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Will a novel antibody fix the anticoagulant-bleeding problem?
It seems inescapable: If patients are made less able to form blood clots, they bleed more.
Bleeding is the perennial problem for anticoagulants. Whether it’s the traditional anticoagulants (heparin, warfarin, and the low-molecular-weight heparins) or new drugs (fondaparinux, dabigatran, rivaroxaban, and apixaban), as the anticoagulant’s potency or dosage increases to stop blood clots from forming, the inevitable downside is increased bleeding.
Maybe not.
A newly developed, synthetic human IgG antibody appears, in animal and in vitro models, to allow normal clotting to occur and stop bleeding at vessel tears and cuts, while short-circuiting pathologic clotting in intravascular spaces – the sorts of clots that cause venous thromboembolisms, myocardial infarctions, and strokes.
"It seems too good to be true. It’s beyond comprehension," said Dr. Trevor Baglin, the University of Cambridge, England, hematologist who discovered the first identified, naturally occurring example of this antibody, in IgA form, in a patient he initially saw in 2008. "All we can do is go forward and see if it genuinely is as good as it seems," he said while presenting his group’s initial animal findings with the antibody at the Congress of the International Society on Thrombosis and Haemostasis in Amsterdam earlier this month.
The antibody – which has been patented, synthesized, and is in extensive preclinical testing – has been named ichorcumab. In Greek mythology, "ichor" was the blood factor in gods that made them immortal.
The secret behind ichorcumab is that it binds to and inactivates exosite 1, the part of the thrombin molecule that cleaves fibrinogen into fibrin, an effective brake on clotting. Study results suggest that whether the exosite 1 portion of thrombin is exposed or hidden at various body sites accounts for ichorcumab’s varied effects.
"Our hypothesis is that exosite 1 is protected from the antibody [when a thrombin molecule sits] on a cell or clot surface, so hemostasis is unaffected, but thrombosis occurs in the luminal space, where exosite 1 is exposed an available to the antibody," Dr. Baglin explained.
"While before we thought of just one type of clot, [the work with ichorcumab so far] suggests there is not one clotting mechanism but two," he noted, one that leads to clot formation that stops bleeding, and a second mechanism that produces clots that cause thrombosis. Ichorcumab blocks the bad clots but not the good ones, because the clots form at different locations that affect the way that exosite 1 on thrombin is exposed.
It may sound farfetched, but it’s a way for the researchers to explain the curious patient whom Dr. Baglin first met in 2008, a 53-year old woman who spontaneously makes and carries the IgA prototype of ichorcumab in her blood.
Dr. Baglin said that he consulted on her case after a preprocedural clotting screen revealed that her blood was unclottable by standard tests, yet she had no history of any bleeding disorder. In fact, her history showed that she had undergone knee surgery (when no clotting screen had been done) 5 months before Dr. Baglin first saw her without any hint of a bleeding incident. She subsequently cut the tip of a finger while slicing with a mandolin, but her bleeding stopped spontaneously.
The patient goes through life with this antibody in her blood at a level of about 3 g/L with no bleeding problems whatsoever; yet in a mouse model, a substantially lower level of the mimic antibody, ichorcumab, effectively blocked thrombosis. In the mouse model, this effective dose of ichorcumab does not cause bleeding if the mouse’s tail is cut.
Dr. Baglin and his associates started a company in Cambridge, XO1, to fund the preclinical work and eventually commercialize ichorcumab. They believe it will be another 2 years before any person receives a dose of the antibody.
–BY MITCHEL L. ZOLER
On Twitter @mitchelzoler
It seems inescapable: If patients are made less able to form blood clots, they bleed more.
Bleeding is the perennial problem for anticoagulants. Whether it’s the traditional anticoagulants (heparin, warfarin, and the low-molecular-weight heparins) or new drugs (fondaparinux, dabigatran, rivaroxaban, and apixaban), as the anticoagulant’s potency or dosage increases to stop blood clots from forming, the inevitable downside is increased bleeding.
Maybe not.
A newly developed, synthetic human IgG antibody appears, in animal and in vitro models, to allow normal clotting to occur and stop bleeding at vessel tears and cuts, while short-circuiting pathologic clotting in intravascular spaces – the sorts of clots that cause venous thromboembolisms, myocardial infarctions, and strokes.
