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Emergency Ultrasound: Tendon Evaluation With Ultrasonography
The vast majority of musculotendinous injuries occur secondary to violent contraction or excessive stretching.1 Ligamentous injuries, on the other hand, are due to an abnormal motion of joints. The magnitude of inciting forces results in a spectrum of pathology, ranging from a minor tear to a complete disruption of structures.
Ultrasonography provides a detailed assessment of soft tissue anatomy and dynamic functionality, and in some instances can be comparable or even superior to magnetic resonance imaging2 because the structural characteristics of certain tendons make them ideal for imaging via ultrasonography. We describe some of these characteristics and highlight their utility in diagnostic imaging.
Anatomical Structure
Tendons consist of tightly packed type I collagen fibers forming subfascicles that are arranged in a parallel distribution as fascicles. These bundles are held together by loose soft tissue, and the entire structure is covered by a thick fibroelastic epitendineum sheath. This linear distribution of structures yields a uniquely linear “fibrillary” pattern when viewed along the longitudinal axis of the structure (Figure 1a). In the short-axis view, the tendon appears as a well-circumscribed structure with speckled pattern of hyperechoic foci (Figure 1b). 3
Imaging Technique
The optimal scanning technique involves the use of a high-frequency linear transducer. Higher frequencies yield more detailed images, but may be limited in patients with deeper structures due to body habitus. A key concept in tendon evaluation is an artifact known as “anisotropy.” This refers to change in appearance of the tendon based on the incident angle of the ultrasound beam. For example, when the probe is held perpendicular to the structure of interest, parallel fibers will reflect the emitted beam toward the probe and thus appear as hyperechoic and speckled, a characteristic of these fibers (Figures 1a and 1b). Contrarily, if the probe is held at a nonperpendicular angle, the reflected beam will not return to the probe, resulting in a hypoechoic appearance (Figure 2).
Pathology
Tendon strains result in varying degrees of fibrous tearing. These tears can range from first-degree tears (a few fibers) to third-degree tears (complete disruption). Partial tears result in focal hematoma formation (Figure 3a) at the region of disruption, appearing on ultrasound as a hypoechoic fluid collection within a hyperechoic fibrillary or speckled tendon structure. If the disruption occurs along the surface of the tendon, a focus of anechoic fluid may be seen surrounding the tendon. Complete tendon ruptures, on the other hand, appear as a hypoechoic void with retracted tendon fragments visualized on either side4 (Figures 3b and 3c). Although complete tears can be more apparent clinically in areas in which a group of tendons performs a cohesive movement (ie, rotator cuff), ultrasound can significantly reduce the rate of delayed diagnosis when physical examination is equivocal.
In the appropriate clinical setting, ultrasonography can provide rapid and dynamic assessment of musculotendinous injuries. Lower extremity injuries, including those affecting the Achilles (Figure 1), quadriceps, (Figures 4a and 4b) and patellar tendons (Figure 5), are easier clinical applications.
Assessment of rotator cuff tendons, although more difficult, can provide a specific assessment of shoulder pain.5 In such scenarios, ultrasound can serve a very useful role as an adjunct to the physical examination.
An important point to recognize is that tendons will appear hypoechoic at the insertion point on bone (anthesis) due to increased curvature resulting in lack of anisotropy. This can appear as a pathological finding, but can be accounted for by simply performing a heel-toe or tilt maneuver to arrange the beam perpendicular to the tendon fibers (Figures 6a and 6b).
Summary
Musculotendinous injuries many times present as nonspecific symptoms of pain and/or swelling. In the case of an equivocal physical examination, musculotendinous injuries can be diagnosed with increased accuracy through the use of ultrasound. Understanding the artifactual component of tendon ultrasound can aid the clinician in diagnosing these injuries, enhancing patient care and satisfaction.
1. Geiderman J, Katz D. Geneneral principles in orthopedic injuries. In: Marx JA, Hockberger RS, Walls RM, Biros MH, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. Philadelphia, PA: Elsevier Saunders; 2014:49:511-533.
2. Jacobson, Jon A. Musculoskeletal sonography and MR imaging. A role for both imaging methods. Radiol Clin North Am. 1999;37(4):713-735.
3. O’Neill J, ed. Musculoskeletal Ultrasound: Anatomy and Technique. New York, NY: Springer Science+Business Media. 2008:3-17.
4. Dawson M, Mallin M. Introduction to bedside ultrasound. Vol 1. Emergency ultrasound solutions. Lexington, KY: Emergency Ultrasound Solutions; 2012;25:245-248. https://www.aci.health.nsw.gov.au/__data/assets/pdf_file/0009/327852/Introduction_to_Bedside_Ultrasound_Volume_1_-_Matt_and_Mike.pdf. Accessed April 12, 2017.
5. Tran G, Hensor EM, Ray A, Kingsbury SR, O’Connor P, Conaghan PG. Ultrasound-detected pathologies cluster into groups with different clinical outcomes: data from 3000 community referrals for shoulder pain. Arthritis Res Ther. 2017;19(1):30. doi:10.1186/s13075-017-1235-y.
The vast majority of musculotendinous injuries occur secondary to violent contraction or excessive stretching.1 Ligamentous injuries, on the other hand, are due to an abnormal motion of joints. The magnitude of inciting forces results in a spectrum of pathology, ranging from a minor tear to a complete disruption of structures.
Ultrasonography provides a detailed assessment of soft tissue anatomy and dynamic functionality, and in some instances can be comparable or even superior to magnetic resonance imaging2 because the structural characteristics of certain tendons make them ideal for imaging via ultrasonography. We describe some of these characteristics and highlight their utility in diagnostic imaging.
Anatomical Structure
Tendons consist of tightly packed type I collagen fibers forming subfascicles that are arranged in a parallel distribution as fascicles. These bundles are held together by loose soft tissue, and the entire structure is covered by a thick fibroelastic epitendineum sheath. This linear distribution of structures yields a uniquely linear “fibrillary” pattern when viewed along the longitudinal axis of the structure (Figure 1a). In the short-axis view, the tendon appears as a well-circumscribed structure with speckled pattern of hyperechoic foci (Figure 1b). 3
Imaging Technique
The optimal scanning technique involves the use of a high-frequency linear transducer. Higher frequencies yield more detailed images, but may be limited in patients with deeper structures due to body habitus. A key concept in tendon evaluation is an artifact known as “anisotropy.” This refers to change in appearance of the tendon based on the incident angle of the ultrasound beam. For example, when the probe is held perpendicular to the structure of interest, parallel fibers will reflect the emitted beam toward the probe and thus appear as hyperechoic and speckled, a characteristic of these fibers (Figures 1a and 1b). Contrarily, if the probe is held at a nonperpendicular angle, the reflected beam will not return to the probe, resulting in a hypoechoic appearance (Figure 2).
Pathology
Tendon strains result in varying degrees of fibrous tearing. These tears can range from first-degree tears (a few fibers) to third-degree tears (complete disruption). Partial tears result in focal hematoma formation (Figure 3a) at the region of disruption, appearing on ultrasound as a hypoechoic fluid collection within a hyperechoic fibrillary or speckled tendon structure. If the disruption occurs along the surface of the tendon, a focus of anechoic fluid may be seen surrounding the tendon. Complete tendon ruptures, on the other hand, appear as a hypoechoic void with retracted tendon fragments visualized on either side4 (Figures 3b and 3c). Although complete tears can be more apparent clinically in areas in which a group of tendons performs a cohesive movement (ie, rotator cuff), ultrasound can significantly reduce the rate of delayed diagnosis when physical examination is equivocal.
In the appropriate clinical setting, ultrasonography can provide rapid and dynamic assessment of musculotendinous injuries. Lower extremity injuries, including those affecting the Achilles (Figure 1), quadriceps, (Figures 4a and 4b) and patellar tendons (Figure 5), are easier clinical applications.
Assessment of rotator cuff tendons, although more difficult, can provide a specific assessment of shoulder pain.5 In such scenarios, ultrasound can serve a very useful role as an adjunct to the physical examination.
An important point to recognize is that tendons will appear hypoechoic at the insertion point on bone (anthesis) due to increased curvature resulting in lack of anisotropy. This can appear as a pathological finding, but can be accounted for by simply performing a heel-toe or tilt maneuver to arrange the beam perpendicular to the tendon fibers (Figures 6a and 6b).
Summary
Musculotendinous injuries many times present as nonspecific symptoms of pain and/or swelling. In the case of an equivocal physical examination, musculotendinous injuries can be diagnosed with increased accuracy through the use of ultrasound. Understanding the artifactual component of tendon ultrasound can aid the clinician in diagnosing these injuries, enhancing patient care and satisfaction.
The vast majority of musculotendinous injuries occur secondary to violent contraction or excessive stretching.1 Ligamentous injuries, on the other hand, are due to an abnormal motion of joints. The magnitude of inciting forces results in a spectrum of pathology, ranging from a minor tear to a complete disruption of structures.
Ultrasonography provides a detailed assessment of soft tissue anatomy and dynamic functionality, and in some instances can be comparable or even superior to magnetic resonance imaging2 because the structural characteristics of certain tendons make them ideal for imaging via ultrasonography. We describe some of these characteristics and highlight their utility in diagnostic imaging.
Anatomical Structure
Tendons consist of tightly packed type I collagen fibers forming subfascicles that are arranged in a parallel distribution as fascicles. These bundles are held together by loose soft tissue, and the entire structure is covered by a thick fibroelastic epitendineum sheath. This linear distribution of structures yields a uniquely linear “fibrillary” pattern when viewed along the longitudinal axis of the structure (Figure 1a). In the short-axis view, the tendon appears as a well-circumscribed structure with speckled pattern of hyperechoic foci (Figure 1b). 3
Imaging Technique
The optimal scanning technique involves the use of a high-frequency linear transducer. Higher frequencies yield more detailed images, but may be limited in patients with deeper structures due to body habitus. A key concept in tendon evaluation is an artifact known as “anisotropy.” This refers to change in appearance of the tendon based on the incident angle of the ultrasound beam. For example, when the probe is held perpendicular to the structure of interest, parallel fibers will reflect the emitted beam toward the probe and thus appear as hyperechoic and speckled, a characteristic of these fibers (Figures 1a and 1b). Contrarily, if the probe is held at a nonperpendicular angle, the reflected beam will not return to the probe, resulting in a hypoechoic appearance (Figure 2).
Pathology
Tendon strains result in varying degrees of fibrous tearing. These tears can range from first-degree tears (a few fibers) to third-degree tears (complete disruption). Partial tears result in focal hematoma formation (Figure 3a) at the region of disruption, appearing on ultrasound as a hypoechoic fluid collection within a hyperechoic fibrillary or speckled tendon structure. If the disruption occurs along the surface of the tendon, a focus of anechoic fluid may be seen surrounding the tendon. Complete tendon ruptures, on the other hand, appear as a hypoechoic void with retracted tendon fragments visualized on either side4 (Figures 3b and 3c). Although complete tears can be more apparent clinically in areas in which a group of tendons performs a cohesive movement (ie, rotator cuff), ultrasound can significantly reduce the rate of delayed diagnosis when physical examination is equivocal.
In the appropriate clinical setting, ultrasonography can provide rapid and dynamic assessment of musculotendinous injuries. Lower extremity injuries, including those affecting the Achilles (Figure 1), quadriceps, (Figures 4a and 4b) and patellar tendons (Figure 5), are easier clinical applications.
Assessment of rotator cuff tendons, although more difficult, can provide a specific assessment of shoulder pain.5 In such scenarios, ultrasound can serve a very useful role as an adjunct to the physical examination.
An important point to recognize is that tendons will appear hypoechoic at the insertion point on bone (anthesis) due to increased curvature resulting in lack of anisotropy. This can appear as a pathological finding, but can be accounted for by simply performing a heel-toe or tilt maneuver to arrange the beam perpendicular to the tendon fibers (Figures 6a and 6b).
Summary
Musculotendinous injuries many times present as nonspecific symptoms of pain and/or swelling. In the case of an equivocal physical examination, musculotendinous injuries can be diagnosed with increased accuracy through the use of ultrasound. Understanding the artifactual component of tendon ultrasound can aid the clinician in diagnosing these injuries, enhancing patient care and satisfaction.
1. Geiderman J, Katz D. Geneneral principles in orthopedic injuries. In: Marx JA, Hockberger RS, Walls RM, Biros MH, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. Philadelphia, PA: Elsevier Saunders; 2014:49:511-533.
2. Jacobson, Jon A. Musculoskeletal sonography and MR imaging. A role for both imaging methods. Radiol Clin North Am. 1999;37(4):713-735.
3. O’Neill J, ed. Musculoskeletal Ultrasound: Anatomy and Technique. New York, NY: Springer Science+Business Media. 2008:3-17.
4. Dawson M, Mallin M. Introduction to bedside ultrasound. Vol 1. Emergency ultrasound solutions. Lexington, KY: Emergency Ultrasound Solutions; 2012;25:245-248. https://www.aci.health.nsw.gov.au/__data/assets/pdf_file/0009/327852/Introduction_to_Bedside_Ultrasound_Volume_1_-_Matt_and_Mike.pdf. Accessed April 12, 2017.
5. Tran G, Hensor EM, Ray A, Kingsbury SR, O’Connor P, Conaghan PG. Ultrasound-detected pathologies cluster into groups with different clinical outcomes: data from 3000 community referrals for shoulder pain. Arthritis Res Ther. 2017;19(1):30. doi:10.1186/s13075-017-1235-y.
1. Geiderman J, Katz D. Geneneral principles in orthopedic injuries. In: Marx JA, Hockberger RS, Walls RM, Biros MH, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. Philadelphia, PA: Elsevier Saunders; 2014:49:511-533.
2. Jacobson, Jon A. Musculoskeletal sonography and MR imaging. A role for both imaging methods. Radiol Clin North Am. 1999;37(4):713-735.
3. O’Neill J, ed. Musculoskeletal Ultrasound: Anatomy and Technique. New York, NY: Springer Science+Business Media. 2008:3-17.
4. Dawson M, Mallin M. Introduction to bedside ultrasound. Vol 1. Emergency ultrasound solutions. Lexington, KY: Emergency Ultrasound Solutions; 2012;25:245-248. https://www.aci.health.nsw.gov.au/__data/assets/pdf_file/0009/327852/Introduction_to_Bedside_Ultrasound_Volume_1_-_Matt_and_Mike.pdf. Accessed April 12, 2017.
5. Tran G, Hensor EM, Ray A, Kingsbury SR, O’Connor P, Conaghan PG. Ultrasound-detected pathologies cluster into groups with different clinical outcomes: data from 3000 community referrals for shoulder pain. Arthritis Res Ther. 2017;19(1):30. doi:10.1186/s13075-017-1235-y.
Hospitalists get hands-on training at POC ultrasound pre-course
Hospitalists participated in a double-header of hands-on point-of-care ultrasound training here on Monday, looking to gain an edge in expertise in a role that’s becoming more and more common.
Nearly 100 hospitalists and other health care professionals heard talks on the fundamental principles of ultrasound and cardiac, lung and vascular, and abdominal ultrasound. The highlights of the sessions were two 80-minute hands-on segments using the probes.
“This course has grown and grown – this is the largest we’ve ever done,” said pre-course director Nilam Soni, MD, MS, FHM, associate professor of medicine at the University of Texas Health Science Center San Antonio.
A morning and afternoon session were held, each attended by 48 registrants. Because of high demand, the society added 12 spots to each session – and there was still a wait list, said Ricardo Franco-Sadud, MD, the other director of the course and associate professor of medicine at the Medical College of Wisconsin, Milwaukee.
“The idea is to give you the most amount of time with the probe in their hand,” Dr. Franco said.
In one of the hands-on sessions, Adam Merando, MD, a hospitalist and associate program director of the internal medicine residency program at Saint Louis University, slid and rocked the probe on the stomach of a volunteer as the picture came into view.
“Now we’re getting an image,” his bedside instructor, Brandon Boesch, DO, a hospitalist at Highland Hospital in Oakland, Calif., told him. Dr. Merando had found the liver.
He eventually found the main target, the inferior vena cava, and assessed its diameter in relation to the breathing of the “patient.” This information is used to gauge how responsive acute circulatory failure patients are to fluid therapy.
At one point, with another learner, the image shifted.
“You see how it feels like your hand is not moving, but the image is changing?” Dr. Boesch said. “That’s part of the fine motor skill.”
Kirk Spencer, MD, professor of medicine and a cardiologist at the University of Chicago and perennial participant in the course, said it’s a great way for hospitalists who were hesitant about learning ultrasound to get over the hump.
Benji Mathews, MD, assistant professor of medicine at the University of Minnesota, Minneapolis, another bedside instructor, said the enthusiasm about the course is well founded.
“This is one of the few technologies that brings you back to the bedside.”
Hospitalists participated in a double-header of hands-on point-of-care ultrasound training here on Monday, looking to gain an edge in expertise in a role that’s becoming more and more common.
Nearly 100 hospitalists and other health care professionals heard talks on the fundamental principles of ultrasound and cardiac, lung and vascular, and abdominal ultrasound. The highlights of the sessions were two 80-minute hands-on segments using the probes.
“This course has grown and grown – this is the largest we’ve ever done,” said pre-course director Nilam Soni, MD, MS, FHM, associate professor of medicine at the University of Texas Health Science Center San Antonio.
A morning and afternoon session were held, each attended by 48 registrants. Because of high demand, the society added 12 spots to each session – and there was still a wait list, said Ricardo Franco-Sadud, MD, the other director of the course and associate professor of medicine at the Medical College of Wisconsin, Milwaukee.
“The idea is to give you the most amount of time with the probe in their hand,” Dr. Franco said.
In one of the hands-on sessions, Adam Merando, MD, a hospitalist and associate program director of the internal medicine residency program at Saint Louis University, slid and rocked the probe on the stomach of a volunteer as the picture came into view.
“Now we’re getting an image,” his bedside instructor, Brandon Boesch, DO, a hospitalist at Highland Hospital in Oakland, Calif., told him. Dr. Merando had found the liver.
He eventually found the main target, the inferior vena cava, and assessed its diameter in relation to the breathing of the “patient.” This information is used to gauge how responsive acute circulatory failure patients are to fluid therapy.
At one point, with another learner, the image shifted.
“You see how it feels like your hand is not moving, but the image is changing?” Dr. Boesch said. “That’s part of the fine motor skill.”
Kirk Spencer, MD, professor of medicine and a cardiologist at the University of Chicago and perennial participant in the course, said it’s a great way for hospitalists who were hesitant about learning ultrasound to get over the hump.
Benji Mathews, MD, assistant professor of medicine at the University of Minnesota, Minneapolis, another bedside instructor, said the enthusiasm about the course is well founded.
“This is one of the few technologies that brings you back to the bedside.”
