condition are mesothelioma, hepatocellular carcinoma, and certain types of gastrointestinal adenocarcinoma.

Other conditions associated with clubbing include:

• Cardiovascular disease such as congenital cyanotic heart disease and infective endocarditis
• Gastrointestinal conditions such as cirrhosis, primary sclerosing cholangitis, Crohn disease, and ulcerative colitis
• Infections such as lung abscess and empyema.

Clubbing is generally bilaterally symmetrical. Asymmetric clubbing is rare and usually indicates impaired regional blood flow due to vascular disease. Unilateral clubbing or hypertrophic osteoarthropathy restricted to 1 upper limb can result from an anomaly of the aortic arch or from a subclavian or brachial artery aneurysm. Clubbing affecting predominantly the lower limbs has been reported in coarctation of aorta and patent ductus arteriosus.⁶ Rare cases of unidigital clubbing are reported in sarcoidosis.⁷

The importance of recognizing hypertrophic osteoarthropathy cannot be overemphasized. If any of the manifestations of the syndrome become evident in a previously healthy person, a thorough evaluation for an underlying disease should be done.

Clubbing should be differentiated from pseudoclubbing, which is seen in conditions such as hyperparathyroidism and scleroderma. The central mechanism for nail deformity in pseudoclubbing is acro-osteolysis with the resulting collapse of the subungual soft tissues. The important features differentiating it from true clubbing are preservation of the angle between the nail bed and proximal nail fold and asymmetric finger involvement.⁸

MANAGEMENT

The management of primary hypertrophic osteoarthropathy focuses on relieving the symptoms of periosteitis. Secondary forms require a detailed evaluation to rule out the underlying disease. In refractory cases, a bone-modifying agent (eg, zoledronic acid),⁹ octreotide,¹⁰ nonsteroidal anti-inflammatory drugs, or vagotomy¹¹ may help.

A   43-year-old woman presented to the  clinic complaining of bilateral ankle joint pain for 2 months. She denied a history of fever, weight loss, addictions, cough, or trauma. On physical examinatio, she had swelling of the ankle and wrist joints and digital clubbing (Figure 1). Active movement of the ankles and wrists was restricted due to pain. The examination was otherwise unremarkable.

Radiography of both ankles showed a lamellar type periosteal reaction suggestive of periostitis (Figure 2). Computed tomography of the chest revealed a spiculated mass over the right lower lobe. Biopsy study of the mass was positive for squamous cell carcinoma. She was referred to the oncology center for further management.

FEATURES OF HYPERTROPHIC OSTEOARTHROPATHY

Digital clubbing is one of the oldest signs in clinical medicine. It is characterized by bulbous enlargement of the terminal segments of the fingers and toes due to proliferation of subungual connective tissue. It usually appears as a painless finger deformity and is clinically appreciated as a loss of the normal angle between the nail bed and proximal nail fold.

Hypertrophic osteoarthropathy is a symptomatic form of clubbing associated with proliferative periostosis of the distal end of long tubular bones, commonly those adjacent to the wrist and ankle joints.¹ The laminated appearance of these bones on radiography is due to the excess connective tissue secondary to new osteoid material deposited under the periosteum.

There is evidence to suggest that clubbing and hypertrophic osteoarthropathy represent different stages of the same disease process.² In most cases, finger deformity is the first manifestation; as the disease progresses, periostosis becomes evident.

Hypertrophic osteoarthropathy can be classified as primary or secondary. The primary form, also known as primary pachydermoperiostosis, is rare and constitutes only 3% of all cases.³ The exact cause is not yet known; it occurs as a hereditary disease with autosomal dominant inheritance with variable penetrance. Congenital clubbing without periostosis is of no clinical significance.⁴

CONDITIONS ASSOCIATED WITH CLUBBING

Primary bronchogenic carcinoma is the most common cause of clubbing and hypertrophic osteoarthropathy. In one retrospective series, 4.5% of patients with lung cancer had radiologic evidence of hypertrophic osteoarthropathy.⁵ Other malignancies associated with this condition are mesothelioma, hepatocellular carcinoma, and certain types of gastrointestinal adenocarcinoma.

Other conditions associated with clubbing include:

• Cardiovascular disease such as congenital cyanotic heart disease and infective endocarditis
• Gastrointestinal conditions such as cirrhosis, primary sclerosing cholangitis, Crohn disease, and ulcerative colitis
• Infections such as lung abscess and empyema.

Clubbing is generally bilaterally symmetrical. Asymmetric clubbing is rare and usually indicates impaired regional blood flow due to vascular disease. Unilateral clubbing or hypertrophic osteoarthropathy restricted to 1 upper limb can result from an anomaly of the aortic arch or from a subclavian or brachial artery aneurysm. Clubbing affecting predominantly the lower limbs has been reported in coarctation of aorta and patent ductus arteriosus.⁶ Rare cases of unidigital clubbing are reported in sarcoidosis.⁷

The importance of recognizing hypertrophic osteoarthropathy cannot be overemphasized. If any of the manifestations of the syndrome become evident in a previously healthy person, a thorough evaluation for an underlying disease should be done.

Clubbing should be differentiated from pseudoclubbing, which is seen in conditions such as hyperparathyroidism and scleroderma. The central mechanism for nail deformity in pseudoclubbing is acro-osteolysis with the resulting collapse of the subungual soft tissues. The important features differentiating it from true clubbing are preservation of the angle between the nail bed and proximal nail fold and asymmetric finger involvement.⁸

MANAGEMENT

The management of primary hypertrophic osteoarthropathy focuses on relieving the symptoms of periosteitis. Secondary forms require a detailed evaluation to rule out the underlying disease. In refractory cases, a bone-modifying agent (eg, zoledronic acid),⁹ octreotide,¹⁰ nonsteroidal anti-inflammatory drugs, or vagotomy¹¹ may help.

Laboratory studies revealed leukocytosis with a left shift. Chest radiographs were negative for pneumonia. A magnetic resonance image (MRI) of the lumbar spine was obtained to evaluate for diskitis osteomyelitis. A radiograph of the pelvis was also obtained to evaluate the patient’s THAs, and a computed tomography scan (CT) of the abdomen and pelvis with contrast was obtained for further evaluation. Representative CT, radiographic, and MRI images are shown at left (Figures 1-3).

What is the suspected diagnosis?

Answer

The MRI of the lumbar spine demonstrated no evidence of diskitis osteomyelitis. However, T₂-weighted axial images showed enlarged heterogeneous bilateral psoas muscles with bright signal, indicating the presence of fluid (white arrows, Figure 4).

On the pelvic radiographs, both femoral heads appeared off-center within the acetabular cups (red arrows, Figure 5). This eccentric positioning indicated wear of the polyethylene in the THAs that normally occupies the space between the acetabular cup and the femoral head. In addition, focal lucency in the right acetabulum indicated breakdown of the bone, a condition referred to as osteolysis (white asterisk, Figure 5).