"It seems too good to be true. It’s beyond comprehension," said Dr. Trevor Baglin, the University of Cambridge, England, hematologist who discovered the first identified, naturally occurring example of this antibody, in IgA form, in a patient he initially saw in 2008. "All we can do is go forward and see if it genuinely is as good as it seems," he said while presenting his group’s initial animal findings with the antibody at the Congress of the International Society on Thrombosis and Haemostasis in Amsterdam earlier this month.
The antibody – which has been patented, synthesized, and is in extensive preclinical testing – has been named ichorcumab. In Greek mythology, "ichor" was the blood factor in gods that made them immortal.
The secret behind ichorcumab is that it binds to and inactivates exosite 1, the part of the thrombin molecule that cleaves fibrinogen into fibrin, an effective brake on clotting. Study results suggest that whether the exosite 1 portion of thrombin is exposed or hidden at various body sites accounts for ichorcumab’s varied effects.
"Our hypothesis is that exosite 1 is protected from the antibody [when a thrombin molecule sits] on a cell or clot surface, so hemostasis is unaffected, but thrombosis occurs in the luminal space, where exosite 1 is exposed an available to the antibody," Dr. Baglin explained.
"While before we thought of just one type of clot, [the work with ichorcumab so far] suggests there is not one clotting mechanism but two," he noted, one that leads to clot formation that stops bleeding, and a second mechanism that produces clots that cause thrombosis. Ichorcumab blocks the bad clots but not the good ones, because the clots form at different locations that affect the way that exosite 1 on thrombin is exposed.
It may sound farfetched, but it’s a way for the researchers to explain the curious patient whom Dr. Baglin first met in 2008, a 53-year old woman who spontaneously makes and carries the IgA prototype of ichorcumab in her blood.
Dr. Baglin said that he consulted on her case after a preprocedural clotting screen revealed that her blood was unclottable by standard tests, yet she had no history of any bleeding disorder. In fact, her history showed that she had undergone knee surgery (when no clotting screen had been done) 5 months before Dr. Baglin first saw her without any hint of a bleeding incident. She subsequently cut the tip of a finger while slicing with a mandolin, but her bleeding stopped spontaneously.
The patient goes through life with this antibody in her blood at a level of about 3 g/L with no bleeding problems whatsoever; yet in a mouse model, a substantially lower level of the mimic antibody, ichorcumab, effectively blocked thrombosis. In the mouse model, this effective dose of ichorcumab does not cause bleeding if the mouse’s tail is cut.
Dr. Baglin and his associates started a company in Cambridge, XO1, to fund the preclinical work and eventually commercialize ichorcumab. They believe it will be another 2 years before any person receives a dose of the antibody.
–BY MITCHEL L. ZOLER
On Twitter @mitchelzoler
It seems inescapable: If patients are made less able to form blood clots, they bleed more.
Bleeding is the perennial problem for anticoagulants. Whether it’s the traditional anticoagulants (heparin, warfarin, and the low-molecular-weight heparins) or new drugs (fondaparinux, dabigatran, rivaroxaban, and apixaban), as the anticoagulant’s potency or dosage increases to stop blood clots from forming, the inevitable downside is increased bleeding.
Maybe not.
A newly developed, synthetic human IgG antibody appears, in animal and in vitro models, to allow normal clotting to occur and stop bleeding at vessel tears and cuts, while short-circuiting pathologic clotting in intravascular spaces – the sorts of clots that cause venous thromboembolisms, myocardial infarctions, and strokes.
"It seems too good to be true. It’s beyond comprehension," said Dr. Trevor Baglin, the University of Cambridge, England, hematologist who discovered the first identified, naturally occurring example of this antibody, in IgA form, in a patient he initially saw in 2008. "All we can do is go forward and see if it genuinely is as good as it seems," he said while presenting his group’s initial animal findings with the antibody at the Congress of the International Society on Thrombosis and Haemostasis in Amsterdam earlier this month.
The antibody – which has been patented, synthesized, and is in extensive preclinical testing – has been named ichorcumab. In Greek mythology, "ichor" was the blood factor in gods that made them immortal.
The secret behind ichorcumab is that it binds to and inactivates exosite 1, the part of the thrombin molecule that cleaves fibrinogen into fibrin, an effective brake on clotting. Study results suggest that whether the exosite 1 portion of thrombin is exposed or hidden at various body sites accounts for ichorcumab’s varied effects.
"Our hypothesis is that exosite 1 is protected from the antibody [when a thrombin molecule sits] on a cell or clot surface, so hemostasis is unaffected, but thrombosis occurs in the luminal space, where exosite 1 is exposed an available to the antibody," Dr. Baglin explained.
