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Magnetic Resonance Imaging of Complications of Anterior Cruciate Ligament Reconstruction
Magnetic resonance imaging (MRI) is the preferred modality in the evaluation of complications of anterior cruciate ligament reconstruction (ACL-R).1-3 ACL-R complications may be broadly characterized as those resulting in decreased range of motion (ROM), eg, arthrofibrosis and impingement, and those resulting in increased laxity, ie, graft disruption.4 Short tau inversion recovery (STIR) sequences best minimize artifact related to field inhomogeneity in the presence of metal-containing fixation devices. Patients with contraindications to MRI may undergo high-resolution computed tomographic arthrography of the knee for evaluation of postoperative graft abnormalities.1
Arthrofibrosis refers to focal or diffuse synovial scar tissue, which may limit ROM. Preoperative irritation, preoperative limited ROM, and reconstruction within 4 weeks of trauma may all play a role in the development of arthrofibrosis.5,6 The focal form, cyclops lesion, named for its arthroscopic appearance, has been reported in 1% to 10% of patients with ACL-R.1 On MRI, focal arthrofibrosis may be seen as a focal or diffuse intermediate signal lesion in the anterior intercondylar notch extending linearly along the intercondylar roof1 (Figure 1).
MRI can be used to accurately determine the position of the femoral and tibial tunnels. Correct femoral tunnel position results in isometry of the graft during full ROM of the knee. Graft impingement can occur when the tibial tunnel is placed too far anteriorly such that the graft contacts the roof of the intercondylar notch before the knee is able to fully extend.7 A tibial tunnel placed anterior to the intersection of the Blumensaat line and the tibia is at higher risk for impingement.1,4 Impingement may be accompanied by signal change in the graft on intermediate-weighted and fluid-sensitive sequences. The signal abnormality is usually focal and persists longer than the expected signal changes related to revascularization of immature grafts within the first year (Figure 2). If left untreated, impingement may progress to graft rupture.4
Complete graft rupture is diagnosed on the basis of discontinuity of the graft fibers. MRI findings include fluid-filled defect or absence of intact graft fibers. Other reliable signs include large joint effusion, anterior tibial translation, pivot-shift–type marrow edema pattern, and horizontal orientation, laxity, or resorption of the graft fibers.1,8,9 The diagnosis of partial graft rupture may be challenging, as there are several other causes of increased graft signal, including revascularization (within 12 months after procedure), signal heterogeneity between individual bundles of hamstring grafts, and focal signal changes related to impingment (Figures 3, 4).
Fluid within the tunnels is a normal finding after surgery and typically resolves within the first 18 months.1 Cyst formation within the tibial tunnel is an uncommon complication of ACL-R and may be incidental to or present with clinical symptoms caused by extension into the pretibial soft tissues or expansion of the tunnel (Figure 5). Communication of cyst with joint space is important, as a noncommunicating cyst requires simple excision without need for bone grafting.7
Hardware-related complications (eg, loosening of fixation devices) are uncommon but may require revision surgery (Figure 6). Septic arthritis after ACL-R has a cumulative incidence of 0.1% to 0.9% and may be difficult to diagnose clinically because of the lack of classic symptoms of a septic joint.1 Diagnosis requires joint aspiration.
MRI is reliably and accurately used to assess ACL-R complications. The clinical history helps in stratifying complications that result in decreased ROM or increased laxity.
1. Bencardino JT, Beltran J, Feldman MI, Rose DJ. MR imaging of complications of anterior cruciate ligament graft reconstruction. Radiographics. 2009;29(7):2115-2126.
2. Recht MP, Kramer J. MR imaging of the postoperative knee: a pictorial essay. Radiographics. 2002;22(4):765-774.
3. Papakonstantinou O, Chung CB, Chanchairujira K, Resnick DL. Complications of anterior cruciate ligament reconstruction: MR imaging. Eur Radiol. 2003;13(5):1106-1117.
4. Meyers AB, Haims AH, Menn K, Moukaddam H. Imaging of anterior cruciate ligament repair and its complications. AJR Am J Roentgenol. 2010;194(2):476-484.
5. Kwok CS, Harrison T, Servant C. The optimal timing for anterior cruciate ligament reconstruction with respect to the risk of postoperative stiffness. Arthroscopy. 2013;29(3):556-565.
6. Mayr HO, Weig TG, Plitz W. Arthrofibrosis following ACL reconstruction—reasons and outcome. Arch Orthop Trauma Surg. 2004;124(8):518-522.
7. Ghazikhanian V, Beltran J, Nikac V, Feldman M, Bencardino JT. Tibial tunnel and pretibial cysts following ACL graft reconstruction: MR imaging diagnosis. Skeletal Radiol. 2012;41(11):1375-1379.
8. Collins MS, Unruh KP, Bond JR, Mandrekar JN. Magnetic resonance imaging of surgically confirmed anterior cruciate ligament graft disruption. Skeletal Radiol. 2008;37(3):233-243.
9. Saupe N, White LM, Chiavaras MM, et al. Anterior cruciate ligament reconstruction grafts: MR imaging features at long-term follow-up—correlation with functional and clinical evaluation. Radiology. 2008;249(2):581-590.
Magnetic resonance imaging (MRI) is the preferred modality in the evaluation of complications of anterior cruciate ligament reconstruction (ACL-R).1-3 ACL-R complications may be broadly characterized as those resulting in decreased range of motion (ROM), eg, arthrofibrosis and impingement, and those resulting in increased laxity, ie, graft disruption.4 Short tau inversion recovery (STIR) sequences best minimize artifact related to field inhomogeneity in the presence of metal-containing fixation devices. Patients with contraindications to MRI may undergo high-resolution computed tomographic arthrography of the knee for evaluation of postoperative graft abnormalities.1
Arthrofibrosis refers to focal or diffuse synovial scar tissue, which may limit ROM. Preoperative irritation, preoperative limited ROM, and reconstruction within 4 weeks of trauma may all play a role in the development of arthrofibrosis.5,6 The focal form, cyclops lesion, named for its arthroscopic appearance, has been reported in 1% to 10% of patients with ACL-R.1 On MRI, focal arthrofibrosis may be seen as a focal or diffuse intermediate signal lesion in the anterior intercondylar notch extending linearly along the intercondylar roof1 (Figure 1).
MRI can be used to accurately determine the position of the femoral and tibial tunnels. Correct femoral tunnel position results in isometry of the graft during full ROM of the knee. Graft impingement can occur when the tibial tunnel is placed too far anteriorly such that the graft contacts the roof of the intercondylar notch before the knee is able to fully extend.7 A tibial tunnel placed anterior to the intersection of the Blumensaat line and the tibia is at higher risk for impingement.1,4 Impingement may be accompanied by signal change in the graft on intermediate-weighted and fluid-sensitive sequences. The signal abnormality is usually focal and persists longer than the expected signal changes related to revascularization of immature grafts within the first year (Figure 2). If left untreated, impingement may progress to graft rupture.4
Complete graft rupture is diagnosed on the basis of discontinuity of the graft fibers. MRI findings include fluid-filled defect or absence of intact graft fibers. Other reliable signs include large joint effusion, anterior tibial translation, pivot-shift–type marrow edema pattern, and horizontal orientation, laxity, or resorption of the graft fibers.1,8,9 The diagnosis of partial graft rupture may be challenging, as there are several other causes of increased graft signal, including revascularization (within 12 months after procedure), signal heterogeneity between individual bundles of hamstring grafts, and focal signal changes related to impingment (Figures 3, 4).
Fluid within the tunnels is a normal finding after surgery and typically resolves within the first 18 months.1 Cyst formation within the tibial tunnel is an uncommon complication of ACL-R and may be incidental to or present with clinical symptoms caused by extension into the pretibial soft tissues or expansion of the tunnel (Figure 5). Communication of cyst with joint space is important, as a noncommunicating cyst requires simple excision without need for bone grafting.7
Hardware-related complications (eg, loosening of fixation devices) are uncommon but may require revision surgery (Figure 6). Septic arthritis after ACL-R has a cumulative incidence of 0.1% to 0.9% and may be difficult to diagnose clinically because of the lack of classic symptoms of a septic joint.1 Diagnosis requires joint aspiration.
MRI is reliably and accurately used to assess ACL-R complications. The clinical history helps in stratifying complications that result in decreased ROM or increased laxity.
Magnetic resonance imaging (MRI) is the preferred modality in the evaluation of complications of anterior cruciate ligament reconstruction (ACL-R).1-3 ACL-R complications may be broadly characterized as those resulting in decreased range of motion (ROM), eg, arthrofibrosis and impingement, and those resulting in increased laxity, ie, graft disruption.4 Short tau inversion recovery (STIR) sequences best minimize artifact related to field inhomogeneity in the presence of metal-containing fixation devices. Patients with contraindications to MRI may undergo high-resolution computed tomographic arthrography of the knee for evaluation of postoperative graft abnormalities.1
Arthrofibrosis refers to focal or diffuse synovial scar tissue, which may limit ROM. Preoperative irritation, preoperative limited ROM, and reconstruction within 4 weeks of trauma may all play a role in the development of arthrofibrosis.5,6 The focal form, cyclops lesion, named for its arthroscopic appearance, has been reported in 1% to 10% of patients with ACL-R.1 On MRI, focal arthrofibrosis may be seen as a focal or diffuse intermediate signal lesion in the anterior intercondylar notch extending linearly along the intercondylar roof1 (Figure 1).
MRI can be used to accurately determine the position of the femoral and tibial tunnels. Correct femoral tunnel position results in isometry of the graft during full ROM of the knee. Graft impingement can occur when the tibial tunnel is placed too far anteriorly such that the graft contacts the roof of the intercondylar notch before the knee is able to fully extend.7 A tibial tunnel placed anterior to the intersection of the Blumensaat line and the tibia is at higher risk for impingement.1,4 Impingement may be accompanied by signal change in the graft on intermediate-weighted and fluid-sensitive sequences. The signal abnormality is usually focal and persists longer than the expected signal changes related to revascularization of immature grafts within the first year (Figure 2). If left untreated, impingement may progress to graft rupture.4
Complete graft rupture is diagnosed on the basis of discontinuity of the graft fibers. MRI findings include fluid-filled defect or absence of intact graft fibers. Other reliable signs include large joint effusion, anterior tibial translation, pivot-shift–type marrow edema pattern, and horizontal orientation, laxity, or resorption of the graft fibers.1,8,9 The diagnosis of partial graft rupture may be challenging, as there are several other causes of increased graft signal, including revascularization (within 12 months after procedure), signal heterogeneity between individual bundles of hamstring grafts, and focal signal changes related to impingment (Figures 3, 4).
Fluid within the tunnels is a normal finding after surgery and typically resolves within the first 18 months.1 Cyst formation within the tibial tunnel is an uncommon complication of ACL-R and may be incidental to or present with clinical symptoms caused by extension into the pretibial soft tissues or expansion of the tunnel (Figure 5). Communication of cyst with joint space is important, as a noncommunicating cyst requires simple excision without need for bone grafting.7
Hardware-related complications (eg, loosening of fixation devices) are uncommon but may require revision surgery (Figure 6). Septic arthritis after ACL-R has a cumulative incidence of 0.1% to 0.9% and may be difficult to diagnose clinically because of the lack of classic symptoms of a septic joint.1 Diagnosis requires joint aspiration.
MRI is reliably and accurately used to assess ACL-R complications. The clinical history helps in stratifying complications that result in decreased ROM or increased laxity.
1. Bencardino JT, Beltran J, Feldman MI, Rose DJ. MR imaging of complications of anterior cruciate ligament graft reconstruction. Radiographics. 2009;29(7):2115-2126.
2. Recht MP, Kramer J. MR imaging of the postoperative knee: a pictorial essay. Radiographics. 2002;22(4):765-774.
3. Papakonstantinou O, Chung CB, Chanchairujira K, Resnick DL. Complications of anterior cruciate ligament reconstruction: MR imaging. Eur Radiol. 2003;13(5):1106-1117.
4. Meyers AB, Haims AH, Menn K, Moukaddam H. Imaging of anterior cruciate ligament repair and its complications. AJR Am J Roentgenol. 2010;194(2):476-484.
5. Kwok CS, Harrison T, Servant C. The optimal timing for anterior cruciate ligament reconstruction with respect to the risk of postoperative stiffness. Arthroscopy. 2013;29(3):556-565.
6. Mayr HO, Weig TG, Plitz W. Arthrofibrosis following ACL reconstruction—reasons and outcome. Arch Orthop Trauma Surg. 2004;124(8):518-522.
7. Ghazikhanian V, Beltran J, Nikac V, Feldman M, Bencardino JT. Tibial tunnel and pretibial cysts following ACL graft reconstruction: MR imaging diagnosis. Skeletal Radiol. 2012;41(11):1375-1379.
8. Collins MS, Unruh KP, Bond JR, Mandrekar JN. Magnetic resonance imaging of surgically confirmed anterior cruciate ligament graft disruption. Skeletal Radiol. 2008;37(3):233-243.
9. Saupe N, White LM, Chiavaras MM, et al. Anterior cruciate ligament reconstruction grafts: MR imaging features at long-term follow-up—correlation with functional and clinical evaluation. Radiology. 2008;249(2):581-590.
1. Bencardino JT, Beltran J, Feldman MI, Rose DJ. MR imaging of complications of anterior cruciate ligament graft reconstruction. Radiographics. 2009;29(7):2115-2126.
2. Recht MP, Kramer J. MR imaging of the postoperative knee: a pictorial essay. Radiographics. 2002;22(4):765-774.
3. Papakonstantinou O, Chung CB, Chanchairujira K, Resnick DL. Complications of anterior cruciate ligament reconstruction: MR imaging. Eur Radiol. 2003;13(5):1106-1117.
4. Meyers AB, Haims AH, Menn K, Moukaddam H. Imaging of anterior cruciate ligament repair and its complications. AJR Am J Roentgenol. 2010;194(2):476-484.
5. Kwok CS, Harrison T, Servant C. The optimal timing for anterior cruciate ligament reconstruction with respect to the risk of postoperative stiffness. Arthroscopy. 2013;29(3):556-565.
6. Mayr HO, Weig TG, Plitz W. Arthrofibrosis following ACL reconstruction—reasons and outcome. Arch Orthop Trauma Surg. 2004;124(8):518-522.
7. Ghazikhanian V, Beltran J, Nikac V, Feldman M, Bencardino JT. Tibial tunnel and pretibial cysts following ACL graft reconstruction: MR imaging diagnosis. Skeletal Radiol. 2012;41(11):1375-1379.
8. Collins MS, Unruh KP, Bond JR, Mandrekar JN. Magnetic resonance imaging of surgically confirmed anterior cruciate ligament graft disruption. Skeletal Radiol. 2008;37(3):233-243.