An abdominopelvic CT scan with contrast was performed and confirmed the findings of polyethylene wear and osteolysis. The CT scan also demonstrated large bilateral hip joint effusions (white arrows, Figure 6), decompressed along distended bilateral iliopsoas bursae (red asterisks, Figure 6), and communicating with the bilateral psoas muscle collections (red arrows, Figure 6).

Osteolysis With Iliopsoas Bursitis

Bursae are fluid-filled sacs lined by synovial tissue located throughout the body to reduce friction at sites of movement between muscles, bones, and tendons. Bursitis develops when these sacs become inflamed and/or infected and fill with fluid. The iliopsoas bursa lies between the anterior capsule of the hip and the psoas tendon, iliacus tendon, and muscle fibers.^1,2 This bursa frequently communicates with the hip joint.^3,4 Iliopsoas bursal distension has been reported following THA in the setting of polyethylene wear,⁵ and aseptic bursitis is a commonly seen incidental finding at the time of revision surgery.⁶

In this patient, long-standing polyethylene-induced synovitis had markedly expanded the hip joints and iliopsoas bursae, eventually resulting in superinfection, which accounted for the patient’s symptoms.

Treatment

Based on the imaging findings, interventional radiology services were contacted. The interventional radiologist drained the bilateral psoas abscesses. Cultures of the fluid were positive for both methicillin-resistant Staphylococcus aureus (MRSA) and methicillin-susceptible S aureus (MSSA). The patient was admitted to the hospital for treatment of MRSA and MSSA with intravenous antibiotic therapy. He recovered from the infection and was discharged on hospital day 2, with instructions to follow up with an orthopedic surgeon to discuss eventual revision of the bilateral THAs.

Laboratory studies revealed leukocytosis with a left shift. Chest radiographs were negative for pneumonia. A magnetic resonance image (MRI) of the lumbar spine was obtained to evaluate for diskitis osteomyelitis. A radiograph of the pelvis was also obtained to evaluate the patient’s THAs, and a computed tomography scan (CT) of the abdomen and pelvis with contrast was obtained for further evaluation. Representative CT, radiographic, and MRI images are shown at left (Figures 1-3).

What is the suspected diagnosis?

Answer

The MRI of the lumbar spine demonstrated no evidence of diskitis osteomyelitis. However, T₂-weighted axial images showed enlarged heterogeneous bilateral psoas muscles with bright signal, indicating the presence of fluid (white arrows, Figure 4).

On the pelvic radiographs, both femoral heads appeared off-center within the acetabular cups (red arrows, Figure 5). This eccentric positioning indicated wear of the polyethylene in the THAs that normally occupies the space between the acetabular cup and the femoral head. In addition, focal lucency in the right acetabulum indicated breakdown of the bone, a condition referred to as osteolysis (white asterisk, Figure 5).

An abdominopelvic CT scan with contrast was performed and confirmed the findings of polyethylene wear and osteolysis. The CT scan also demonstrated large bilateral hip joint effusions (white arrows, Figure 6), decompressed along distended bilateral iliopsoas bursae (red asterisks, Figure 6), and communicating with the bilateral psoas muscle collections (red arrows, Figure 6).

Osteolysis With Iliopsoas Bursitis

Bursae are fluid-filled sacs lined by synovial tissue located throughout the body to reduce friction at sites of movement between muscles, bones, and tendons. Bursitis develops when these sacs become inflamed and/or infected and fill with fluid. The iliopsoas bursa lies between the anterior capsule of the hip and the psoas tendon, iliacus tendon, and muscle fibers.^1,2 This bursa frequently communicates with the hip joint.^3,4 Iliopsoas bursal distension has been reported following THA in the setting of polyethylene wear,⁵ and aseptic bursitis is a commonly seen incidental finding at the time of revision surgery.⁶

In this patient, long-standing polyethylene-induced synovitis had markedly expanded the hip joints and iliopsoas bursae, eventually resulting in superinfection, which accounted for the patient’s symptoms.

Treatment

Based on the imaging findings, interventional radiology services were contacted. The interventional radiologist drained the bilateral psoas abscesses. Cultures of the fluid were positive for both methicillin-resistant Staphylococcus aureus (MRSA) and methicillin-susceptible S aureus (MSSA). The patient was admitted to the hospital for treatment of MRSA and MSSA with intravenous antibiotic therapy. He recovered from the infection and was discharged on hospital day 2, with instructions to follow up with an orthopedic surgeon to discuss eventual revision of the bilateral THAs.

Laboratory studies revealed leukocytosis with a left shift. Chest radiographs were negative for pneumonia. A magnetic resonance image (MRI) of the lumbar spine was obtained to evaluate for diskitis osteomyelitis. A radiograph of the pelvis was also obtained to evaluate the patient’s THAs, and a computed tomography scan (CT) of the abdomen and pelvis with contrast was obtained for further evaluation. Representative CT, radiographic, and MRI images are shown at left (Figures 1-3).

What is the suspected diagnosis?

Answer

The MRI of the lumbar spine demonstrated no evidence of diskitis osteomyelitis. However, T₂-weighted axial images showed enlarged heterogeneous bilateral psoas muscles with bright signal, indicating the presence of fluid (white arrows, Figure 4).

On the pelvic radiographs, both femoral heads appeared off-center within the acetabular cups (red arrows, Figure 5). This eccentric positioning indicated wear of the polyethylene in the THAs that normally occupies the space between the acetabular cup and the femoral head. In addition, focal lucency in the right acetabulum indicated breakdown of the bone, a condition referred to as osteolysis (white asterisk, Figure 5).

An abdominopelvic CT scan with contrast was performed and confirmed the findings of polyethylene wear and osteolysis. The CT scan also demonstrated large bilateral hip joint effusions (white arrows, Figure 6), decompressed along distended bilateral iliopsoas bursae (red asterisks, Figure 6), and communicating with the bilateral psoas muscle collections (red arrows, Figure 6).

Osteolysis With Iliopsoas Bursitis

Bursae are fluid-filled sacs lined by synovial tissue located throughout the body to reduce friction at sites of movement between muscles, bones, and tendons. Bursitis develops when these sacs become inflamed and/or infected and fill with fluid. The iliopsoas bursa lies between the anterior capsule of the hip and the psoas tendon, iliacus tendon, and muscle fibers.^1,2 This bursa frequently communicates with the hip joint.^3,4 Iliopsoas bursal distension has been reported following THA in the setting of polyethylene wear,⁵ and aseptic bursitis is a commonly seen incidental finding at the time of revision surgery.⁶

In this patient, long-standing polyethylene-induced synovitis had markedly expanded the hip joints and iliopsoas bursae, eventually resulting in superinfection, which accounted for the patient’s symptoms.