"While before we thought of just one type of clot, [the work with ichorcumab so far] suggests there is not one clotting mechanism but two," he noted, one that leads to clot formation that stops bleeding, and a second mechanism that produces clots that cause thrombosis. Ichorcumab blocks the bad clots but not the good ones, because the clots form at different locations that affect the way that exosite 1 on thrombin is exposed.
It may sound farfetched, but it’s a way for the researchers to explain the curious patient whom Dr. Baglin first met in 2008, a 53-year old woman who spontaneously makes and carries the IgA prototype of ichorcumab in her blood.
Dr. Baglin said that he consulted on her case after a preprocedural clotting screen revealed that her blood was unclottable by standard tests, yet she had no history of any bleeding disorder. In fact, her history showed that she had undergone knee surgery (when no clotting screen had been done) 5 months before Dr. Baglin first saw her without any hint of a bleeding incident. She subsequently cut the tip of a finger while slicing with a mandolin, but her bleeding stopped spontaneously.
The patient goes through life with this antibody in her blood at a level of about 3 g/L with no bleeding problems whatsoever; yet in a mouse model, a substantially lower level of the mimic antibody, ichorcumab, effectively blocked thrombosis. In the mouse model, this effective dose of ichorcumab does not cause bleeding if the mouse’s tail is cut.
Dr. Baglin and his associates started a company in Cambridge, XO1, to fund the preclinical work and eventually commercialize ichorcumab. They believe it will be another 2 years before any person receives a dose of the antibody.
–BY MITCHEL L. ZOLER
On Twitter @mitchelzoler
Risks for poorer outcomes of ASO for TGA
Neoaortic root dilation and neoaortic valve regurgitation are common complications in infants with transposition of the great arteries who undergo an arterial switch operation for repair, and the risk of developing these changes in the neoaorta increases over time, according to the results of a retrospective database study of patients at Children’s Hospital of Wisconsin.
In addition, when dilation occurs, the dimensions may progressively enlarge over time, making it important to maintain lifelong surveillance of this population.
Although perioperative mortality and long-term survival (assessed up to 30 years) has improved in more recent eras for use of an arterial switch operation (ASO) for transposition of the great arteries (TGA), these long-term studies have also shown important late complications that may contribute to late morbidity and the need for reoperation, according to Dr. Jennifer G. Co-Vu and her colleagues at the Medical College of Wisconsin, Milwaukee.
They performed their study to determine the prevalence of neoaortic root dilation and neoaortic valve regurgitation in patients treated at their institution and to determine risk factors involved in the development of these late complications.
Out of 247 patients with TGA treated with an ASO at the hospital, there were 124 patients who had at least one available postoperative transthoracic echocardiogram at least 1 year after the ASO. Median age of these patients was 0.2 months at the time of their ASO and 7.2 years at their last follow-up; 71% were boys (Ann. Thorac. Surg. 2013;95:1654-9).
Retrospective measurements of the neoaortic annulus and root were performed on all available transthoracic echocardiograms and the severity of neoaortic valve regurgitation was determined by assessing the width of the color Doppler jet of regurgitation measured at the level of the valve in the parasternal long-axis view. A jet width of 1-4 mm was defined as trivial to mild; 4-6 mm was defined as moderate; and greater than 6 mm indicated severe regurgitation, according to the researchers. Significant regurgitation was defined as moderate or severe. Significant neoaortic annulus dilation was defined as a z score of 2.5 or greater.
They evaluated potential risk factors for the development of neoaortic root dilation, annulus dilation, and neoaortic valve regurgitation.
Significant neoaortic root dilation developed in 88 of 124 (66%) of the patients during follow-up, with the probability of being free from a root diameter z score of 2.5 or greater of 84%, 67%, 47%, and 32% at 1, 5, 10, and 15 years, respectively. Significant risk factors predicting neoaortic root dilation using multivariate analysis were a history of double outlet right ventricle (DORV), previous pulmonary artery (PA) banding, and length of follow-up. A history of ventricular septal defect (VSD), coarctation, left ventricular outflow tract obstruction, and age at ASO were not significant risk factors.