9. Saupe N, White LM, Chiavaras MM, et al. Anterior cruciate ligament reconstruction grafts: MR imaging features at long-term follow-up—correlation with functional and clinical evaluation. Radiology. 2008;249(2):581-590.
Increased prevalence of pancreatic cysts due to MRI improvements
The apparent increase in the prevalence of incidental pancreatic cysts in recent years may be tied to improvements in MRI scanning technology, results of a study suggest.
Researchers conducted a retrospective analysis of data from 500 patients who underwent an MRI for nonpancreatic indications at a single center between 2005 and 2014; 50 were sampled from each year in chronological order.
A total of 208 patients (41.6%) were found to have an incidental cyst, of which less than a quarter were described in the original MRI report, according to a paper published online in Clinical Gastroenterology and Hepatology.
Analysis showed a very strong association between the type of imaging hardware and software, and the presence of cysts; older hardware found pancreatic cysts in 30.3% of patients and the newest hardware found cysts in 56.3% of patients.
However, MRI field strength was not associated with the frequency of lesion discovery (Clin Gastro Hepatol. 2015 Sep 11. doi: 10.1016/j.cgh.2015.08.038).
Most cysts were relatively small, with a median size of 4 mm. Nearly half of the patients with a cyst only had one described.
Nearly two-thirds of these cysts (62%) had an uncertain diagnosis, but 35% of patients were diagnosed with an intraductal papillary mucinous neoplasm, and one patient showed radiologic evidence of subacute pancreatitis.
When compared to the rest of the cohort, individuals with pancreatic cysts were more likely to be older, have diabetes mellitus, or have a personal history of cancer, particularly nonmelanoma skin cancer and hepatocellular carcinoma.
“Our study demonstrates the relationship between the higher trend of incidental pancreatic cysts observed in the recent years and the improvements in the technical features of MRIs,” wrote Dr. Maria Moris and colleagues from the Mayo Clinic, Jacksonville.
The authors said the real prevalence of pancreatic cystic lesions is estimated to range from 0.2% to 44.7%.
Their finding of a prevalence of 41.6% was higher than that found in similar imaging studies, but the authors suggested some of this may be due to the lack of a size cutoff in their study, as opposed to a 5-mm cutoff used in one earlier study that found a prevalence of 10%.
“Moreover, we believe that we may have even underestimated the real prevalence because of the absence of magnetic resonance cholangiopancreatography sequences (only 19% of the examinations), and the lack of 3-T studies (6% of the MRIs),” they wrote.
The median size of the lesions was lower than those found in previous studies.
“This smaller size was unexpected because, as a result of the exclusion criteria applied, the technical features of the MRIs were not the most specific for [pancreatic cystic lesion] PCL visualization,” the authors wrote, suggesting that this may have been due to the radiologist’s experience in this field.
The study was funded by the Joyce E. Baker Foundation for Research at Mayo Clinic in Jacksonville. One author disclosed grants or travel support from Olympus, Boston Scientific, and Cosmo Pharmaceuticals. There were no other conflicts of interest declared.
The apparent increase in the prevalence of incidental pancreatic cysts in recent years may be tied to improvements in MRI scanning technology, results of a study suggest.
Researchers conducted a retrospective analysis of data from 500 patients who underwent an MRI for nonpancreatic indications at a single center between 2005 and 2014; 50 were sampled from each year in chronological order.
A total of 208 patients (41.6%) were found to have an incidental cyst, of which less than a quarter were described in the original MRI report, according to a paper published online in Clinical Gastroenterology and Hepatology.
Analysis showed a very strong association between the type of imaging hardware and software, and the presence of cysts; older hardware found pancreatic cysts in 30.3% of patients and the newest hardware found cysts in 56.3% of patients.
However, MRI field strength was not associated with the frequency of lesion discovery (Clin Gastro Hepatol. 2015 Sep 11. doi: 10.1016/j.cgh.2015.08.038).
Most cysts were relatively small, with a median size of 4 mm. Nearly half of the patients with a cyst only had one described.
Nearly two-thirds of these cysts (62%) had an uncertain diagnosis, but 35% of patients were diagnosed with an intraductal papillary mucinous neoplasm, and one patient showed radiologic evidence of subacute pancreatitis.
When compared to the rest of the cohort, individuals with pancreatic cysts were more likely to be older, have diabetes mellitus, or have a personal history of cancer, particularly nonmelanoma skin cancer and hepatocellular carcinoma.
“Our study demonstrates the relationship between the higher trend of incidental pancreatic cysts observed in the recent years and the improvements in the technical features of MRIs,” wrote Dr. Maria Moris and colleagues from the Mayo Clinic, Jacksonville.
The authors said the real prevalence of pancreatic cystic lesions is estimated to range from 0.2% to 44.7%.
Their finding of a prevalence of 41.6% was higher than that found in similar imaging studies, but the authors suggested some of this may be due to the lack of a size cutoff in their study, as opposed to a 5-mm cutoff used in one earlier study that found a prevalence of 10%.
“Moreover, we believe that we may have even underestimated the real prevalence because of the absence of magnetic resonance cholangiopancreatography sequences (only 19% of the examinations), and the lack of 3-T studies (6% of the MRIs),” they wrote.
The median size of the lesions was lower than those found in previous studies.
“This smaller size was unexpected because, as a result of the exclusion criteria applied, the technical features of the MRIs were not the most specific for [pancreatic cystic lesion] PCL visualization,” the authors wrote, suggesting that this may have been due to the radiologist’s experience in this field.
The study was funded by the Joyce E. Baker Foundation for Research at Mayo Clinic in Jacksonville. One author disclosed grants or travel support from Olympus, Boston Scientific, and Cosmo Pharmaceuticals. There were no other conflicts of interest declared.
The apparent increase in the prevalence of incidental pancreatic cysts in recent years may be tied to improvements in MRI scanning technology, results of a study suggest.
Researchers conducted a retrospective analysis of data from 500 patients who underwent an MRI for nonpancreatic indications at a single center between 2005 and 2014; 50 were sampled from each year in chronological order.
A total of 208 patients (41.6%) were found to have an incidental cyst, of which less than a quarter were described in the original MRI report, according to a paper published online in Clinical Gastroenterology and Hepatology.
Analysis showed a very strong association between the type of imaging hardware and software, and the presence of cysts; older hardware found pancreatic cysts in 30.3% of patients and the newest hardware found cysts in 56.3% of patients.
However, MRI field strength was not associated with the frequency of lesion discovery (Clin Gastro Hepatol. 2015 Sep 11. doi: 10.1016/j.cgh.2015.08.038).
Most cysts were relatively small, with a median size of 4 mm. Nearly half of the patients with a cyst only had one described.
Nearly two-thirds of these cysts (62%) had an uncertain diagnosis, but 35% of patients were diagnosed with an intraductal papillary mucinous neoplasm, and one patient showed radiologic evidence of subacute pancreatitis.
When compared to the rest of the cohort, individuals with pancreatic cysts were more likely to be older, have diabetes mellitus, or have a personal history of cancer, particularly nonmelanoma skin cancer and hepatocellular carcinoma.
“Our study demonstrates the relationship between the higher trend of incidental pancreatic cysts observed in the recent years and the improvements in the technical features of MRIs,” wrote Dr. Maria Moris and colleagues from the Mayo Clinic, Jacksonville.
The authors said the real prevalence of pancreatic cystic lesions is estimated to range from 0.2% to 44.7%.
Their finding of a prevalence of 41.6% was higher than that found in similar imaging studies, but the authors suggested some of this may be due to the lack of a size cutoff in their study, as opposed to a 5-mm cutoff used in one earlier study that found a prevalence of 10%.
“Moreover, we believe that we may have even underestimated the real prevalence because of the absence of magnetic resonance cholangiopancreatography sequences (only 19% of the examinations), and the lack of 3-T studies (6% of the MRIs),” they wrote.
The median size of the lesions was lower than those found in previous studies.
“This smaller size was unexpected because, as a result of the exclusion criteria applied, the technical features of the MRIs were not the most specific for [pancreatic cystic lesion] PCL visualization,” the authors wrote, suggesting that this may have been due to the radiologist’s experience in this field.
The study was funded by the Joyce E. Baker Foundation for Research at Mayo Clinic in Jacksonville. One author disclosed grants or travel support from Olympus, Boston Scientific, and Cosmo Pharmaceuticals. There were no other conflicts of interest declared.
FROM CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
Key clinical point: The apparent increase of the prevalence of incidental pancreatic cysts in recent years may be tied to improvements in MRI scanning technology.
Major finding: Older MRI hardware found pancreatic cysts in 30.3% of patients and the newest hardware found cysts in 56.3% of patients.
Data source: A retrospective analysis of data from 500 patients who underwent an MRI for nonpancreatic indications.
Disclosures: The study was funded by the Joyce E. Baker Foundation for Research at Mayo Clinic in Jacksonville, Fla. One author disclosed grants or travel support from Olympus, Boston Scientific, and Cosmo Pharmaceuticals. There were no other conflicts of interest declared.
Emergency Ultrasound: Renal Evaluation
Background
Technique
The study is performed with a curvilinear probe placed in the left and right midaxillary region along the lower costal margin. To obtain a longitudinal view of the kidneys, the probe marker should point toward the head of the bed (Figure 1). The clinician should then slide the probe until the kidney comes into view just caudal to either the liver on the right or the spleen on the left. It is important to remember that the kidneys are retroperitoneal; as such, the probe should be pointed toward the bed to ensure visualization.
Hydronephrosis
Ureteral or bladder outlet obstruction can lead to unilateral or bilateral renal hydronephrosis, which can present on a spectrum ranging from mild to severe. As fluid appears black on ultrasound, hydronephrosis will appear black in what is normally an echogenic center of the kidney. The higher the degree of hydronephrosis, the larger the area of black; in cases of severe hydronephrosis, there is thinning of the renal parenchyma and most of the kidney is taken up by dilated calyces (Figure 3). If there is uncertainty during evaluation, color Doppler may be employed to differentiate the vascular renal hilum from hydronephrosis (Figure 4).
Ureteral Stones
Ureteral stones are not typically visualized by ultrasound. However, intrarenal stones can be found. These will appear as hyperechoic structures within the central area of the kidney with acoustic shadowing artifact noted underneath them. Additionally, while scanning the bladder, one can sometimes find a stone lodged in the ureteropelvic junction (UPJ). One can also look for “ureteral jets,” seen as periodic flow of urine within the bladder using color/power Doppler (Figure 5).
Pearls/Pitfalls
Dr Meer is an assistant professor and director of emergency ultrasound, department of emergency medicine, Emory University School of Medicine, Atlanta, Georgia. Dr Beck is an assistant professor, department of emergency medicine, Emory University School of Medicine, Atlanta, Georgia. Dr Taylor is an assistant professor and director of postgraduate medical education, department of emergency medicine, Emory University School of Medicine, Atlanta, Georgia.
- Smith-Bindman R, Aubin C, Bailitz J, et al. Ultrasonography versus computed tomography for suspected nephrolithiasis. N Engl J Med. 2014;371(12):1100-1110.
Background
Technique
The study is performed with a curvilinear probe placed in the left and right midaxillary region along the lower costal margin. To obtain a longitudinal view of the kidneys, the probe marker should point toward the head of the bed (Figure 1). The clinician should then slide the probe until the kidney comes into view just caudal to either the liver on the right or the spleen on the left. It is important to remember that the kidneys are retroperitoneal; as such, the probe should be pointed toward the bed to ensure visualization.
Hydronephrosis
Ureteral or bladder outlet obstruction can lead to unilateral or bilateral renal hydronephrosis, which can present on a spectrum ranging from mild to severe. As fluid appears black on ultrasound, hydronephrosis will appear black in what is normally an echogenic center of the kidney. The higher the degree of hydronephrosis, the larger the area of black; in cases of severe hydronephrosis, there is thinning of the renal parenchyma and most of the kidney is taken up by dilated calyces (Figure 3). If there is uncertainty during evaluation, color Doppler may be employed to differentiate the vascular renal hilum from hydronephrosis (Figure 4).
Ureteral Stones
Ureteral stones are not typically visualized by ultrasound. However, intrarenal stones can be found. These will appear as hyperechoic structures within the central area of the kidney with acoustic shadowing artifact noted underneath them. Additionally, while scanning the bladder, one can sometimes find a stone lodged in the ureteropelvic junction (UPJ). One can also look for “ureteral jets,” seen as periodic flow of urine within the bladder using color/power Doppler (Figure 5).
Pearls/Pitfalls
Dr Meer is an assistant professor and director of emergency ultrasound, department of emergency medicine, Emory University School of Medicine, Atlanta, Georgia. Dr Beck is an assistant professor, department of emergency medicine, Emory University School of Medicine, Atlanta, Georgia. Dr Taylor is an assistant professor and director of postgraduate medical education, department of emergency medicine, Emory University School of Medicine, Atlanta, Georgia.
Background
Technique
The study is performed with a curvilinear probe placed in the left and right midaxillary region along the lower costal margin. To obtain a longitudinal view of the kidneys, the probe marker should point toward the head of the bed (Figure 1). The clinician should then slide the probe until the kidney comes into view just caudal to either the liver on the right or the spleen on the left. It is important to remember that the kidneys are retroperitoneal; as such, the probe should be pointed toward the bed to ensure visualization.
Hydronephrosis
Ureteral or bladder outlet obstruction can lead to unilateral or bilateral renal hydronephrosis, which can present on a spectrum ranging from mild to severe. As fluid appears black on ultrasound, hydronephrosis will appear black in what is normally an echogenic center of the kidney. The higher the degree of hydronephrosis, the larger the area of black; in cases of severe hydronephrosis, there is thinning of the renal parenchyma and most of the kidney is taken up by dilated calyces (Figure 3). If there is uncertainty during evaluation, color Doppler may be employed to differentiate the vascular renal hilum from hydronephrosis (Figure 4).
Ureteral Stones
Ureteral stones are not typically visualized by ultrasound. However, intrarenal stones can be found. These will appear as hyperechoic structures within the central area of the kidney with acoustic shadowing artifact noted underneath them. Additionally, while scanning the bladder, one can sometimes find a stone lodged in the ureteropelvic junction (UPJ). One can also look for “ureteral jets,” seen as periodic flow of urine within the bladder using color/power Doppler (Figure 5).
Pearls/Pitfalls
Dr Meer is an assistant professor and director of emergency ultrasound, department of emergency medicine, Emory University School of Medicine, Atlanta, Georgia. Dr Beck is an assistant professor, department of emergency medicine, Emory University School of Medicine, Atlanta, Georgia. Dr Taylor is an assistant professor and director of postgraduate medical education, department of emergency medicine, Emory University School of Medicine, Atlanta, Georgia.