Treatment

Based on the imaging findings, interventional radiology services were contacted. The interventional radiologist drained the bilateral psoas abscesses. Cultures of the fluid were positive for both methicillin-resistant Staphylococcus aureus (MRSA) and methicillin-susceptible S aureus (MSSA). The patient was admitted to the hospital for treatment of MRSA and MSSA with intravenous antibiotic therapy. He recovered from the infection and was discharged on hospital day 2, with instructions to follow up with an orthopedic surgeon to discuss eventual revision of the bilateral THAs.

The diagnosis of aortic dissection is often challenging due to its various presentations and the frequent absence of classic findings. This high-morbidity and high-mortality condition may present with nonspecific chest, back, or abdominal pain, and is often associated with hypotension.¹ Point-of-care (POC) ultrasound in the ED allows for rapid diagnosis of this time-sensitive disease.

Case

A 70-year-old woman presented to the ED for evaluation of acute sharp chest pain, which she stated began while she was exercising earlier that day. The pain was substernal and radiated to her upper back. The patient also described associated lightheadedness and dyspnea, but denied any focal weakness or paresthesias. Her vital signs were remarkable for a blood pressure of 90/31 mm Hg and a heart rate of 42 beats/min. A bedside ultrasound of the patient’s aortic root and abdominal aorta was performed to assess for evidence of aortic dissection.

Imaging Technique

To evaluate for aortic dissection using POC ultrasound, views of the aortic root and the abdominal aorta should be obtained with the patient in the supine position. The phased array (cardiac) probe is used to obtain the parasternal long axis (PSLA) view of the heart to visualize the aortic root. The PSLA view is obtained by placing the probe in the third or fourth intercostal space, adjacent to the left sternal border, with the probe parallel to the long axis of the left ventricle (Figure 1). The American Society of Echocardiography recommends measuring the aortic diameter at the sinus of Valsalva, but measurement of the largest visible portion of the aortic root may be more practical.^2,3 Measurement of the aortic root diameter should occur at end diastole.^2,3 Tricks for better visualization of the aortic root include tilting the probe tail 10° toward the patient’s right elbow (ie, aiming the probe footprint toward the patient’s left shoulder), or placing the patient in the left lateral decubitus position. Values greater than 4 cm indicate aortic root dilatation.⁴ Figure 2 demonstrates the PSLA view in our patient, showing the dilated aortic root, which measured roughly 5 cm. 

The abdominal aorta is best visualized using a low-frequency curvilinear (abdominal) probe. The aorta should be visualized in the transverse plane from the diaphragm to its bifurcation by placing the probe in the epigastrium and slowly moving it inferiorly to the level of the umbilicus (Figure 3). The aorta can then be visualized in the longitudinal plane by rotating the probe clockwise until it is parallel with the long axis of the aorta (Figure 4). Visualization of an intimal flap is the most common sonographic finding associated with an abdominal aortic dissection. In our patient, an intimal flap was visualized in both the transverse and longitudinal views (Figures 5 and 6).

Discussion

Aortic dissection is a medical emergency—one that has a reported in-hospital mortality of 27.4%.¹ Therefore, prompt diagnosis of an aortic dissection in the ED is crucial to improving patient outcomes. Traditionally, emergency physicians (EPs) have relied on aortography and contrast-enhanced computed tomography (CT) to diagnose aortic dissection. However, both of these modalities require a considerable length of time, injection of contrast material, and often transportation of the patient from the ED.

Point-of-care ultrasound provides a fast and noninvasive tool for the diagnosis of aortic dissection. Several recent case reports and case series have highlighted the utility of POC ultrasound to diagnose aortic dissection in the ED.^5-7

Case Conclusion

After the results of the POC transthoracic and transabdominal ultrasound were reviewed, we promptly consulted the vascular surgery team. They performed a CT scan verifying a DeBakey type I aortic dissection involving both the ascending aorta and the descending aorta. The patient was subsequently taken to the operating room for definitive repair with a graft. She was discharged home on hospital day 9 in good condition.

Summary

Point-of-care ultrasound is a useful bedside tool for the rapid diagnosis of aortic dissection in the ED. The aortic root dilatation seen on the PSLA view and the presence of an intimal flap seen on either transthoracic or transabdominal views of the aorta are both highly sensitive for aortic dissection.

The diagnosis of aortic dissection is often challenging due to its various presentations and the frequent absence of classic findings. This high-morbidity and high-mortality condition may present with nonspecific chest, back, or abdominal pain, and is often associated with hypotension.¹ Point-of-care (POC) ultrasound in the ED allows for rapid diagnosis of this time-sensitive disease.

Case

A 70-year-old woman presented to the ED for evaluation of acute sharp chest pain, which she stated began while she was exercising earlier that day. The pain was substernal and radiated to her upper back. The patient also described associated lightheadedness and dyspnea, but denied any focal weakness or paresthesias. Her vital signs were remarkable for a blood pressure of 90/31 mm Hg and a heart rate of 42 beats/min. A bedside ultrasound of the patient’s aortic root and abdominal aorta was performed to assess for evidence of aortic dissection.

Imaging Technique

To evaluate for aortic dissection using POC ultrasound, views of the aortic root and the abdominal aorta should be obtained with the patient in the supine position. The phased array (cardiac) probe is used to obtain the parasternal long axis (PSLA) view of the heart to visualize the aortic root. The PSLA view is obtained by placing the probe in the third or fourth intercostal space, adjacent to the left sternal border, with the probe parallel to the long axis of the left ventricle (Figure 1). The American Society of Echocardiography recommends measuring the aortic diameter at the sinus of Valsalva, but measurement of the largest visible portion of the aortic root may be more practical.^2,3 Measurement of the aortic root diameter should occur at end diastole.^2,3 Tricks for better visualization of the aortic root include tilting the probe tail 10° toward the patient’s right elbow (ie, aiming the probe footprint toward the patient’s left shoulder), or placing the patient in the left lateral decubitus position. Values greater than 4 cm indicate aortic root dilatation.⁴ Figure 2 demonstrates the PSLA view in our patient, showing the dilated aortic root, which measured roughly 5 cm. 

The abdominal aorta is best visualized using a low-frequency curvilinear (abdominal) probe. The aorta should be visualized in the transverse plane from the diaphragm to its bifurcation by placing the probe in the epigastrium and slowly moving it inferiorly to the level of the umbilicus (Figure 3). The aorta can then be visualized in the longitudinal plane by rotating the probe clockwise until it is parallel with the long axis of the aorta (Figure 4). Visualization of an intimal flap is the most common sonographic finding associated with an abdominal aortic dissection. In our patient, an intimal flap was visualized in both the transverse and longitudinal views (Figures 5 and 6).