Significant annulus dilation occurred in 54% of patients, with significant risk factors including a history of VSD, history of DORV, and the presence of a dilated neoaortic root. History of PA banding and length of follow-up were not significant. Moderate or severe neoaortic valve regurgitation occurred in 17 of 124 (14%) of the patients, with a probability of being free of these levels of regurgitation of 96%, 92%, 89%, and 75% at 1, 5, 10, and 15 years, respectively. The significant risk factors for regurgitation were history of DORV, VSD, left ventricular outflow tract obstruction, and length of follow-up. No patient in the series required reintervention on the neoaorta.
The authors had no disclosures.
Most people living with congenital heart disease are now adults. Unfortunately the majority of these adults, for unclear reasons, are not receiving expert care by congenital heart specialists. Perhaps some of these adults have a misperception that they are cured. Dr. Co-Vu and coauthors at the Medical College of Wisconsin confirm that the highly successful arterial switch operation is not a "cure."
| Dr. Williams |
Their important, carefully executed echo study demonstrates important progressive increases in measured diameters of the neoaortic annulus and neoaortic root over the first 15 years of life. The
authors point out that the dilation has not as yet led to a need for reintervention, and the late prevalence of neoaortic regurgitation is not high, although it too is slowly increasing over time. Their message is a clarion call for lifelong clinical surveillance following an arterial switch operation – a message that should be applied to all patients with congenital heart disease.
Dr. William G. Williams is executive director of the Congenital Heart Surgeons’ Society Data Center, Toronto, and emeritus professor of surgery, University of Toronto, and an associate medical editor for Thoracic Surgery News.
Most people living with congenital heart disease are now adults. Unfortunately the majority of these adults, for unclear reasons, are not receiving expert care by congenital heart specialists. Perhaps some of these adults have a misperception that they are cured. Dr. Co-Vu and coauthors at the Medical College of Wisconsin confirm that the highly successful arterial switch operation is not a "cure."
| Dr. Williams |
Their important, carefully executed echo study demonstrates important progressive increases in measured diameters of the neoaortic annulus and neoaortic root over the first 15 years of life. The
authors point out that the dilation has not as yet led to a need for reintervention, and the late prevalence of neoaortic regurgitation is not high, although it too is slowly increasing over time. Their message is a clarion call for lifelong clinical surveillance following an arterial switch operation – a message that should be applied to all patients with congenital heart disease.
Dr. William G. Williams is executive director of the Congenital Heart Surgeons’ Society Data Center, Toronto, and emeritus professor of surgery, University of Toronto, and an associate medical editor for Thoracic Surgery News.
Most people living with congenital heart disease are now adults. Unfortunately the majority of these adults, for unclear reasons, are not receiving expert care by congenital heart specialists. Perhaps some of these adults have a misperception that they are cured. Dr. Co-Vu and coauthors at the Medical College of Wisconsin confirm that the highly successful arterial switch operation is not a "cure."
| Dr. Williams |
Their important, carefully executed echo study demonstrates important progressive increases in measured diameters of the neoaortic annulus and neoaortic root over the first 15 years of life. The
authors point out that the dilation has not as yet led to a need for reintervention, and the late prevalence of neoaortic regurgitation is not high, although it too is slowly increasing over time. Their message is a clarion call for lifelong clinical surveillance following an arterial switch operation – a message that should be applied to all patients with congenital heart disease.
Dr. William G. Williams is executive director of the Congenital Heart Surgeons’ Society Data Center, Toronto, and emeritus professor of surgery, University of Toronto, and an associate medical editor for Thoracic Surgery News.
Neoaortic root dilation and neoaortic valve regurgitation are common complications in infants with transposition of the great arteries who undergo an arterial switch operation for repair, and the risk of developing these changes in the neoaorta increases over time, according to the results of a retrospective database study of patients at Children’s Hospital of Wisconsin.
In addition, when dilation occurs, the dimensions may progressively enlarge over time, making it important to maintain lifelong surveillance of this population.
Although perioperative mortality and long-term survival (assessed up to 30 years) has improved in more recent eras for use of an arterial switch operation (ASO) for transposition of the great arteries (TGA), these long-term studies have also shown important late complications that may contribute to late morbidity and the need for reoperation, according to Dr. Jennifer G. Co-Vu and her colleagues at the Medical College of Wisconsin, Milwaukee.
They performed their study to determine the prevalence of neoaortic root dilation and neoaortic valve regurgitation in patients treated at their institution and to determine risk factors involved in the development of these late complications.
Out of 247 patients with TGA treated with an ASO at the hospital, there were 124 patients who had at least one available postoperative transthoracic echocardiogram at least 1 year after the ASO. Median age of these patients was 0.2 months at the time of their ASO and 7.2 years at their last follow-up; 71% were boys (Ann. Thorac. Surg. 2013;95:1654-9).