- Smith-Bindman R, Aubin C, Bailitz J, et al. Ultrasonography versus computed tomography for suspected nephrolithiasis. N Engl J Med. 2014;371(12):1100-1110.
- Smith-Bindman R, Aubin C, Bailitz J, et al. Ultrasonography versus computed tomography for suspected nephrolithiasis. N Engl J Med. 2014;371(12):1100-1110.
Case Report: An Unusual Case of Morel-Lavallée Lesion of the Upper Extremity
Case
A 32-year-old previously healthy woman presented to the ED with right upper arm pain and swelling of 6 days duration. According to the patient, the swelling began 2 days after she sustained a work-related injury at a coin-manufacturing factory. She stated that her right arm had gotten caught inside of a rolling press while she was cleaning it. The roller had stopped over her upper arm, trapping it between the roller and the platform for several minutes before it was extricated. She was brought to the ED by emergency medical services for evaluation immediately following this incident. At this first visit to the ED, the patient complained of mild pain in her right arm. Physical examination at that time revealed mild diffuse swelling extending from her hand to her distal humerus, with mild pain on passive flexion, and extension without associated numbness or tingling. Plain films of her right upper extremity were ordered, the results of which were relatively unremarkable. She was evaluated by an orthopedist, who ruled out compartment syndrome based on her benign physical examination and soft compartments. She was ultimately discharged and told to follow up with her primary care provider.
Over the course of 48 hours from the first ED visit, the patient developed large bullae on the dorsal and volar aspect of her forearm, elbow, and upper arm with associated pain. In addition to dark discolorations of the skin over her affected arm, she noticed that the bullae had become numerous and discolored. These symptoms continued to grow progressively worse, prompting her second presentation to the ED.
The patient was taken to the operating room and underwent debridement and resection of the circumferential necrotic skin and subcutaneous tissue in her right arm, and the placement of a skin graft with overlying wound vacuum-assisted closure. During the procedure, a large amount of serosanguinous fluid was drained and cultured, and was found to be sterile. Due to the size of her injury, she underwent two additional episodes of debridement and graft placement over the course of the next 2 weeks.
Discussion
First described in the 1850s by the French physician Maurice Morel-Lavallée, Morel-Lavallée lesion is a rare, traumatic, soft-tissue injury.1 It is an internal degloving injury wherein the skin and subcutaneous tissue have been forcibly separated from the underlying fascia as a result of shear stress. The lymphatic and blood vessels between the layers are also disrupted in this process, resulting in the accumulation of blood and lymphatic fluid as well as subcutaneous debris in the potential space that forms. Excess accumulation over time can compromise blood supply to the overlying skin and cause necrosis.2 Morel-Lavallée lesion is missed on initial evaluation in up to one-third of the cases and may have a delay in presentation ranging from hours to months after the inciting injury.3
Morel-Lavallée lesions typically involve the flank, hips, thigh, and prepatellar regions as a result of shear injuries sustained from bicycle falls and motor vehicle accidents.4 These lesions are often associated with concomitant acetabular and pelvic fractures.5 Involvement of the upper extremities is unusual. Typically, presentation consists of a fluctuant and painful mass underneath the skin which increases over time. The overlying skin may show the mechanism of the original injury, for example, as abrasions after a crush injury. The excessive skin necrosis and hemorrhagic bullae seen in this particular case is a very rare presentation.
Differential Diagnosis
The differential diagnosis includes compartment syndrome, coma blisters, a missed fracture, bullous pemphigoid, bullous drug reactions, and linear immunoglobulin A disease. Most of these conditions were easily ruled out in this case as the patient was previously healthy and not on any medications. The lesions in this case could have been confused with coma blisters, which are similar in appearance, self-limiting, and can develop on the extremities. However, coma blisters are classically associated with toxicity from various central nervous system depressants, as well as reduced consciousness from other causes—all of which were readily ruled-out based on the patient’s history. Moreover, the Morel-Lavallée lesion is a degloving injury of the subcutaneous tissue from the fascia underneath, whereas the pathology of coma blisters includes subepidermal bullae formation as well as immunoglobulin and complement deposition.6
Diagnostic Imaging
Morel-Lavallée lesion can often be confirmed via several imaging modalities, including ultrasound, CT, 3D CT, or magnetic resonance imaging (MRI).3,7 Ultrasound will usually show a well-circumscribed hypoechoic fluid collection with hyperechoic fat globules from the subcutaneous tissue, whereas CT tends to show an encapsulated mass with fluid collection underneath. In MRI, Morel-Lavallée lesion often appears as a hypointense T1-sequence and hyperintense T2-sequence similar to most other fluid collections. There may be variable T1- and T2-intensities with subcutaneous tissues in the fluid collection.2
Management
Despite recognition of this disease entity, controversies still exist regarding management. Case reports have demonstrated a relatively high rate of infected fluid collections depending on the chronicity of the injury.8 A recent algorithm to management described by Nickerson et al4 proposes that for patients with viable skin, percutaneous aspiration of more than 50 cc of fluid from these lesions should be treated with more extensive operative intervention based on the increased likelihood of recurrence. Patients without viable skin require formal debridement with possible skin grafting.
Other treatment options include conservative management, surgical drainage, sclerodesis, and extensive open surgery.8-10 Management is always case-based and dependent upon the size of the lesion and associated injuries.
Conclusion
This case represents an example of Morel-Lavallée lesions in their most severe and atypical form. It also serves as a reminder that vigilance and knowledge of this disease process is important in helping to diagnose this rare but potentially devastating condition. The key to recognizing this injury lies in keeping this disease process in the differential diagnosis of traumatic injuries with suspicious mechanism involving significant shear forces. Significant physical examination findings may not be present initially and evolve over a time period of hours to days. Once this injury is identified, management hinges on the size of the lesion and affected body part. Despite timely interventions, Morel-Lavallée lesions may result in significant morbidity and functional disability.
Dr Ye is an emergency medicine resident at the Brown Alpert Medical School in Providence, Rhode Island. Dr Rosenberg is a clinical assistant professor at Brown Alpert Medical School, and an emergency medicine attending physican at Rhode Island Hospital and The Miriam Hospital, Providence, Rhode Island.
- Morel-Lavallée M. Epanchements traumatique de serosite. Arc Générales Méd. 1853;691-731.
- Chokshi F, Jose J, Clifford P. Morel Lavallée Lesion. Am J Orthop (Belle Mead NJ). 2010;39(5): 252-253.
- Bonilla-Yoon I, Masih S, Patel DB, et al. The Morel-Lavallée lesion: pathophysiology, clinical presentation, imaging features, and treatment options. Emerg Radiol. 2014;21(1):35-43.
- Nickerson T, Zielinski M, Jenkins D, Schiller HJ. The Mayo Clinic experience with Morel-Lavallée lesions: establishment of a practice management guideline. J Trauma Acute Care Surg. 2014:76(2);493-497.
- Powers ML, Hatem SF, Sundaram M. Morel-Lavallee lesion. Orthopedics. 2007;30(4):322-323.
- Agarwal A, Bansal M, Conner K. Coma blisters with hypoxemic respiratory failure. Dermatol Online Journal. 2012:18(3);10.
- Reddix RN, Carrol E, Webb LX. Early diagnosis of a Morel-Lavallee lesion using three-dimensional computed tomography reconstructions: a case report. J Trauma. 2009;67(2):e57-e59.
- Lin HL, Lee WC, Kuo LC, Chen CW. Closed internal degloving injury with conservative treatment. Am J Emerg Med. 2008:26(2);254.e5-e6.
- Luria S, Applbaum Y,Weil Y, Liebergall M, Peyser A. Talc sclerodhesis of persistent Morel-Lavallée lesions (posttraumatic pseudocysts): case report of 4 patients. J Orthop Trauma. 2006;20(6):435-438.
- Penaud A, Quignon R, Danin A, Bahé L, Zakine G. Alcohol sclerodhesis: an innovative treatment for chronic Morel-Lavallée lesions. J Plast Reconstr Aesthet Surg. 2011;64(10): e262-264.
Case
A 32-year-old previously healthy woman presented to the ED with right upper arm pain and swelling of 6 days duration. According to the patient, the swelling began 2 days after she sustained a work-related injury at a coin-manufacturing factory. She stated that her right arm had gotten caught inside of a rolling press while she was cleaning it. The roller had stopped over her upper arm, trapping it between the roller and the platform for several minutes before it was extricated. She was brought to the ED by emergency medical services for evaluation immediately following this incident. At this first visit to the ED, the patient complained of mild pain in her right arm. Physical examination at that time revealed mild diffuse swelling extending from her hand to her distal humerus, with mild pain on passive flexion, and extension without associated numbness or tingling. Plain films of her right upper extremity were ordered, the results of which were relatively unremarkable. She was evaluated by an orthopedist, who ruled out compartment syndrome based on her benign physical examination and soft compartments. She was ultimately discharged and told to follow up with her primary care provider.
Over the course of 48 hours from the first ED visit, the patient developed large bullae on the dorsal and volar aspect of her forearm, elbow, and upper arm with associated pain. In addition to dark discolorations of the skin over her affected arm, she noticed that the bullae had become numerous and discolored. These symptoms continued to grow progressively worse, prompting her second presentation to the ED.
The patient was taken to the operating room and underwent debridement and resection of the circumferential necrotic skin and subcutaneous tissue in her right arm, and the placement of a skin graft with overlying wound vacuum-assisted closure. During the procedure, a large amount of serosanguinous fluid was drained and cultured, and was found to be sterile. Due to the size of her injury, she underwent two additional episodes of debridement and graft placement over the course of the next 2 weeks.
Discussion
First described in the 1850s by the French physician Maurice Morel-Lavallée, Morel-Lavallée lesion is a rare, traumatic, soft-tissue injury.1 It is an internal degloving injury wherein the skin and subcutaneous tissue have been forcibly separated from the underlying fascia as a result of shear stress. The lymphatic and blood vessels between the layers are also disrupted in this process, resulting in the accumulation of blood and lymphatic fluid as well as subcutaneous debris in the potential space that forms. Excess accumulation over time can compromise blood supply to the overlying skin and cause necrosis.2 Morel-Lavallée lesion is missed on initial evaluation in up to one-third of the cases and may have a delay in presentation ranging from hours to months after the inciting injury.3
Morel-Lavallée lesions typically involve the flank, hips, thigh, and prepatellar regions as a result of shear injuries sustained from bicycle falls and motor vehicle accidents.4 These lesions are often associated with concomitant acetabular and pelvic fractures.5 Involvement of the upper extremities is unusual. Typically, presentation consists of a fluctuant and painful mass underneath the skin which increases over time. The overlying skin may show the mechanism of the original injury, for example, as abrasions after a crush injury. The excessive skin necrosis and hemorrhagic bullae seen in this particular case is a very rare presentation.
Differential Diagnosis
The differential diagnosis includes compartment syndrome, coma blisters, a missed fracture, bullous pemphigoid, bullous drug reactions, and linear immunoglobulin A disease. Most of these conditions were easily ruled out in this case as the patient was previously healthy and not on any medications. The lesions in this case could have been confused with coma blisters, which are similar in appearance, self-limiting, and can develop on the extremities. However, coma blisters are classically associated with toxicity from various central nervous system depressants, as well as reduced consciousness from other causes—all of which were readily ruled-out based on the patient’s history. Moreover, the Morel-Lavallée lesion is a degloving injury of the subcutaneous tissue from the fascia underneath, whereas the pathology of coma blisters includes subepidermal bullae formation as well as immunoglobulin and complement deposition.6
Diagnostic Imaging
Morel-Lavallée lesion can often be confirmed via several imaging modalities, including ultrasound, CT, 3D CT, or magnetic resonance imaging (MRI).3,7 Ultrasound will usually show a well-circumscribed hypoechoic fluid collection with hyperechoic fat globules from the subcutaneous tissue, whereas CT tends to show an encapsulated mass with fluid collection underneath. In MRI, Morel-Lavallée lesion often appears as a hypointense T1-sequence and hyperintense T2-sequence similar to most other fluid collections. There may be variable T1- and T2-intensities with subcutaneous tissues in the fluid collection.2
Management
Despite recognition of this disease entity, controversies still exist regarding management. Case reports have demonstrated a relatively high rate of infected fluid collections depending on the chronicity of the injury.8 A recent algorithm to management described by Nickerson et al4 proposes that for patients with viable skin, percutaneous aspiration of more than 50 cc of fluid from these lesions should be treated with more extensive operative intervention based on the increased likelihood of recurrence. Patients without viable skin require formal debridement with possible skin grafting.
Other treatment options include conservative management, surgical drainage, sclerodesis, and extensive open surgery.8-10 Management is always case-based and dependent upon the size of the lesion and associated injuries.
Conclusion
This case represents an example of Morel-Lavallée lesions in their most severe and atypical form. It also serves as a reminder that vigilance and knowledge of this disease process is important in helping to diagnose this rare but potentially devastating condition. The key to recognizing this injury lies in keeping this disease process in the differential diagnosis of traumatic injuries with suspicious mechanism involving significant shear forces. Significant physical examination findings may not be present initially and evolve over a time period of hours to days. Once this injury is identified, management hinges on the size of the lesion and affected body part. Despite timely interventions, Morel-Lavallée lesions may result in significant morbidity and functional disability.
Dr Ye is an emergency medicine resident at the Brown Alpert Medical School in Providence, Rhode Island. Dr Rosenberg is a clinical assistant professor at Brown Alpert Medical School, and an emergency medicine attending physican at Rhode Island Hospital and The Miriam Hospital, Providence, Rhode Island.
Case
A 32-year-old previously healthy woman presented to the ED with right upper arm pain and swelling of 6 days duration. According to the patient, the swelling began 2 days after she sustained a work-related injury at a coin-manufacturing factory. She stated that her right arm had gotten caught inside of a rolling press while she was cleaning it. The roller had stopped over her upper arm, trapping it between the roller and the platform for several minutes before it was extricated. She was brought to the ED by emergency medical services for evaluation immediately following this incident. At this first visit to the ED, the patient complained of mild pain in her right arm. Physical examination at that time revealed mild diffuse swelling extending from her hand to her distal humerus, with mild pain on passive flexion, and extension without associated numbness or tingling. Plain films of her right upper extremity were ordered, the results of which were relatively unremarkable. She was evaluated by an orthopedist, who ruled out compartment syndrome based on her benign physical examination and soft compartments. She was ultimately discharged and told to follow up with her primary care provider.