Discussion

Aortic dissection is a medical emergency—one that has a reported in-hospital mortality of 27.4%.¹ Therefore, prompt diagnosis of an aortic dissection in the ED is crucial to improving patient outcomes. Traditionally, emergency physicians (EPs) have relied on aortography and contrast-enhanced computed tomography (CT) to diagnose aortic dissection. However, both of these modalities require a considerable length of time, injection of contrast material, and often transportation of the patient from the ED.

Point-of-care ultrasound provides a fast and noninvasive tool for the diagnosis of aortic dissection. Several recent case reports and case series have highlighted the utility of POC ultrasound to diagnose aortic dissection in the ED.^5-7

Case Conclusion

After the results of the POC transthoracic and transabdominal ultrasound were reviewed, we promptly consulted the vascular surgery team. They performed a CT scan verifying a DeBakey type I aortic dissection involving both the ascending aorta and the descending aorta. The patient was subsequently taken to the operating room for definitive repair with a graft. She was discharged home on hospital day 9 in good condition.

Summary

Point-of-care ultrasound is a useful bedside tool for the rapid diagnosis of aortic dissection in the ED. The aortic root dilatation seen on the PSLA view and the presence of an intimal flap seen on either transthoracic or transabdominal views of the aorta are both highly sensitive for aortic dissection.

The diagnosis of aortic dissection is often challenging due to its various presentations and the frequent absence of classic findings. This high-morbidity and high-mortality condition may present with nonspecific chest, back, or abdominal pain, and is often associated with hypotension.¹ Point-of-care (POC) ultrasound in the ED allows for rapid diagnosis of this time-sensitive disease.

Case

A 70-year-old woman presented to the ED for evaluation of acute sharp chest pain, which she stated began while she was exercising earlier that day. The pain was substernal and radiated to her upper back. The patient also described associated lightheadedness and dyspnea, but denied any focal weakness or paresthesias. Her vital signs were remarkable for a blood pressure of 90/31 mm Hg and a heart rate of 42 beats/min. A bedside ultrasound of the patient’s aortic root and abdominal aorta was performed to assess for evidence of aortic dissection.

Imaging Technique

To evaluate for aortic dissection using POC ultrasound, views of the aortic root and the abdominal aorta should be obtained with the patient in the supine position. The phased array (cardiac) probe is used to obtain the parasternal long axis (PSLA) view of the heart to visualize the aortic root. The PSLA view is obtained by placing the probe in the third or fourth intercostal space, adjacent to the left sternal border, with the probe parallel to the long axis of the left ventricle (Figure 1). The American Society of Echocardiography recommends measuring the aortic diameter at the sinus of Valsalva, but measurement of the largest visible portion of the aortic root may be more practical.^2,3 Measurement of the aortic root diameter should occur at end diastole.^2,3 Tricks for better visualization of the aortic root include tilting the probe tail 10° toward the patient’s right elbow (ie, aiming the probe footprint toward the patient’s left shoulder), or placing the patient in the left lateral decubitus position. Values greater than 4 cm indicate aortic root dilatation.⁴ Figure 2 demonstrates the PSLA view in our patient, showing the dilated aortic root, which measured roughly 5 cm. 

The abdominal aorta is best visualized using a low-frequency curvilinear (abdominal) probe. The aorta should be visualized in the transverse plane from the diaphragm to its bifurcation by placing the probe in the epigastrium and slowly moving it inferiorly to the level of the umbilicus (Figure 3). The aorta can then be visualized in the longitudinal plane by rotating the probe clockwise until it is parallel with the long axis of the aorta (Figure 4). Visualization of an intimal flap is the most common sonographic finding associated with an abdominal aortic dissection. In our patient, an intimal flap was visualized in both the transverse and longitudinal views (Figures 5 and 6).

Discussion

Aortic dissection is a medical emergency—one that has a reported in-hospital mortality of 27.4%.¹ Therefore, prompt diagnosis of an aortic dissection in the ED is crucial to improving patient outcomes. Traditionally, emergency physicians (EPs) have relied on aortography and contrast-enhanced computed tomography (CT) to diagnose aortic dissection. However, both of these modalities require a considerable length of time, injection of contrast material, and often transportation of the patient from the ED.

Point-of-care ultrasound provides a fast and noninvasive tool for the diagnosis of aortic dissection. Several recent case reports and case series have highlighted the utility of POC ultrasound to diagnose aortic dissection in the ED.^5-7

Case Conclusion

After the results of the POC transthoracic and transabdominal ultrasound were reviewed, we promptly consulted the vascular surgery team. They performed a CT scan verifying a DeBakey type I aortic dissection involving both the ascending aorta and the descending aorta. The patient was subsequently taken to the operating room for definitive repair with a graft. She was discharged home on hospital day 9 in good condition.

Summary

Point-of-care ultrasound is a useful bedside tool for the rapid diagnosis of aortic dissection in the ED. The aortic root dilatation seen on the PSLA view and the presence of an intimal flap seen on either transthoracic or transabdominal views of the aorta are both highly sensitive for aortic dissection.

Arthrex Synergy MSK Ultrasound by Clarius(http://www.synergy-ultrasound.com/)

Arthrex Synergy MSK Ultrasound by Clarius is a new wireless ultrasound scanner that can connect to any iOS or Android device through a secure WiFi Direct connection. The scanner sets up the connection to an app on the device. Ultrasound and wireless technology have been around for decades, but combinations thereof have produced poor results. The main challenge has been to create and wirelessly transmit high-quality images without latency to a display while maintaining a reasonably sized transducer. Handheld ultrasound transducers scan effectively and process the scanned information in compact form. Recent advances in image processing and proprietary imaging algorithms now allow creation of high-resolution images comparable to those produced by most midrange or high-range machines costing $30,000 to $50,000. This new unit costs about $12,000. Ultrasound use has increased over the past decade. Numerous studies have found improved accuracy, efficacy, and outcomes of injections, and reduced pain, with ultrasound-guided injections over blind injections, and cost savings over magnetic resonance imaging.^1-12

Three scanners are capable of targeting different tissue types and depths. We prefer the Synergy MSK Linear Ultrasound by Clarius, a linear transducer that can evaluate tissue to depths of 7 cm and use frequencies from 4 MHz to 13 MHz. Its battery holds a standby charge for 7 days and can be actively used for 45 minutes. The unit has a magnesium shell; with the battery removed, the unit can be completely immersed in liquid without being damaged, which allows for easy cleaning and, potentially, sterilization with a soak solution. Color Doppler (for blood-flow assessment) and proprietary advanced needle visualization technology will be available in June.

The app is simply controlled with typical smart-device gestures. Depth control requires a finger swipe, and zoom takes a pinch. Other controls, such as optimal gain and frequency settings, are automated. Images and videos can be stored on the device and uploaded either to the Clarius Cloud or to a PACS (picture archiving and communication system) device. New features will allow the device to use a Synergy arthroscopy tower (Arthrex) as its display for surgeons and anesthesiologists in the surgical suite.