Hospitalists participated in a double-header of hands-on point-of-care ultrasound training here on Monday, looking to gain an edge in expertise in a role that’s becoming more and more common.
Nearly 100 hospitalists and other health care professionals heard talks on the fundamental principles of ultrasound and cardiac, lung and vascular, and abdominal ultrasound. The highlights of the sessions were two 80-minute hands-on segments using the probes.
“This course has grown and grown – this is the largest we’ve ever done,” said pre-course director Nilam Soni, MD, MS, FHM, associate professor of medicine at the University of Texas Health Science Center San Antonio.
A morning and afternoon session were held, each attended by 48 registrants. Because of high demand, the society added 12 spots to each session – and there was still a wait list, said Ricardo Franco-Sadud, MD, the other director of the course and associate professor of medicine at the Medical College of Wisconsin, Milwaukee.
“The idea is to give you the most amount of time with the probe in their hand,” Dr. Franco said.
In one of the hands-on sessions, Adam Merando, MD, a hospitalist and associate program director of the internal medicine residency program at Saint Louis University, slid and rocked the probe on the stomach of a volunteer as the picture came into view.
“Now we’re getting an image,” his bedside instructor, Brandon Boesch, DO, a hospitalist at Highland Hospital in Oakland, Calif., told him. Dr. Merando had found the liver.
He eventually found the main target, the inferior vena cava, and assessed its diameter in relation to the breathing of the “patient.” This information is used to gauge how responsive acute circulatory failure patients are to fluid therapy.
At one point, with another learner, the image shifted.
“You see how it feels like your hand is not moving, but the image is changing?” Dr. Boesch said. “That’s part of the fine motor skill.”
Kirk Spencer, MD, professor of medicine and a cardiologist at the University of Chicago and perennial participant in the course, said it’s a great way for hospitalists who were hesitant about learning ultrasound to get over the hump.
Benji Mathews, MD, assistant professor of medicine at the University of Minnesota, Minneapolis, another bedside instructor, said the enthusiasm about the course is well founded.
“This is one of the few technologies that brings you back to the bedside.”
Measuring Malalignment on Imaging in the Treatment of Patellofemoral Instability
Take-Home Points
- Radiographic assessment of TT position is most commonly performed by measuring TT-TG distance, which is the distance between the extensor mechanism attachment at the TT and the center of the TG.
- TT-TG distances of more than 15 mm or 20 mm have been reported as indications for TT osteotomy.
- TT-TG distance criteria should serve as a guide, rather than a rigid threshold, in the context of imaging and patient factors when deciding whether to perform TT osteotomy for patellar instability.
- Factors such as knee flexion angle, imaging modality, and landmarks used for the measurements should be considered when using TT-TG distance as an indication for surgery.
- There has been significant variability in reported TT-TG measurements. A surgeon using this measurement should understand how it is obtained because many technical factors are involved.
Assessment of malalignment is an important factor in determining surgical treatment options for patellar instability. Although soft-tissue reconstruction of the medial soft-tissue stabilizers is often performed to address patellar instability, bony malalignment may increase stress on the medial soft tissues; therefore, it must be adequately identified and addressed.
Bony malalignment, which is often thought of as lateralization of the tibial tubercle (TT), can be influenced by tibiofemoral alignment, external tibial torsion, and femoral anteversion.
Clinically, coronal alignment can be assessed with a measurement such as quadriceps (Q) angle, but this has been reported to have low interrater reliability and high variability in the reported optimal conditions and positions in which the measurement should be made.1-3An anatomically lateralized TT pulls the extensor mechanism laterally with respect to the trochlear groove (TG), and this can accentuate problems related to patellofemoral instability. A recent biomechanical study found that increased TT lateralization significantly increased lateral patellar translation and tilt in the setting of medial patellofemoral ligament (MPFL) deficiency.4 Although MPFL reconstruction restored patellar kinematics and contact mechanics, this restoration did not occur when the TT was lateralized more than 10 mm relative to its normal position.
Realigning the extensor mechanism by moving the TT medially decreases the lateralizing forces on the patella and the stress on the soft-tissue restraints. This raises the issues of when to correct a lateralized TT and how to identify and measure malalignment.
Radiographic assessment of TT position is most commonly performed by measuring TT-TG distance, which is the distance between the extensor mechanism attachment at the TT and the center of the TG. Originally described on radiographs and subsequently on computed tomography (CT) and magnetic resonance imaging (MRI) scans, distances of more than 15 mm or 20 mm have been reported as indications for TT osteotomy.5,6However, there has been significant variability in reported TT-TG measurements. Studies have found that TT-TG distance is 3.8 mm larger on CT scans than on MRI scans.7 Furthermore, factors such as knee flexion angle at time of imaging have been found to reduce TT-TG distance.1 More recently, patient size and TT-TG ratios relative to patellar and trochlear width were identified as important factors in assessing TT-TG distance.8 Therefore, TT-TG distance measurements should serve as a guide rather than a rigid threshold in the context of imaging and patient factors when deciding whether to perform TT osteotomy for patellar instability.
What You Need to Know About Measuring Patellofemoral Malalignment
TT-TG distance can guide decisions about performing a medializing TT osteotomy for patellar instability because the measurement can aid in assessing bony malalignment caused by an anatomically lateralized tubercle. TT-TG distance can be used to determine when and how far to move the tubercle in TT osteotomy.
Background
A normal TT-TG value is approximately 10 mm. The measurement originally used bony landmarks, including the deepest part of the bony TG and the anterior-most part of the TT, as described by Goutallier and colleagues.9 In their original study, Dejour and colleagues5 found that patients with recurrent symptoms of patellar instability had TT-TG distances >20 mm.
Increased TT-TG distance has been shown to correlate with patellar position, including increased lateral shift and lateral tilt of the patella. In a study using dynamic CT scans of patients with recurrent patellar instability, we found that TT-TG distance increased with knee extension, and that this increase correlated with the lateral shift and lateral tilt of the patella.10An excessively lateralized TT can be corrected with a medializing osteotomy that reduces TT-TG distance to within the normal range. TT surgery can be performed with flat osteotomy, as described by Elmslie and Trillat,11 or with oblique osteotomy, as described by Fulkerson,6 to obtain concomitant anteriorization. In a computational study, Elias and colleagues12 found that medializing TT osteotomy not only reduced TT-TG distance but led to correction of lateral patellar tilt and displacement. Patellofemoral contact forces have also shown to be reduced with anteromedialization.6Although reported outcomes of TT osteotomy have been excellent for patients with patellar instability, the procedure has higher risks and longer rehabilitation relative to a soft-tissue procedure alone. Reported risks associated with TT osteotomy include fracture, nonunion, delayed union, painful screws, and deep vein thrombosis.6,10,13,14Understanding the limitations of and variability in radiographic assessments of TT and TG positions can help when deciding whether to perform TT osteotomy for patellar instability.
Discussion
When considering TT osteotomy for patellar instability, some surgeons use a TT-TG distance of more than 15 mm or 20 mm as a threshold for performing medialization. The variability is based on the multiple patient and imaging factors that can influence TT-TG distance measurement.
Several TG and TT landmarks have been used to measure TT-TG distance. The deepest part of the TG, based on bony anatomy, was used originally, but the cartilaginous landmark at the deepest part of the cartilaginous TG has also been described.15 Similarly, on the TT, the original description of TT-TG distance, by Goutallier and colleagues,9 involved the anterior-most part of the TT on CT scan, though the central part of the TT has also been described.15 We found a 4.2-mm difference in TT-TG distance with use of different landmarks (central tubercle, anterior tubercle) within the same study population.16 Therefore, within a practice, the distance used as an indication for TT osteotomy should be measured consistently.
Knee flexion angle at the time of imaging can also affect measurement of TT-TG distance. Several authors have reported smaller TT-TG distance with increased knee flexion angle.10,16,17 In a study of patients with symptomatic patellar instability, we found that TT-TG distance decreases by an estimated 1 mm for every 4.4° of knee flexion >0°.10 In measurements of TT-TG distance, the sagittal view can be used to assess knee flexion angle because positioning protocols and patient comfort at the time of imaging may produce variable knee flexion angles.
Given the variability that occurs in TT-TG distance with knee flexion angles, some surgeons use TT–posterior cruciate ligament (PCL) distance as another measurement of TT lateralization.18 This measurement is made with both tibial landmarks, from the TT to the medial border of the PCL insertion on the tibia, and theoretically eliminates knee flexion angle as a measurement factor. Seitlinger and colleagues18 found that values >24 mm were associated with symptoms of patellar instability. More study is needed to determine the precise indications for TT osteotomy with use of this measurement.
In addition to patient positioning during knee imaging, patient size should be considered when TT-TG distance is used for malalignment measurement. Camp and colleagues8 discussed the importance of “individualizing” TT-TG distance on the basis of patient size and bony structure. They reported that the ratio of TT-TG distance to trochlear width or patellar width more effectively predicted recurrent patellar instability than TT-TG distance alone.
Measurement of TT-TG distance is valuable in planning surgical treatment for patellar instability because it quantifies a component of malalignment and aids in deciding whether to perform TT osteotomy. However, this distance should be understood in the context of many measurement factors to allow for an individualized procedure that addresses the specific contributors to patellar instability in each patient.
Am J Orthop. 2017;46(3):148-151. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. France L, Nester C. Effect of errors in the identification of anatomical landmarks on the accuracy of Q angle values. Clin Biomech (Bristol, Avon). 2001;16(8):710-713.
2. Greene CC, Edwards TB, Wade MR, Carson EW. Reliability of the quadriceps angle measurement. Am J Knee Surg. 2001;14(2):97-103.
3. Smith TO, Hunt NJ, Donell ST. The reliability and validity of the Q-angle: a systematic review. Knee Surg Sports Traumatol Arthrosc. 2008;16(12):1068-1079.
4. Stephen JM, Dodds AL, Lumpaopong P, Kader D, Williams A, Amis AA. The ability of medial patellofemoral ligament reconstruction to correct patellar kinematics and contact mechanics in the presence of a lateralized tibial tubercle. Am J Sports Med. 2015;43(9):2198-2207.
5. Dejour H, Walch G, Nove-Josserand L, Guier C. Factors of patellar instability: an anatomic radiographic study. Knee Surg Sports Traumatol Arthrosc. 1994;2(1):19-26.
6. Fulkerson JP. Anteromedialization of the tibial tuberosity for patellofemoral malalignment. Clin Orthop Relat Res. 1983;177:176-181.
7. Camp CL, Stuart MJ, Krych AJ, et al. CT and MRI measurements of tibial tubercle-trochlear groove distances are not equivalent in patients with patellar instability. Am J Sports Med. 2013;41(8):1835-1840.
8. Camp CL, Heidenreich MJ, Dahm DL, Stuart MJ, Levy BA, Krych AJ. Individualizing the tibial tubercle-trochlear groove distance: patellar instability ratios that predict recurrent instability. Am J Sports Med. 2016;44(2):393-399.
9. Goutallier D, Bernageau J, Lecudonnec B. [The measurement of the tibial tuberosity. Patella groove distanced technique and results (author’s transl)]. Rev Chir Orthop Reparatrice Appar Mot. 1978;64(5):423-428.
10. Tanaka MJ, Elias JJ, Williams AA, Carrino JA, Cosgarea AJ. Correlation between changes in tibial tuberosity-trochlear groove distance and patellar position during active knee extension on dynamic kinematic computed tomography imaging. Arthroscopy. 2015;31(9):1748-1755.
11. Trillat A, Dejour H, Couette A. [Diagnosis and treatment of recurrent dislocations of the patella]. Rev Chir Orthop Reparatrice Appar Motur. 1964;50(6):813-824.
12. Elias JJ, Carrino JA, Saranathan A, Guseila LM, Tanaka MJ, Cosgarea AJ. Variations in kinematics and function following patellar stabilization including tibial tuberosity realignment. Knee Surg Sports Traumatol Arthrosc. 2014;22(10):2350-2356.
13. Sherman SL, Erickson BJ, Cvetanovich GL, et al. Tibial tuberosity osteotomy: indications, techniques, and outcomes. Am J Sports Med. 2014;42(8):2006-2017.
14. Wilcox JJ, Snow BJ, Aoki SK, Hung M, Burks RT. Does landmark selection affect the reliability of tibial tubercle-trochlear groove measurements using MRI? Clin Orthop Relat Res. 2012;470(8):2253-2260.
15. Schoettle PB, Zanetti M, Seifert B, Pfirrmann CWA, Fucentese SF, Romero J. The tibial tuberosity-trochlear groove distance; a comparative study between CT and MRI scanning. Knee. 2006;13(1):26-31.
16. Williams AA, Tanaka MJ, Elias JJ, et al. Measuring tibial tuberosity-trochlear groove distance on CT: Where to begin? Presented at the American Academy of Orthopaedic Surgeons Annual Meeting, New Orleans, LA, March 11-15, 2014.
17. Dietrich TJ, Betz M, Pfirrmann CWA, Koch PP, Fucentese SF. End-stage extension of the knee and its influence on tibial tuberosity-trochlear groove distance (TTTG) in asymptomatic volunteers. Knee Surg Sports Traumatol Arthrosc. 2014;22(1):214-218.
18. Seitlinger G, Scheurecker G, Hogler R, Labey L, Innocenti B, Hofmann S. Tibial tubercle-posterior cruciate ligament distance: a new measurement to define the position of the tibial tubercle in patients with patellar dislocation. Am J Sports Med. 2012;40(5):1119-1125.
Take-Home Points
- Radiographic assessment of TT position is most commonly performed by measuring TT-TG distance, which is the distance between the extensor mechanism attachment at the TT and the center of the TG.
- TT-TG distances of more than 15 mm or 20 mm have been reported as indications for TT osteotomy.
- TT-TG distance criteria should serve as a guide, rather than a rigid threshold, in the context of imaging and patient factors when deciding whether to perform TT osteotomy for patellar instability.
- Factors such as knee flexion angle, imaging modality, and landmarks used for the measurements should be considered when using TT-TG distance as an indication for surgery.
- There has been significant variability in reported TT-TG measurements. A surgeon using this measurement should understand how it is obtained because many technical factors are involved.
Assessment of malalignment is an important factor in determining surgical treatment options for patellar instability. Although soft-tissue reconstruction of the medial soft-tissue stabilizers is often performed to address patellar instability, bony malalignment may increase stress on the medial soft tissues; therefore, it must be adequately identified and addressed.
Bony malalignment, which is often thought of as lateralization of the tibial tubercle (TT), can be influenced by tibiofemoral alignment, external tibial torsion, and femoral anteversion.
Clinically, coronal alignment can be assessed with a measurement such as quadriceps (Q) angle, but this has been reported to have low interrater reliability and high variability in the reported optimal conditions and positions in which the measurement should be made.1-3An anatomically lateralized TT pulls the extensor mechanism laterally with respect to the trochlear groove (TG), and this can accentuate problems related to patellofemoral instability. A recent biomechanical study found that increased TT lateralization significantly increased lateral patellar translation and tilt in the setting of medial patellofemoral ligament (MPFL) deficiency.4 Although MPFL reconstruction restored patellar kinematics and contact mechanics, this restoration did not occur when the TT was lateralized more than 10 mm relative to its normal position.
Realigning the extensor mechanism by moving the TT medially decreases the lateralizing forces on the patella and the stress on the soft-tissue restraints. This raises the issues of when to correct a lateralized TT and how to identify and measure malalignment.
Radiographic assessment of TT position is most commonly performed by measuring TT-TG distance, which is the distance between the extensor mechanism attachment at the TT and the center of the TG. Originally described on radiographs and subsequently on computed tomography (CT) and magnetic resonance imaging (MRI) scans, distances of more than 15 mm or 20 mm have been reported as indications for TT osteotomy.5,6However, there has been significant variability in reported TT-TG measurements. Studies have found that TT-TG distance is 3.8 mm larger on CT scans than on MRI scans.7 Furthermore, factors such as knee flexion angle at time of imaging have been found to reduce TT-TG distance.1 More recently, patient size and TT-TG ratios relative to patellar and trochlear width were identified as important factors in assessing TT-TG distance.8 Therefore, TT-TG distance measurements should serve as a guide rather than a rigid threshold in the context of imaging and patient factors when deciding whether to perform TT osteotomy for patellar instability.
What You Need to Know About Measuring Patellofemoral Malalignment
TT-TG distance can guide decisions about performing a medializing TT osteotomy for patellar instability because the measurement can aid in assessing bony malalignment caused by an anatomically lateralized tubercle. TT-TG distance can be used to determine when and how far to move the tubercle in TT osteotomy.
Background
A normal TT-TG value is approximately 10 mm. The measurement originally used bony landmarks, including the deepest part of the bony TG and the anterior-most part of the TT, as described by Goutallier and colleagues.9 In their original study, Dejour and colleagues5 found that patients with recurrent symptoms of patellar instability had TT-TG distances >20 mm.
Increased TT-TG distance has been shown to correlate with patellar position, including increased lateral shift and lateral tilt of the patella. In a study using dynamic CT scans of patients with recurrent patellar instability, we found that TT-TG distance increased with knee extension, and that this increase correlated with the lateral shift and lateral tilt of the patella.10An excessively lateralized TT can be corrected with a medializing osteotomy that reduces TT-TG distance to within the normal range. TT surgery can be performed with flat osteotomy, as described by Elmslie and Trillat,11 or with oblique osteotomy, as described by Fulkerson,6 to obtain concomitant anteriorization. In a computational study, Elias and colleagues12 found that medializing TT osteotomy not only reduced TT-TG distance but led to correction of lateral patellar tilt and displacement. Patellofemoral contact forces have also shown to be reduced with anteromedialization.6Although reported outcomes of TT osteotomy have been excellent for patients with patellar instability, the procedure has higher risks and longer rehabilitation relative to a soft-tissue procedure alone. Reported risks associated with TT osteotomy include fracture, nonunion, delayed union, painful screws, and deep vein thrombosis.6,10,13,14Understanding the limitations of and variability in radiographic assessments of TT and TG positions can help when deciding whether to perform TT osteotomy for patellar instability.
Discussion
When considering TT osteotomy for patellar instability, some surgeons use a TT-TG distance of more than 15 mm or 20 mm as a threshold for performing medialization. The variability is based on the multiple patient and imaging factors that can influence TT-TG distance measurement.
Several TG and TT landmarks have been used to measure TT-TG distance. The deepest part of the TG, based on bony anatomy, was used originally, but the cartilaginous landmark at the deepest part of the cartilaginous TG has also been described.15 Similarly, on the TT, the original description of TT-TG distance, by Goutallier and colleagues,9 involved the anterior-most part of the TT on CT scan, though the central part of the TT has also been described.15 We found a 4.2-mm difference in TT-TG distance with use of different landmarks (central tubercle, anterior tubercle) within the same study population.16 Therefore, within a practice, the distance used as an indication for TT osteotomy should be measured consistently.