Over the course of 48 hours from the first ED visit, the patient developed large bullae on the dorsal and volar aspect of her forearm, elbow, and upper arm with associated pain. In addition to dark discolorations of the skin over her affected arm, she noticed that the bullae had become numerous and discolored. These symptoms continued to grow progressively worse, prompting her second presentation to the ED.
The patient was taken to the operating room and underwent debridement and resection of the circumferential necrotic skin and subcutaneous tissue in her right arm, and the placement of a skin graft with overlying wound vacuum-assisted closure. During the procedure, a large amount of serosanguinous fluid was drained and cultured, and was found to be sterile. Due to the size of her injury, she underwent two additional episodes of debridement and graft placement over the course of the next 2 weeks.
Discussion
First described in the 1850s by the French physician Maurice Morel-Lavallée, Morel-Lavallée lesion is a rare, traumatic, soft-tissue injury.1 It is an internal degloving injury wherein the skin and subcutaneous tissue have been forcibly separated from the underlying fascia as a result of shear stress. The lymphatic and blood vessels between the layers are also disrupted in this process, resulting in the accumulation of blood and lymphatic fluid as well as subcutaneous debris in the potential space that forms. Excess accumulation over time can compromise blood supply to the overlying skin and cause necrosis.2 Morel-Lavallée lesion is missed on initial evaluation in up to one-third of the cases and may have a delay in presentation ranging from hours to months after the inciting injury.3
Morel-Lavallée lesions typically involve the flank, hips, thigh, and prepatellar regions as a result of shear injuries sustained from bicycle falls and motor vehicle accidents.4 These lesions are often associated with concomitant acetabular and pelvic fractures.5 Involvement of the upper extremities is unusual. Typically, presentation consists of a fluctuant and painful mass underneath the skin which increases over time. The overlying skin may show the mechanism of the original injury, for example, as abrasions after a crush injury. The excessive skin necrosis and hemorrhagic bullae seen in this particular case is a very rare presentation.
Differential Diagnosis
The differential diagnosis includes compartment syndrome, coma blisters, a missed fracture, bullous pemphigoid, bullous drug reactions, and linear immunoglobulin A disease. Most of these conditions were easily ruled out in this case as the patient was previously healthy and not on any medications. The lesions in this case could have been confused with coma blisters, which are similar in appearance, self-limiting, and can develop on the extremities. However, coma blisters are classically associated with toxicity from various central nervous system depressants, as well as reduced consciousness from other causes—all of which were readily ruled-out based on the patient’s history. Moreover, the Morel-Lavallée lesion is a degloving injury of the subcutaneous tissue from the fascia underneath, whereas the pathology of coma blisters includes subepidermal bullae formation as well as immunoglobulin and complement deposition.6
Diagnostic Imaging
Morel-Lavallée lesion can often be confirmed via several imaging modalities, including ultrasound, CT, 3D CT, or magnetic resonance imaging (MRI).3,7 Ultrasound will usually show a well-circumscribed hypoechoic fluid collection with hyperechoic fat globules from the subcutaneous tissue, whereas CT tends to show an encapsulated mass with fluid collection underneath. In MRI, Morel-Lavallée lesion often appears as a hypointense T1-sequence and hyperintense T2-sequence similar to most other fluid collections. There may be variable T1- and T2-intensities with subcutaneous tissues in the fluid collection.2
Management
Despite recognition of this disease entity, controversies still exist regarding management. Case reports have demonstrated a relatively high rate of infected fluid collections depending on the chronicity of the injury.8 A recent algorithm to management described by Nickerson et al4 proposes that for patients with viable skin, percutaneous aspiration of more than 50 cc of fluid from these lesions should be treated with more extensive operative intervention based on the increased likelihood of recurrence. Patients without viable skin require formal debridement with possible skin grafting.
Other treatment options include conservative management, surgical drainage, sclerodesis, and extensive open surgery.8-10 Management is always case-based and dependent upon the size of the lesion and associated injuries.
Conclusion
This case represents an example of Morel-Lavallée lesions in their most severe and atypical form. It also serves as a reminder that vigilance and knowledge of this disease process is important in helping to diagnose this rare but potentially devastating condition. The key to recognizing this injury lies in keeping this disease process in the differential diagnosis of traumatic injuries with suspicious mechanism involving significant shear forces. Significant physical examination findings may not be present initially and evolve over a time period of hours to days. Once this injury is identified, management hinges on the size of the lesion and affected body part. Despite timely interventions, Morel-Lavallée lesions may result in significant morbidity and functional disability.
Dr Ye is an emergency medicine resident at the Brown Alpert Medical School in Providence, Rhode Island. Dr Rosenberg is a clinical assistant professor at Brown Alpert Medical School, and an emergency medicine attending physican at Rhode Island Hospital and The Miriam Hospital, Providence, Rhode Island.
- Morel-Lavallée M. Epanchements traumatique de serosite. Arc Générales Méd. 1853;691-731.
- Chokshi F, Jose J, Clifford P. Morel Lavallée Lesion. Am J Orthop (Belle Mead NJ). 2010;39(5): 252-253.
- Bonilla-Yoon I, Masih S, Patel DB, et al. The Morel-Lavallée lesion: pathophysiology, clinical presentation, imaging features, and treatment options. Emerg Radiol. 2014;21(1):35-43.
- Nickerson T, Zielinski M, Jenkins D, Schiller HJ. The Mayo Clinic experience with Morel-Lavallée lesions: establishment of a practice management guideline. J Trauma Acute Care Surg. 2014:76(2);493-497.
- Powers ML, Hatem SF, Sundaram M. Morel-Lavallee lesion. Orthopedics. 2007;30(4):322-323.
- Agarwal A, Bansal M, Conner K. Coma blisters with hypoxemic respiratory failure. Dermatol Online Journal. 2012:18(3);10.
- Reddix RN, Carrol E, Webb LX. Early diagnosis of a Morel-Lavallee lesion using three-dimensional computed tomography reconstructions: a case report. J Trauma. 2009;67(2):e57-e59.
- Lin HL, Lee WC, Kuo LC, Chen CW. Closed internal degloving injury with conservative treatment. Am J Emerg Med. 2008:26(2);254.e5-e6.
- Luria S, Applbaum Y,Weil Y, Liebergall M, Peyser A. Talc sclerodhesis of persistent Morel-Lavallée lesions (posttraumatic pseudocysts): case report of 4 patients. J Orthop Trauma. 2006;20(6):435-438.
- Penaud A, Quignon R, Danin A, Bahé L, Zakine G. Alcohol sclerodhesis: an innovative treatment for chronic Morel-Lavallée lesions. J Plast Reconstr Aesthet Surg. 2011;64(10): e262-264.
- Morel-Lavallée M. Epanchements traumatique de serosite. Arc Générales Méd. 1853;691-731.
- Chokshi F, Jose J, Clifford P. Morel Lavallée Lesion. Am J Orthop (Belle Mead NJ). 2010;39(5): 252-253.
- Bonilla-Yoon I, Masih S, Patel DB, et al. The Morel-Lavallée lesion: pathophysiology, clinical presentation, imaging features, and treatment options. Emerg Radiol. 2014;21(1):35-43.
- Nickerson T, Zielinski M, Jenkins D, Schiller HJ. The Mayo Clinic experience with Morel-Lavallée lesions: establishment of a practice management guideline. J Trauma Acute Care Surg. 2014:76(2);493-497.
- Powers ML, Hatem SF, Sundaram M. Morel-Lavallee lesion. Orthopedics. 2007;30(4):322-323.
- Agarwal A, Bansal M, Conner K. Coma blisters with hypoxemic respiratory failure. Dermatol Online Journal. 2012:18(3);10.
- Reddix RN, Carrol E, Webb LX. Early diagnosis of a Morel-Lavallee lesion using three-dimensional computed tomography reconstructions: a case report. J Trauma. 2009;67(2):e57-e59.
- Lin HL, Lee WC, Kuo LC, Chen CW. Closed internal degloving injury with conservative treatment. Am J Emerg Med. 2008:26(2);254.e5-e6.
- Luria S, Applbaum Y,Weil Y, Liebergall M, Peyser A. Talc sclerodhesis of persistent Morel-Lavallée lesions (posttraumatic pseudocysts): case report of 4 patients. J Orthop Trauma. 2006;20(6):435-438.
- Penaud A, Quignon R, Danin A, Bahé L, Zakine G. Alcohol sclerodhesis: an innovative treatment for chronic Morel-Lavallée lesions. J Plast Reconstr Aesthet Surg. 2011;64(10): e262-264.
An alerting sign: Enlarged cardiac silhouette
A 75-year-old woman with a history of hypertension and left-lung lobectomy for a carcinoid tumor 10 years ago presented with a 2-week history of progressive cough, dyspnea, and fatigue. Her heart rate was 159 beats per minute with an irregularly irregular rhythm, and her respiratory rate was 36 breaths per minute. Her blood pressure was 140/90 mm Hg. Examination revealed decreased breath sounds and dullness on percussion at the left lung base, jugular venous distention with a positive hepatojugular reflux sign, and an enlarged liver. Electrocardiography showed atrial fibrillation. Chest radiography (Figure 1) revealed enlargement of the cardiac silhouette, with a disproportionately increased transverse diameter, and an obscured left costophrenic angle. A radiograph taken 13 months earlier (Figure 1) had shown a normal cardiothoracic ratio.
EVALUATION OF PERICARDIAL EFFUSION
Pericardial effusion should be suspected in patients presenting with symptoms of impaired cardiac function such as fatigue, dyspnea, nausea, palpitations, lightheadedness, cough, and hoarseness. Patients may also present with chest pain, often decreased by sitting up and leaning forward and exacerbated by lying supine.
Physical examination may reveal distant heart sounds, an absent or displaced apical impulse, dullness and increased fremitus beneath the angle of the left scapula (the Ewart sign), pulsus paradoxus, and nonspecific findings such as tachycardia and hypotension. Jugular venous distention, hepatojugular reflux, and peripheral edema suggest impaired cardiac function.
A chest radiograph showing unexplained new symmetric cardiomegaly (which is often globe-shaped) without signs of pulmonary congestion1 or with a left dominant pleural effusion is an indicator of pericardial effusion, as in our patient. Pericardial fluid may be seen outlining the heart between the epicardial and mediastinal fat, posterior to the sternum in a lateral view.
Other common causes of cardiomegaly include hypertension, congestive heart failure, valvular disease, cardiomyopathy, ischemic heart disease, and pulmonary disease.
Once pericardial effusion is suspected, the next step is to confirm its presence and determine its hemodynamic significance. Transthoracic echocardiography is the imaging test of choice to confirm effusion, as it can be done rapidly and in unstable patients.2
If transthoracic echocardiography is nondiagnostic but suspicion is high, further evaluation may include transesophageal echocardiography,3 computed tomography, or magnetic resonance imaging.
MAKING THE DIAGNOSIS
Pericardial effusion can occur as part of various diseases involving the pericardium, eg, acute pericarditis, myocarditis, autoimmune disease, postmyocardial infarction, malignancy, aortic dissection, and chest trauma. It can also be associated with certain drugs.
In our patient, echocardiography (Figure 2, Figure 3) demonstrated a large amount of pericardial fluid, and 820 mL of red fluid was aspirated by pericardiocentesis, resulting in relief of her respiratory symptoms. Subcostal two-dimensional echocardiography demonstrated rocking of the heart and intermittent right-ventricular collapse (watch video at www.ccjm.org). Flow cytometry demonstrated 10% kappa+ monoclonal cells. Bone marrow biopsy with immunohistochemical staining revealed infiltration by CD20+, CD5+, CD23+, and BCL1– cells, compatible with small lymphocytic lymphoma.
MALIGNANT PERICARDIAL EFFUSION
Pericardial disease can be the first manifestation of malignancy,4 more often when the patient presents with a large pericardial effusion or tamponade. Malignant tumors of the lung, breast, and esophagus—as well as lymphoma, leukemia, and melanoma—often spread to the pericardium directly or through the lymphatic vessels or bloodstream.4 In our patient, corticosteroid treatment was initiated, and echocardiography at a follow-up visit 2 months later showed no pericardial fluid.
- Khandaker MH, Espinosa RE, Nishimura RA, et al. Pericardial disease: diagnosis and management. Mayo Clin Proc 2010; 85:572–593.
- Cheitlin MD, Armstrong WF, Aurigemma GP, et al; American College of Cardiology; American Heart Association; American Society of Echocardiography. ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASE Committee to Update the 1997 Guidelines for the Clinical Application of Echocardiography). Circulation 2003; 108:1146–1162.
- Verhaert D, Gabriel RS, Johnston D, Lytle BW, Desai MY, Klein AL. The role of multimodality imaging in the management of pericardial disease. Circ Cardiovascular Imaging 2010; 3:333–343.
- Burazor I, Imazio M, Markel G, Adler Y. Malignant pericardial effusion. Cardiology 2013; 124:224–232.
A 75-year-old woman with a history of hypertension and left-lung lobectomy for a carcinoid tumor 10 years ago presented with a 2-week history of progressive cough, dyspnea, and fatigue. Her heart rate was 159 beats per minute with an irregularly irregular rhythm, and her respiratory rate was 36 breaths per minute. Her blood pressure was 140/90 mm Hg. Examination revealed decreased breath sounds and dullness on percussion at the left lung base, jugular venous distention with a positive hepatojugular reflux sign, and an enlarged liver. Electrocardiography showed atrial fibrillation. Chest radiography (Figure 1) revealed enlargement of the cardiac silhouette, with a disproportionately increased transverse diameter, and an obscured left costophrenic angle. A radiograph taken 13 months earlier (Figure 1) had shown a normal cardiothoracic ratio.
EVALUATION OF PERICARDIAL EFFUSION
Pericardial effusion should be suspected in patients presenting with symptoms of impaired cardiac function such as fatigue, dyspnea, nausea, palpitations, lightheadedness, cough, and hoarseness. Patients may also present with chest pain, often decreased by sitting up and leaning forward and exacerbated by lying supine.
Physical examination may reveal distant heart sounds, an absent or displaced apical impulse, dullness and increased fremitus beneath the angle of the left scapula (the Ewart sign), pulsus paradoxus, and nonspecific findings such as tachycardia and hypotension. Jugular venous distention, hepatojugular reflux, and peripheral edema suggest impaired cardiac function.
A chest radiograph showing unexplained new symmetric cardiomegaly (which is often globe-shaped) without signs of pulmonary congestion1 or with a left dominant pleural effusion is an indicator of pericardial effusion, as in our patient. Pericardial fluid may be seen outlining the heart between the epicardial and mediastinal fat, posterior to the sternum in a lateral view.
Other common causes of cardiomegaly include hypertension, congestive heart failure, valvular disease, cardiomyopathy, ischemic heart disease, and pulmonary disease.