This technology finally allows ultrasound to be used in the operating room without the hassles of cumbersome machines and the potential contamination by the sleeves covering the cord that connects the transducer and the base unit (Figure 1).

Arthrex Synergy MSK Ultrasound by Clarius(http://www.synergy-ultrasound.com/)

Arthrex Synergy MSK Ultrasound by Clarius is a new wireless ultrasound scanner that can connect to any iOS or Android device through a secure WiFi Direct connection. The scanner sets up the connection to an app on the device. Ultrasound and wireless technology have been around for decades, but combinations thereof have produced poor results. The main challenge has been to create and wirelessly transmit high-quality images without latency to a display while maintaining a reasonably sized transducer. Handheld ultrasound transducers scan effectively and process the scanned information in compact form. Recent advances in image processing and proprietary imaging algorithms now allow creation of high-resolution images comparable to those produced by most midrange or high-range machines costing $30,000 to $50,000. This new unit costs about $12,000. Ultrasound use has increased over the past decade. Numerous studies have found improved accuracy, efficacy, and outcomes of injections, and reduced pain, with ultrasound-guided injections over blind injections, and cost savings over magnetic resonance imaging.^1-12

Three scanners are capable of targeting different tissue types and depths. We prefer the Synergy MSK Linear Ultrasound by Clarius, a linear transducer that can evaluate tissue to depths of 7 cm and use frequencies from 4 MHz to 13 MHz. Its battery holds a standby charge for 7 days and can be actively used for 45 minutes. The unit has a magnesium shell; with the battery removed, the unit can be completely immersed in liquid without being damaged, which allows for easy cleaning and, potentially, sterilization with a soak solution. Color Doppler (for blood-flow assessment) and proprietary advanced needle visualization technology will be available in June.

The app is simply controlled with typical smart-device gestures. Depth control requires a finger swipe, and zoom takes a pinch. Other controls, such as optimal gain and frequency settings, are automated. Images and videos can be stored on the device and uploaded either to the Clarius Cloud or to a PACS (picture archiving and communication system) device. New features will allow the device to use a Synergy arthroscopy tower (Arthrex) as its display for surgeons and anesthesiologists in the surgical suite.

This technology finally allows ultrasound to be used in the operating room without the hassles of cumbersome machines and the potential contamination by the sleeves covering the cord that connects the transducer and the base unit (Figure 1).

Arthrex Synergy MSK Ultrasound by Clarius(http://www.synergy-ultrasound.com/)

Arthrex Synergy MSK Ultrasound by Clarius is a new wireless ultrasound scanner that can connect to any iOS or Android device through a secure WiFi Direct connection. The scanner sets up the connection to an app on the device. Ultrasound and wireless technology have been around for decades, but combinations thereof have produced poor results. The main challenge has been to create and wirelessly transmit high-quality images without latency to a display while maintaining a reasonably sized transducer. Handheld ultrasound transducers scan effectively and process the scanned information in compact form. Recent advances in image processing and proprietary imaging algorithms now allow creation of high-resolution images comparable to those produced by most midrange or high-range machines costing $30,000 to $50,000. This new unit costs about $12,000. Ultrasound use has increased over the past decade. Numerous studies have found improved accuracy, efficacy, and outcomes of injections, and reduced pain, with ultrasound-guided injections over blind injections, and cost savings over magnetic resonance imaging.^1-12

Three scanners are capable of targeting different tissue types and depths. We prefer the Synergy MSK Linear Ultrasound by Clarius, a linear transducer that can evaluate tissue to depths of 7 cm and use frequencies from 4 MHz to 13 MHz. Its battery holds a standby charge for 7 days and can be actively used for 45 minutes. The unit has a magnesium shell; with the battery removed, the unit can be completely immersed in liquid without being damaged, which allows for easy cleaning and, potentially, sterilization with a soak solution. Color Doppler (for blood-flow assessment) and proprietary advanced needle visualization technology will be available in June.

The app is simply controlled with typical smart-device gestures. Depth control requires a finger swipe, and zoom takes a pinch. Other controls, such as optimal gain and frequency settings, are automated. Images and videos can be stored on the device and uploaded either to the Clarius Cloud or to a PACS (picture archiving and communication system) device. New features will allow the device to use a Synergy arthroscopy tower (Arthrex) as its display for surgeons and anesthesiologists in the surgical suite.

This technology finally allows ultrasound to be used in the operating room without the hassles of cumbersome machines and the potential contamination by the sleeves covering the cord that connects the transducer and the base unit (Figure 1).

A 58-year-old man with end-stage renal disease due to diabetic nephropathy was admitted with aggravated exertional dyspnea and intermittent chest pain for 1 week. He had been on hemodialysis for 15 years.

His blood pressure was 124/69 mm Hg, pulse 96 beats per minute, and temperature 35.8°C. On physical examination, he had bilateral diffuse crackles, elevated jugular venous pressure (9.5 cm H₂O) with positive hepatojugular reflux, and apparent dependent pedal edema. The Kussmaul sign was not observed.

Cardiac enzymes were in the normal range (creatine kinase 73 U/L, troponin I 0.032 ng/mL), but the brain-natriuretic peptide level was elevated at 340 pg/mL. Other laboratory findings included calcium 9 mg/dL (reference range 8.4–10.2 mg/dL), inorganic phosphate 5 mg/dL (2.5–4.5 mg/dL), and intact parathyroid hormone 1,457 pg/mL (10–69 pg/mL).

Electrocardiography showed sinus tachycardia with low voltage in diffuse leads and generalized flattening of the T wave. Chest radiography showed a bilateral reticulo­nodular pattern, mild costo­phrenic angle obliteration, and notable calcifications along the cardiac contour. Thoracic computed tomography showed a porcelain-like encasement of the heart (Figure 1). Transthoracic echocardiography showed thickened pericardium, pericardial calcification, and mild interventricular septal bounce in diastole, with no dyskinesia of ventricular wall motion. We decided not to perform an invasive hemodynamic assessment.