Retrospective measurements of the neoaortic annulus and root were performed on all available transthoracic echocardiograms and the severity of neoaortic valve regurgitation was determined by assessing the width of the color Doppler jet of regurgitation measured at the level of the valve in the parasternal long-axis view. A jet width of 1-4 mm was defined as trivial to mild; 4-6 mm was defined as moderate; and greater than 6 mm indicated severe regurgitation, according to the researchers. Significant regurgitation was defined as moderate or severe. Significant neoaortic annulus dilation was defined as a z score of 2.5 or greater.
They evaluated potential risk factors for the development of neoaortic root dilation, annulus dilation, and neoaortic valve regurgitation.
Significant neoaortic root dilation developed in 88 of 124 (66%) of the patients during follow-up, with the probability of being free from a root diameter z score of 2.5 or greater of 84%, 67%, 47%, and 32% at 1, 5, 10, and 15 years, respectively. Significant risk factors predicting neoaortic root dilation using multivariate analysis were a history of double outlet right ventricle (DORV), previous pulmonary artery (PA) banding, and length of follow-up. A history of ventricular septal defect (VSD), coarctation, left ventricular outflow tract obstruction, and age at ASO were not significant risk factors.
Significant annulus dilation occurred in 54% of patients, with significant risk factors including a history of VSD, history of DORV, and the presence of a dilated neoaortic root. History of PA banding and length of follow-up were not significant. Moderate or severe neoaortic valve regurgitation occurred in 17 of 124 (14%) of the patients, with a probability of being free of these levels of regurgitation of 96%, 92%, 89%, and 75% at 1, 5, 10, and 15 years, respectively. The significant risk factors for regurgitation were history of DORV, VSD, left ventricular outflow tract obstruction, and length of follow-up. No patient in the series required reintervention on the neoaorta.
The authors had no disclosures.
Neoaortic root dilation and neoaortic valve regurgitation are common complications in infants with transposition of the great arteries who undergo an arterial switch operation for repair, and the risk of developing these changes in the neoaorta increases over time, according to the results of a retrospective database study of patients at Children’s Hospital of Wisconsin.
In addition, when dilation occurs, the dimensions may progressively enlarge over time, making it important to maintain lifelong surveillance of this population.
Although perioperative mortality and long-term survival (assessed up to 30 years) has improved in more recent eras for use of an arterial switch operation (ASO) for transposition of the great arteries (TGA), these long-term studies have also shown important late complications that may contribute to late morbidity and the need for reoperation, according to Dr. Jennifer G. Co-Vu and her colleagues at the Medical College of Wisconsin, Milwaukee.
They performed their study to determine the prevalence of neoaortic root dilation and neoaortic valve regurgitation in patients treated at their institution and to determine risk factors involved in the development of these late complications.
Out of 247 patients with TGA treated with an ASO at the hospital, there were 124 patients who had at least one available postoperative transthoracic echocardiogram at least 1 year after the ASO. Median age of these patients was 0.2 months at the time of their ASO and 7.2 years at their last follow-up; 71% were boys (Ann. Thorac. Surg. 2013;95:1654-9).
Retrospective measurements of the neoaortic annulus and root were performed on all available transthoracic echocardiograms and the severity of neoaortic valve regurgitation was determined by assessing the width of the color Doppler jet of regurgitation measured at the level of the valve in the parasternal long-axis view. A jet width of 1-4 mm was defined as trivial to mild; 4-6 mm was defined as moderate; and greater than 6 mm indicated severe regurgitation, according to the researchers. Significant regurgitation was defined as moderate or severe. Significant neoaortic annulus dilation was defined as a z score of 2.5 or greater.
They evaluated potential risk factors for the development of neoaortic root dilation, annulus dilation, and neoaortic valve regurgitation.
Significant neoaortic root dilation developed in 88 of 124 (66%) of the patients during follow-up, with the probability of being free from a root diameter z score of 2.5 or greater of 84%, 67%, 47%, and 32% at 1, 5, 10, and 15 years, respectively. Significant risk factors predicting neoaortic root dilation using multivariate analysis were a history of double outlet right ventricle (DORV), previous pulmonary artery (PA) banding, and length of follow-up. A history of ventricular septal defect (VSD), coarctation, left ventricular outflow tract obstruction, and age at ASO were not significant risk factors.