Knee flexion angle at the time of imaging can also affect measurement of TT-TG distance. Several authors have reported smaller TT-TG distance with increased knee flexion angle.10,16,17 In a study of patients with symptomatic patellar instability, we found that TT-TG distance decreases by an estimated 1 mm for every 4.4° of knee flexion >0°.10 In measurements of TT-TG distance, the sagittal view can be used to assess knee flexion angle because positioning protocols and patient comfort at the time of imaging may produce variable knee flexion angles.
Given the variability that occurs in TT-TG distance with knee flexion angles, some surgeons use TT–posterior cruciate ligament (PCL) distance as another measurement of TT lateralization.18 This measurement is made with both tibial landmarks, from the TT to the medial border of the PCL insertion on the tibia, and theoretically eliminates knee flexion angle as a measurement factor. Seitlinger and colleagues18 found that values >24 mm were associated with symptoms of patellar instability. More study is needed to determine the precise indications for TT osteotomy with use of this measurement.
In addition to patient positioning during knee imaging, patient size should be considered when TT-TG distance is used for malalignment measurement. Camp and colleagues8 discussed the importance of “individualizing” TT-TG distance on the basis of patient size and bony structure. They reported that the ratio of TT-TG distance to trochlear width or patellar width more effectively predicted recurrent patellar instability than TT-TG distance alone.
Measurement of TT-TG distance is valuable in planning surgical treatment for patellar instability because it quantifies a component of malalignment and aids in deciding whether to perform TT osteotomy. However, this distance should be understood in the context of many measurement factors to allow for an individualized procedure that addresses the specific contributors to patellar instability in each patient.
Am J Orthop. 2017;46(3):148-151. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
Take-Home Points
- Radiographic assessment of TT position is most commonly performed by measuring TT-TG distance, which is the distance between the extensor mechanism attachment at the TT and the center of the TG.
- TT-TG distances of more than 15 mm or 20 mm have been reported as indications for TT osteotomy.
- TT-TG distance criteria should serve as a guide, rather than a rigid threshold, in the context of imaging and patient factors when deciding whether to perform TT osteotomy for patellar instability.
- Factors such as knee flexion angle, imaging modality, and landmarks used for the measurements should be considered when using TT-TG distance as an indication for surgery.
- There has been significant variability in reported TT-TG measurements. A surgeon using this measurement should understand how it is obtained because many technical factors are involved.
Assessment of malalignment is an important factor in determining surgical treatment options for patellar instability. Although soft-tissue reconstruction of the medial soft-tissue stabilizers is often performed to address patellar instability, bony malalignment may increase stress on the medial soft tissues; therefore, it must be adequately identified and addressed.
Bony malalignment, which is often thought of as lateralization of the tibial tubercle (TT), can be influenced by tibiofemoral alignment, external tibial torsion, and femoral anteversion.
Clinically, coronal alignment can be assessed with a measurement such as quadriceps (Q) angle, but this has been reported to have low interrater reliability and high variability in the reported optimal conditions and positions in which the measurement should be made.1-3An anatomically lateralized TT pulls the extensor mechanism laterally with respect to the trochlear groove (TG), and this can accentuate problems related to patellofemoral instability. A recent biomechanical study found that increased TT lateralization significantly increased lateral patellar translation and tilt in the setting of medial patellofemoral ligament (MPFL) deficiency.4 Although MPFL reconstruction restored patellar kinematics and contact mechanics, this restoration did not occur when the TT was lateralized more than 10 mm relative to its normal position.
Realigning the extensor mechanism by moving the TT medially decreases the lateralizing forces on the patella and the stress on the soft-tissue restraints. This raises the issues of when to correct a lateralized TT and how to identify and measure malalignment.
Radiographic assessment of TT position is most commonly performed by measuring TT-TG distance, which is the distance between the extensor mechanism attachment at the TT and the center of the TG. Originally described on radiographs and subsequently on computed tomography (CT) and magnetic resonance imaging (MRI) scans, distances of more than 15 mm or 20 mm have been reported as indications for TT osteotomy.5,6However, there has been significant variability in reported TT-TG measurements. Studies have found that TT-TG distance is 3.8 mm larger on CT scans than on MRI scans.7 Furthermore, factors such as knee flexion angle at time of imaging have been found to reduce TT-TG distance.1 More recently, patient size and TT-TG ratios relative to patellar and trochlear width were identified as important factors in assessing TT-TG distance.8 Therefore, TT-TG distance measurements should serve as a guide rather than a rigid threshold in the context of imaging and patient factors when deciding whether to perform TT osteotomy for patellar instability.
What You Need to Know About Measuring Patellofemoral Malalignment
TT-TG distance can guide decisions about performing a medializing TT osteotomy for patellar instability because the measurement can aid in assessing bony malalignment caused by an anatomically lateralized tubercle. TT-TG distance can be used to determine when and how far to move the tubercle in TT osteotomy.
Background
A normal TT-TG value is approximately 10 mm. The measurement originally used bony landmarks, including the deepest part of the bony TG and the anterior-most part of the TT, as described by Goutallier and colleagues.9 In their original study, Dejour and colleagues5 found that patients with recurrent symptoms of patellar instability had TT-TG distances >20 mm.
Increased TT-TG distance has been shown to correlate with patellar position, including increased lateral shift and lateral tilt of the patella. In a study using dynamic CT scans of patients with recurrent patellar instability, we found that TT-TG distance increased with knee extension, and that this increase correlated with the lateral shift and lateral tilt of the patella.10An excessively lateralized TT can be corrected with a medializing osteotomy that reduces TT-TG distance to within the normal range. TT surgery can be performed with flat osteotomy, as described by Elmslie and Trillat,11 or with oblique osteotomy, as described by Fulkerson,6 to obtain concomitant anteriorization. In a computational study, Elias and colleagues12 found that medializing TT osteotomy not only reduced TT-TG distance but led to correction of lateral patellar tilt and displacement. Patellofemoral contact forces have also shown to be reduced with anteromedialization.6Although reported outcomes of TT osteotomy have been excellent for patients with patellar instability, the procedure has higher risks and longer rehabilitation relative to a soft-tissue procedure alone. Reported risks associated with TT osteotomy include fracture, nonunion, delayed union, painful screws, and deep vein thrombosis.6,10,13,14Understanding the limitations of and variability in radiographic assessments of TT and TG positions can help when deciding whether to perform TT osteotomy for patellar instability.
Discussion
When considering TT osteotomy for patellar instability, some surgeons use a TT-TG distance of more than 15 mm or 20 mm as a threshold for performing medialization. The variability is based on the multiple patient and imaging factors that can influence TT-TG distance measurement.
Several TG and TT landmarks have been used to measure TT-TG distance. The deepest part of the TG, based on bony anatomy, was used originally, but the cartilaginous landmark at the deepest part of the cartilaginous TG has also been described.15 Similarly, on the TT, the original description of TT-TG distance, by Goutallier and colleagues,9 involved the anterior-most part of the TT on CT scan, though the central part of the TT has also been described.15 We found a 4.2-mm difference in TT-TG distance with use of different landmarks (central tubercle, anterior tubercle) within the same study population.16 Therefore, within a practice, the distance used as an indication for TT osteotomy should be measured consistently.
Knee flexion angle at the time of imaging can also affect measurement of TT-TG distance. Several authors have reported smaller TT-TG distance with increased knee flexion angle.10,16,17 In a study of patients with symptomatic patellar instability, we found that TT-TG distance decreases by an estimated 1 mm for every 4.4° of knee flexion >0°.10 In measurements of TT-TG distance, the sagittal view can be used to assess knee flexion angle because positioning protocols and patient comfort at the time of imaging may produce variable knee flexion angles.
Given the variability that occurs in TT-TG distance with knee flexion angles, some surgeons use TT–posterior cruciate ligament (PCL) distance as another measurement of TT lateralization.18 This measurement is made with both tibial landmarks, from the TT to the medial border of the PCL insertion on the tibia, and theoretically eliminates knee flexion angle as a measurement factor. Seitlinger and colleagues18 found that values >24 mm were associated with symptoms of patellar instability. More study is needed to determine the precise indications for TT osteotomy with use of this measurement.
In addition to patient positioning during knee imaging, patient size should be considered when TT-TG distance is used for malalignment measurement. Camp and colleagues8 discussed the importance of “individualizing” TT-TG distance on the basis of patient size and bony structure. They reported that the ratio of TT-TG distance to trochlear width or patellar width more effectively predicted recurrent patellar instability than TT-TG distance alone.
Measurement of TT-TG distance is valuable in planning surgical treatment for patellar instability because it quantifies a component of malalignment and aids in deciding whether to perform TT osteotomy. However, this distance should be understood in the context of many measurement factors to allow for an individualized procedure that addresses the specific contributors to patellar instability in each patient.
Am J Orthop. 2017;46(3):148-151. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. France L, Nester C. Effect of errors in the identification of anatomical landmarks on the accuracy of Q angle values. Clin Biomech (Bristol, Avon). 2001;16(8):710-713.
2. Greene CC, Edwards TB, Wade MR, Carson EW. Reliability of the quadriceps angle measurement. Am J Knee Surg. 2001;14(2):97-103.
3. Smith TO, Hunt NJ, Donell ST. The reliability and validity of the Q-angle: a systematic review. Knee Surg Sports Traumatol Arthrosc. 2008;16(12):1068-1079.
4. Stephen JM, Dodds AL, Lumpaopong P, Kader D, Williams A, Amis AA. The ability of medial patellofemoral ligament reconstruction to correct patellar kinematics and contact mechanics in the presence of a lateralized tibial tubercle. Am J Sports Med. 2015;43(9):2198-2207.
5. Dejour H, Walch G, Nove-Josserand L, Guier C. Factors of patellar instability: an anatomic radiographic study. Knee Surg Sports Traumatol Arthrosc. 1994;2(1):19-26.
6. Fulkerson JP. Anteromedialization of the tibial tuberosity for patellofemoral malalignment. Clin Orthop Relat Res. 1983;177:176-181.
7. Camp CL, Stuart MJ, Krych AJ, et al. CT and MRI measurements of tibial tubercle-trochlear groove distances are not equivalent in patients with patellar instability. Am J Sports Med. 2013;41(8):1835-1840.
8. Camp CL, Heidenreich MJ, Dahm DL, Stuart MJ, Levy BA, Krych AJ. Individualizing the tibial tubercle-trochlear groove distance: patellar instability ratios that predict recurrent instability. Am J Sports Med. 2016;44(2):393-399.
9. Goutallier D, Bernageau J, Lecudonnec B. [The measurement of the tibial tuberosity. Patella groove distanced technique and results (author’s transl)]. Rev Chir Orthop Reparatrice Appar Mot. 1978;64(5):423-428.
10. Tanaka MJ, Elias JJ, Williams AA, Carrino JA, Cosgarea AJ. Correlation between changes in tibial tuberosity-trochlear groove distance and patellar position during active knee extension on dynamic kinematic computed tomography imaging. Arthroscopy. 2015;31(9):1748-1755.
11. Trillat A, Dejour H, Couette A. [Diagnosis and treatment of recurrent dislocations of the patella]. Rev Chir Orthop Reparatrice Appar Motur. 1964;50(6):813-824.
12. Elias JJ, Carrino JA, Saranathan A, Guseila LM, Tanaka MJ, Cosgarea AJ. Variations in kinematics and function following patellar stabilization including tibial tuberosity realignment. Knee Surg Sports Traumatol Arthrosc. 2014;22(10):2350-2356.
13. Sherman SL, Erickson BJ, Cvetanovich GL, et al. Tibial tuberosity osteotomy: indications, techniques, and outcomes. Am J Sports Med. 2014;42(8):2006-2017.
14. Wilcox JJ, Snow BJ, Aoki SK, Hung M, Burks RT. Does landmark selection affect the reliability of tibial tubercle-trochlear groove measurements using MRI? Clin Orthop Relat Res. 2012;470(8):2253-2260.
15. Schoettle PB, Zanetti M, Seifert B, Pfirrmann CWA, Fucentese SF, Romero J. The tibial tuberosity-trochlear groove distance; a comparative study between CT and MRI scanning. Knee. 2006;13(1):26-31.
16. Williams AA, Tanaka MJ, Elias JJ, et al. Measuring tibial tuberosity-trochlear groove distance on CT: Where to begin? Presented at the American Academy of Orthopaedic Surgeons Annual Meeting, New Orleans, LA, March 11-15, 2014.
17. Dietrich TJ, Betz M, Pfirrmann CWA, Koch PP, Fucentese SF. End-stage extension of the knee and its influence on tibial tuberosity-trochlear groove distance (TTTG) in asymptomatic volunteers. Knee Surg Sports Traumatol Arthrosc. 2014;22(1):214-218.
18. Seitlinger G, Scheurecker G, Hogler R, Labey L, Innocenti B, Hofmann S. Tibial tubercle-posterior cruciate ligament distance: a new measurement to define the position of the tibial tubercle in patients with patellar dislocation. Am J Sports Med. 2012;40(5):1119-1125.
1. France L, Nester C. Effect of errors in the identification of anatomical landmarks on the accuracy of Q angle values. Clin Biomech (Bristol, Avon). 2001;16(8):710-713.
2. Greene CC, Edwards TB, Wade MR, Carson EW. Reliability of the quadriceps angle measurement. Am J Knee Surg. 2001;14(2):97-103.
3. Smith TO, Hunt NJ, Donell ST. The reliability and validity of the Q-angle: a systematic review. Knee Surg Sports Traumatol Arthrosc. 2008;16(12):1068-1079.
4. Stephen JM, Dodds AL, Lumpaopong P, Kader D, Williams A, Amis AA. The ability of medial patellofemoral ligament reconstruction to correct patellar kinematics and contact mechanics in the presence of a lateralized tibial tubercle. Am J Sports Med. 2015;43(9):2198-2207.
5. Dejour H, Walch G, Nove-Josserand L, Guier C. Factors of patellar instability: an anatomic radiographic study. Knee Surg Sports Traumatol Arthrosc. 1994;2(1):19-26.
6. Fulkerson JP. Anteromedialization of the tibial tuberosity for patellofemoral malalignment. Clin Orthop Relat Res. 1983;177:176-181.
7. Camp CL, Stuart MJ, Krych AJ, et al. CT and MRI measurements of tibial tubercle-trochlear groove distances are not equivalent in patients with patellar instability. Am J Sports Med. 2013;41(8):1835-1840.
8. Camp CL, Heidenreich MJ, Dahm DL, Stuart MJ, Levy BA, Krych AJ. Individualizing the tibial tubercle-trochlear groove distance: patellar instability ratios that predict recurrent instability. Am J Sports Med. 2016;44(2):393-399.
9. Goutallier D, Bernageau J, Lecudonnec B. [The measurement of the tibial tuberosity. Patella groove distanced technique and results (author’s transl)]. Rev Chir Orthop Reparatrice Appar Mot. 1978;64(5):423-428.
10. Tanaka MJ, Elias JJ, Williams AA, Carrino JA, Cosgarea AJ. Correlation between changes in tibial tuberosity-trochlear groove distance and patellar position during active knee extension on dynamic kinematic computed tomography imaging. Arthroscopy. 2015;31(9):1748-1755.
11. Trillat A, Dejour H, Couette A. [Diagnosis and treatment of recurrent dislocations of the patella]. Rev Chir Orthop Reparatrice Appar Motur. 1964;50(6):813-824.
12. Elias JJ, Carrino JA, Saranathan A, Guseila LM, Tanaka MJ, Cosgarea AJ. Variations in kinematics and function following patellar stabilization including tibial tuberosity realignment. Knee Surg Sports Traumatol Arthrosc. 2014;22(10):2350-2356.
13. Sherman SL, Erickson BJ, Cvetanovich GL, et al. Tibial tuberosity osteotomy: indications, techniques, and outcomes. Am J Sports Med. 2014;42(8):2006-2017.
14. Wilcox JJ, Snow BJ, Aoki SK, Hung M, Burks RT. Does landmark selection affect the reliability of tibial tubercle-trochlear groove measurements using MRI? Clin Orthop Relat Res. 2012;470(8):2253-2260.
15. Schoettle PB, Zanetti M, Seifert B, Pfirrmann CWA, Fucentese SF, Romero J. The tibial tuberosity-trochlear groove distance; a comparative study between CT and MRI scanning. Knee. 2006;13(1):26-31.
16. Williams AA, Tanaka MJ, Elias JJ, et al. Measuring tibial tuberosity-trochlear groove distance on CT: Where to begin? Presented at the American Academy of Orthopaedic Surgeons Annual Meeting, New Orleans, LA, March 11-15, 2014.
17. Dietrich TJ, Betz M, Pfirrmann CWA, Koch PP, Fucentese SF. End-stage extension of the knee and its influence on tibial tuberosity-trochlear groove distance (TTTG) in asymptomatic volunteers. Knee Surg Sports Traumatol Arthrosc. 2014;22(1):214-218.
18. Seitlinger G, Scheurecker G, Hogler R, Labey L, Innocenti B, Hofmann S. Tibial tubercle-posterior cruciate ligament distance: a new measurement to define the position of the tibial tubercle in patients with patellar dislocation. Am J Sports Med. 2012;40(5):1119-1125.
Ultrasound-Guided Percutaneous Repair of Medial Patellofemoral Ligament: Surgical Technique and Outcomes
Take-Home Points
- Use ultrasound to identify integrity and location of MPFL tear.
- Anatomic repair allows native tissue to reintegrate into bone.
- Repairs done early can prevent complications of recurrent instability.
- Repair maintains biological and proprioceptive qualities of tissue.
- 10Ultrasound-guided percutaneous repair is quick and effective.
The medial patellofemoral ligament (MPFL) is the primary passive restraint to lateral patellar excursion1-5 and helps control patellar tilt and rotation.6,7 More than 90% of lateral patellar dislocations cause the MPFL to rupture, and roughly 90% of these detachments involve the femoral insertion.4 Ensuing patellar instability often results from MPFL insufficiency. It has been suggested that re-creating the anatomy and functionality of this ligament is of utmost importance in restoring normal patellar biomechanics.1-5,7,8
Anatomical risk factors for recurrent patellar instability include patella alta, increased tibial tuberosity-trochlear groove (TT-TG) distance, trochlear dysplasia, and torsional abnormalities.1-4,6 A medial reefing technique with a lateral tissue release traditionally was used to restore proper kinematics, but was shown to have associated postoperative issues.9
Methods
Patient Demographics
Dr. Hirahara developed this technique in 2013 and performed it 11 times between 2013 and 2016. Of the 11 patients, 1 was excluded from our retrospective analysis because of trochlear dysplasia, now considered a relative contraindication. Of the remaining 10 patients, 5 (50%) had the repair performed on the right knee. Eight patients (80%) were female. Mean (SD) age was 17.21 (3.53) years. One patient had concurrent femur- and patella-side detachments; otherwise, 6 (60%) of 10 repairs were performed exclusively at the patella. We grade patellar instability according to amount of glide based on patellar width and quadrants. Normal lateral displacement was usually 1 to 2 quadrants of lateral glide relative to the contralateral side. Before surgery, 6 (60%) of the 10 patients presented with lateral glide of 3 quadrants, and 3 (30%) presented with lateral glide of 4 quadrants. All had patellar instability apprehension on physical examination.