CAUSES OF PERICARDIAL CALCIFICATION

Pericardial calcification, abnormal calcium deposits in response to inflammation,¹ has become more widely reported as the use of chest computed tomography has become more widespread. The common identifiable causes of pericardial calcification include recurrent or chronic pericarditis, radiation therapy for Hodgkin lymphoma or breast cancer, tuberculosis, and end-stage kidney disease.^2,3 Other possible causes are retention of uremic metabolites, metastatic calcification induced by secondary hyperparathyroidism, and calcium-phosphate deposition induced by hyperphosphatemia.⁴

In chronic kidney disease, the amount of pericardial fluid and fibrinous pericardial deposition is thought to contribute to increased pericardial thickness and constriction. In some patients, pericardial calcification and thickening would lead to constrictive pericarditis, which could be confirmed by echocardiography and cardiac catheterization. About 25% to 50% of cases of pericardial calcification are complicated by constrictive pericarditis.^5,6 Constrictive pericarditis occurs in up to 4% of patients with end-stage renal disease, even with successful dialysis.⁷

Partial clinical improvement may be obtained with intensive hemodialysis, strict volume control, and decreased catabolism in patients with multiple comorbidities.⁸ However, the definite treatment is total pericardiectomy, which reduces symptoms substantially and offers a favorable long-term outcome.⁷

SECONDARY HYPERPARATHYROIDISM

Secondary hyperparathyroidism is a common complication in patients with end-stage renal disease and is characterized by derangements in the homeostasis of calcium, phosphorus, and vitamin D.⁹

Because renal function is decreased, phosphate is retained and calcitriol synthesis is reduced, resulting in hypocalcemia, which induces parathyroid gland hyperplasia and parathyroid hormone secretion.¹⁰ Moreover, some patents with long-standing secondary hyperparathyroidism may develop tertiary hyperparathyroidism associated with autonomous parathyroid hormone secretion, hypercalcemia, and hyperphosphatemia.¹¹

The Kidney Disease: Improving Global Outcomes (KDIGO) Work Group recommends screening for and managing secondary hyperparathyroidism in all patients with stage 3 chronic kidney disease (estimated glomerular filtration rate < 60 mL/min). In patients with stage 5 chronic kidney disease or on dialysis, the serum calcium and phosphorus levels should be monitored every 1 to 3 months and the parathyroid hormone levels every 3 to 6 months.¹²

According to KDIGO guidelines, the target level of calcium is less than 10.2 mg/dL, and the target phosphorus level is less than 4.6 mg/dL. The level of parathyroid hormone should be maintained at 2 to 9 times the upper limit of normal for the assay.

The management of secondary hyperparathyroidism includes a low-phosphorus diet, calcium-containing or calcium-free phosphate binders, a calcitriol supplement, and calcimimetics. If medical treatment fails and manifestations are significant, parathyroidectomy may be indicated.¹³

A 58-year-old man with end-stage renal disease due to diabetic nephropathy was admitted with aggravated exertional dyspnea and intermittent chest pain for 1 week. He had been on hemodialysis for 15 years.

His blood pressure was 124/69 mm Hg, pulse 96 beats per minute, and temperature 35.8°C. On physical examination, he had bilateral diffuse crackles, elevated jugular venous pressure (9.5 cm H₂O) with positive hepatojugular reflux, and apparent dependent pedal edema. The Kussmaul sign was not observed.

Cardiac enzymes were in the normal range (creatine kinase 73 U/L, troponin I 0.032 ng/mL), but the brain-natriuretic peptide level was elevated at 340 pg/mL. Other laboratory findings included calcium 9 mg/dL (reference range 8.4–10.2 mg/dL), inorganic phosphate 5 mg/dL (2.5–4.5 mg/dL), and intact parathyroid hormone 1,457 pg/mL (10–69 pg/mL).

Electrocardiography showed sinus tachycardia with low voltage in diffuse leads and generalized flattening of the T wave. Chest radiography showed a bilateral reticulo­nodular pattern, mild costo­phrenic angle obliteration, and notable calcifications along the cardiac contour. Thoracic computed tomography showed a porcelain-like encasement of the heart (Figure 1). Transthoracic echocardiography showed thickened pericardium, pericardial calcification, and mild interventricular septal bounce in diastole, with no dyskinesia of ventricular wall motion. We decided not to perform an invasive hemodynamic assessment.

CAUSES OF PERICARDIAL CALCIFICATION

Pericardial calcification, abnormal calcium deposits in response to inflammation,¹ has become more widely reported as the use of chest computed tomography has become more widespread. The common identifiable causes of pericardial calcification include recurrent or chronic pericarditis, radiation therapy for Hodgkin lymphoma or breast cancer, tuberculosis, and end-stage kidney disease.^2,3 Other possible causes are retention of uremic metabolites, metastatic calcification induced by secondary hyperparathyroidism, and calcium-phosphate deposition induced by hyperphosphatemia.⁴

In chronic kidney disease, the amount of pericardial fluid and fibrinous pericardial deposition is thought to contribute to increased pericardial thickness and constriction. In some patients, pericardial calcification and thickening would lead to constrictive pericarditis, which could be confirmed by echocardiography and cardiac catheterization. About 25% to 50% of cases of pericardial calcification are complicated by constrictive pericarditis.^5,6 Constrictive pericarditis occurs in up to 4% of patients with end-stage renal disease, even with successful dialysis.⁷

Partial clinical improvement may be obtained with intensive hemodialysis, strict volume control, and decreased catabolism in patients with multiple comorbidities.⁸ However, the definite treatment is total pericardiectomy, which reduces symptoms substantially and offers a favorable long-term outcome.⁷

SECONDARY HYPERPARATHYROIDISM

Secondary hyperparathyroidism is a common complication in patients with end-stage renal disease and is characterized by derangements in the homeostasis of calcium, phosphorus, and vitamin D.⁹

Because renal function is decreased, phosphate is retained and calcitriol synthesis is reduced, resulting in hypocalcemia, which induces parathyroid gland hyperplasia and parathyroid hormone secretion.¹⁰ Moreover, some patents with long-standing secondary hyperparathyroidism may develop tertiary hyperparathyroidism associated with autonomous parathyroid hormone secretion, hypercalcemia, and hyperphosphatemia.¹¹

The Kidney Disease: Improving Global Outcomes (KDIGO) Work Group recommends screening for and managing secondary hyperparathyroidism in all patients with stage 3 chronic kidney disease (estimated glomerular filtration rate < 60 mL/min). In patients with stage 5 chronic kidney disease or on dialysis, the serum calcium and phosphorus levels should be monitored every 1 to 3 months and the parathyroid hormone levels every 3 to 6 months.¹²

According to KDIGO guidelines, the target level of calcium is less than 10.2 mg/dL, and the target phosphorus level is less than 4.6 mg/dL. The level of parathyroid hormone should be maintained at 2 to 9 times the upper limit of normal for the assay.

The management of secondary hyperparathyroidism includes a low-phosphorus diet, calcium-containing or calcium-free phosphate binders, a calcitriol supplement, and calcimimetics. If medical treatment fails and manifestations are significant, parathyroidectomy may be indicated.¹³

A 58-year-old man with end-stage renal disease due to diabetic nephropathy was admitted with aggravated exertional dyspnea and intermittent chest pain for 1 week. He had been on hemodialysis for 15 years.

His blood pressure was 124/69 mm Hg, pulse 96 beats per minute, and temperature 35.8°C. On physical examination, he had bilateral diffuse crackles, elevated jugular venous pressure (9.5 cm H₂O) with positive hepatojugular reflux, and apparent dependent pedal edema. The Kussmaul sign was not observed.