Once pericardial effusion is suspected, the next step is to confirm its presence and determine its hemodynamic significance. Transthoracic echocardiography is the imaging test of choice to confirm effusion, as it can be done rapidly and in unstable patients.2
If transthoracic echocardiography is nondiagnostic but suspicion is high, further evaluation may include transesophageal echocardiography,3 computed tomography, or magnetic resonance imaging.
MAKING THE DIAGNOSIS
Pericardial effusion can occur as part of various diseases involving the pericardium, eg, acute pericarditis, myocarditis, autoimmune disease, postmyocardial infarction, malignancy, aortic dissection, and chest trauma. It can also be associated with certain drugs.
In our patient, echocardiography (Figure 2, Figure 3) demonstrated a large amount of pericardial fluid, and 820 mL of red fluid was aspirated by pericardiocentesis, resulting in relief of her respiratory symptoms. Subcostal two-dimensional echocardiography demonstrated rocking of the heart and intermittent right-ventricular collapse (watch video at www.ccjm.org). Flow cytometry demonstrated 10% kappa+ monoclonal cells. Bone marrow biopsy with immunohistochemical staining revealed infiltration by CD20+, CD5+, CD23+, and BCL1– cells, compatible with small lymphocytic lymphoma.
MALIGNANT PERICARDIAL EFFUSION
Pericardial disease can be the first manifestation of malignancy,4 more often when the patient presents with a large pericardial effusion or tamponade. Malignant tumors of the lung, breast, and esophagus—as well as lymphoma, leukemia, and melanoma—often spread to the pericardium directly or through the lymphatic vessels or bloodstream.4 In our patient, corticosteroid treatment was initiated, and echocardiography at a follow-up visit 2 months later showed no pericardial fluid.
A 75-year-old woman with a history of hypertension and left-lung lobectomy for a carcinoid tumor 10 years ago presented with a 2-week history of progressive cough, dyspnea, and fatigue. Her heart rate was 159 beats per minute with an irregularly irregular rhythm, and her respiratory rate was 36 breaths per minute. Her blood pressure was 140/90 mm Hg. Examination revealed decreased breath sounds and dullness on percussion at the left lung base, jugular venous distention with a positive hepatojugular reflux sign, and an enlarged liver. Electrocardiography showed atrial fibrillation. Chest radiography (Figure 1) revealed enlargement of the cardiac silhouette, with a disproportionately increased transverse diameter, and an obscured left costophrenic angle. A radiograph taken 13 months earlier (Figure 1) had shown a normal cardiothoracic ratio.
EVALUATION OF PERICARDIAL EFFUSION
Pericardial effusion should be suspected in patients presenting with symptoms of impaired cardiac function such as fatigue, dyspnea, nausea, palpitations, lightheadedness, cough, and hoarseness. Patients may also present with chest pain, often decreased by sitting up and leaning forward and exacerbated by lying supine.
Physical examination may reveal distant heart sounds, an absent or displaced apical impulse, dullness and increased fremitus beneath the angle of the left scapula (the Ewart sign), pulsus paradoxus, and nonspecific findings such as tachycardia and hypotension. Jugular venous distention, hepatojugular reflux, and peripheral edema suggest impaired cardiac function.
A chest radiograph showing unexplained new symmetric cardiomegaly (which is often globe-shaped) without signs of pulmonary congestion1 or with a left dominant pleural effusion is an indicator of pericardial effusion, as in our patient. Pericardial fluid may be seen outlining the heart between the epicardial and mediastinal fat, posterior to the sternum in a lateral view.
Other common causes of cardiomegaly include hypertension, congestive heart failure, valvular disease, cardiomyopathy, ischemic heart disease, and pulmonary disease.
Once pericardial effusion is suspected, the next step is to confirm its presence and determine its hemodynamic significance. Transthoracic echocardiography is the imaging test of choice to confirm effusion, as it can be done rapidly and in unstable patients.2
If transthoracic echocardiography is nondiagnostic but suspicion is high, further evaluation may include transesophageal echocardiography,3 computed tomography, or magnetic resonance imaging.
MAKING THE DIAGNOSIS
Pericardial effusion can occur as part of various diseases involving the pericardium, eg, acute pericarditis, myocarditis, autoimmune disease, postmyocardial infarction, malignancy, aortic dissection, and chest trauma. It can also be associated with certain drugs.
In our patient, echocardiography (Figure 2, Figure 3) demonstrated a large amount of pericardial fluid, and 820 mL of red fluid was aspirated by pericardiocentesis, resulting in relief of her respiratory symptoms. Subcostal two-dimensional echocardiography demonstrated rocking of the heart and intermittent right-ventricular collapse (watch video at www.ccjm.org). Flow cytometry demonstrated 10% kappa+ monoclonal cells. Bone marrow biopsy with immunohistochemical staining revealed infiltration by CD20+, CD5+, CD23+, and BCL1– cells, compatible with small lymphocytic lymphoma.
MALIGNANT PERICARDIAL EFFUSION
Pericardial disease can be the first manifestation of malignancy,4 more often when the patient presents with a large pericardial effusion or tamponade. Malignant tumors of the lung, breast, and esophagus—as well as lymphoma, leukemia, and melanoma—often spread to the pericardium directly or through the lymphatic vessels or bloodstream.4 In our patient, corticosteroid treatment was initiated, and echocardiography at a follow-up visit 2 months later showed no pericardial fluid.
- Khandaker MH, Espinosa RE, Nishimura RA, et al. Pericardial disease: diagnosis and management. Mayo Clin Proc 2010; 85:572–593.
- Cheitlin MD, Armstrong WF, Aurigemma GP, et al; American College of Cardiology; American Heart Association; American Society of Echocardiography. ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASE Committee to Update the 1997 Guidelines for the Clinical Application of Echocardiography). Circulation 2003; 108:1146–1162.
- Verhaert D, Gabriel RS, Johnston D, Lytle BW, Desai MY, Klein AL. The role of multimodality imaging in the management of pericardial disease. Circ Cardiovascular Imaging 2010; 3:333–343.
- Burazor I, Imazio M, Markel G, Adler Y. Malignant pericardial effusion. Cardiology 2013; 124:224–232.
- Khandaker MH, Espinosa RE, Nishimura RA, et al. Pericardial disease: diagnosis and management. Mayo Clin Proc 2010; 85:572–593.
- Cheitlin MD, Armstrong WF, Aurigemma GP, et al; American College of Cardiology; American Heart Association; American Society of Echocardiography. ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASE Committee to Update the 1997 Guidelines for the Clinical Application of Echocardiography). Circulation 2003; 108:1146–1162.
- Verhaert D, Gabriel RS, Johnston D, Lytle BW, Desai MY, Klein AL. The role of multimodality imaging in the management of pericardial disease. Circ Cardiovascular Imaging 2010; 3:333–343.
- Burazor I, Imazio M, Markel G, Adler Y. Malignant pericardial effusion. Cardiology 2013; 124:224–232.
Brown tumor of the pelvis
A 39-year-old man presented with acute left hip pain and inability to bear weight following a minor trauma. The patient had a history of polycystic kidney disease and was on dialysis. Five years ago he had undergone bilateral nephrectomy and a renal transplantation that subsequently failed.
On examination, the active and passive range of motion of the left hip were limited due to pain. His serum laboratory values were:
- Parathyroid hormone 259.7 pmol/L (reference range 1.5–9.3)
- Calcium 2.32 mmol/L (1.15–1.32)
- Phosphate 3.26 mmol/L (0.8–1.45).
Computed tomography of the pelvis revealed an exophytic calcified lesion with multiple cystic spaces and fluid-fluid levels centered on the left pubis, extending medially into the right pubis and laterally into the left adductor muscle group. An acute pathologic fracture was documented in the left inferior pubic ramus (Figure 1). Other radiographic signs of long-standing hyperparathyroidism were present, including subperiosteal bone resorption at the radial side of the middle phalanges and the clavicle epiphysis.
The differential diagnosis of the pelvic lesion included giant cell tumor of bone with aneurysmal bone-cyst-like changes, osteitis fibrosa cystica, and, less likely, metastatic bone disease. Biopsy of the lesion showed clusters of osteoclast-type giant cells on a background of spindle cells and fibrous stroma that in this clinical context was consistent with the diagnosis of brown tumor (Figure 2).1
BROWN TUMOR
Brown tumor has been reported in fewer than 2% of patients with primary hyperparathyroidism and in 1.5% to 1.7% of those with secondary hyperparathyroidism (ie, from chronic renal failure, malabsorption, vitamin D deficiency, or hypocalcemia).2–4 An excess of parathyroid hormone increases the number and activity of osteoclasts, which are responsible for the lytic lesions. Brown tumor is the localized form of osteitis fibrosa cystica and is the most characteristic of the many skeletal changes that accompany secondary hyperparathyroidism.
Brown tumor is named for its color, which results from hemorrhages with accumulation of hemosiderin within the vascularized fibrous tissue. The tumor most commonly affects the pelvis, ribs, long-bone shafts, clavicle, and mandible.5 Clinical symptoms are nonspecific and depend on the size and location of the lesion.
Medical management of secondary hyperparathyroidism in dialysis patients involves some combination of phosphate binders (either calcium-containing or non-calcium-containing binders), calcitriol or synthetic vitamin D analogs, and a calcimimetic. Parathyroidectomy is required if drug therapy is ineffective. Surgical excision of brown tumor should be considered in patients who have large bone defects with spontaneous fracture risk or increasing pain. Our patient declined surgical intervention.
- Davies AM, Evans N, Mangham DC, Grimer RJ. MR imaging of brown tumour with fluid-fluid levels: a report of three cases. Eur Radiol 2001; 11:1445–1449.
- Silverberg SJ, Bilezikian JP. Evaluation and management of primary hyperparathyroidism. J Clin Endocrinol Metab 1996; 81:2036–2040.
- Bohlman ME, Kim YC, Eagan J, Spees EK. Brown tumor in secondary hyperparathyroidism causing acute paraplegia. Am J Med 1986; 81:545–547.
- Demay MB, Rosenthal DI, Deshpande V. Case records of the Massachusetts General Hospital. Case 16-2008. A 46-year-old woman with bone pain. N Engl J Med 2008; 358:2266–2274.
- Perlman JS, Pletcher SD, Schmidt BL, Eisele DW. Pathology quiz case 2. Giant cell lesion (brown tumor) of the mandible, associated with primary hyperparathyroidism (HPT). Arch Otolaryngol Head Neck Surg 2004; 130:793–794.
A 39-year-old man presented with acute left hip pain and inability to bear weight following a minor trauma. The patient had a history of polycystic kidney disease and was on dialysis. Five years ago he had undergone bilateral nephrectomy and a renal transplantation that subsequently failed.
On examination, the active and passive range of motion of the left hip were limited due to pain. His serum laboratory values were:
- Parathyroid hormone 259.7 pmol/L (reference range 1.5–9.3)
- Calcium 2.32 mmol/L (1.15–1.32)
- Phosphate 3.26 mmol/L (0.8–1.45).
Computed tomography of the pelvis revealed an exophytic calcified lesion with multiple cystic spaces and fluid-fluid levels centered on the left pubis, extending medially into the right pubis and laterally into the left adductor muscle group. An acute pathologic fracture was documented in the left inferior pubic ramus (Figure 1). Other radiographic signs of long-standing hyperparathyroidism were present, including subperiosteal bone resorption at the radial side of the middle phalanges and the clavicle epiphysis.
The differential diagnosis of the pelvic lesion included giant cell tumor of bone with aneurysmal bone-cyst-like changes, osteitis fibrosa cystica, and, less likely, metastatic bone disease. Biopsy of the lesion showed clusters of osteoclast-type giant cells on a background of spindle cells and fibrous stroma that in this clinical context was consistent with the diagnosis of brown tumor (Figure 2).1
BROWN TUMOR
Brown tumor has been reported in fewer than 2% of patients with primary hyperparathyroidism and in 1.5% to 1.7% of those with secondary hyperparathyroidism (ie, from chronic renal failure, malabsorption, vitamin D deficiency, or hypocalcemia).2–4 An excess of parathyroid hormone increases the number and activity of osteoclasts, which are responsible for the lytic lesions. Brown tumor is the localized form of osteitis fibrosa cystica and is the most characteristic of the many skeletal changes that accompany secondary hyperparathyroidism.
Brown tumor is named for its color, which results from hemorrhages with accumulation of hemosiderin within the vascularized fibrous tissue. The tumor most commonly affects the pelvis, ribs, long-bone shafts, clavicle, and mandible.5 Clinical symptoms are nonspecific and depend on the size and location of the lesion.
Medical management of secondary hyperparathyroidism in dialysis patients involves some combination of phosphate binders (either calcium-containing or non-calcium-containing binders), calcitriol or synthetic vitamin D analogs, and a calcimimetic. Parathyroidectomy is required if drug therapy is ineffective. Surgical excision of brown tumor should be considered in patients who have large bone defects with spontaneous fracture risk or increasing pain. Our patient declined surgical intervention.
A 39-year-old man presented with acute left hip pain and inability to bear weight following a minor trauma. The patient had a history of polycystic kidney disease and was on dialysis. Five years ago he had undergone bilateral nephrectomy and a renal transplantation that subsequently failed.
On examination, the active and passive range of motion of the left hip were limited due to pain. His serum laboratory values were:
- Parathyroid hormone 259.7 pmol/L (reference range 1.5–9.3)
- Calcium 2.32 mmol/L (1.15–1.32)
- Phosphate 3.26 mmol/L (0.8–1.45).
Computed tomography of the pelvis revealed an exophytic calcified lesion with multiple cystic spaces and fluid-fluid levels centered on the left pubis, extending medially into the right pubis and laterally into the left adductor muscle group. An acute pathologic fracture was documented in the left inferior pubic ramus (Figure 1). Other radiographic signs of long-standing hyperparathyroidism were present, including subperiosteal bone resorption at the radial side of the middle phalanges and the clavicle epiphysis.
The differential diagnosis of the pelvic lesion included giant cell tumor of bone with aneurysmal bone-cyst-like changes, osteitis fibrosa cystica, and, less likely, metastatic bone disease. Biopsy of the lesion showed clusters of osteoclast-type giant cells on a background of spindle cells and fibrous stroma that in this clinical context was consistent with the diagnosis of brown tumor (Figure 2).1
BROWN TUMOR
Brown tumor has been reported in fewer than 2% of patients with primary hyperparathyroidism and in 1.5% to 1.7% of those with secondary hyperparathyroidism (ie, from chronic renal failure, malabsorption, vitamin D deficiency, or hypocalcemia).2–4 An excess of parathyroid hormone increases the number and activity of osteoclasts, which are responsible for the lytic lesions. Brown tumor is the localized form of osteitis fibrosa cystica and is the most characteristic of the many skeletal changes that accompany secondary hyperparathyroidism.