Significant annulus dilation occurred in 54% of patients, with significant risk factors including a history of VSD, history of DORV, and the presence of a dilated neoaortic root. History of PA banding and length of follow-up were not significant. Moderate or severe neoaortic valve regurgitation occurred in 17 of 124 (14%) of the patients, with a probability of being free of these levels of regurgitation of 96%, 92%, 89%, and 75% at 1, 5, 10, and 15 years, respectively. The significant risk factors for regurgitation were history of DORV, VSD, left ventricular outflow tract obstruction, and length of follow-up. No patient in the series required reintervention on the neoaorta.
The authors had no disclosures.
Imperforate hymen in your adolescent patient: Don’t miss the diagnosis
Many gynecologists encounter imperforate hymen, a congenital vaginal anomaly, in general practice. As such, it is important to have a basic understanding of the condition and to be aware of appropriate screening, evaluation, and management. This knowledge will allow you to differentiate imperforate hymen from more complex anomalies—preventing significant morbidity that could result from performing the wrong surgical procedure on this condition—and to provide optimal surgical management.
How often and why does it occur?
Imperforate hymen occurs in approximately 1/1000 newborn girls. It is the most common obstructive anomaly of the female reproductive tract.1,2
The hymen consists of fibrous connective tissue attached to the vaginal wall. In the perinatal period, the hymen serves to separate the vaginal lumen from the urogenital sinus (UGS); this is usually perforated during embryonic life by canalization of the most caudal portion of the vaginal plate at the UGS. This establishes a connection between the lumen of the vaginal canal and the vaginal vestibule.3 Failure of the hymen to perforate completely in the perinatal period can result in varying anomalies, including imperforate (FIGURE 1), microperforate, cribiform, or septated hymen.
Figure 1. Imperforate hymen
How does it present?
Its presentation is variable and frequently asymptomatic in infants and children.4 As a result, the diagnosis is often delayed until puberty.3
In infancy. Newborns typically will present with a hymenal bulge from hydrocolpos or mucocolpos, which result from maternal estrogen secretion on the newborn’s vaginal epithelium.5 This is usually asymptomatic and self limited.
Rarely, large hydrocolpos/mucocolpos may become symptomatic and can lead to urinary obstruction, or they can present as an abdominal mass or intestinal obstruction.4
In adolescence. The majority of adolescents will present with cyclic or persistent pelvic pain and primary amenorrhea. If significant hematometra is present, an abdominal mass also may be palpated. In extreme cases, the patient may present with mass effect symptoms, including back pain, pain with defecation, constipation, nausea and vomiting, urinary retention, or hydronephrosis.6 Retrograde passage of blood into the fallopian tubes can cause hematosalpinx, which can lead to endometriosis and adhesion formation. Blood also may pass freely into the peritoneal cavity, forming hemoperitoneum.3
Related article: Your age-based guide to comprehensive well-woman care
Robert L. Barbieri, MD (October 2012)
Imperforate hymen, vaginal septum, or distal vaginal atresia?
When in doubt, refer. Imperforate hymen can be confused with distal vaginal atresia or low transverse vaginal septum. Often, the patient may present with similar signs and symptoms in all 3 cases. Accurately differentiating imperforate hymen from the former two more complex congenital anomalies prior to surgery is of utmost importance because management is very different, and performing the wrong procedure can result in serious morbidity. As such, it is important to appropriately define the anatomy and refer the complex cases to a specialist comfortable and skilled in managing congenital anomalies, usually a pediatric and adolescent gynecologist or reproductive endocrinologist.
Imperforate hymen
Examination of the external genitalia reveals a perineal bulge secondary to hematocolpos.7 This finding, coupled with a rectal examination and pelvic ultrasonography is usually sufficient to make the diagnosis.6,8 However, magnetic resonance imaging (MRI) of the pelvis should be obtained in cases where the diagnosis is uncertain or the physical exam is more consistent with vaginal septum or agenesis.
Transverse vaginal septum
A reverse septum results from failure of the müllerian duct derivatives and UGS to fuse or canalize. This can occur in the lower, middle, or upper portion of the vagina, and septa may be thick or thin.6 Low transverse septa are more easily confused with imperforate hymen. Examination usually reveals a normal hymen with a short vagina posteriorly. In cases of extreme hematocolpos, vaginal septa also may present with a perineal bulge but, again, this will be posterior to a normal hymen.