Cardiac enzymes were in the normal range (creatine kinase 73 U/L, troponin I 0.032 ng/mL), but the brain-natriuretic peptide level was elevated at 340 pg/mL. Other laboratory findings included calcium 9 mg/dL (reference range 8.4–10.2 mg/dL), inorganic phosphate 5 mg/dL (2.5–4.5 mg/dL), and intact parathyroid hormone 1,457 pg/mL (10–69 pg/mL).

Electrocardiography showed sinus tachycardia with low voltage in diffuse leads and generalized flattening of the T wave. Chest radiography showed a bilateral reticulo­nodular pattern, mild costo­phrenic angle obliteration, and notable calcifications along the cardiac contour. Thoracic computed tomography showed a porcelain-like encasement of the heart (Figure 1). Transthoracic echocardiography showed thickened pericardium, pericardial calcification, and mild interventricular septal bounce in diastole, with no dyskinesia of ventricular wall motion. We decided not to perform an invasive hemodynamic assessment.

CAUSES OF PERICARDIAL CALCIFICATION

Pericardial calcification, abnormal calcium deposits in response to inflammation,¹ has become more widely reported as the use of chest computed tomography has become more widespread. The common identifiable causes of pericardial calcification include recurrent or chronic pericarditis, radiation therapy for Hodgkin lymphoma or breast cancer, tuberculosis, and end-stage kidney disease.^2,3 Other possible causes are retention of uremic metabolites, metastatic calcification induced by secondary hyperparathyroidism, and calcium-phosphate deposition induced by hyperphosphatemia.⁴

In chronic kidney disease, the amount of pericardial fluid and fibrinous pericardial deposition is thought to contribute to increased pericardial thickness and constriction. In some patients, pericardial calcification and thickening would lead to constrictive pericarditis, which could be confirmed by echocardiography and cardiac catheterization. About 25% to 50% of cases of pericardial calcification are complicated by constrictive pericarditis.^5,6 Constrictive pericarditis occurs in up to 4% of patients with end-stage renal disease, even with successful dialysis.⁷

Partial clinical improvement may be obtained with intensive hemodialysis, strict volume control, and decreased catabolism in patients with multiple comorbidities.⁸ However, the definite treatment is total pericardiectomy, which reduces symptoms substantially and offers a favorable long-term outcome.⁷

SECONDARY HYPERPARATHYROIDISM

Secondary hyperparathyroidism is a common complication in patients with end-stage renal disease and is characterized by derangements in the homeostasis of calcium, phosphorus, and vitamin D.⁹

Because renal function is decreased, phosphate is retained and calcitriol synthesis is reduced, resulting in hypocalcemia, which induces parathyroid gland hyperplasia and parathyroid hormone secretion.¹⁰ Moreover, some patents with long-standing secondary hyperparathyroidism may develop tertiary hyperparathyroidism associated with autonomous parathyroid hormone secretion, hypercalcemia, and hyperphosphatemia.¹¹

The Kidney Disease: Improving Global Outcomes (KDIGO) Work Group recommends screening for and managing secondary hyperparathyroidism in all patients with stage 3 chronic kidney disease (estimated glomerular filtration rate < 60 mL/min). In patients with stage 5 chronic kidney disease or on dialysis, the serum calcium and phosphorus levels should be monitored every 1 to 3 months and the parathyroid hormone levels every 3 to 6 months.¹²

According to KDIGO guidelines, the target level of calcium is less than 10.2 mg/dL, and the target phosphorus level is less than 4.6 mg/dL. The level of parathyroid hormone should be maintained at 2 to 9 times the upper limit of normal for the assay.

The management of secondary hyperparathyroidism includes a low-phosphorus diet, calcium-containing or calcium-free phosphate binders, a calcitriol supplement, and calcimimetics. If medical treatment fails and manifestations are significant, parathyroidectomy may be indicated.¹³

A 35-year-old woman with a history of migraine presented with a headache that had worsened over the past 2 weeks. The headache was occipital and was associated with blurred vision, photophobia, tingling of the hands, episodes of flashing lights and images, and difficulty concentrating. The headache was similar to her typical migraines, but with the addition of flashing lights and images.

Her medical history included a cystic mass in the right occipital lobe that had been found incidentally on magnetic resonance imaging (MRI) during a workup for pituitary adenoma. The mass was thought to be a congenital lesion or arachnoid cyst, and intermittent screening had been recommended.

The patient had grown up in Honduras and had lived in the jungle until age 12, when she moved to the United States.

EVALUATION AND MANAGEMENT

Physical examination was remarkable for partial visual field loss in the periphery of the left temporal quadrant in both eyes (partial homonymous hemianopia). Repeat MRI showed a cystic lesion with scolex (the anterior end of a tapeworm) in the right occipital lobe, with surrounding edema (Figure 1).

Cystic brain lesions are associated with arachnoid cyst, glioma, and malignancy, but the presence of the scolex placed neurocysticercosis as the leading diagnosis. Testing for cysticercus antibody was negative. This test was done in the hope of confirming our high suspicion; while a negative test result does not exclude this diagnosis, a positive test would have been helpful to corroborate what we suspected. However, her imaging and clinical features were sufficient to warrant treating her for neurocysticercosis

She was treated with albendazole 400 mg twice a day for 10 days, and prednisone 1 mg/kg/day for 10 days followed by a taper. Because of the frequency with which neurocysticercosis causes seizures, an anti­epileptic drug is also recommended, at least until active lesions have subsided.¹ In this patient, levetiracetam 1,000 mg twice a day was prescribed for 6 months for seizure prophylaxis.

Repeat MRI 2 months later showed improvement (Figure 2). Her acute neurologic signs and symptoms had resolved, but she continued to be followed for chronic migraines (Figure 3). She has had no seizures despite weaning from levetiracetam.

TAPEWORM AND MIGRAINE

Neurocysticercosis is caused by the cestode Taenia solium, acquired by eating undercooked pork contaminated with the cysts or eggs.¹ The oncospheres released by the eggs migrate through the host body and encyst in end organs.

Neuroimaging can show 4 stages of the cysts—vesicular with living larva, colloidal with larva degeneration, granulonodular with thickening of the cyst, and calcification.¹

For patients who have lived in or visited high-risk areas of the world such as Central America, South America, sub-Saharan Africa, India, and Asia, it is important to include neurocysticercosis in the differential diagnosis of migraine with focal deficits or migraine with an evolving quality. Encysted larvae can remain asymptomatic for years but can cause brain edema, often leading to seizures.

Serum testing for cysticercus antibody can indicate acute infection, chronic infection, and possibly the immune response to treatment; however, serum testing has limited sensitivity in patients who have single or calcified lesions.² A negative test result does not exclude infection and is more likely to be a false negative in patients with a single or calcified lesion.