Brown tumor is named for its color, which results from hemorrhages with accumulation of hemosiderin within the vascularized fibrous tissue. The tumor most commonly affects the pelvis, ribs, long-bone shafts, clavicle, and mandible.5 Clinical symptoms are nonspecific and depend on the size and location of the lesion.
Medical management of secondary hyperparathyroidism in dialysis patients involves some combination of phosphate binders (either calcium-containing or non-calcium-containing binders), calcitriol or synthetic vitamin D analogs, and a calcimimetic. Parathyroidectomy is required if drug therapy is ineffective. Surgical excision of brown tumor should be considered in patients who have large bone defects with spontaneous fracture risk or increasing pain. Our patient declined surgical intervention.
- Davies AM, Evans N, Mangham DC, Grimer RJ. MR imaging of brown tumour with fluid-fluid levels: a report of three cases. Eur Radiol 2001; 11:1445–1449.
- Silverberg SJ, Bilezikian JP. Evaluation and management of primary hyperparathyroidism. J Clin Endocrinol Metab 1996; 81:2036–2040.
- Bohlman ME, Kim YC, Eagan J, Spees EK. Brown tumor in secondary hyperparathyroidism causing acute paraplegia. Am J Med 1986; 81:545–547.
- Demay MB, Rosenthal DI, Deshpande V. Case records of the Massachusetts General Hospital. Case 16-2008. A 46-year-old woman with bone pain. N Engl J Med 2008; 358:2266–2274.
- Perlman JS, Pletcher SD, Schmidt BL, Eisele DW. Pathology quiz case 2. Giant cell lesion (brown tumor) of the mandible, associated with primary hyperparathyroidism (HPT). Arch Otolaryngol Head Neck Surg 2004; 130:793–794.
- Davies AM, Evans N, Mangham DC, Grimer RJ. MR imaging of brown tumour with fluid-fluid levels: a report of three cases. Eur Radiol 2001; 11:1445–1449.
- Silverberg SJ, Bilezikian JP. Evaluation and management of primary hyperparathyroidism. J Clin Endocrinol Metab 1996; 81:2036–2040.
- Bohlman ME, Kim YC, Eagan J, Spees EK. Brown tumor in secondary hyperparathyroidism causing acute paraplegia. Am J Med 1986; 81:545–547.
- Demay MB, Rosenthal DI, Deshpande V. Case records of the Massachusetts General Hospital. Case 16-2008. A 46-year-old woman with bone pain. N Engl J Med 2008; 358:2266–2274.
- Perlman JS, Pletcher SD, Schmidt BL, Eisele DW. Pathology quiz case 2. Giant cell lesion (brown tumor) of the mandible, associated with primary hyperparathyroidism (HPT). Arch Otolaryngol Head Neck Surg 2004; 130:793–794.
AHA: Coronary calcium personalizes ACC/AHA risk calculator
ORLANDO – Combining the coronary artery calcium score with the ACC/AHA cardiovascular risk calculator tool enables physicians to refine their decision making about who to recommend for statin therapy, Dr. Salman Waheed reported at the American Heart Association scientific sessions.
He presented an analysis of 1,225 asymptomatic adults followed for a median of 3.9 years in the observational arm of the St. Francis Health Study, an early landmark prospective study of the relationship between electron beam CT coronary artery calcium (CAC) score and cardiovascular event risk.
The 217 subjects who today would not be recommended for statin therapy on the basis of a 10-year atherosclerotic cardiovascular disease risk of 5%-7.4% as determined by the risk calculator included in the 2013 ACC/AHA cholesterol management guidelines (Circulation. 2014 Jun 24;129[25 Suppl 2]:S1-45) would be reclassified as warranting statin therapy if they had a CAC greater than 0, as was the case for 169 of the 217 (78%). Indeed, the presence of a CAC of 1 or more boosted their estimated 10-year risk to 10.8%.
On the other hand, there were 510 patients who would be classified as high risk by the ACC/AHA clinical risk calculator, with a 10-year risk of 7.5%-20%. Taking their CAC score into account would result in 73 being reclassified as low risk and becoming no longer statin candidates because their CAC of 0 was associated with a 10-year event risk of less than 1%. In contrast, for the 447 remaining subjects with a CAC greater than 0, the 10-year risk climbed to 21.9%, according to Dr. Waheed of the University of Kansas, Kansas City.
The composite outcome utilized in this analysis from the St. Francis Heart Study was comprised of nonfatal MI, coronary death, stroke, peripheral arterial revascularization, or coronary revascularization. Of note, heart failure wasn’t included.
Among the 545 subjects deemed at low cardiovascular risk because they weren’t eligible for statin therapy according to the 2013 ACC/AHA guidelines, 209 would be recategorized as high risk on the basis of a CAC score at or above the 80th percentile adjusted for age and gender. The adjusted risk of a cardiovascular event in the high CAC/low clinical risk group was 24.9-fold greater than in the low CAC/low clinical risk group.
“Among those eligible for statin therapy based upon current guidelines, high CAC portends a sixfold higher outcome risk than low CAC,” Dr. Waheed added.
The magnitude of CAC progression over the course of 4 years was similar across the baseline risk categories; however, the absolute CAC progression was greater among those with a high CAC at baseline.
Audience member Dr. Daniel S. Berman observed that the results of Dr. Waheed’s study are highly concordant with an earlier report from the Multi-Ethnic Study of Atherosclerosis in which a CAC of 0 was quite common in patients for whom statins would be recommended under the current ACC/AHA guidelines.
“Your data support the idea that stratification based upon CAC could more personalize the statin recommendations,” said Dr. Berman, chief of cardiac imaging and nuclear cardiology at Cedars-Sinai Medical Center and professor of medicine at the University of California, Los Angeles.
Another audience member, Dr. Donald M. Lloyd-Jones, one of the architects of the current guidelines, commented that the analyses from the St. Francis Heart Study and the Multi-Ethnic Study of Atherosclerosis suggest CAC screening coupled with the ACC/AHA risk score provides added value in a select group of patients.
“Your analysis continues to reinforce the point that we probably shouldn’t be doing universal CAC screening because in the people with a 10-year risk of less than 5% the yield is low and the CAC didn’t change anything, while in the people with a 10-year risk of 20% or higher the yield is incredibly high and the CAC didn’t change anything,” observed Dr. Lloyd-Jones, professor and chair of the department of preventive medicine at Northwestern University, Chicago.
“So CAC really is for those intermediate-risk folks where we’re on the bubble, where we might consider withholding therapy. And I’d love to see a trial to show that’s safe, by the way, but maybe that day will come. But we certainly would be comfortable up-classifying somebody if more CAC is present than there should be,” he added.
Dr. Waheed reported having no financial conflicts regarding his study.
ORLANDO – Combining the coronary artery calcium score with the ACC/AHA cardiovascular risk calculator tool enables physicians to refine their decision making about who to recommend for statin therapy, Dr. Salman Waheed reported at the American Heart Association scientific sessions.
He presented an analysis of 1,225 asymptomatic adults followed for a median of 3.9 years in the observational arm of the St. Francis Health Study, an early landmark prospective study of the relationship between electron beam CT coronary artery calcium (CAC) score and cardiovascular event risk.
The 217 subjects who today would not be recommended for statin therapy on the basis of a 10-year atherosclerotic cardiovascular disease risk of 5%-7.4% as determined by the risk calculator included in the 2013 ACC/AHA cholesterol management guidelines (Circulation. 2014 Jun 24;129[25 Suppl 2]:S1-45) would be reclassified as warranting statin therapy if they had a CAC greater than 0, as was the case for 169 of the 217 (78%). Indeed, the presence of a CAC of 1 or more boosted their estimated 10-year risk to 10.8%.
On the other hand, there were 510 patients who would be classified as high risk by the ACC/AHA clinical risk calculator, with a 10-year risk of 7.5%-20%. Taking their CAC score into account would result in 73 being reclassified as low risk and becoming no longer statin candidates because their CAC of 0 was associated with a 10-year event risk of less than 1%. In contrast, for the 447 remaining subjects with a CAC greater than 0, the 10-year risk climbed to 21.9%, according to Dr. Waheed of the University of Kansas, Kansas City.
The composite outcome utilized in this analysis from the St. Francis Heart Study was comprised of nonfatal MI, coronary death, stroke, peripheral arterial revascularization, or coronary revascularization. Of note, heart failure wasn’t included.
Among the 545 subjects deemed at low cardiovascular risk because they weren’t eligible for statin therapy according to the 2013 ACC/AHA guidelines, 209 would be recategorized as high risk on the basis of a CAC score at or above the 80th percentile adjusted for age and gender. The adjusted risk of a cardiovascular event in the high CAC/low clinical risk group was 24.9-fold greater than in the low CAC/low clinical risk group.
“Among those eligible for statin therapy based upon current guidelines, high CAC portends a sixfold higher outcome risk than low CAC,” Dr. Waheed added.
The magnitude of CAC progression over the course of 4 years was similar across the baseline risk categories; however, the absolute CAC progression was greater among those with a high CAC at baseline.
Audience member Dr. Daniel S. Berman observed that the results of Dr. Waheed’s study are highly concordant with an earlier report from the Multi-Ethnic Study of Atherosclerosis in which a CAC of 0 was quite common in patients for whom statins would be recommended under the current ACC/AHA guidelines.
“Your data support the idea that stratification based upon CAC could more personalize the statin recommendations,” said Dr. Berman, chief of cardiac imaging and nuclear cardiology at Cedars-Sinai Medical Center and professor of medicine at the University of California, Los Angeles.
Another audience member, Dr. Donald M. Lloyd-Jones, one of the architects of the current guidelines, commented that the analyses from the St. Francis Heart Study and the Multi-Ethnic Study of Atherosclerosis suggest CAC screening coupled with the ACC/AHA risk score provides added value in a select group of patients.
“Your analysis continues to reinforce the point that we probably shouldn’t be doing universal CAC screening because in the people with a 10-year risk of less than 5% the yield is low and the CAC didn’t change anything, while in the people with a 10-year risk of 20% or higher the yield is incredibly high and the CAC didn’t change anything,” observed Dr. Lloyd-Jones, professor and chair of the department of preventive medicine at Northwestern University, Chicago.
“So CAC really is for those intermediate-risk folks where we’re on the bubble, where we might consider withholding therapy. And I’d love to see a trial to show that’s safe, by the way, but maybe that day will come. But we certainly would be comfortable up-classifying somebody if more CAC is present than there should be,” he added.
Dr. Waheed reported having no financial conflicts regarding his study.
ORLANDO – Combining the coronary artery calcium score with the ACC/AHA cardiovascular risk calculator tool enables physicians to refine their decision making about who to recommend for statin therapy, Dr. Salman Waheed reported at the American Heart Association scientific sessions.
He presented an analysis of 1,225 asymptomatic adults followed for a median of 3.9 years in the observational arm of the St. Francis Health Study, an early landmark prospective study of the relationship between electron beam CT coronary artery calcium (CAC) score and cardiovascular event risk.
The 217 subjects who today would not be recommended for statin therapy on the basis of a 10-year atherosclerotic cardiovascular disease risk of 5%-7.4% as determined by the risk calculator included in the 2013 ACC/AHA cholesterol management guidelines (Circulation. 2014 Jun 24;129[25 Suppl 2]:S1-45) would be reclassified as warranting statin therapy if they had a CAC greater than 0, as was the case for 169 of the 217 (78%). Indeed, the presence of a CAC of 1 or more boosted their estimated 10-year risk to 10.8%.
On the other hand, there were 510 patients who would be classified as high risk by the ACC/AHA clinical risk calculator, with a 10-year risk of 7.5%-20%. Taking their CAC score into account would result in 73 being reclassified as low risk and becoming no longer statin candidates because their CAC of 0 was associated with a 10-year event risk of less than 1%. In contrast, for the 447 remaining subjects with a CAC greater than 0, the 10-year risk climbed to 21.9%, according to Dr. Waheed of the University of Kansas, Kansas City.
The composite outcome utilized in this analysis from the St. Francis Heart Study was comprised of nonfatal MI, coronary death, stroke, peripheral arterial revascularization, or coronary revascularization. Of note, heart failure wasn’t included.
Among the 545 subjects deemed at low cardiovascular risk because they weren’t eligible for statin therapy according to the 2013 ACC/AHA guidelines, 209 would be recategorized as high risk on the basis of a CAC score at or above the 80th percentile adjusted for age and gender. The adjusted risk of a cardiovascular event in the high CAC/low clinical risk group was 24.9-fold greater than in the low CAC/low clinical risk group.
“Among those eligible for statin therapy based upon current guidelines, high CAC portends a sixfold higher outcome risk than low CAC,” Dr. Waheed added.
The magnitude of CAC progression over the course of 4 years was similar across the baseline risk categories; however, the absolute CAC progression was greater among those with a high CAC at baseline.
Audience member Dr. Daniel S. Berman observed that the results of Dr. Waheed’s study are highly concordant with an earlier report from the Multi-Ethnic Study of Atherosclerosis in which a CAC of 0 was quite common in patients for whom statins would be recommended under the current ACC/AHA guidelines.
“Your data support the idea that stratification based upon CAC could more personalize the statin recommendations,” said Dr. Berman, chief of cardiac imaging and nuclear cardiology at Cedars-Sinai Medical Center and professor of medicine at the University of California, Los Angeles.
Another audience member, Dr. Donald M. Lloyd-Jones, one of the architects of the current guidelines, commented that the analyses from the St. Francis Heart Study and the Multi-Ethnic Study of Atherosclerosis suggest CAC screening coupled with the ACC/AHA risk score provides added value in a select group of patients.
“Your analysis continues to reinforce the point that we probably shouldn’t be doing universal CAC screening because in the people with a 10-year risk of less than 5% the yield is low and the CAC didn’t change anything, while in the people with a 10-year risk of 20% or higher the yield is incredibly high and the CAC didn’t change anything,” observed Dr. Lloyd-Jones, professor and chair of the department of preventive medicine at Northwestern University, Chicago.
“So CAC really is for those intermediate-risk folks where we’re on the bubble, where we might consider withholding therapy. And I’d love to see a trial to show that’s safe, by the way, but maybe that day will come. But we certainly would be comfortable up-classifying somebody if more CAC is present than there should be,” he added.
Dr. Waheed reported having no financial conflicts regarding his study.
AT THE AHA SCIENTIFIC SESSIONS
Key clinical point: Measuring coronary artery calcium provides added value in refining the 10-year atherosclerotic cardiovascular disease risk, especially in patients with an intermediate-risk score on the ACC/AHA risk calculator.