Surgical Indications
Before surgery, MPFL integrity is determined by ultrasound evaluation. Repair is considered if the MPFL has a femur- or patella-side tear and is of adequate quantity and quality, and if there are minimal or no arthritic changes (Table 2).
Surgical Technique
The patient is brought to the operating room and placed supine. Patellar stability of the affected knee is assessed and compared with that of the contralateral side with patellar glide. The knee is prepared and draped in usual sterile fashion. With the knee flexed at 90º, a tourniquet is inflated. Diagnostic arthroscopy is performed with standard anteromedial and anterolateral portals, and, if necessary, arthroscopic procedures are performed.
Femoral Attachment Repair
With the leg in extension, ultrasound is used to identify the tear at the femoral attachment (watch part 1 of the video). A spinal needle is placed at the femoral insertion, typically just anterior and distal to the adductor tubercle (Figure 4).10
Patellar Attachment Repair
With the leg in extension, ultrasound is used to identify where the MPFL is detached from the patella (watch part 2 of the video). A spinal needle is placed at the detachment site (Figure 5). A scalpel is used to make a 1-cm incision down to the patella.
In this description, we showcase knotless and knotted techniques for each repair site. Either method is appropriate for the 2 repair sites. Owing to the superficial nature of the attachment sites—they may have very little fat, particularly at the patella—knot stacks are more prominent, can be felt after surgery, and have the potential to irritate surrounding tissues. Therefore, we prefer knotless fixation for both sites.
Rehabilitation
Rehabilitation after MPFL repair is much like rehabilitation after quadriceps tendon repair. The patient is locked in a brace in full extension when up and moving. Early weight-bearing and minimal use of assistive devices (crutches) are allowed because, when the leg is in full extension, there is no tension at the repair sites. Rehabilitation begins within 1 week, and normal daily function is quickly attained. The protocol emphasizes pain-free motion and suitable patellar mobility, and allows the immobilizing brace to be unlocked for exercise and sitting. During the first 4 weeks, quadriceps activation is limited; progression to full ROM occurs by 4 to 6 weeks. During the strengthening phase, loading the knee in early flexion should be avoided. Return to heavy lifting, physical activity, and sports is delayed until after 6 months in order to allow the construct to mature and integrate. Once the patient has satisfied all the strength, ROM, and functional outcome measurements, a brace is no longer required during sports and normal activity.
Results
Mean tourniquet time for each procedure, which includes diagnostic arthroscopy and ultrasound-guided percutaneous repair, was 26.9 minutes.
Discussion
Conservative management typically is recommended for acute patellar dislocations. In the event of failed conservative management or chronic patellar instability, surgical intervention is indicated. Studies have found that conservative management has recurrent-dislocation rates of 35% at 3-year follow-up and 73% at 6-year follow-up, and recurrent dislocations significantly increase patients’ risk of developing chondral and bony damage.13 MPFL repair is designed to restore proper patellar tracking and kinematics while maintaining the anatomical tissue. Lateral patellar dislocations often cause the MPFL to rupture; tears are reported in more than 90% of incidents.4 The significant rate indicates that, even after a single patellar dislocation, the MPFL should be evaluated. The MPFL contributes 50% to 60% of the medial stabilizing force during patellar tracking1,7,14 and is the primary restraint to lateral patellar excursion and excessive patellar tilt and rotation.1-5 Its absence plays a key role in recurrent lateral patellar instability. With this structure being so important, proper identification and intervention are vital. Studies have established that redislocation rates are significantly higher for nonoperatively (vs operatively) treated primary patellar dislocations.13 Simple and accurate percutaneous repair of the MPFL should be performed early to avoid the long-term complications of recurrent instability that could damage the cartilage and bone of the patella and trochlea.
The primary advantage of this technique is its novel use of musculoskeletal ultrasound to accurately identify anatomy and pathology and the placement of anatomical repairs. Accurate preoperative and intraoperative assessment of MPFL anatomy is vital to the success of a procedure. Descriptions of MPFL anatomy suggest discrepancies in the exact locations of the femoral and patellar attachments.2,5,7,10,12,15,16 Tanaka5 noted that, even within paired knees, there was “marked variability” in the MPFL insertions. McCarthy and colleagues10 contended the femoral attachment of the MPFL is just anterior and distal to the adductor tubercle, the landmark addressed in this technique. Steensen and colleagues16 described this attachment site as being statistically the “single most important point affecting isometry” of the MPFL. Sallay and colleagues4 asserted that an overwhelming majority of MPFL tears (87%) occur at the adductor tubercle. The variable distribution of tear locations and the importance of re-creating patient anatomy further highlight the need for individualized treatment, which is afforded by ultrasound. Fluoroscopy has been inadequate in identifying MPFL anatomy; this modality is difficult, cumbersome, inaccurate, and inconsistent.11,12 Conversely, ultrasound provides real-time visualization of anatomy and allows for precise identification of MPFL attachments and accurate placement of suture anchors for repair during surgery (Figures 3, 4).
For femur-side and patella-side tears, repairs can and should be performed. For midsubstance tears, however, repair is not feasible, and reconstruction is appropriate. MPFL repair is superior to reconstruction in several ways. Repair is a simple percutaneous procedure that had a mean tourniquet time of 26.9 minutes in this study. For tissue that is quantitatively and qualitatively adequate, repair allows the structure to reintegrate into bone without total reconstruction. In the event of multiple tears, the percutaneous procedure allows for repair of each attachment. As the MPFL sits between the second and third tissue layers of the medial knee, reconstruction can be difficult and invasive and require establishment of a between-layers plane, which can disrupt adjacent tissue.4,7,17 Repair also maintains native tissue and its neurovascular and proprioceptive properties.
Reconstruction of the MPFL has become the gold-standard treatment for recurrent lateral patellar instability but has limitations and complications.3,7,12,17 Reconstruction techniques use either surface anatomy palpation (requiring large incisions) or fluoroscopy to identify tunnel placement locations, and accurate placement has often been difficult and inconsistent. Our repair technique has several advantages over reconstruction. It does not burn any bridges; it allows for subsequent reconstruction. It does not require a graft and, using small suture anchors instead of large sockets and anchors, involves less bone loss. It also allows for early repair of tears—patients can return to activities, sports, and work quicker—and avoids the risk of chondral and bony damage with recurrent dislocations. According to our review of the MPFL repairs performed by Dr. Hirahara starting in 2013, the procedure is quick and successful and has outstanding outcomes.
Another treatment option for recurrent lateral patellar instability combines reefing of the medial patellofemoral tissues with a lateral release. This combination has had several postoperative complications and is no longer indicated.9 TT transfer and trochleoplasty procedures have been developed to address different aspects of patellar instability, increased TT-TG distance, and dysplastic trochlea (Table 2). Both types of procedures are highly invasive and difficult to perform, requiring technical expertise. They are best used when warranted by the anatomy, but this is uncommon. The technique we have presented allows for easy and reliable repair of dislocations in the absence of associated pathology that would require larger, more complex surgery. The ease of use and accuracy of musculoskeletal ultrasound make this technique superior to others.
Conclusion
The MPFL is a vital static stabilizer of the patella and as such should be evaluated in the setting of patellar injury. The novel preoperative and intraoperative use of musculoskeletal ultrasound described in this article allows for easy real-time identification of the MPFL and simple and accurate percutaneous repair of torn structures. Nonoperative treatments of acute patellar dislocations have higher rates of recurrent dislocations, which put patella and trochlea at risk for bony and chondral damage. Given appropriate tear location and tissue quality, repairs should be considered early and before reconstruction. To our knowledge, a reliable, easily reproducible MPFL repair was not described until now. We have reported on use of such a technique and on its promising patient outcomes, which should be considered when addressing MPFL injuries.
Am J Orthop. 2017;46(3):152-157. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Desio SM, Burks RT, Bachus KN. Soft tissue restraints to lateral patellar translation in the human knee. Am J Sports Med. 1998;26(1):59-65.
2. Nomura E, Inoue M, Osada N. Anatomical analysis of the medial patellofemoral ligament of the knee, especially the femoral attachment. Knee Surg Sports Traumatol Arthrosc. 2005;13(7):510-515.
3. Petri M, Ettinger M, Stuebig T, et al. Current concepts for patellar dislocation. Arch Trauma Res. 2015;4(3):e29301.
4. Sallay PI, Poggi J, Speer KP, Garrett WE. Acute dislocation of the patella. A correlative pathoanatomic study. Am J Sports Med. 1996;24(1):52-60.
5. Tanaka MJ. Variability in the patellar attachment of the medial patellofemoral ligament. Arthroscopy. 2016;32(8):1667-1670.
6. Philippot R, Boyer B, Testa R, Farizon F, Moyen B. The role of the medial ligamentous structures on patellar tracking during knee flexion. Knee Surg Sports Traumatol Arthrosc. 2012;20(2):331-336.
7. Philippot R, Chouteau J, Wegrzyn J, Testa R, Fessy MH, Moyen B. Medial patellofemoral ligament anatomy: implications for its surgical reconstruction. Knee Surg Sports Traumatol Arthrosc. 2009;17(5):475-479.
8. Ahmad CS, Stein BE, Matuz D, Henry JH. Immediate surgical repair of the medial patellar stabilizers for acute patellar dislocation. A review of eight cases. Am J Sports Med. 2000;28(6):804-810.
9. Song GY, Hong L, Zhang H, Zhang J, Li Y, Feng H. Iatrogenic medial patellar instability following lateral retinacular release of the knee joint. Knee Surg Sports Traumatol Arthrosc. 2016;24(9):2825-2830.
10. McCarthy M, Ridley TJ, Bollier M, Wolf B, Albright J, Amendola A. Femoral tunnel placement in medial patellofemoral ligament reconstruction. Iowa Orthop J. 2013;33:58-63.
11. Redfern J, Kamath G, Burks R. Anatomical confirmation of the use of radiographic landmarks in medial patellofemoral ligament reconstruction. Am J Sports Med. 2010;38(2):293-297.
12. Barnett AJ, Howells NR, Burston BJ, Ansari A, Clark D, Eldridge JD. Radiographic landmarks for tunnel placement in reconstruction of the medial patellofemoral ligament. Knee Surg Sports Traumatol Arthrosc. 2012;20(12):2380-2384.
13. Regalado G, Lintula H, Kokki H, Kröger H, Väätäinen U, Eskelinen M. Six-year outcome after non-surgical versus surgical treatment of acute primary patellar dislocation in adolescents: a prospective randomized trial. Knee Surg Sports Traumatol Arthrosc. 2016;24(1):6-11.
14. Sandmeier RH, Burks RT, Bachus KN, Billings A. The effect of reconstruction of the medial patellofemoral ligament on patellar tracking. Am J Sports Med. 2000;28(3):345-349.
15. Baldwin JL. The anatomy of the medial patellofemoral ligament. Am J Sports Med. 2009;37(12):2355-2361.
16. Steensen RN, Dopirak RM, McDonald WG 3rd. The anatomy and isometry of the medial patellofemoral ligament: implications for reconstruction. Am J Sports Med. 2004;32(6):1509-1513.
17. Godin JA, Karas V, Visgauss JD, Garrett WE. Medial patellofemoral ligament reconstruction using a femoral loop button fixation technique. Arthrosc Tech. 2015;4(5):e601-e607.
Take-Home Points
- Use ultrasound to identify integrity and location of MPFL tear.
- Anatomic repair allows native tissue to reintegrate into bone.
- Repairs done early can prevent complications of recurrent instability.
- Repair maintains biological and proprioceptive qualities of tissue.
- 10Ultrasound-guided percutaneous repair is quick and effective.
The medial patellofemoral ligament (MPFL) is the primary passive restraint to lateral patellar excursion1-5 and helps control patellar tilt and rotation.6,7 More than 90% of lateral patellar dislocations cause the MPFL to rupture, and roughly 90% of these detachments involve the femoral insertion.4 Ensuing patellar instability often results from MPFL insufficiency. It has been suggested that re-creating the anatomy and functionality of this ligament is of utmost importance in restoring normal patellar biomechanics.1-5,7,8
Anatomical risk factors for recurrent patellar instability include patella alta, increased tibial tuberosity-trochlear groove (TT-TG) distance, trochlear dysplasia, and torsional abnormalities.1-4,6 A medial reefing technique with a lateral tissue release traditionally was used to restore proper kinematics, but was shown to have associated postoperative issues.9
Methods
Patient Demographics
Dr. Hirahara developed this technique in 2013 and performed it 11 times between 2013 and 2016. Of the 11 patients, 1 was excluded from our retrospective analysis because of trochlear dysplasia, now considered a relative contraindication. Of the remaining 10 patients, 5 (50%) had the repair performed on the right knee. Eight patients (80%) were female. Mean (SD) age was 17.21 (3.53) years. One patient had concurrent femur- and patella-side detachments; otherwise, 6 (60%) of 10 repairs were performed exclusively at the patella. We grade patellar instability according to amount of glide based on patellar width and quadrants. Normal lateral displacement was usually 1 to 2 quadrants of lateral glide relative to the contralateral side. Before surgery, 6 (60%) of the 10 patients presented with lateral glide of 3 quadrants, and 3 (30%) presented with lateral glide of 4 quadrants. All had patellar instability apprehension on physical examination.
Surgical Indications
Before surgery, MPFL integrity is determined by ultrasound evaluation. Repair is considered if the MPFL has a femur- or patella-side tear and is of adequate quantity and quality, and if there are minimal or no arthritic changes (Table 2).
Surgical Technique
The patient is brought to the operating room and placed supine. Patellar stability of the affected knee is assessed and compared with that of the contralateral side with patellar glide. The knee is prepared and draped in usual sterile fashion. With the knee flexed at 90º, a tourniquet is inflated. Diagnostic arthroscopy is performed with standard anteromedial and anterolateral portals, and, if necessary, arthroscopic procedures are performed.
Femoral Attachment Repair
With the leg in extension, ultrasound is used to identify the tear at the femoral attachment (watch part 1 of the video). A spinal needle is placed at the femoral insertion, typically just anterior and distal to the adductor tubercle (Figure 4).10
Patellar Attachment Repair
With the leg in extension, ultrasound is used to identify where the MPFL is detached from the patella (watch part 2 of the video). A spinal needle is placed at the detachment site (Figure 5). A scalpel is used to make a 1-cm incision down to the patella.
In this description, we showcase knotless and knotted techniques for each repair site. Either method is appropriate for the 2 repair sites. Owing to the superficial nature of the attachment sites—they may have very little fat, particularly at the patella—knot stacks are more prominent, can be felt after surgery, and have the potential to irritate surrounding tissues. Therefore, we prefer knotless fixation for both sites.
Rehabilitation
Rehabilitation after MPFL repair is much like rehabilitation after quadriceps tendon repair. The patient is locked in a brace in full extension when up and moving. Early weight-bearing and minimal use of assistive devices (crutches) are allowed because, when the leg is in full extension, there is no tension at the repair sites. Rehabilitation begins within 1 week, and normal daily function is quickly attained. The protocol emphasizes pain-free motion and suitable patellar mobility, and allows the immobilizing brace to be unlocked for exercise and sitting. During the first 4 weeks, quadriceps activation is limited; progression to full ROM occurs by 4 to 6 weeks. During the strengthening phase, loading the knee in early flexion should be avoided. Return to heavy lifting, physical activity, and sports is delayed until after 6 months in order to allow the construct to mature and integrate. Once the patient has satisfied all the strength, ROM, and functional outcome measurements, a brace is no longer required during sports and normal activity.
Results
Mean tourniquet time for each procedure, which includes diagnostic arthroscopy and ultrasound-guided percutaneous repair, was 26.9 minutes.
Discussion
Conservative management typically is recommended for acute patellar dislocations. In the event of failed conservative management or chronic patellar instability, surgical intervention is indicated. Studies have found that conservative management has recurrent-dislocation rates of 35% at 3-year follow-up and 73% at 6-year follow-up, and recurrent dislocations significantly increase patients’ risk of developing chondral and bony damage.13 MPFL repair is designed to restore proper patellar tracking and kinematics while maintaining the anatomical tissue. Lateral patellar dislocations often cause the MPFL to rupture; tears are reported in more than 90% of incidents.4 The significant rate indicates that, even after a single patellar dislocation, the MPFL should be evaluated. The MPFL contributes 50% to 60% of the medial stabilizing force during patellar tracking1,7,14 and is the primary restraint to lateral patellar excursion and excessive patellar tilt and rotation.1-5 Its absence plays a key role in recurrent lateral patellar instability. With this structure being so important, proper identification and intervention are vital. Studies have established that redislocation rates are significantly higher for nonoperatively (vs operatively) treated primary patellar dislocations.13 Simple and accurate percutaneous repair of the MPFL should be performed early to avoid the long-term complications of recurrent instability that could damage the cartilage and bone of the patella and trochlea.
The primary advantage of this technique is its novel use of musculoskeletal ultrasound to accurately identify anatomy and pathology and the placement of anatomical repairs. Accurate preoperative and intraoperative assessment of MPFL anatomy is vital to the success of a procedure. Descriptions of MPFL anatomy suggest discrepancies in the exact locations of the femoral and patellar attachments.2,5,7,10,12,15,16 Tanaka5 noted that, even within paired knees, there was “marked variability” in the MPFL insertions. McCarthy and colleagues10 contended the femoral attachment of the MPFL is just anterior and distal to the adductor tubercle, the landmark addressed in this technique. Steensen and colleagues16 described this attachment site as being statistically the “single most important point affecting isometry” of the MPFL. Sallay and colleagues4 asserted that an overwhelming majority of MPFL tears (87%) occur at the adductor tubercle. The variable distribution of tear locations and the importance of re-creating patient anatomy further highlight the need for individualized treatment, which is afforded by ultrasound. Fluoroscopy has been inadequate in identifying MPFL anatomy; this modality is difficult, cumbersome, inaccurate, and inconsistent.11,12 Conversely, ultrasound provides real-time visualization of anatomy and allows for precise identification of MPFL attachments and accurate placement of suture anchors for repair during surgery (Figures 3, 4).