Distal vaginal atresia
This condition occurs during embryonic development when the UGS fails to contribute to the lower portion of the vagina (FIGURE 2).5 In cases of distal vaginal atresia there is a lack of vaginal orifice, or only a vaginal dimple may be present.5,6 Rectovaginal examination will reveal a palpable mass if the upper vagina is distended with blood.6
Figure 2. Lower vaginal atresia
MRI is vital to firm diagnosis
In addition to pelvic ultrasonography, pelvic MRI is necessary to delineate the anatomy with both vaginal septum (FIGURE 3) and lower vaginal atresia (FIGURE 4), as preoperative evaluation of location and thickness of a vaginal septum as well as measurement of the total length of agenesis is imperative.6-8 Misdiagnosis of the vaginal septa or atresia as an imperforate hymen can lead to significant scarring and stenosis and can make corrective surgical procedures difficult or suboptimal.
| Figure 3. MRI of transverse vaginal septum |
Figure 4. MRI of lower vaginal atresia
Surgical management: hymenectomy
Imperforate hymen is managed surgically with hymenectomy. Repair is generally reserved for the newborn period or, ideally, in adolescence, as at puberty the presence of estrogen aids in surgical repair and healing.5 Simple aspiration of hematocolpos/ mucocolpos can lead to ascending infection, and pyocolpos and should be avoided.6
The goal of hymenectomy is to:
-
open the hymeneal membrane to allow egress of fluid and menstrual flow
-
allow for tampon use
The procedure is relatively straightforward and usually is performed under general anesthesia, although regional anesthesia also is an option.
Steps to the varying hymenectomy incisions
Cruciate incision
1. Incise the hymen at the 2-, 4-, 8-, and 10-o’clock positions into four quadrants.
2. Excise the quadrants along the lateral wall of the vagina.
Elliptical incision
1. Make a circumferential incision with the Bovie electrocautery, incising the hymenal membrane close to the hymenal ring.
U-incision
1. Similar to the elliptical incision, use the Bovie electrocautery to incise the tissue close to the hymenal ring posterior and laterally in a “u” shape.
2. Make a horizontal incision superiorly to remove the extra tissue.
Vertical incision
This incision has been described in cases where there is an attempt to spare the hymen for religious or cultural preference.
1. Make a midline vertical hymenotomy less than 1 cm. Drain the borders of the hymen.
2. Apply suture obliquely to form a circular opening.
References
1. Dominguez C, Rock J, Horowitz I. Surgical conditions of the vagina and urethra. In: TeLinde’s Operative Gynecology. 10th ed. Philadelphia, PA: Lippincott Williams and Wilkins; 1997.
2. Basaran M, Usal D, Aydemir C. Hymen sparing surgery for imperforate hymen: case reports and review of literature. J Pediatr Adolesc Gynecol. 2009;22(4):e61–e64.
Tips to a successful procedure
Ensure adequate suctioning. Before starting the procedure, insert a Foley catheter to completely drain the bladder and delineate the urethra. Making an initial incision into the hymen usually results in the expulsion of the old blood and mucus, which can be very thick and viscous; therefore, it is important to have adequate suction tubing.
Prevent scarring. After evacuating the old blood and mucus, excise the hymeneal membrane with a cruciate incision as is traditionally described. Alternatively, some experts use an elliptical incision or u-incision. (See “Steps to the varying hymenectomy incisions”.) Prevent excision of the hymenal tissue too close to the vaginal mucosa, as this can lead to scarring and stenosis and dyspareunia.3
Suturing the mucosal margins is likely unnecessary in adolescent patients. After excision of the hymenal tissue, one option is to suture the mucosal margins of the hymenal ring in an interrupted fashion with a fine, delayed-absorbable suture. Alternatively, at our institution, where we employ the u-incision (FIGURE 5), we assure hemostasis of the mucosal margins and do not suture the margins. Suturing the margins is believed to prevent adherence of the edges; however, in the pubertal girl, adherence is unlikely secondary to estrogen exposure.
Figure 5. Surgical correction with u-incision
Avoid infection; do not irrigate. We do not recommend that you irrigate the vagina and perform unnecessary uterine manipulation, as this may introduce bacteria into the dilated cervix and uterus.3,8
Septate/microperforate/cribiform hymen
These other hymeneal anomalies also may require surgical correction if they become clinically significant. Patients may present with difficulty inserting or removing a tampon, insertional dyspareunia, or incomplete drainage of menstrual blood.6
Imaging is usually not indicated to diagnose these hymenal anomalies, as physical examination will reveal a patent vaginal tract. A moistened Q-tip can be placed into the orifice or behind the septate hymen for confirmation (FIGURE 6).