Major finding: Seventy-eight percent of a group of patients for whom statin therapy wouldn’t be recommended under the current ACC/AHA guidelines because their estimated 10-year event risk was 5%-7.5% would be reclassified as warranting statin therapy because their coronary artery calcium score was greater than 0, pushing their estimated risk to 10.8%.
Data source: A retrospective analysis of data on 1,225 asymptomatic adults followed prospectively with coronary artery calcium measurements in the St. Francis Health Study.
Disclosures: The study presenter reported having no financial conflicts of interest.
AHA: PCI renal complications keep climbing
ORLANDO – Cases of contrast-induced nephropathy increased dramatically among Medicare patients undergoing percutaneous coronary intervention (PCI) during a recent 5-year period, despite the increased attention that has been drawn to the problem.
“These findings suggest that despite a longstanding focus on preventing CIN [contrast-induced nephropathy], the complication is increasing steadily and new efforts to reduce PCI-related CIN are warranted,” Dr. Phillip P. Brown said at the American Heart Association scientific sessions.
A fresh approach is a priority for Medicare, in part because new-onset renal failure requiring hemodialysis as a result of CIN increases health care costs substantially for the remainder of the patient’s life, noted Dr. Brown of Cardiac Data Solutions in Atlanta.
He presented a retrospective analysis of Medicare data files for 2009-2013. Among 1,552,960 Medicare beneficiaries who underwent PCI without valve surgery or coronary artery bypass graft surgery, 275,471 were admitted for nonelective PCI.
The rate of new hemodialysis as a complication of nonelective PCI increased by 24.8% annually during the study period, climbing to an incidence of 1.15% in 2013. Among patients admitted for elective PCI, the rate of new-onset renal failure requiring hemodialysis essentially doubled from 1% to 2% during the 5-year period.
The rate of new-onset acute renal failure as a complication of nonelective PCI increased by an average of 6.9% annually, reaching 7.67% in 2013. The increase in acute renal failure as a complication of elective PCI was even steeper: an average of 10.6% per year.
In addition to the rising rates of acute renal failure and need for dialysis as a complication of PCI, the proportion of patients who presented with prior dialysis or acute renal failure at admission for the procedure also rose year by year. In 2013, acute renal failure was present at admission in 6.12% of patients undergoing elective and 7.02% having nonelective PCI. Prior dialysis at admission was present in 2.61% and 0.94%, respectively.
Dr. Brown reported having no financial conflicts regarding this descriptive study.
ORLANDO – Cases of contrast-induced nephropathy increased dramatically among Medicare patients undergoing percutaneous coronary intervention (PCI) during a recent 5-year period, despite the increased attention that has been drawn to the problem.
“These findings suggest that despite a longstanding focus on preventing CIN [contrast-induced nephropathy], the complication is increasing steadily and new efforts to reduce PCI-related CIN are warranted,” Dr. Phillip P. Brown said at the American Heart Association scientific sessions.
A fresh approach is a priority for Medicare, in part because new-onset renal failure requiring hemodialysis as a result of CIN increases health care costs substantially for the remainder of the patient’s life, noted Dr. Brown of Cardiac Data Solutions in Atlanta.
He presented a retrospective analysis of Medicare data files for 2009-2013. Among 1,552,960 Medicare beneficiaries who underwent PCI without valve surgery or coronary artery bypass graft surgery, 275,471 were admitted for nonelective PCI.
The rate of new hemodialysis as a complication of nonelective PCI increased by 24.8% annually during the study period, climbing to an incidence of 1.15% in 2013. Among patients admitted for elective PCI, the rate of new-onset renal failure requiring hemodialysis essentially doubled from 1% to 2% during the 5-year period.
The rate of new-onset acute renal failure as a complication of nonelective PCI increased by an average of 6.9% annually, reaching 7.67% in 2013. The increase in acute renal failure as a complication of elective PCI was even steeper: an average of 10.6% per year.
In addition to the rising rates of acute renal failure and need for dialysis as a complication of PCI, the proportion of patients who presented with prior dialysis or acute renal failure at admission for the procedure also rose year by year. In 2013, acute renal failure was present at admission in 6.12% of patients undergoing elective and 7.02% having nonelective PCI. Prior dialysis at admission was present in 2.61% and 0.94%, respectively.
Dr. Brown reported having no financial conflicts regarding this descriptive study.
ORLANDO – Cases of contrast-induced nephropathy increased dramatically among Medicare patients undergoing percutaneous coronary intervention (PCI) during a recent 5-year period, despite the increased attention that has been drawn to the problem.
“These findings suggest that despite a longstanding focus on preventing CIN [contrast-induced nephropathy], the complication is increasing steadily and new efforts to reduce PCI-related CIN are warranted,” Dr. Phillip P. Brown said at the American Heart Association scientific sessions.
A fresh approach is a priority for Medicare, in part because new-onset renal failure requiring hemodialysis as a result of CIN increases health care costs substantially for the remainder of the patient’s life, noted Dr. Brown of Cardiac Data Solutions in Atlanta.
He presented a retrospective analysis of Medicare data files for 2009-2013. Among 1,552,960 Medicare beneficiaries who underwent PCI without valve surgery or coronary artery bypass graft surgery, 275,471 were admitted for nonelective PCI.
The rate of new hemodialysis as a complication of nonelective PCI increased by 24.8% annually during the study period, climbing to an incidence of 1.15% in 2013. Among patients admitted for elective PCI, the rate of new-onset renal failure requiring hemodialysis essentially doubled from 1% to 2% during the 5-year period.
The rate of new-onset acute renal failure as a complication of nonelective PCI increased by an average of 6.9% annually, reaching 7.67% in 2013. The increase in acute renal failure as a complication of elective PCI was even steeper: an average of 10.6% per year.
In addition to the rising rates of acute renal failure and need for dialysis as a complication of PCI, the proportion of patients who presented with prior dialysis or acute renal failure at admission for the procedure also rose year by year. In 2013, acute renal failure was present at admission in 6.12% of patients undergoing elective and 7.02% having nonelective PCI. Prior dialysis at admission was present in 2.61% and 0.94%, respectively.
Dr. Brown reported having no financial conflicts regarding this descriptive study.
AT THE AHA SCIENTIFIC SESSIONS
Key clinical point: Renal complication rates in Medicare patients undergoing PCI continue to rise dramatically.
Major finding: The combined rate of acute renal failure and need for hemodialysis as a complication of elective PCI in Medicare patients climbed by 18% per year during a recent 5-year period and by nearly 32% annually in those undergoing nonelective PCI.
Data source: A retrospective study of 1.5 million Medicare beneficiaries who underwent elective or nonelective PCI during 2009-2013.
Disclosures: The presenter of this study reported having no financial conflicts.
Glial fibrillary acidic protein may help identify youth with TBI
Glial fibrillary acidic protein appears to be a candidate biomarker for detecting traumatic intracranial lesions on head CT after mild to moderate head trauma in youth, a study showed.
Previous studies have found that head CT scans in children less than 5 years old may contribute to the risk for brain cancer and leukemia because children are more sensitive to ionizing radiation. Ninety-nine different pediatric biomarkers have been researched for traumatic brain injury (TBI); some studies have indicated glial fibrillary acidic protein (GFAP) may be a promising biomarker for mild to moderate TBI in adults.
Dr. Linda Papa of the department of emergency medicine at Orlando Regional Medical Center and colleagues compared the GFAP level in the serum of children and youth evaluated for mild to moderate TBI with pediatric trauma patients without brain injury to see how these levels were related to evidence of traumatic lesions on head CT. Their results were published in Academic Emergency Medicine (2015 Nov;22[11]:1274-82. doi: 10.1111/acem.12795).
They conducted a prospective cohort study of 197 children and youth who presented with a Glasgow Coma Scale (GCS) score of 9-15 after blunt head trauma. The 60 control patients included those without head trauma and a GSC score of 15. A head CT scan was obtained in 152 patients, with 11% demonstrating traumatic intracranial lesions. Serum samples were drawn within 6 hours of injury, at a mean 3.3 hours in those with head injury and 4.1 hours in those without head injury.
Children with traumatic intracranial lesions on CT scan had higher median GFAP levels (1.01, interquartile range = 0.59-1.48), compared with those without lesions on CT (0.18, IQR = 0.06-0.47).
When GFAP was used to detect traumatic lesions on head CT, the area under the receiver operating characteristic curve (AUC) was 0.82 (95% confidence interval, 0.71-0.93); it was 0.80 (95% CI, 0.68-0.92) for those with a GCS of 15, and 0.83 (95% CI, 0.56-1.00) in those younger than 5 years old.
Using a cutoff level of 0.15 ng/mL for GFAP, Dr. Papa and colleagues noted a negative predictive value of 98%, a specificity of 47%, and a sensitivity of 94% for detecting intracranial lesions.
Several limitations to the study included not having research assistants available to enroll participants 24/7, a lack of long-term outcome data, and a small cohort without any participants requiring neurosurgical intervention.
The next steps would involve clinical validation with a large, multicenter study.
This study was supported by an award from the National Institute of Neurological Disorders and Stroke. Dr. Papa reported consulting for Banyan Biomarkers.
Out of the 99 markers studied previously, glial fibrillary acidic protein appears to be the most promising in adults. The authors wanted to examine its usefulness in children.
Dr. Gregory L. Landry |
This serum marker may be helpful to clinicians in deciding who needs a CT scan and who does not, but a larger study is still needed.
Serum markers seem to be most useful in patients with moderate to severe head trauma. The typical sports concussion (mild traumatic brain injury) does not cause enough damage to raise serum markers, and so far studies of markers in that group have shown that they are not helpful in determining severity of the injury.
Dr. Gregory L. Landry is affiliated with the University of Wisconsin–Madison, specializing in pediatric and adolescent primary care sports medicine. These comments were taken from an interview with Dr. Landry, who said he had no relevant financial disclosures.
Out of the 99 markers studied previously, glial fibrillary acidic protein appears to be the most promising in adults. The authors wanted to examine its usefulness in children.
Dr. Gregory L. Landry |
This serum marker may be helpful to clinicians in deciding who needs a CT scan and who does not, but a larger study is still needed.
Serum markers seem to be most useful in patients with moderate to severe head trauma. The typical sports concussion (mild traumatic brain injury) does not cause enough damage to raise serum markers, and so far studies of markers in that group have shown that they are not helpful in determining severity of the injury.
Dr. Gregory L. Landry is affiliated with the University of Wisconsin–Madison, specializing in pediatric and adolescent primary care sports medicine. These comments were taken from an interview with Dr. Landry, who said he had no relevant financial disclosures.
Out of the 99 markers studied previously, glial fibrillary acidic protein appears to be the most promising in adults. The authors wanted to examine its usefulness in children.
Dr. Gregory L. Landry |
This serum marker may be helpful to clinicians in deciding who needs a CT scan and who does not, but a larger study is still needed.
Serum markers seem to be most useful in patients with moderate to severe head trauma. The typical sports concussion (mild traumatic brain injury) does not cause enough damage to raise serum markers, and so far studies of markers in that group have shown that they are not helpful in determining severity of the injury.
Dr. Gregory L. Landry is affiliated with the University of Wisconsin–Madison, specializing in pediatric and adolescent primary care sports medicine. These comments were taken from an interview with Dr. Landry, who said he had no relevant financial disclosures.
Glial fibrillary acidic protein appears to be a candidate biomarker for detecting traumatic intracranial lesions on head CT after mild to moderate head trauma in youth, a study showed.
Previous studies have found that head CT scans in children less than 5 years old may contribute to the risk for brain cancer and leukemia because children are more sensitive to ionizing radiation. Ninety-nine different pediatric biomarkers have been researched for traumatic brain injury (TBI); some studies have indicated glial fibrillary acidic protein (GFAP) may be a promising biomarker for mild to moderate TBI in adults.
Dr. Linda Papa of the department of emergency medicine at Orlando Regional Medical Center and colleagues compared the GFAP level in the serum of children and youth evaluated for mild to moderate TBI with pediatric trauma patients without brain injury to see how these levels were related to evidence of traumatic lesions on head CT. Their results were published in Academic Emergency Medicine (2015 Nov;22[11]:1274-82. doi: 10.1111/acem.12795).
They conducted a prospective cohort study of 197 children and youth who presented with a Glasgow Coma Scale (GCS) score of 9-15 after blunt head trauma. The 60 control patients included those without head trauma and a GSC score of 15. A head CT scan was obtained in 152 patients, with 11% demonstrating traumatic intracranial lesions. Serum samples were drawn within 6 hours of injury, at a mean 3.3 hours in those with head injury and 4.1 hours in those without head injury.
Children with traumatic intracranial lesions on CT scan had higher median GFAP levels (1.01, interquartile range = 0.59-1.48), compared with those without lesions on CT (0.18, IQR = 0.06-0.47).
When GFAP was used to detect traumatic lesions on head CT, the area under the receiver operating characteristic curve (AUC) was 0.82 (95% confidence interval, 0.71-0.93); it was 0.80 (95% CI, 0.68-0.92) for those with a GCS of 15, and 0.83 (95% CI, 0.56-1.00) in those younger than 5 years old.
Using a cutoff level of 0.15 ng/mL for GFAP, Dr. Papa and colleagues noted a negative predictive value of 98%, a specificity of 47%, and a sensitivity of 94% for detecting intracranial lesions.
Several limitations to the study included not having research assistants available to enroll participants 24/7, a lack of long-term outcome data, and a small cohort without any participants requiring neurosurgical intervention.
The next steps would involve clinical validation with a large, multicenter study.
This study was supported by an award from the National Institute of Neurological Disorders and Stroke. Dr. Papa reported consulting for Banyan Biomarkers.
Glial fibrillary acidic protein appears to be a candidate biomarker for detecting traumatic intracranial lesions on head CT after mild to moderate head trauma in youth, a study showed.
Previous studies have found that head CT scans in children less than 5 years old may contribute to the risk for brain cancer and leukemia because children are more sensitive to ionizing radiation. Ninety-nine different pediatric biomarkers have been researched for traumatic brain injury (TBI); some studies have indicated glial fibrillary acidic protein (GFAP) may be a promising biomarker for mild to moderate TBI in adults.
Dr. Linda Papa of the department of emergency medicine at Orlando Regional Medical Center and colleagues compared the GFAP level in the serum of children and youth evaluated for mild to moderate TBI with pediatric trauma patients without brain injury to see how these levels were related to evidence of traumatic lesions on head CT. Their results were published in Academic Emergency Medicine (2015 Nov;22[11]:1274-82. doi: 10.1111/acem.12795).