For femur-side and patella-side tears, repairs can and should be performed. For midsubstance tears, however, repair is not feasible, and reconstruction is appropriate. MPFL repair is superior to reconstruction in several ways. Repair is a simple percutaneous procedure that had a mean tourniquet time of 26.9 minutes in this study. For tissue that is quantitatively and qualitatively adequate, repair allows the structure to reintegrate into bone without total reconstruction. In the event of multiple tears, the percutaneous procedure allows for repair of each attachment. As the MPFL sits between the second and third tissue layers of the medial knee, reconstruction can be difficult and invasive and require establishment of a between-layers plane, which can disrupt adjacent tissue.4,7,17 Repair also maintains native tissue and its neurovascular and proprioceptive properties.
Reconstruction of the MPFL has become the gold-standard treatment for recurrent lateral patellar instability but has limitations and complications.3,7,12,17 Reconstruction techniques use either surface anatomy palpation (requiring large incisions) or fluoroscopy to identify tunnel placement locations, and accurate placement has often been difficult and inconsistent. Our repair technique has several advantages over reconstruction. It does not burn any bridges; it allows for subsequent reconstruction. It does not require a graft and, using small suture anchors instead of large sockets and anchors, involves less bone loss. It also allows for early repair of tears—patients can return to activities, sports, and work quicker—and avoids the risk of chondral and bony damage with recurrent dislocations. According to our review of the MPFL repairs performed by Dr. Hirahara starting in 2013, the procedure is quick and successful and has outstanding outcomes.
Another treatment option for recurrent lateral patellar instability combines reefing of the medial patellofemoral tissues with a lateral release. This combination has had several postoperative complications and is no longer indicated.9 TT transfer and trochleoplasty procedures have been developed to address different aspects of patellar instability, increased TT-TG distance, and dysplastic trochlea (Table 2). Both types of procedures are highly invasive and difficult to perform, requiring technical expertise. They are best used when warranted by the anatomy, but this is uncommon. The technique we have presented allows for easy and reliable repair of dislocations in the absence of associated pathology that would require larger, more complex surgery. The ease of use and accuracy of musculoskeletal ultrasound make this technique superior to others.
Conclusion
The MPFL is a vital static stabilizer of the patella and as such should be evaluated in the setting of patellar injury. The novel preoperative and intraoperative use of musculoskeletal ultrasound described in this article allows for easy real-time identification of the MPFL and simple and accurate percutaneous repair of torn structures. Nonoperative treatments of acute patellar dislocations have higher rates of recurrent dislocations, which put patella and trochlea at risk for bony and chondral damage. Given appropriate tear location and tissue quality, repairs should be considered early and before reconstruction. To our knowledge, a reliable, easily reproducible MPFL repair was not described until now. We have reported on use of such a technique and on its promising patient outcomes, which should be considered when addressing MPFL injuries.
Am J Orthop. 2017;46(3):152-157. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
Take-Home Points
- Use ultrasound to identify integrity and location of MPFL tear.
- Anatomic repair allows native tissue to reintegrate into bone.
- Repairs done early can prevent complications of recurrent instability.
- Repair maintains biological and proprioceptive qualities of tissue.
- 10Ultrasound-guided percutaneous repair is quick and effective.
The medial patellofemoral ligament (MPFL) is the primary passive restraint to lateral patellar excursion1-5 and helps control patellar tilt and rotation.6,7 More than 90% of lateral patellar dislocations cause the MPFL to rupture, and roughly 90% of these detachments involve the femoral insertion.4 Ensuing patellar instability often results from MPFL insufficiency. It has been suggested that re-creating the anatomy and functionality of this ligament is of utmost importance in restoring normal patellar biomechanics.1-5,7,8
Anatomical risk factors for recurrent patellar instability include patella alta, increased tibial tuberosity-trochlear groove (TT-TG) distance, trochlear dysplasia, and torsional abnormalities.1-4,6 A medial reefing technique with a lateral tissue release traditionally was used to restore proper kinematics, but was shown to have associated postoperative issues.9
Methods
Patient Demographics
Dr. Hirahara developed this technique in 2013 and performed it 11 times between 2013 and 2016. Of the 11 patients, 1 was excluded from our retrospective analysis because of trochlear dysplasia, now considered a relative contraindication. Of the remaining 10 patients, 5 (50%) had the repair performed on the right knee. Eight patients (80%) were female. Mean (SD) age was 17.21 (3.53) years. One patient had concurrent femur- and patella-side detachments; otherwise, 6 (60%) of 10 repairs were performed exclusively at the patella. We grade patellar instability according to amount of glide based on patellar width and quadrants. Normal lateral displacement was usually 1 to 2 quadrants of lateral glide relative to the contralateral side. Before surgery, 6 (60%) of the 10 patients presented with lateral glide of 3 quadrants, and 3 (30%) presented with lateral glide of 4 quadrants. All had patellar instability apprehension on physical examination.
Surgical Indications
Before surgery, MPFL integrity is determined by ultrasound evaluation. Repair is considered if the MPFL has a femur- or patella-side tear and is of adequate quantity and quality, and if there are minimal or no arthritic changes (Table 2).
Surgical Technique
The patient is brought to the operating room and placed supine. Patellar stability of the affected knee is assessed and compared with that of the contralateral side with patellar glide. The knee is prepared and draped in usual sterile fashion. With the knee flexed at 90º, a tourniquet is inflated. Diagnostic arthroscopy is performed with standard anteromedial and anterolateral portals, and, if necessary, arthroscopic procedures are performed.
Femoral Attachment Repair
With the leg in extension, ultrasound is used to identify the tear at the femoral attachment (watch part 1 of the video). A spinal needle is placed at the femoral insertion, typically just anterior and distal to the adductor tubercle (Figure 4).10
Patellar Attachment Repair
With the leg in extension, ultrasound is used to identify where the MPFL is detached from the patella (watch part 2 of the video). A spinal needle is placed at the detachment site (Figure 5). A scalpel is used to make a 1-cm incision down to the patella.
In this description, we showcase knotless and knotted techniques for each repair site. Either method is appropriate for the 2 repair sites. Owing to the superficial nature of the attachment sites—they may have very little fat, particularly at the patella—knot stacks are more prominent, can be felt after surgery, and have the potential to irritate surrounding tissues. Therefore, we prefer knotless fixation for both sites.
Rehabilitation
Rehabilitation after MPFL repair is much like rehabilitation after quadriceps tendon repair. The patient is locked in a brace in full extension when up and moving. Early weight-bearing and minimal use of assistive devices (crutches) are allowed because, when the leg is in full extension, there is no tension at the repair sites. Rehabilitation begins within 1 week, and normal daily function is quickly attained. The protocol emphasizes pain-free motion and suitable patellar mobility, and allows the immobilizing brace to be unlocked for exercise and sitting. During the first 4 weeks, quadriceps activation is limited; progression to full ROM occurs by 4 to 6 weeks. During the strengthening phase, loading the knee in early flexion should be avoided. Return to heavy lifting, physical activity, and sports is delayed until after 6 months in order to allow the construct to mature and integrate. Once the patient has satisfied all the strength, ROM, and functional outcome measurements, a brace is no longer required during sports and normal activity.
Results
Mean tourniquet time for each procedure, which includes diagnostic arthroscopy and ultrasound-guided percutaneous repair, was 26.9 minutes.
Discussion
Conservative management typically is recommended for acute patellar dislocations. In the event of failed conservative management or chronic patellar instability, surgical intervention is indicated. Studies have found that conservative management has recurrent-dislocation rates of 35% at 3-year follow-up and 73% at 6-year follow-up, and recurrent dislocations significantly increase patients’ risk of developing chondral and bony damage.13 MPFL repair is designed to restore proper patellar tracking and kinematics while maintaining the anatomical tissue. Lateral patellar dislocations often cause the MPFL to rupture; tears are reported in more than 90% of incidents.4 The significant rate indicates that, even after a single patellar dislocation, the MPFL should be evaluated. The MPFL contributes 50% to 60% of the medial stabilizing force during patellar tracking1,7,14 and is the primary restraint to lateral patellar excursion and excessive patellar tilt and rotation.1-5 Its absence plays a key role in recurrent lateral patellar instability. With this structure being so important, proper identification and intervention are vital. Studies have established that redislocation rates are significantly higher for nonoperatively (vs operatively) treated primary patellar dislocations.13 Simple and accurate percutaneous repair of the MPFL should be performed early to avoid the long-term complications of recurrent instability that could damage the cartilage and bone of the patella and trochlea.
The primary advantage of this technique is its novel use of musculoskeletal ultrasound to accurately identify anatomy and pathology and the placement of anatomical repairs. Accurate preoperative and intraoperative assessment of MPFL anatomy is vital to the success of a procedure. Descriptions of MPFL anatomy suggest discrepancies in the exact locations of the femoral and patellar attachments.2,5,7,10,12,15,16 Tanaka5 noted that, even within paired knees, there was “marked variability” in the MPFL insertions. McCarthy and colleagues10 contended the femoral attachment of the MPFL is just anterior and distal to the adductor tubercle, the landmark addressed in this technique. Steensen and colleagues16 described this attachment site as being statistically the “single most important point affecting isometry” of the MPFL. Sallay and colleagues4 asserted that an overwhelming majority of MPFL tears (87%) occur at the adductor tubercle. The variable distribution of tear locations and the importance of re-creating patient anatomy further highlight the need for individualized treatment, which is afforded by ultrasound. Fluoroscopy has been inadequate in identifying MPFL anatomy; this modality is difficult, cumbersome, inaccurate, and inconsistent.11,12 Conversely, ultrasound provides real-time visualization of anatomy and allows for precise identification of MPFL attachments and accurate placement of suture anchors for repair during surgery (Figures 3, 4).
For femur-side and patella-side tears, repairs can and should be performed. For midsubstance tears, however, repair is not feasible, and reconstruction is appropriate. MPFL repair is superior to reconstruction in several ways. Repair is a simple percutaneous procedure that had a mean tourniquet time of 26.9 minutes in this study. For tissue that is quantitatively and qualitatively adequate, repair allows the structure to reintegrate into bone without total reconstruction. In the event of multiple tears, the percutaneous procedure allows for repair of each attachment. As the MPFL sits between the second and third tissue layers of the medial knee, reconstruction can be difficult and invasive and require establishment of a between-layers plane, which can disrupt adjacent tissue.4,7,17 Repair also maintains native tissue and its neurovascular and proprioceptive properties.
Reconstruction of the MPFL has become the gold-standard treatment for recurrent lateral patellar instability but has limitations and complications.3,7,12,17 Reconstruction techniques use either surface anatomy palpation (requiring large incisions) or fluoroscopy to identify tunnel placement locations, and accurate placement has often been difficult and inconsistent. Our repair technique has several advantages over reconstruction. It does not burn any bridges; it allows for subsequent reconstruction. It does not require a graft and, using small suture anchors instead of large sockets and anchors, involves less bone loss. It also allows for early repair of tears—patients can return to activities, sports, and work quicker—and avoids the risk of chondral and bony damage with recurrent dislocations. According to our review of the MPFL repairs performed by Dr. Hirahara starting in 2013, the procedure is quick and successful and has outstanding outcomes.
Another treatment option for recurrent lateral patellar instability combines reefing of the medial patellofemoral tissues with a lateral release. This combination has had several postoperative complications and is no longer indicated.9 TT transfer and trochleoplasty procedures have been developed to address different aspects of patellar instability, increased TT-TG distance, and dysplastic trochlea (Table 2). Both types of procedures are highly invasive and difficult to perform, requiring technical expertise. They are best used when warranted by the anatomy, but this is uncommon. The technique we have presented allows for easy and reliable repair of dislocations in the absence of associated pathology that would require larger, more complex surgery. The ease of use and accuracy of musculoskeletal ultrasound make this technique superior to others.
Conclusion
The MPFL is a vital static stabilizer of the patella and as such should be evaluated in the setting of patellar injury. The novel preoperative and intraoperative use of musculoskeletal ultrasound described in this article allows for easy real-time identification of the MPFL and simple and accurate percutaneous repair of torn structures. Nonoperative treatments of acute patellar dislocations have higher rates of recurrent dislocations, which put patella and trochlea at risk for bony and chondral damage. Given appropriate tear location and tissue quality, repairs should be considered early and before reconstruction. To our knowledge, a reliable, easily reproducible MPFL repair was not described until now. We have reported on use of such a technique and on its promising patient outcomes, which should be considered when addressing MPFL injuries.
Am J Orthop. 2017;46(3):152-157. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Desio SM, Burks RT, Bachus KN. Soft tissue restraints to lateral patellar translation in the human knee. Am J Sports Med. 1998;26(1):59-65.
2. Nomura E, Inoue M, Osada N. Anatomical analysis of the medial patellofemoral ligament of the knee, especially the femoral attachment. Knee Surg Sports Traumatol Arthrosc. 2005;13(7):510-515.
3. Petri M, Ettinger M, Stuebig T, et al. Current concepts for patellar dislocation. Arch Trauma Res. 2015;4(3):e29301.
4. Sallay PI, Poggi J, Speer KP, Garrett WE. Acute dislocation of the patella. A correlative pathoanatomic study. Am J Sports Med. 1996;24(1):52-60.
5. Tanaka MJ. Variability in the patellar attachment of the medial patellofemoral ligament. Arthroscopy. 2016;32(8):1667-1670.
6. Philippot R, Boyer B, Testa R, Farizon F, Moyen B. The role of the medial ligamentous structures on patellar tracking during knee flexion. Knee Surg Sports Traumatol Arthrosc. 2012;20(2):331-336.
7. Philippot R, Chouteau J, Wegrzyn J, Testa R, Fessy MH, Moyen B. Medial patellofemoral ligament anatomy: implications for its surgical reconstruction. Knee Surg Sports Traumatol Arthrosc. 2009;17(5):475-479.
8. Ahmad CS, Stein BE, Matuz D, Henry JH. Immediate surgical repair of the medial patellar stabilizers for acute patellar dislocation. A review of eight cases. Am J Sports Med. 2000;28(6):804-810.
9. Song GY, Hong L, Zhang H, Zhang J, Li Y, Feng H. Iatrogenic medial patellar instability following lateral retinacular release of the knee joint. Knee Surg Sports Traumatol Arthrosc. 2016;24(9):2825-2830.
10. McCarthy M, Ridley TJ, Bollier M, Wolf B, Albright J, Amendola A. Femoral tunnel placement in medial patellofemoral ligament reconstruction. Iowa Orthop J. 2013;33:58-63.
11. Redfern J, Kamath G, Burks R. Anatomical confirmation of the use of radiographic landmarks in medial patellofemoral ligament reconstruction. Am J Sports Med. 2010;38(2):293-297.
12. Barnett AJ, Howells NR, Burston BJ, Ansari A, Clark D, Eldridge JD. Radiographic landmarks for tunnel placement in reconstruction of the medial patellofemoral ligament. Knee Surg Sports Traumatol Arthrosc. 2012;20(12):2380-2384.
13. Regalado G, Lintula H, Kokki H, Kröger H, Väätäinen U, Eskelinen M. Six-year outcome after non-surgical versus surgical treatment of acute primary patellar dislocation in adolescents: a prospective randomized trial. Knee Surg Sports Traumatol Arthrosc. 2016;24(1):6-11.
14. Sandmeier RH, Burks RT, Bachus KN, Billings A. The effect of reconstruction of the medial patellofemoral ligament on patellar tracking. Am J Sports Med. 2000;28(3):345-349.
15. Baldwin JL. The anatomy of the medial patellofemoral ligament. Am J Sports Med. 2009;37(12):2355-2361.
16. Steensen RN, Dopirak RM, McDonald WG 3rd. The anatomy and isometry of the medial patellofemoral ligament: implications for reconstruction. Am J Sports Med. 2004;32(6):1509-1513.
17. Godin JA, Karas V, Visgauss JD, Garrett WE. Medial patellofemoral ligament reconstruction using a femoral loop button fixation technique. Arthrosc Tech. 2015;4(5):e601-e607.
1. Desio SM, Burks RT, Bachus KN. Soft tissue restraints to lateral patellar translation in the human knee. Am J Sports Med. 1998;26(1):59-65.
2. Nomura E, Inoue M, Osada N. Anatomical analysis of the medial patellofemoral ligament of the knee, especially the femoral attachment. Knee Surg Sports Traumatol Arthrosc. 2005;13(7):510-515.
3. Petri M, Ettinger M, Stuebig T, et al. Current concepts for patellar dislocation. Arch Trauma Res. 2015;4(3):e29301.
4. Sallay PI, Poggi J, Speer KP, Garrett WE. Acute dislocation of the patella. A correlative pathoanatomic study. Am J Sports Med. 1996;24(1):52-60.
5. Tanaka MJ. Variability in the patellar attachment of the medial patellofemoral ligament. Arthroscopy. 2016;32(8):1667-1670.
6. Philippot R, Boyer B, Testa R, Farizon F, Moyen B. The role of the medial ligamentous structures on patellar tracking during knee flexion. Knee Surg Sports Traumatol Arthrosc. 2012;20(2):331-336.
7. Philippot R, Chouteau J, Wegrzyn J, Testa R, Fessy MH, Moyen B. Medial patellofemoral ligament anatomy: implications for its surgical reconstruction. Knee Surg Sports Traumatol Arthrosc. 2009;17(5):475-479.
8. Ahmad CS, Stein BE, Matuz D, Henry JH. Immediate surgical repair of the medial patellar stabilizers for acute patellar dislocation. A review of eight cases. Am J Sports Med. 2000;28(6):804-810.
9. Song GY, Hong L, Zhang H, Zhang J, Li Y, Feng H. Iatrogenic medial patellar instability following lateral retinacular release of the knee joint. Knee Surg Sports Traumatol Arthrosc. 2016;24(9):2825-2830.
10. McCarthy M, Ridley TJ, Bollier M, Wolf B, Albright J, Amendola A. Femoral tunnel placement in medial patellofemoral ligament reconstruction. Iowa Orthop J. 2013;33:58-63.
11. Redfern J, Kamath G, Burks R. Anatomical confirmation of the use of radiographic landmarks in medial patellofemoral ligament reconstruction. Am J Sports Med. 2010;38(2):293-297.
12. Barnett AJ, Howells NR, Burston BJ, Ansari A, Clark D, Eldridge JD. Radiographic landmarks for tunnel placement in reconstruction of the medial patellofemoral ligament. Knee Surg Sports Traumatol Arthrosc. 2012;20(12):2380-2384.
13. Regalado G, Lintula H, Kokki H, Kröger H, Väätäinen U, Eskelinen M. Six-year outcome after non-surgical versus surgical treatment of acute primary patellar dislocation in adolescents: a prospective randomized trial. Knee Surg Sports Traumatol Arthrosc. 2016;24(1):6-11.