Current treatment guidelines recommend albendazole 400 mg twice daily along with dexamethasone or prednisolone to decrease the number of cysts and the development of lesional epilepsy.¹ Albendazole in combination with praziquantel 50 mg/kg/day kills more cysts than albendazole alone and should be considered in patients with more than 2 cysts.³

A 35-year-old woman with a history of migraine presented with a headache that had worsened over the past 2 weeks. The headache was occipital and was associated with blurred vision, photophobia, tingling of the hands, episodes of flashing lights and images, and difficulty concentrating. The headache was similar to her typical migraines, but with the addition of flashing lights and images.

Her medical history included a cystic mass in the right occipital lobe that had been found incidentally on magnetic resonance imaging (MRI) during a workup for pituitary adenoma. The mass was thought to be a congenital lesion or arachnoid cyst, and intermittent screening had been recommended.

The patient had grown up in Honduras and had lived in the jungle until age 12, when she moved to the United States.

EVALUATION AND MANAGEMENT

Physical examination was remarkable for partial visual field loss in the periphery of the left temporal quadrant in both eyes (partial homonymous hemianopia). Repeat MRI showed a cystic lesion with scolex (the anterior end of a tapeworm) in the right occipital lobe, with surrounding edema (Figure 1).

Cystic brain lesions are associated with arachnoid cyst, glioma, and malignancy, but the presence of the scolex placed neurocysticercosis as the leading diagnosis. Testing for cysticercus antibody was negative. This test was done in the hope of confirming our high suspicion; while a negative test result does not exclude this diagnosis, a positive test would have been helpful to corroborate what we suspected. However, her imaging and clinical features were sufficient to warrant treating her for neurocysticercosis

She was treated with albendazole 400 mg twice a day for 10 days, and prednisone 1 mg/kg/day for 10 days followed by a taper. Because of the frequency with which neurocysticercosis causes seizures, an anti­epileptic drug is also recommended, at least until active lesions have subsided.¹ In this patient, levetiracetam 1,000 mg twice a day was prescribed for 6 months for seizure prophylaxis.

Repeat MRI 2 months later showed improvement (Figure 2). Her acute neurologic signs and symptoms had resolved, but she continued to be followed for chronic migraines (Figure 3). She has had no seizures despite weaning from levetiracetam.

TAPEWORM AND MIGRAINE

Neurocysticercosis is caused by the cestode Taenia solium, acquired by eating undercooked pork contaminated with the cysts or eggs.¹ The oncospheres released by the eggs migrate through the host body and encyst in end organs.

Neuroimaging can show 4 stages of the cysts—vesicular with living larva, colloidal with larva degeneration, granulonodular with thickening of the cyst, and calcification.¹

For patients who have lived in or visited high-risk areas of the world such as Central America, South America, sub-Saharan Africa, India, and Asia, it is important to include neurocysticercosis in the differential diagnosis of migraine with focal deficits or migraine with an evolving quality. Encysted larvae can remain asymptomatic for years but can cause brain edema, often leading to seizures.

Serum testing for cysticercus antibody can indicate acute infection, chronic infection, and possibly the immune response to treatment; however, serum testing has limited sensitivity in patients who have single or calcified lesions.² A negative test result does not exclude infection and is more likely to be a false negative in patients with a single or calcified lesion.

Current treatment guidelines recommend albendazole 400 mg twice daily along with dexamethasone or prednisolone to decrease the number of cysts and the development of lesional epilepsy.¹ Albendazole in combination with praziquantel 50 mg/kg/day kills more cysts than albendazole alone and should be considered in patients with more than 2 cysts.³

A 35-year-old woman with a history of migraine presented with a headache that had worsened over the past 2 weeks. The headache was occipital and was associated with blurred vision, photophobia, tingling of the hands, episodes of flashing lights and images, and difficulty concentrating. The headache was similar to her typical migraines, but with the addition of flashing lights and images.

Her medical history included a cystic mass in the right occipital lobe that had been found incidentally on magnetic resonance imaging (MRI) during a workup for pituitary adenoma. The mass was thought to be a congenital lesion or arachnoid cyst, and intermittent screening had been recommended.

The patient had grown up in Honduras and had lived in the jungle until age 12, when she moved to the United States.

EVALUATION AND MANAGEMENT

Physical examination was remarkable for partial visual field loss in the periphery of the left temporal quadrant in both eyes (partial homonymous hemianopia). Repeat MRI showed a cystic lesion with scolex (the anterior end of a tapeworm) in the right occipital lobe, with surrounding edema (Figure 1).

Cystic brain lesions are associated with arachnoid cyst, glioma, and malignancy, but the presence of the scolex placed neurocysticercosis as the leading diagnosis. Testing for cysticercus antibody was negative. This test was done in the hope of confirming our high suspicion; while a negative test result does not exclude this diagnosis, a positive test would have been helpful to corroborate what we suspected. However, her imaging and clinical features were sufficient to warrant treating her for neurocysticercosis

She was treated with albendazole 400 mg twice a day for 10 days, and prednisone 1 mg/kg/day for 10 days followed by a taper. Because of the frequency with which neurocysticercosis causes seizures, an anti­epileptic drug is also recommended, at least until active lesions have subsided.¹ In this patient, levetiracetam 1,000 mg twice a day was prescribed for 6 months for seizure prophylaxis.

Repeat MRI 2 months later showed improvement (Figure 2). Her acute neurologic signs and symptoms had resolved, but she continued to be followed for chronic migraines (Figure 3). She has had no seizures despite weaning from levetiracetam.

TAPEWORM AND MIGRAINE

Neurocysticercosis is caused by the cestode Taenia solium, acquired by eating undercooked pork contaminated with the cysts or eggs.¹ The oncospheres released by the eggs migrate through the host body and encyst in end organs.

Neuroimaging can show 4 stages of the cysts—vesicular with living larva, colloidal with larva degeneration, granulonodular with thickening of the cyst, and calcification.¹

For patients who have lived in or visited high-risk areas of the world such as Central America, South America, sub-Saharan Africa, India, and Asia, it is important to include neurocysticercosis in the differential diagnosis of migraine with focal deficits or migraine with an evolving quality. Encysted larvae can remain asymptomatic for years but can cause brain edema, often leading to seizures.

Serum testing for cysticercus antibody can indicate acute infection, chronic infection, and possibly the immune response to treatment; however, serum testing has limited sensitivity in patients who have single or calcified lesions.² A negative test result does not exclude infection and is more likely to be a false negative in patients with a single or calcified lesion.

Current treatment guidelines recommend albendazole 400 mg twice daily along with dexamethasone or prednisolone to decrease the number of cysts and the development of lesional epilepsy.¹ Albendazole in combination with praziquantel 50 mg/kg/day kills more cysts than albendazole alone and should be considered in patients with more than 2 cysts.³