They conducted a prospective cohort study of 197 children and youth who presented with a Glasgow Coma Scale (GCS) score of 9-15 after blunt head trauma. The 60 control patients included those without head trauma and a GSC score of 15. A head CT scan was obtained in 152 patients, with 11% demonstrating traumatic intracranial lesions. Serum samples were drawn within 6 hours of injury, at a mean 3.3 hours in those with head injury and 4.1 hours in those without head injury.
Children with traumatic intracranial lesions on CT scan had higher median GFAP levels (1.01, interquartile range = 0.59-1.48), compared with those without lesions on CT (0.18, IQR = 0.06-0.47).
When GFAP was used to detect traumatic lesions on head CT, the area under the receiver operating characteristic curve (AUC) was 0.82 (95% confidence interval, 0.71-0.93); it was 0.80 (95% CI, 0.68-0.92) for those with a GCS of 15, and 0.83 (95% CI, 0.56-1.00) in those younger than 5 years old.
Using a cutoff level of 0.15 ng/mL for GFAP, Dr. Papa and colleagues noted a negative predictive value of 98%, a specificity of 47%, and a sensitivity of 94% for detecting intracranial lesions.
Several limitations to the study included not having research assistants available to enroll participants 24/7, a lack of long-term outcome data, and a small cohort without any participants requiring neurosurgical intervention.
The next steps would involve clinical validation with a large, multicenter study.
This study was supported by an award from the National Institute of Neurological Disorders and Stroke. Dr. Papa reported consulting for Banyan Biomarkers.
FROM ACADEMIC EMERGENCY MEDICINE
Key clinical point: GFAP appears to be associated with severity of injury and identification of lesions on head CT scan after head trauma in youth.
Major finding: The negative predictive value was 98%, the specificity was 47%, and the sensitivity was 94% for detecting intracranial lesions when a GFAP cutoff level of 0.15 ng/mL was used.
Data source: A prospective controlled cohort study of children and youth who presented with a Glasgow Coma Scale score of 9-15 after blunt head trauma.
Disclosures: This study was supported by an award from the National Institute of Neurological Disorders and Stroke. Dr. Papa reported consulting for Banyan Biomarkers.
In angiography, intracoronary contrast damaged kidneys more than IV contrast
SAN DIEGO – Contrast agents administered through the coronary vessels for invasive angiography led to significantly more kidney damage than contrast agents administered intravenously for coronary computed tomography angiography, according to a randomized study.
In the Coronary Artery Disease-Management (CAD-Man) study, contrast-induced kidney injury was two to three times more likely after intracoronary than after intravenous contrast administration, explained study investigators Dr. Eva Schönenberger and Dr. Marc Dewey of Charité Medical University, Berlin.
Contrast agents used to detect and treat blockages in coronary arteries are known to damage the kidneys in 2%-20% of patients. In the United States, about 4 million doses of contrast are administered directly into the coronary vessels during invasive catheterization, and 40 million into superficial veins, said Dr. Dewey, Heisenberg Professor of Radiology at the German Research Foundation and vice chair of the department of radiology at Charité.
That makes contrast administration a significant clinical decision for physicians, he added, not just because of potential for harm, but also the potential for added costs.
CAD-Man included 326 patients with suspected coronary disease. Researchers randomized 161 patients to intracoronary contrast agent (ICA) for invasive coronary angiography and 165 patients to IV contrast agent for coronary computed tomography angiography (CTA). All patients received the same contrast agent.
Blood samples were taken at baseline before the procedure, and at two time points after: between 18 and 24 hours, and between 46 and 50 hours. Baseline creatinine levels were similar in the two groups. The researchers defined contrast-associated nephrotoxicity as an increase in creatinine of at least 0.5 mg/dL, or 25%.
At follow-up, 21 of 158 ICA patients (13%) and 9 of 160 CTA patients (6%) had contrast-associated nephropathy, a significant difference (P less than .05). In patients without coronary disease, 13% of ICA patients and 4% of CTA patients developed contrast-associated nephropathy, also a significant difference (P less than .05).
Catheter administration concentrates more contrast in the heart and above the kidneys than intravenous administration, Dr. Schönenberger explained at the meeting sponsored by the American Society of Nephrology. Thus, the increased kidney damage in invasive-angiography patients may be due to higher dosages of contrast in their kidneys.
Physicians “have to keep in mind that putting contrast agents directly into the coronaries might produce more of an increase of creatinine, and more acute kidney injury, than just giving it through an IV,” explained Dr. Schönenberger, a nephrologist in the department of anesthesiology and operative intensive care medicine at Charité.
Physicians should take this information into consideration when deciding how to administer contrast for patients suspected of having coronary artery disease, Dr. Dewey noted. “In addition to being noninvasive, cardiac CT may thus also have the advantage of reducing kidney risk.”
Cost should be a big concern as well. Dr. Dewey referred to published literature indicating that contrast-induced kidney injury can lead to “longer hospital and intensive care unit stays, [increased] dialysis, cost of adverse events, and higher mortality rates. The in-hospital cost was $10,000 per contrast-induced acute kidney injury, and the 1-year cost of treatment was more than $11,000.”
Because CAD-Man’s last patient was enrolled in mid-September, the data are still being analyzed, Dr. Schönenberger noted. Therefore, some confounders may be discovered that influenced the results.
For example, cardiologists may select their sicker patients for invasive procedures in order to be ready to insert stents, so there may not be as much flexibility in which approach to use.
Also unclear is the amount of contrast used for each patient in each arm of this study. Some physicians may have used more contrast for patients suspected of having disease that was harder to detect, although that part of the analysis remains under review, Dr. Dewey and Dr. Schönenberger said.
It remains unclear whether the nephrotoxicity found in the invasive angiography group was all due to the contrast, Dr. Schönenberger noted, or whether some of it might have been caused by small particles of hardened cholesterol spreading to blood vessels in the kidneys – a process known as atheroembolic renal disease. That, too, is under review.
The contrast agent used in the study, low-osmolar nonionic Xenetix 350, is used in 96 countries but is not approved by the U.S. Food and Drug Administration, Dr. Schönenberger said. However, it is very similar to those agents that are in use in the United States, she added.
The study was funded by the German Research Foundation through the Heisenberg Professorship Program. The researchers reported no financial disclosures.
SAN DIEGO – Contrast agents administered through the coronary vessels for invasive angiography led to significantly more kidney damage than contrast agents administered intravenously for coronary computed tomography angiography, according to a randomized study.
In the Coronary Artery Disease-Management (CAD-Man) study, contrast-induced kidney injury was two to three times more likely after intracoronary than after intravenous contrast administration, explained study investigators Dr. Eva Schönenberger and Dr. Marc Dewey of Charité Medical University, Berlin.
Contrast agents used to detect and treat blockages in coronary arteries are known to damage the kidneys in 2%-20% of patients. In the United States, about 4 million doses of contrast are administered directly into the coronary vessels during invasive catheterization, and 40 million into superficial veins, said Dr. Dewey, Heisenberg Professor of Radiology at the German Research Foundation and vice chair of the department of radiology at Charité.
That makes contrast administration a significant clinical decision for physicians, he added, not just because of potential for harm, but also the potential for added costs.
CAD-Man included 326 patients with suspected coronary disease. Researchers randomized 161 patients to intracoronary contrast agent (ICA) for invasive coronary angiography and 165 patients to IV contrast agent for coronary computed tomography angiography (CTA). All patients received the same contrast agent.
Blood samples were taken at baseline before the procedure, and at two time points after: between 18 and 24 hours, and between 46 and 50 hours. Baseline creatinine levels were similar in the two groups. The researchers defined contrast-associated nephrotoxicity as an increase in creatinine of at least 0.5 mg/dL, or 25%.
At follow-up, 21 of 158 ICA patients (13%) and 9 of 160 CTA patients (6%) had contrast-associated nephropathy, a significant difference (P less than .05). In patients without coronary disease, 13% of ICA patients and 4% of CTA patients developed contrast-associated nephropathy, also a significant difference (P less than .05).
Catheter administration concentrates more contrast in the heart and above the kidneys than intravenous administration, Dr. Schönenberger explained at the meeting sponsored by the American Society of Nephrology. Thus, the increased kidney damage in invasive-angiography patients may be due to higher dosages of contrast in their kidneys.
Physicians “have to keep in mind that putting contrast agents directly into the coronaries might produce more of an increase of creatinine, and more acute kidney injury, than just giving it through an IV,” explained Dr. Schönenberger, a nephrologist in the department of anesthesiology and operative intensive care medicine at Charité.
Physicians should take this information into consideration when deciding how to administer contrast for patients suspected of having coronary artery disease, Dr. Dewey noted. “In addition to being noninvasive, cardiac CT may thus also have the advantage of reducing kidney risk.”
Cost should be a big concern as well. Dr. Dewey referred to published literature indicating that contrast-induced kidney injury can lead to “longer hospital and intensive care unit stays, [increased] dialysis, cost of adverse events, and higher mortality rates. The in-hospital cost was $10,000 per contrast-induced acute kidney injury, and the 1-year cost of treatment was more than $11,000.”
Because CAD-Man’s last patient was enrolled in mid-September, the data are still being analyzed, Dr. Schönenberger noted. Therefore, some confounders may be discovered that influenced the results.
For example, cardiologists may select their sicker patients for invasive procedures in order to be ready to insert stents, so there may not be as much flexibility in which approach to use.
Also unclear is the amount of contrast used for each patient in each arm of this study. Some physicians may have used more contrast for patients suspected of having disease that was harder to detect, although that part of the analysis remains under review, Dr. Dewey and Dr. Schönenberger said.
It remains unclear whether the nephrotoxicity found in the invasive angiography group was all due to the contrast, Dr. Schönenberger noted, or whether some of it might have been caused by small particles of hardened cholesterol spreading to blood vessels in the kidneys – a process known as atheroembolic renal disease. That, too, is under review.
The contrast agent used in the study, low-osmolar nonionic Xenetix 350, is used in 96 countries but is not approved by the U.S. Food and Drug Administration, Dr. Schönenberger said. However, it is very similar to those agents that are in use in the United States, she added.
The study was funded by the German Research Foundation through the Heisenberg Professorship Program. The researchers reported no financial disclosures.
SAN DIEGO – Contrast agents administered through the coronary vessels for invasive angiography led to significantly more kidney damage than contrast agents administered intravenously for coronary computed tomography angiography, according to a randomized study.
In the Coronary Artery Disease-Management (CAD-Man) study, contrast-induced kidney injury was two to three times more likely after intracoronary than after intravenous contrast administration, explained study investigators Dr. Eva Schönenberger and Dr. Marc Dewey of Charité Medical University, Berlin.
Contrast agents used to detect and treat blockages in coronary arteries are known to damage the kidneys in 2%-20% of patients. In the United States, about 4 million doses of contrast are administered directly into the coronary vessels during invasive catheterization, and 40 million into superficial veins, said Dr. Dewey, Heisenberg Professor of Radiology at the German Research Foundation and vice chair of the department of radiology at Charité.
That makes contrast administration a significant clinical decision for physicians, he added, not just because of potential for harm, but also the potential for added costs.
CAD-Man included 326 patients with suspected coronary disease. Researchers randomized 161 patients to intracoronary contrast agent (ICA) for invasive coronary angiography and 165 patients to IV contrast agent for coronary computed tomography angiography (CTA). All patients received the same contrast agent.
Blood samples were taken at baseline before the procedure, and at two time points after: between 18 and 24 hours, and between 46 and 50 hours. Baseline creatinine levels were similar in the two groups. The researchers defined contrast-associated nephrotoxicity as an increase in creatinine of at least 0.5 mg/dL, or 25%.
At follow-up, 21 of 158 ICA patients (13%) and 9 of 160 CTA patients (6%) had contrast-associated nephropathy, a significant difference (P less than .05). In patients without coronary disease, 13% of ICA patients and 4% of CTA patients developed contrast-associated nephropathy, also a significant difference (P less than .05).
Catheter administration concentrates more contrast in the heart and above the kidneys than intravenous administration, Dr. Schönenberger explained at the meeting sponsored by the American Society of Nephrology. Thus, the increased kidney damage in invasive-angiography patients may be due to higher dosages of contrast in their kidneys.
Physicians “have to keep in mind that putting contrast agents directly into the coronaries might produce more of an increase of creatinine, and more acute kidney injury, than just giving it through an IV,” explained Dr. Schönenberger, a nephrologist in the department of anesthesiology and operative intensive care medicine at Charité.
Physicians should take this information into consideration when deciding how to administer contrast for patients suspected of having coronary artery disease, Dr. Dewey noted. “In addition to being noninvasive, cardiac CT may thus also have the advantage of reducing kidney risk.”
Cost should be a big concern as well. Dr. Dewey referred to published literature indicating that contrast-induced kidney injury can lead to “longer hospital and intensive care unit stays, [increased] dialysis, cost of adverse events, and higher mortality rates. The in-hospital cost was $10,000 per contrast-induced acute kidney injury, and the 1-year cost of treatment was more than $11,000.”
Because CAD-Man’s last patient was enrolled in mid-September, the data are still being analyzed, Dr. Schönenberger noted. Therefore, some confounders may be discovered that influenced the results.
For example, cardiologists may select their sicker patients for invasive procedures in order to be ready to insert stents, so there may not be as much flexibility in which approach to use.
Also unclear is the amount of contrast used for each patient in each arm of this study. Some physicians may have used more contrast for patients suspected of having disease that was harder to detect, although that part of the analysis remains under review, Dr. Dewey and Dr. Schönenberger said.
It remains unclear whether the nephrotoxicity found in the invasive angiography group was all due to the contrast, Dr. Schönenberger noted, or whether some of it might have been caused by small particles of hardened cholesterol spreading to blood vessels in the kidneys – a process known as atheroembolic renal disease. That, too, is under review.
The contrast agent used in the study, low-osmolar nonionic Xenetix 350, is used in 96 countries but is not approved by the U.S. Food and Drug Administration, Dr. Schönenberger said. However, it is very similar to those agents that are in use in the United States, she added.
The study was funded by the German Research Foundation through the Heisenberg Professorship Program. The researchers reported no financial disclosures.
AT KIDNEY WEEK 2015
Key clinical point: Patients undergoing angiography with intracoronary contrast agent instead of IV contrast agent may be at greater risk of kidney injury.
Major finding: Kidney injury was two to three times more likely after intracoronary than after intravenous contrast administration in patients undergoing angiography for suspected heart disease.
Data source: A randomized study of 326 patients with atypical angina pectoris who were scheduled for angiography.
Disclosures: The study was funded by the German Research Foundation through the Heisenberg Professorship Program. The researchers reported no financial disclosures.