14. Sandmeier RH, Burks RT, Bachus KN, Billings A. The effect of reconstruction of the medial patellofemoral ligament on patellar tracking. Am J Sports Med. 2000;28(3):345-349.
15. Baldwin JL. The anatomy of the medial patellofemoral ligament. Am J Sports Med. 2009;37(12):2355-2361.
16. Steensen RN, Dopirak RM, McDonald WG 3rd. The anatomy and isometry of the medial patellofemoral ligament: implications for reconstruction. Am J Sports Med. 2004;32(6):1509-1513.
17. Godin JA, Karas V, Visgauss JD, Garrett WE. Medial patellofemoral ligament reconstruction using a femoral loop button fixation technique. Arthrosc Tech. 2015;4(5):e601-e607.
A broken pacemaker lead in a 69-year-old woman
A 69-year-old woman presented with fatigue, cough, and lightheadedness. She had a history of atrial fibrillation and complete heart block, for which she had a pacemaker (dual-pacing, dual-sensing, dual-response, and rate-adaptive mode) inserted in 2005. Her heart rate was 30 beats per minute.
A chest radiograph showed a fractured right ventricular pacemaker lead (Figure 1). Electrocardiography showed sinus rhythm with a high-grade atrioventricular block (Figure 2). Pacemaker interrogation confirmed the diagnosis of lead fracture. A new lead was placed, and the old lead was abandoned.
HOW LEADS BREAK
The rate of lead fracture ranges from 0.1% to 4.2% per patient-year, and the annual failure rate increases progressively with time after implantation.1,2
Extrinsic pressure on the lead can eventually break it. This can happen between the first rib and clavicle, in “subclavian crush” injury, or with any anatomical abnormality that narrows the thoracic outlet. Typically, classic subclavian crush results from entrapment of the pacemaker leads by the subclavius muscle or the costoclavicular ligament as the lead follows the needle course of the antecedent access puncture of the subclavian vein. This results in intermittent flexing of the lead and potential lead fracture3 and was likely the cause of lead fracture in our patient.
The risk of fracture is higher in patients under the age of 50, those who perform intense physical activity, women, and patients with greater left ventricular ejection fraction.4,5 Certain leads are prone to fracture due to design flaws. One of these was the Medtronic Sprint Fidelis cardioverter defibrillator lead, which was recalled in 2007.5
DETECTING LEAD FRACTURE
Symptoms of lead fracture vary, depending on the patient’s pacemaker-dependency and on the degree of loss of capture (ie, the degree to which the heart fails to respond to the pacemaker’s signals), and may include lightheadedness, syncope, and extracardiac stimulation.
The electrical integrity of a lead can be tested by measuring the circuit impedance, which normally ranges from 300 to 1,000 ohms.6 An insulation failure results in very low impedance, while a disrupted circuit due to lead fracture commonly causes a sudden rather than gradual increase in impedance.6
Simple imaging studies such as chest radiography or fluoroscopy may establish the diagnosis of lead fracture. One should carefully trace every lead along its entire course and look for any conductor discontinuity, kinks, or sharp bends.6
REMOVE THE OLD LEAD, OR LEAVE IT IN PLACE?
The treatment for lead fracture is usually to put in a new lead, with or without extracting the old one.
In view of the potential complications of lead removal such as cardiac perforation or vascular tear, lead abandonment with placement of a new lead may be performed.7 There are no controlled clinical studies comparing lead abandonment vs lead extraction.8 However, extraction is currently recommended only in patients in whom the old lead causes life-threatening arrhythmias, interferes with the operation of implanted cardiac devices, interferes with radiation therapy or needed surgery, or, due to its design or failure, poses an immediate threat to the patient if left in place.7 Lead removal is reasonable in patients who require specific imaging studies such as magnetic resonance imaging with no available imaging alternative for the diagnosis.7
In our patient, a new lead was placed without removing the fractured lead, with no complications. Afterward, the patient’s heart rhythm was observed to be appropriately paced, and she was discharged home the following day.
- Alt E, Völker R, Blömer H. Lead fracture in pacemaker patients. Thorac Cardiovasc Surg 1987; 35:101–104.
- Kleemann T, Becker T, Doenges K, et al. Annual rate of transvenous defibrillation lead defects in implantable cardioverter-defibrillators over a period of > 10 years. Circulation 2007; 115:2474–2480.
- Magney JE, Flynn DM, Parsons JA, et al. Anatomical mechanisms explaining damage to pacemaker leads, defibrillator leads, and failure of central venous catheters adjacent to the sternoclavicular joint. Pacing Clin Electrophysiol 1993; 16:445–457.
- Farwell D, Green MS, Lemery R, Gollob MH, Birnie DH. Accelerating risk of Fidelis lead fracture. Heart Rhythm 2008; 5:1375–1379.
- Morrison TB, Rea RF, Hodge DO, et al. Risk factors for implantable defibrillator lead fracture in a recalled and a nonrecalled lead. J Cardiovasc Electrophysiol 2010; 21:671–677.
- Swerdlow CD, Ellenbogen KA. Implantable cardioverter-defibrillator leads: design, diagnostics, and management. Circulation 2013; 128:2062–2071.
- Wilkoff BL, Love CJ, Byrd CL, et al; Heart Rhythm Society; American Heart Association. Transvenous lead extraction: Heart Rhythm Society expert consensus on facilities, training, indications, and patient management: this document was endorsed by the American Heart Association (AHA). Heart Rhythm 2009; 6:1085–1104.
- Maytin M, Epstein LM, Henrikson CA. Lead extraction is preferred for lead revisions and system upgrades: when less is more. Circ Arrhythm Electrophysiol 2010; 3:413–424.
A 69-year-old woman presented with fatigue, cough, and lightheadedness. She had a history of atrial fibrillation and complete heart block, for which she had a pacemaker (dual-pacing, dual-sensing, dual-response, and rate-adaptive mode) inserted in 2005. Her heart rate was 30 beats per minute.
A chest radiograph showed a fractured right ventricular pacemaker lead (Figure 1). Electrocardiography showed sinus rhythm with a high-grade atrioventricular block (Figure 2). Pacemaker interrogation confirmed the diagnosis of lead fracture. A new lead was placed, and the old lead was abandoned.
HOW LEADS BREAK
The rate of lead fracture ranges from 0.1% to 4.2% per patient-year, and the annual failure rate increases progressively with time after implantation.1,2
Extrinsic pressure on the lead can eventually break it. This can happen between the first rib and clavicle, in “subclavian crush” injury, or with any anatomical abnormality that narrows the thoracic outlet. Typically, classic subclavian crush results from entrapment of the pacemaker leads by the subclavius muscle or the costoclavicular ligament as the lead follows the needle course of the antecedent access puncture of the subclavian vein. This results in intermittent flexing of the lead and potential lead fracture3 and was likely the cause of lead fracture in our patient.
The risk of fracture is higher in patients under the age of 50, those who perform intense physical activity, women, and patients with greater left ventricular ejection fraction.4,5 Certain leads are prone to fracture due to design flaws. One of these was the Medtronic Sprint Fidelis cardioverter defibrillator lead, which was recalled in 2007.5
DETECTING LEAD FRACTURE
Symptoms of lead fracture vary, depending on the patient’s pacemaker-dependency and on the degree of loss of capture (ie, the degree to which the heart fails to respond to the pacemaker’s signals), and may include lightheadedness, syncope, and extracardiac stimulation.
The electrical integrity of a lead can be tested by measuring the circuit impedance, which normally ranges from 300 to 1,000 ohms.6 An insulation failure results in very low impedance, while a disrupted circuit due to lead fracture commonly causes a sudden rather than gradual increase in impedance.6
Simple imaging studies such as chest radiography or fluoroscopy may establish the diagnosis of lead fracture. One should carefully trace every lead along its entire course and look for any conductor discontinuity, kinks, or sharp bends.6
REMOVE THE OLD LEAD, OR LEAVE IT IN PLACE?
The treatment for lead fracture is usually to put in a new lead, with or without extracting the old one.
In view of the potential complications of lead removal such as cardiac perforation or vascular tear, lead abandonment with placement of a new lead may be performed.7 There are no controlled clinical studies comparing lead abandonment vs lead extraction.8 However, extraction is currently recommended only in patients in whom the old lead causes life-threatening arrhythmias, interferes with the operation of implanted cardiac devices, interferes with radiation therapy or needed surgery, or, due to its design or failure, poses an immediate threat to the patient if left in place.7 Lead removal is reasonable in patients who require specific imaging studies such as magnetic resonance imaging with no available imaging alternative for the diagnosis.7
In our patient, a new lead was placed without removing the fractured lead, with no complications. Afterward, the patient’s heart rhythm was observed to be appropriately paced, and she was discharged home the following day.
A 69-year-old woman presented with fatigue, cough, and lightheadedness. She had a history of atrial fibrillation and complete heart block, for which she had a pacemaker (dual-pacing, dual-sensing, dual-response, and rate-adaptive mode) inserted in 2005. Her heart rate was 30 beats per minute.
A chest radiograph showed a fractured right ventricular pacemaker lead (Figure 1). Electrocardiography showed sinus rhythm with a high-grade atrioventricular block (Figure 2). Pacemaker interrogation confirmed the diagnosis of lead fracture. A new lead was placed, and the old lead was abandoned.
HOW LEADS BREAK
The rate of lead fracture ranges from 0.1% to 4.2% per patient-year, and the annual failure rate increases progressively with time after implantation.1,2
Extrinsic pressure on the lead can eventually break it. This can happen between the first rib and clavicle, in “subclavian crush” injury, or with any anatomical abnormality that narrows the thoracic outlet. Typically, classic subclavian crush results from entrapment of the pacemaker leads by the subclavius muscle or the costoclavicular ligament as the lead follows the needle course of the antecedent access puncture of the subclavian vein. This results in intermittent flexing of the lead and potential lead fracture3 and was likely the cause of lead fracture in our patient.
The risk of fracture is higher in patients under the age of 50, those who perform intense physical activity, women, and patients with greater left ventricular ejection fraction.4,5 Certain leads are prone to fracture due to design flaws. One of these was the Medtronic Sprint Fidelis cardioverter defibrillator lead, which was recalled in 2007.5
DETECTING LEAD FRACTURE
Symptoms of lead fracture vary, depending on the patient’s pacemaker-dependency and on the degree of loss of capture (ie, the degree to which the heart fails to respond to the pacemaker’s signals), and may include lightheadedness, syncope, and extracardiac stimulation.
The electrical integrity of a lead can be tested by measuring the circuit impedance, which normally ranges from 300 to 1,000 ohms.6 An insulation failure results in very low impedance, while a disrupted circuit due to lead fracture commonly causes a sudden rather than gradual increase in impedance.6
Simple imaging studies such as chest radiography or fluoroscopy may establish the diagnosis of lead fracture. One should carefully trace every lead along its entire course and look for any conductor discontinuity, kinks, or sharp bends.6
REMOVE THE OLD LEAD, OR LEAVE IT IN PLACE?
The treatment for lead fracture is usually to put in a new lead, with or without extracting the old one.
In view of the potential complications of lead removal such as cardiac perforation or vascular tear, lead abandonment with placement of a new lead may be performed.7 There are no controlled clinical studies comparing lead abandonment vs lead extraction.8 However, extraction is currently recommended only in patients in whom the old lead causes life-threatening arrhythmias, interferes with the operation of implanted cardiac devices, interferes with radiation therapy or needed surgery, or, due to its design or failure, poses an immediate threat to the patient if left in place.7 Lead removal is reasonable in patients who require specific imaging studies such as magnetic resonance imaging with no available imaging alternative for the diagnosis.7
In our patient, a new lead was placed without removing the fractured lead, with no complications. Afterward, the patient’s heart rhythm was observed to be appropriately paced, and she was discharged home the following day.
- Alt E, Völker R, Blömer H. Lead fracture in pacemaker patients. Thorac Cardiovasc Surg 1987; 35:101–104.
- Kleemann T, Becker T, Doenges K, et al. Annual rate of transvenous defibrillation lead defects in implantable cardioverter-defibrillators over a period of > 10 years. Circulation 2007; 115:2474–2480.
- Magney JE, Flynn DM, Parsons JA, et al. Anatomical mechanisms explaining damage to pacemaker leads, defibrillator leads, and failure of central venous catheters adjacent to the sternoclavicular joint. Pacing Clin Electrophysiol 1993; 16:445–457.
- Farwell D, Green MS, Lemery R, Gollob MH, Birnie DH. Accelerating risk of Fidelis lead fracture. Heart Rhythm 2008; 5:1375–1379.
- Morrison TB, Rea RF, Hodge DO, et al. Risk factors for implantable defibrillator lead fracture in a recalled and a nonrecalled lead. J Cardiovasc Electrophysiol 2010; 21:671–677.
- Swerdlow CD, Ellenbogen KA. Implantable cardioverter-defibrillator leads: design, diagnostics, and management. Circulation 2013; 128:2062–2071.
- Wilkoff BL, Love CJ, Byrd CL, et al; Heart Rhythm Society; American Heart Association. Transvenous lead extraction: Heart Rhythm Society expert consensus on facilities, training, indications, and patient management: this document was endorsed by the American Heart Association (AHA). Heart Rhythm 2009; 6:1085–1104.
- Maytin M, Epstein LM, Henrikson CA. Lead extraction is preferred for lead revisions and system upgrades: when less is more. Circ Arrhythm Electrophysiol 2010; 3:413–424.
- Alt E, Völker R, Blömer H. Lead fracture in pacemaker patients. Thorac Cardiovasc Surg 1987; 35:101–104.
- Kleemann T, Becker T, Doenges K, et al. Annual rate of transvenous defibrillation lead defects in implantable cardioverter-defibrillators over a period of > 10 years. Circulation 2007; 115:2474–2480.
- Magney JE, Flynn DM, Parsons JA, et al. Anatomical mechanisms explaining damage to pacemaker leads, defibrillator leads, and failure of central venous catheters adjacent to the sternoclavicular joint. Pacing Clin Electrophysiol 1993; 16:445–457.
- Farwell D, Green MS, Lemery R, Gollob MH, Birnie DH. Accelerating risk of Fidelis lead fracture. Heart Rhythm 2008; 5:1375–1379.
- Morrison TB, Rea RF, Hodge DO, et al. Risk factors for implantable defibrillator lead fracture in a recalled and a nonrecalled lead. J Cardiovasc Electrophysiol 2010; 21:671–677.
- Swerdlow CD, Ellenbogen KA. Implantable cardioverter-defibrillator leads: design, diagnostics, and management. Circulation 2013; 128:2062–2071.
- Wilkoff BL, Love CJ, Byrd CL, et al; Heart Rhythm Society; American Heart Association. Transvenous lead extraction: Heart Rhythm Society expert consensus on facilities, training, indications, and patient management: this document was endorsed by the American Heart Association (AHA). Heart Rhythm 2009; 6:1085–1104.
- Maytin M, Epstein LM, Henrikson CA. Lead extraction is preferred for lead revisions and system upgrades: when less is more. Circ Arrhythm Electrophysiol 2010; 3:413–424.
Which bowel preparation should be used for colonoscopy in patients who have had bariatric surgery?
We routinely use low-volume (2-L) polyethylene glycol electrolyte preparations such as Moviprep and Miralax in split-dose regimens, in which patients drink half of the preparation the day before the procedure and the other half the day of the procedure. In our experience, these are well tolerated by patients with a history of bariatric surgery and provide adequate colon cleansing before colonoscopy.
RATIONALE
Adequate bowel preparation by the ingestion of a cleansing agent is extremely important before colonoscopy: the quality of colon preparation affects the diagnostic accuracy and safety of the procedure, as inadequate bowel preparation has been associated with failure to detect polyps and with a higher rate of adverse events during the procedure.1–3
The most commonly used bowel preparations can be divided into high-volume (which require drinking at least 4 L of a cathartic solution) and low-volume (which require drinking about 2 L).4 Polyethylene glycol electrolyte solutions are among the most commonly used and are available in both high-volume (eg, Golytely, Nulytely) and low-volume (eg, Moviprep, Miralax) forms.
Other low-volume preparations include sodium picosulfate (Prepopik), magnesium citrate, and sodium phosphate tablets. However, these should be avoided in patients with renal insufficiency.4
Prices for bowel preparations vary. For example, the average reported wholesale price of Golytely is $24.56, Moviprep $81.17, and Miralax $10.08.4 However, the final cost depends on the patient’s insurance coverage. Generic formulations are available for some preparations.
After bariatric surgery, patients have a smaller stomach
After bariatric surgery, patients have significantly reduced stomach volume, due either to resection of a part of the stomach (such as in partial gastrectomy) or to diversion of the gastrointestinal (GI) tract to bypass most of the stomach (such as in Roux-en-Y gastric bypass). This causes early satiety with smaller amounts of food and leads to weight loss. However, this restriction in stomach volume also makes it more difficult for the patient to tolerate the intake of large volumes of fluids for bowel cleansing before colonoscopy.
Bariatric surgery patients may require colonoscopy for indications such as colorectal cancer screening, chronic diarrhea, or GI bleeding, all of which are commonly encountered during routine clinical practice.
Guidelines are available
Currently, there are no published data available to support the use of one preparation over another in patients with a history of bariatric surgery. However, for patients who have had bariatric surgery, guidelines from the US Multi-Society Task Force on Colorectal Cancer—endorsed by the three major American gastroenterology societies, ie, the American Gastroenterological Association, the American College of Gastroenterology, and the American Society for Gastrointestinal Endoscopy—recommend either a low-volume solution or, if a high-volume solution is used, extending the duration over which the preparation is consumed.5 In addition, it is recommended that patients consume sugar-free drinks and liquids to avoid dumping syndrome from high sugar content.6
The use of split-dose regimens is also strongly recommended for elective colonoscopy by the US Multi-Society Task Force on Colorectal Cancer.5
Our clinical experience has been in line with the above recommendations.
- Chokshi RV, Hovis CE, Hollander T, Early DS, Wang JS. Prevalence of missed adenomas in patients with inadequate bowel preparation on screening colonoscopy. Gastrointest Endosc 2012; 75:1197–1203.
- Rex DK, Schoenfeld PS, Cohen J, et al. Quality indicators for colonoscopy. Gastrointest Endosc 2015; 81:31–53.
- Wexner SD, Beck DE, Baron TH, et al; American Society of Colon and Rectal Surgeons; American Society for Gastrointestinal Endoscopy; Society of American Gastrointestinal and Endoscopic Surgeons. A consensus document on bowel preparation before colonoscopy: prepared by a task force from the American Society of Colon and Rectal Surgeons (ASCRS), the American Society for Gastrointestinal Endoscopy (ASGE), and the Society of American Gastrointestinal and Endoscopic Surgerons (SAGES). Gastrointest Endosc 2006; 63:894–909.
- ASGE Standards of Practice Committee; Saltzman JR, Cash BD, Pasha SF, et al. Bowel preparation before colonoscopy. Gastrointest Endosc 2015; 81:781–794.
- Johnson DA, Barkun AN, Cohen LB, et al; US Multi-Society Task Force on Colorectal Cancer. Optimizing adequacy of bowel cleansing for colonoscopy: recommendations from the US Multi-Society Task Force on Colorectal Cancer. Gastroenterology 2014; 147:903–924.
- Heber D, Greenway FL, Kaplan LM, Livingston E, Salvador J, Still C; Endocrine Society. Endocrine and nutritional management of the post-bariatric surgery patient: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2010; 95:4823–4843.
We routinely use low-volume (2-L) polyethylene glycol electrolyte preparations such as Moviprep and Miralax in split-dose regimens, in which patients drink half of the preparation the day before the procedure and the other half the day of the procedure. In our experience, these are well tolerated by patients with a history of bariatric surgery and provide adequate colon cleansing before colonoscopy.
RATIONALE
Adequate bowel preparation by the ingestion of a cleansing agent is extremely important before colonoscopy: the quality of colon preparation affects the diagnostic accuracy and safety of the procedure, as inadequate bowel preparation has been associated with failure to detect polyps and with a higher rate of adverse events during the procedure.1–3
The most commonly used bowel preparations can be divided into high-volume (which require drinking at least 4 L of a cathartic solution) and low-volume (which require drinking about 2 L).4 Polyethylene glycol electrolyte solutions are among the most commonly used and are available in both high-volume (eg, Golytely, Nulytely) and low-volume (eg, Moviprep, Miralax) forms.
Other low-volume preparations include sodium picosulfate (Prepopik), magnesium citrate, and sodium phosphate tablets. However, these should be avoided in patients with renal insufficiency.4
Prices for bowel preparations vary. For example, the average reported wholesale price of Golytely is $24.56, Moviprep $81.17, and Miralax $10.08.4 However, the final cost depends on the patient’s insurance coverage. Generic formulations are available for some preparations.
After bariatric surgery, patients have a smaller stomach
After bariatric surgery, patients have significantly reduced stomach volume, due either to resection of a part of the stomach (such as in partial gastrectomy) or to diversion of the gastrointestinal (GI) tract to bypass most of the stomach (such as in Roux-en-Y gastric bypass). This causes early satiety with smaller amounts of food and leads to weight loss. However, this restriction in stomach volume also makes it more difficult for the patient to tolerate the intake of large volumes of fluids for bowel cleansing before colonoscopy.
Bariatric surgery patients may require colonoscopy for indications such as colorectal cancer screening, chronic diarrhea, or GI bleeding, all of which are commonly encountered during routine clinical practice.
Guidelines are available
Currently, there are no published data available to support the use of one preparation over another in patients with a history of bariatric surgery. However, for patients who have had bariatric surgery, guidelines from the US Multi-Society Task Force on Colorectal Cancer—endorsed by the three major American gastroenterology societies, ie, the American Gastroenterological Association, the American College of Gastroenterology, and the American Society for Gastrointestinal Endoscopy—recommend either a low-volume solution or, if a high-volume solution is used, extending the duration over which the preparation is consumed.5 In addition, it is recommended that patients consume sugar-free drinks and liquids to avoid dumping syndrome from high sugar content.6
The use of split-dose regimens is also strongly recommended for elective colonoscopy by the US Multi-Society Task Force on Colorectal Cancer.5
Our clinical experience has been in line with the above recommendations.
We routinely use low-volume (2-L) polyethylene glycol electrolyte preparations such as Moviprep and Miralax in split-dose regimens, in which patients drink half of the preparation the day before the procedure and the other half the day of the procedure. In our experience, these are well tolerated by patients with a history of bariatric surgery and provide adequate colon cleansing before colonoscopy.
RATIONALE
Adequate bowel preparation by the ingestion of a cleansing agent is extremely important before colonoscopy: the quality of colon preparation affects the diagnostic accuracy and safety of the procedure, as inadequate bowel preparation has been associated with failure to detect polyps and with a higher rate of adverse events during the procedure.1–3
The most commonly used bowel preparations can be divided into high-volume (which require drinking at least 4 L of a cathartic solution) and low-volume (which require drinking about 2 L).4 Polyethylene glycol electrolyte solutions are among the most commonly used and are available in both high-volume (eg, Golytely, Nulytely) and low-volume (eg, Moviprep, Miralax) forms.
Other low-volume preparations include sodium picosulfate (Prepopik), magnesium citrate, and sodium phosphate tablets. However, these should be avoided in patients with renal insufficiency.4
Prices for bowel preparations vary. For example, the average reported wholesale price of Golytely is $24.56, Moviprep $81.17, and Miralax $10.08.4 However, the final cost depends on the patient’s insurance coverage. Generic formulations are available for some preparations.
After bariatric surgery, patients have a smaller stomach
After bariatric surgery, patients have significantly reduced stomach volume, due either to resection of a part of the stomach (such as in partial gastrectomy) or to diversion of the gastrointestinal (GI) tract to bypass most of the stomach (such as in Roux-en-Y gastric bypass). This causes early satiety with smaller amounts of food and leads to weight loss. However, this restriction in stomach volume also makes it more difficult for the patient to tolerate the intake of large volumes of fluids for bowel cleansing before colonoscopy.
Bariatric surgery patients may require colonoscopy for indications such as colorectal cancer screening, chronic diarrhea, or GI bleeding, all of which are commonly encountered during routine clinical practice.
Guidelines are available
Currently, there are no published data available to support the use of one preparation over another in patients with a history of bariatric surgery. However, for patients who have had bariatric surgery, guidelines from the US Multi-Society Task Force on Colorectal Cancer—endorsed by the three major American gastroenterology societies, ie, the American Gastroenterological Association, the American College of Gastroenterology, and the American Society for Gastrointestinal Endoscopy—recommend either a low-volume solution or, if a high-volume solution is used, extending the duration over which the preparation is consumed.5 In addition, it is recommended that patients consume sugar-free drinks and liquids to avoid dumping syndrome from high sugar content.6
The use of split-dose regimens is also strongly recommended for elective colonoscopy by the US Multi-Society Task Force on Colorectal Cancer.5
Our clinical experience has been in line with the above recommendations.
- Chokshi RV, Hovis CE, Hollander T, Early DS, Wang JS. Prevalence of missed adenomas in patients with inadequate bowel preparation on screening colonoscopy. Gastrointest Endosc 2012; 75:1197–1203.
- Rex DK, Schoenfeld PS, Cohen J, et al. Quality indicators for colonoscopy. Gastrointest Endosc 2015; 81:31–53.
- Wexner SD, Beck DE, Baron TH, et al; American Society of Colon and Rectal Surgeons; American Society for Gastrointestinal Endoscopy; Society of American Gastrointestinal and Endoscopic Surgeons. A consensus document on bowel preparation before colonoscopy: prepared by a task force from the American Society of Colon and Rectal Surgeons (ASCRS), the American Society for Gastrointestinal Endoscopy (ASGE), and the Society of American Gastrointestinal and Endoscopic Surgerons (SAGES). Gastrointest Endosc 2006; 63:894–909.
- ASGE Standards of Practice Committee; Saltzman JR, Cash BD, Pasha SF, et al. Bowel preparation before colonoscopy. Gastrointest Endosc 2015; 81:781–794.
- Johnson DA, Barkun AN, Cohen LB, et al; US Multi-Society Task Force on Colorectal Cancer. Optimizing adequacy of bowel cleansing for colonoscopy: recommendations from the US Multi-Society Task Force on Colorectal Cancer. Gastroenterology 2014; 147:903–924.
- Heber D, Greenway FL, Kaplan LM, Livingston E, Salvador J, Still C; Endocrine Society. Endocrine and nutritional management of the post-bariatric surgery patient: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2010; 95:4823–4843.
- Chokshi RV, Hovis CE, Hollander T, Early DS, Wang JS. Prevalence of missed adenomas in patients with inadequate bowel preparation on screening colonoscopy. Gastrointest Endosc 2012; 75:1197–1203.
- Rex DK, Schoenfeld PS, Cohen J, et al. Quality indicators for colonoscopy. Gastrointest Endosc 2015; 81:31–53.
- Wexner SD, Beck DE, Baron TH, et al; American Society of Colon and Rectal Surgeons; American Society for Gastrointestinal Endoscopy; Society of American Gastrointestinal and Endoscopic Surgeons. A consensus document on bowel preparation before colonoscopy: prepared by a task force from the American Society of Colon and Rectal Surgeons (ASCRS), the American Society for Gastrointestinal Endoscopy (ASGE), and the Society of American Gastrointestinal and Endoscopic Surgerons (SAGES). Gastrointest Endosc 2006; 63:894–909.
- ASGE Standards of Practice Committee; Saltzman JR, Cash BD, Pasha SF, et al. Bowel preparation before colonoscopy. Gastrointest Endosc 2015; 81:781–794.
- Johnson DA, Barkun AN, Cohen LB, et al; US Multi-Society Task Force on Colorectal Cancer. Optimizing adequacy of bowel cleansing for colonoscopy: recommendations from the US Multi-Society Task Force on Colorectal Cancer. Gastroenterology 2014; 147:903–924.
- Heber D, Greenway FL, Kaplan LM, Livingston E, Salvador J, Still C; Endocrine Society. Endocrine and nutritional management of the post-bariatric surgery patient: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2010; 95:4823–4843.
A second-degree burn after MRI
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
- Dempsey MF, Condon B. Thermal injuries associated with MRI. Clin Radiol 2001; 56:457–465.
- Haik J, Daniel S, Tessone A, Orenstein A, Winkler E. MRI induced fourth-degree burn in an extremity, leading to amputation. Burns 2009; 35:294–296.
- Friedstat J, Moore ME, Goverman J, Fagan SP. An unusual burn during routine magnetic resonance imaging. J Burn Care Res 2013; 34: e110–e111.
- Eising EG, Hughes J, Nolte F, Jentzen W, Bockisch A. Burn injury by nuclear magnetic resonance imaging. Clin Imaging 2010; 34:293–297.
- Landman A, Goldfarb S. Magnetic resonance-induced thermal burn. Ann Emerg Med 2008; 52:308–309.
- Expert Panel on MR Safety; Kanal E, Barkovich AJ, Bell C, et al. ACR guidance document on MR safe practices: 2013. J Magn Reson Imaging 2013; 37:501–530.
- Magnetic resonance safety. Radiol Technol 2010; 81:615–616.
- Shellock FG, Crues JV. MR procedures: biologic effects, safety, and patient care. Radiology 2004; 232:635–652.
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
- Dempsey MF, Condon B. Thermal injuries associated with MRI. Clin Radiol 2001; 56:457–465.
- Haik J, Daniel S, Tessone A, Orenstein A, Winkler E. MRI induced fourth-degree burn in an extremity, leading to amputation. Burns 2009; 35:294–296.
- Friedstat J, Moore ME, Goverman J, Fagan SP. An unusual burn during routine magnetic resonance imaging. J Burn Care Res 2013; 34: e110–e111.
- Eising EG, Hughes J, Nolte F, Jentzen W, Bockisch A. Burn injury by nuclear magnetic resonance imaging. Clin Imaging 2010; 34:293–297.
- Landman A, Goldfarb S. Magnetic resonance-induced thermal burn. Ann Emerg Med 2008; 52:308–309.
- Expert Panel on MR Safety; Kanal E, Barkovich AJ, Bell C, et al. ACR guidance document on MR safe practices: 2013. J Magn Reson Imaging 2013; 37:501–530.
- Magnetic resonance safety. Radiol Technol 2010; 81:615–616.
- Shellock FG, Crues JV. MR procedures: biologic effects, safety, and patient care. Radiology 2004; 232:635–652.
- Dempsey MF, Condon B. Thermal injuries associated with MRI. Clin Radiol 2001; 56:457–465.
- Haik J, Daniel S, Tessone A, Orenstein A, Winkler E. MRI induced fourth-degree burn in an extremity, leading to amputation. Burns 2009; 35:294–296.
- Friedstat J, Moore ME, Goverman J, Fagan SP. An unusual burn during routine magnetic resonance imaging. J Burn Care Res 2013; 34: e110–e111.
- Eising EG, Hughes J, Nolte F, Jentzen W, Bockisch A. Burn injury by nuclear magnetic resonance imaging. Clin Imaging 2010; 34:293–297.
- Landman A, Goldfarb S. Magnetic resonance-induced thermal burn. Ann Emerg Med 2008; 52:308–309.
- Expert Panel on MR Safety; Kanal E, Barkovich AJ, Bell C, et al. ACR guidance document on MR safe practices: 2013. J Magn Reson Imaging 2013; 37:501–530.
- Magnetic resonance safety. Radiol Technol 2010; 81:615–616.
- Shellock FG, Crues JV. MR procedures: biologic effects, safety, and patient care. Radiology 2004; 232:635–652.
Coronary flow reserve reveals hidden cardiovascular risk
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.
When the CFR is markedly low, however, a patient with stable CAD is at high risk for cardiovascular events, even if angiography shows no clinically significant stenosis, added Dr. Di Carli, who is also professor of radiology and medicine at Harvard Medical School, Boston.
Most recently, he and his coinvestigators utilized CFR to provide new insight into the paradox that women have a higher cardiovascular disease death rate than men, even though their prevalence of obstructive CAD is lower.
Their NIH-sponsored study included 329 consecutive patients with a left ventricular ejection fraction greater than 40% – 43% of them women – who underwent coronary angiography several days after noninvasive assessment of CFR via myocardial perfusion positron emission tomography. The women had a lower burden of angiographic CAD and a lower pretest clinical risk score than the men. Nevertheless, during a median of 3 years of follow-up, the women had an adjusted twofold greater risk of the composite endpoint of cardiovascular death, nonfatal MI, or heart failure.
This excess cardiovascular risk in women was independently associated with a very low CFR, defined as less than 1.6. Dr. Di Carli and his coinvestigators calculated that this impaired CFR mediated 40% of the excess risk in women. Thus, a low CFR represents a novel hidden biologic risk for ischemic heart disease (Circulation. 2017 Feb 7;135[6]:566-77).
CFR is defined as the ratio of absolute coronary flow or myocardial perfusion between drug-induced hyperemia and rest. It can be quantified noninvasively using positron emission tomography or MRI.
CFR integrates into a single measure the three components of CAD: the focal stenosis, the diffuse atherosclerotic plaque typically present to a varying degree throughout a target vessel, and microvascular dysfunction.
CFR is a measure of coronary physiology, as is invasive fractional flow reserve (FFR). However, FFR measures only the severity of stenosis and extent of diffuse disease; it doesn’t assess microvascular dysfunction. This is a limitation because it means FFR can give false-negative readings in patients without significant obstructive coronary disease who have severe microvascular dysfunction.
As for angiography, Dr. Di Carli continued, it’s now evident that this purely anatomic assessment is of limited value as a marker of clinical risk and is inadequate to guide management decisions in the setting of stable CAD. After all, angiographically guided revascularization has not reduced cardiovascular events in clinical trials comparing it with optimal medical therapy, as in the COURAGE and BARI-2D trials.
“It’s clear that there’s been a paradigm shift in how we manage patients with stable CAD. For many years the coronary angiogram was the cornerstone of what we did: how we understand the symptoms, the patient’s risk, and ultimately how we proceed with treatment. But there is no benefit in basing treatment solely on what the lesions look like anatomically. That’s why we’ve turned to functional testing of coronary physiology,” he said.
CFR has opened a window on the importance of microvascular dysfunction, which is present in about half of patients with stable CAD and has been shown to predict cardiovascular risk independent of whether or not severe obstructive disease is present.
In an earlier study, Dr. Di Carli and coworkers demonstrated that quantification of CFR enhances stratification for risk of cardiac death among diabetes patients (Circulation. 2012 Oct 9;126[15]:1858-68). The study included 2,783 patients, of whom 1,172 were diabetic, who underwent measurement of CFR and were subsequently followed for a median of 1.4 years, during which 137 cardiac deaths occurred.
Diabetes patients without known CAD who had a low CFR had a high cardiac death rate of 2.8%/year, similar to the 2.0%/year rate in nondiabetic patients with a history of acute MI or revascularization. On the other hand, diabetes patients with a normal CFR and without known CAD had a cardiac mortality rate of only 0.3%/year, comparable to the 0.5% rate in nondiabetics without known CAD who had preserved systolic function and a normal stress perfusion study.
In the future, CFR may aid in decision making as to whether an individual with stable CAD is best treated by percutaneous coronary intervention, surgical revascularization, or guideline-directed medical therapy. For example, if CFR indicates the presence of an isolated severe focal stenosis, and this is confirmed by angiography and FFR, PCI may be the best option, while diffuse disease as demonstrated by CFR may be better treated surgically or using optimal medical therapy. But this needs to be established in prospective clinical trials, added Dr. Di Carli.
He reported having no financial conflicts regarding his presentation.
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.
When the CFR is markedly low, however, a patient with stable CAD is at high risk for cardiovascular events, even if angiography shows no clinically significant stenosis, added Dr. Di Carli, who is also professor of radiology and medicine at Harvard Medical School, Boston.
Most recently, he and his coinvestigators utilized CFR to provide new insight into the paradox that women have a higher cardiovascular disease death rate than men, even though their prevalence of obstructive CAD is lower.
Their NIH-sponsored study included 329 consecutive patients with a left ventricular ejection fraction greater than 40% – 43% of them women – who underwent coronary angiography several days after noninvasive assessment of CFR via myocardial perfusion positron emission tomography. The women had a lower burden of angiographic CAD and a lower pretest clinical risk score than the men. Nevertheless, during a median of 3 years of follow-up, the women had an adjusted twofold greater risk of the composite endpoint of cardiovascular death, nonfatal MI, or heart failure.
This excess cardiovascular risk in women was independently associated with a very low CFR, defined as less than 1.6. Dr. Di Carli and his coinvestigators calculated that this impaired CFR mediated 40% of the excess risk in women. Thus, a low CFR represents a novel hidden biologic risk for ischemic heart disease (Circulation. 2017 Feb 7;135[6]:566-77).
CFR is defined as the ratio of absolute coronary flow or myocardial perfusion between drug-induced hyperemia and rest. It can be quantified noninvasively using positron emission tomography or MRI.
CFR integrates into a single measure the three components of CAD: the focal stenosis, the diffuse atherosclerotic plaque typically present to a varying degree throughout a target vessel, and microvascular dysfunction.
CFR is a measure of coronary physiology, as is invasive fractional flow reserve (FFR). However, FFR measures only the severity of stenosis and extent of diffuse disease; it doesn’t assess microvascular dysfunction. This is a limitation because it means FFR can give false-negative readings in patients without significant obstructive coronary disease who have severe microvascular dysfunction.
As for angiography, Dr. Di Carli continued, it’s now evident that this purely anatomic assessment is of limited value as a marker of clinical risk and is inadequate to guide management decisions in the setting of stable CAD. After all, angiographically guided revascularization has not reduced cardiovascular events in clinical trials comparing it with optimal medical therapy, as in the COURAGE and BARI-2D trials.
“It’s clear that there’s been a paradigm shift in how we manage patients with stable CAD. For many years the coronary angiogram was the cornerstone of what we did: how we understand the symptoms, the patient’s risk, and ultimately how we proceed with treatment. But there is no benefit in basing treatment solely on what the lesions look like anatomically. That’s why we’ve turned to functional testing of coronary physiology,” he said.
CFR has opened a window on the importance of microvascular dysfunction, which is present in about half of patients with stable CAD and has been shown to predict cardiovascular risk independent of whether or not severe obstructive disease is present.
In an earlier study, Dr. Di Carli and coworkers demonstrated that quantification of CFR enhances stratification for risk of cardiac death among diabetes patients (Circulation. 2012 Oct 9;126[15]:1858-68). The study included 2,783 patients, of whom 1,172 were diabetic, who underwent measurement of CFR and were subsequently followed for a median of 1.4 years, during which 137 cardiac deaths occurred.
Diabetes patients without known CAD who had a low CFR had a high cardiac death rate of 2.8%/year, similar to the 2.0%/year rate in nondiabetic patients with a history of acute MI or revascularization. On the other hand, diabetes patients with a normal CFR and without known CAD had a cardiac mortality rate of only 0.3%/year, comparable to the 0.5% rate in nondiabetics without known CAD who had preserved systolic function and a normal stress perfusion study.
In the future, CFR may aid in decision making as to whether an individual with stable CAD is best treated by percutaneous coronary intervention, surgical revascularization, or guideline-directed medical therapy. For example, if CFR indicates the presence of an isolated severe focal stenosis, and this is confirmed by angiography and FFR, PCI may be the best option, while diffuse disease as demonstrated by CFR may be better treated surgically or using optimal medical therapy. But this needs to be established in prospective clinical trials, added Dr. Di Carli.
He reported having no financial conflicts regarding his presentation.
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.
When the CFR is markedly low, however, a patient with stable CAD is at high risk for cardiovascular events, even if angiography shows no clinically significant stenosis, added Dr. Di Carli, who is also professor of radiology and medicine at Harvard Medical School, Boston.
Most recently, he and his coinvestigators utilized CFR to provide new insight into the paradox that women have a higher cardiovascular disease death rate than men, even though their prevalence of obstructive CAD is lower.
Their NIH-sponsored study included 329 consecutive patients with a left ventricular ejection fraction greater than 40% – 43% of them women – who underwent coronary angiography several days after noninvasive assessment of CFR via myocardial perfusion positron emission tomography. The women had a lower burden of angiographic CAD and a lower pretest clinical risk score than the men. Nevertheless, during a median of 3 years of follow-up, the women had an adjusted twofold greater risk of the composite endpoint of cardiovascular death, nonfatal MI, or heart failure.
This excess cardiovascular risk in women was independently associated with a very low CFR, defined as less than 1.6. Dr. Di Carli and his coinvestigators calculated that this impaired CFR mediated 40% of the excess risk in women. Thus, a low CFR represents a novel hidden biologic risk for ischemic heart disease (Circulation. 2017 Feb 7;135[6]:566-77).
CFR is defined as the ratio of absolute coronary flow or myocardial perfusion between drug-induced hyperemia and rest. It can be quantified noninvasively using positron emission tomography or MRI.
CFR integrates into a single measure the three components of CAD: the focal stenosis, the diffuse atherosclerotic plaque typically present to a varying degree throughout a target vessel, and microvascular dysfunction.
CFR is a measure of coronary physiology, as is invasive fractional flow reserve (FFR). However, FFR measures only the severity of stenosis and extent of diffuse disease; it doesn’t assess microvascular dysfunction. This is a limitation because it means FFR can give false-negative readings in patients without significant obstructive coronary disease who have severe microvascular dysfunction.
As for angiography, Dr. Di Carli continued, it’s now evident that this purely anatomic assessment is of limited value as a marker of clinical risk and is inadequate to guide management decisions in the setting of stable CAD. After all, angiographically guided revascularization has not reduced cardiovascular events in clinical trials comparing it with optimal medical therapy, as in the COURAGE and BARI-2D trials.
“It’s clear that there’s been a paradigm shift in how we manage patients with stable CAD. For many years the coronary angiogram was the cornerstone of what we did: how we understand the symptoms, the patient’s risk, and ultimately how we proceed with treatment. But there is no benefit in basing treatment solely on what the lesions look like anatomically. That’s why we’ve turned to functional testing of coronary physiology,” he said.
CFR has opened a window on the importance of microvascular dysfunction, which is present in about half of patients with stable CAD and has been shown to predict cardiovascular risk independent of whether or not severe obstructive disease is present.
In an earlier study, Dr. Di Carli and coworkers demonstrated that quantification of CFR enhances stratification for risk of cardiac death among diabetes patients (Circulation. 2012 Oct 9;126[15]:1858-68). The study included 2,783 patients, of whom 1,172 were diabetic, who underwent measurement of CFR and were subsequently followed for a median of 1.4 years, during which 137 cardiac deaths occurred.
Diabetes patients without known CAD who had a low CFR had a high cardiac death rate of 2.8%/year, similar to the 2.0%/year rate in nondiabetic patients with a history of acute MI or revascularization. On the other hand, diabetes patients with a normal CFR and without known CAD had a cardiac mortality rate of only 0.3%/year, comparable to the 0.5% rate in nondiabetics without known CAD who had preserved systolic function and a normal stress perfusion study.
In the future, CFR may aid in decision making as to whether an individual with stable CAD is best treated by percutaneous coronary intervention, surgical revascularization, or guideline-directed medical therapy. For example, if CFR indicates the presence of an isolated severe focal stenosis, and this is confirmed by angiography and FFR, PCI may be the best option, while diffuse disease as demonstrated by CFR may be better treated surgically or using optimal medical therapy. But this needs to be established in prospective clinical trials, added Dr. Di Carli.
He reported having no financial conflicts regarding his presentation.
EXPERT ANALYSIS FROM THE CARDIOVASCULAR CONFERENCE AT SNOWMASS
When the tail wags the dog: Clinical skills in the age of technology
“... 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.
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.
- Allen RB. Medical Education and the Changing Order: Studies of the New York Academy of Medicine, Committee on Medicine and the Changing Order. New York, NY: Commonwealth Fund, 1946.
- Peterson MC, Holbrook JH, Von Hales D, Smith NL, Staker LV. Contributions of the history, physical examination, and laboratory investigation in making medical diagnoses. West J Med 1992; 156:163–165.
- Roshan M, Rao AP. A study on relative contributions of the history, physical examination and investigations in making medical diagnosis. J Assoc Physicians India 2000; 48:771–775.
- Wagner MM, Bankowitz RA, McNeil M, Challinor SM, Janosky JE, Miller RA. The diagnostic importance of the history and physical examination as determined by the use of a medical decision support system. Proc Am Med Inform Assoc 1989: 139–144.
- Reilly BM. Physical examination in the care of medical inpatients: an observational study. Lancet 2003; 362:1100–1105.
- Verghese A, Charlton B, Kassirer JP, Ramsey M, Ioannidis JPA. Inadequacies of physical examination as a cause of medical errors and adverse events: a collection of vignettes. Am J Med 2015; 128:1322–1324.e3.
- Kondo T, Ohira Y, Uehara T, Noda K, Ikusaka M. An unexpected cause of shoulder pain. Cleve Clin J Med 2017; 84:276–277.
- Deguchi F, Hirakawa S, Gotoh K, Yagi Y, Ohshima S. Prognostic significance of posturally induced crackles. Long-term follow-up of patients after recovery from acute myocardial infarction. Chest 1993; 103:1457–1462.
- Silverman ME, Murrary TJ, Bryan CS, eds. The Quotable Osler. Philadelphia, PA: Am Coll of Physicians; 2008.
- Block L, Habicht R, Wu AW, et al. In the wake of the 2003 and 2011 duty hours regulations, how do internal medicine interns spend their time? J Gen Intern Med 2013; 28:1042–1047.
- Blumenthal D, Causino N, Chang YC, et al. The duration of ambulatory visits to physicians. J Fam Pract 1999; 48:264–271.
- Barton MB, Harris R, Fletcher SW. The rational clinical examination. Does this patient have breast cancer? The screening clinical breast examination: should it be done? How? JAMA 1999; 282:1270–1280.
- Hayward R. VOMIT (victims of modern imaging technology)—an acronym for our times. BMJ 2003; 326:1273.
- Moore FG, Chalk C. The essential neurologic examination: what should medical students be taught? Neurology 2009; 72:2020–2023.
- Simel DL, Rennie D. The rational clinical examination: evidence-based clinical diagnosis. JAMA & Archives Journals. New York, NY: McGraw-Hill Education/Medical; 2009.
- Kravitz RL, Callahan EJ. Patients’ perceptions of omitted examinations and tests: a qualitative analysis. J Gen Intern Med 2000; 15:38–45.
- Thomas L. The Youngest Science: Notes of a Medicine Watcher. New York, NY: Viking Press, 1983.
- Vukanovic-Criley JM, Criley S, Warde CM, et al. Competency in cardiac examination skills in medical students, trainees, physicians, and faculty: a multicenter study. Arch Intern Med 2006; 166:610–616.
- Paauw DS, Wenrich MD, Curtis JR, Carline JD, Ramsey PG. Ability of primary care physicians to recognize physical findings associated with HIV infection. JAMA 1995; 274:1380–1382.
- Brown TM, Fee E. Rudolf Carl Virchow: medical scientist, social reformer, role model. Am J Public Health 2006; 96:2104–2105.
- Osler W. British medicine in Greater Britain. The Medical News 1897; 71:293–298.
“... 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.
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.
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.
- Allen RB. Medical Education and the Changing Order: Studies of the New York Academy of Medicine, Committee on Medicine and the Changing Order. New York, NY: Commonwealth Fund, 1946.
- Peterson MC, Holbrook JH, Von Hales D, Smith NL, Staker LV. Contributions of the history, physical examination, and laboratory investigation in making medical diagnoses. West J Med 1992; 156:163–165.
- Roshan M, Rao AP. A study on relative contributions of the history, physical examination and investigations in making medical diagnosis. J Assoc Physicians India 2000; 48:771–775.
- Wagner MM, Bankowitz RA, McNeil M, Challinor SM, Janosky JE, Miller RA. The diagnostic importance of the history and physical examination as determined by the use of a medical decision support system. Proc Am Med Inform Assoc 1989: 139–144.
- Reilly BM. Physical examination in the care of medical inpatients: an observational study. Lancet 2003; 362:1100–1105.
- Verghese A, Charlton B, Kassirer JP, Ramsey M, Ioannidis JPA. Inadequacies of physical examination as a cause of medical errors and adverse events: a collection of vignettes. Am J Med 2015; 128:1322–1324.e3.
- Kondo T, Ohira Y, Uehara T, Noda K, Ikusaka M. An unexpected cause of shoulder pain. Cleve Clin J Med 2017; 84:276–277.
- Deguchi F, Hirakawa S, Gotoh K, Yagi Y, Ohshima S. Prognostic significance of posturally induced crackles. Long-term follow-up of patients after recovery from acute myocardial infarction. Chest 1993; 103:1457–1462.
- Silverman ME, Murrary TJ, Bryan CS, eds. The Quotable Osler. Philadelphia, PA: Am Coll of Physicians; 2008.
- Block L, Habicht R, Wu AW, et al. In the wake of the 2003 and 2011 duty hours regulations, how do internal medicine interns spend their time? J Gen Intern Med 2013; 28:1042–1047.
- Blumenthal D, Causino N, Chang YC, et al. The duration of ambulatory visits to physicians. J Fam Pract 1999; 48:264–271.
- Barton MB, Harris R, Fletcher SW. The rational clinical examination. Does this patient have breast cancer? The screening clinical breast examination: should it be done? How? JAMA 1999; 282:1270–1280.
- Hayward R. VOMIT (victims of modern imaging technology)—an acronym for our times. BMJ 2003; 326:1273.
- Moore FG, Chalk C. The essential neurologic examination: what should medical students be taught? Neurology 2009; 72:2020–2023.
- Simel DL, Rennie D. The rational clinical examination: evidence-based clinical diagnosis. JAMA & Archives Journals. New York, NY: McGraw-Hill Education/Medical; 2009.
- Kravitz RL, Callahan EJ. Patients’ perceptions of omitted examinations and tests: a qualitative analysis. J Gen Intern Med 2000; 15:38–45.
- Thomas L. The Youngest Science: Notes of a Medicine Watcher. New York, NY: Viking Press, 1983.
- Vukanovic-Criley JM, Criley S, Warde CM, et al. Competency in cardiac examination skills in medical students, trainees, physicians, and faculty: a multicenter study. Arch Intern Med 2006; 166:610–616.
- Paauw DS, Wenrich MD, Curtis JR, Carline JD, Ramsey PG. Ability of primary care physicians to recognize physical findings associated with HIV infection. JAMA 1995; 274:1380–1382.
- Brown TM, Fee E. Rudolf Carl Virchow: medical scientist, social reformer, role model. Am J Public Health 2006; 96:2104–2105.
- Osler W. British medicine in Greater Britain. The Medical News 1897; 71:293–298.
- Allen RB. Medical Education and the Changing Order: Studies of the New York Academy of Medicine, Committee on Medicine and the Changing Order. New York, NY: Commonwealth Fund, 1946.
- Peterson MC, Holbrook JH, Von Hales D, Smith NL, Staker LV. Contributions of the history, physical examination, and laboratory investigation in making medical diagnoses. West J Med 1992; 156:163–165.
- Roshan M, Rao AP. A study on relative contributions of the history, physical examination and investigations in making medical diagnosis. J Assoc Physicians India 2000; 48:771–775.
- Wagner MM, Bankowitz RA, McNeil M, Challinor SM, Janosky JE, Miller RA. The diagnostic importance of the history and physical examination as determined by the use of a medical decision support system. Proc Am Med Inform Assoc 1989: 139–144.
- Reilly BM. Physical examination in the care of medical inpatients: an observational study. Lancet 2003; 362:1100–1105.
- Verghese A, Charlton B, Kassirer JP, Ramsey M, Ioannidis JPA. Inadequacies of physical examination as a cause of medical errors and adverse events: a collection of vignettes. Am J Med 2015; 128:1322–1324.e3.
- Kondo T, Ohira Y, Uehara T, Noda K, Ikusaka M. An unexpected cause of shoulder pain. Cleve Clin J Med 2017; 84:276–277.
- Deguchi F, Hirakawa S, Gotoh K, Yagi Y, Ohshima S. Prognostic significance of posturally induced crackles. Long-term follow-up of patients after recovery from acute myocardial infarction. Chest 1993; 103:1457–1462.
- Silverman ME, Murrary TJ, Bryan CS, eds. The Quotable Osler. Philadelphia, PA: Am Coll of Physicians; 2008.
- Block L, Habicht R, Wu AW, et al. In the wake of the 2003 and 2011 duty hours regulations, how do internal medicine interns spend their time? J Gen Intern Med 2013; 28:1042–1047.
- Blumenthal D, Causino N, Chang YC, et al. The duration of ambulatory visits to physicians. J Fam Pract 1999; 48:264–271.
- Barton MB, Harris R, Fletcher SW. The rational clinical examination. Does this patient have breast cancer? The screening clinical breast examination: should it be done? How? JAMA 1999; 282:1270–1280.
- Hayward R. VOMIT (victims of modern imaging technology)—an acronym for our times. BMJ 2003; 326:1273.
- Moore FG, Chalk C. The essential neurologic examination: what should medical students be taught? Neurology 2009; 72:2020–2023.
- Simel DL, Rennie D. The rational clinical examination: evidence-based clinical diagnosis. JAMA & Archives Journals. New York, NY: McGraw-Hill Education/Medical; 2009.
- Kravitz RL, Callahan EJ. Patients’ perceptions of omitted examinations and tests: a qualitative analysis. J Gen Intern Med 2000; 15:38–45.
- Thomas L. The Youngest Science: Notes of a Medicine Watcher. New York, NY: Viking Press, 1983.
- Vukanovic-Criley JM, Criley S, Warde CM, et al. Competency in cardiac examination skills in medical students, trainees, physicians, and faculty: a multicenter study. Arch Intern Med 2006; 166:610–616.
- Paauw DS, Wenrich MD, Curtis JR, Carline JD, Ramsey PG. Ability of primary care physicians to recognize physical findings associated with HIV infection. JAMA 1995; 274:1380–1382.
- Brown TM, Fee E. Rudolf Carl Virchow: medical scientist, social reformer, role model. Am J Public Health 2006; 96:2104–2105.
- Osler W. British medicine in Greater Britain. The Medical News 1897; 71:293–298.
Blending classic clinical skills with new technology
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.
- Mangione S. Physical Diagnosis Secrets, 2nd ed. Philadelphia: Mosby/Elsevier, 2008.
- Verghese A, Charlton B, Kassirer JP, Ramsey M, Ioannidis JP. Inadequacies of physical examination as a cause of medical errors and adverse events: a collection of vignettes. Am J Med 2015; 128:1322–1324.
- Nishigori H, Masuda K, Kikukawa M, et al. A model teaching session for the hypothesis-driven physical examination. Medical Teacher 2011; 33:410–417.
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.
- Mangione S. Physical Diagnosis Secrets, 2nd ed. Philadelphia: Mosby/Elsevier, 2008.
- Verghese A, Charlton B, Kassirer JP, Ramsey M, Ioannidis JP. Inadequacies of physical examination as a cause of medical errors and adverse events: a collection of vignettes. Am J Med 2015; 128:1322–1324.
- Nishigori H, Masuda K, Kikukawa M, et al. A model teaching session for the hypothesis-driven physical examination. Medical Teacher 2011; 33:410–417.
- Mangione S. Physical Diagnosis Secrets, 2nd ed. Philadelphia: Mosby/Elsevier, 2008.
- Verghese A, Charlton B, Kassirer JP, Ramsey M, Ioannidis JP. Inadequacies of physical examination as a cause of medical errors and adverse events: a collection of vignettes. Am J Med 2015; 128:1322–1324.
- Nishigori H, Masuda K, Kikukawa M, et al. A model teaching session for the hypothesis-driven physical examination. Medical Teacher 2011; 33:410–417.