Surgical correction of a microperforate or cribiform hymen is performed using the same principles as imperforate hymen.
Surgical correction of a septate hymen involves tying and suturing or clamping with a hemostat the upper and lower edges, with the excess hymenal tissue between the sutures then excised.8
Figure 6. Septate hymen
Postop care and follow up
Postoperative analgesia with lidocaine jelly or ice packs is usually sufficient for pain management. Reinforce proper hygienic care measures. At 2- to 3-week follow up, assess the patient for healing and evaluate the size of the hymenal orifice.
Key takeaways
-Differentiating imperforate hymen from low transverse vaginal septum or distal vaginal agenesis prior to surgery is of utmost importance because management is very different, and performing the wrong procedure can result in serious morbidity.
-With imperforate hymen, examination of the external genitalia reveals a perineal bulge secondary to hematocolpos.
-Pelvic MRI is essential to delineate the anatomy with both vaginal septum and agenesis, for preoperative evaluation of location and thickness of septum as well as measurement of total length of agenesis.
-Hymenectomy is relatively straightforward and may be performed using a cruciate, elliptical, or u-incision.
-Care should be taken to prevent excision of hymeneal tissue too close to the vaginal mucosa, as this can lead to scarring and stenosis, and later lead to dyspareunia.
Many gynecologists encounter imperforate hymen, a congenital vaginal anomaly, in general practice. As such, it is important to have a basic understanding of the condition and to be aware of appropriate screening, evaluation, and management. This knowledge will allow you to differentiate imperforate hymen from more complex anomalies—preventing significant morbidity that could result from performing the wrong surgical procedure on this condition—and to provide optimal surgical management.
How often and why does it occur?
Imperforate hymen occurs in approximately 1/1000 newborn girls. It is the most common obstructive anomaly of the female reproductive tract.1,2
The hymen consists of fibrous connective tissue attached to the vaginal wall. In the perinatal period, the hymen serves to separate the vaginal lumen from the urogenital sinus (UGS); this is usually perforated during embryonic life by canalization of the most caudal portion of the vaginal plate at the UGS. This establishes a connection between the lumen of the vaginal canal and the vaginal vestibule.3 Failure of the hymen to perforate completely in the perinatal period can result in varying anomalies, including imperforate (FIGURE 1), microperforate, cribiform, or septated hymen.
Figure 1. Imperforate hymen
How does it present?
Its presentation is variable and frequently asymptomatic in infants and children.4 As a result, the diagnosis is often delayed until puberty.3
In infancy. Newborns typically will present with a hymenal bulge from hydrocolpos or mucocolpos, which result from maternal estrogen secretion on the newborn’s vaginal epithelium.5 This is usually asymptomatic and self limited.
Rarely, large hydrocolpos/mucocolpos may become symptomatic and can lead to urinary obstruction, or they can present as an abdominal mass or intestinal obstruction.4
In adolescence. The majority of adolescents will present with cyclic or persistent pelvic pain and primary amenorrhea. If significant hematometra is present, an abdominal mass also may be palpated. In extreme cases, the patient may present with mass effect symptoms, including back pain, pain with defecation, constipation, nausea and vomiting, urinary retention, or hydronephrosis.6 Retrograde passage of blood into the fallopian tubes can cause hematosalpinx, which can lead to endometriosis and adhesion formation. Blood also may pass freely into the peritoneal cavity, forming hemoperitoneum.3
Related article: Your age-based guide to comprehensive well-woman care
Robert L. Barbieri, MD (October 2012)
Imperforate hymen, vaginal septum, or distal vaginal atresia?
When in doubt, refer. Imperforate hymen can be confused with distal vaginal atresia or low transverse vaginal septum. Often, the patient may present with similar signs and symptoms in all 3 cases. Accurately differentiating imperforate hymen from the former two more complex congenital anomalies prior to surgery is of utmost importance because management is very different, and performing the wrong procedure can result in serious morbidity. As such, it is important to appropriately define the anatomy and refer the complex cases to a specialist comfortable and skilled in managing congenital anomalies, usually a pediatric and adolescent gynecologist or reproductive endocrinologist.
Imperforate hymen
Examination of the external genitalia reveals a perineal bulge secondary to hematocolpos.7 This finding, coupled with a rectal examination and pelvic ultrasonography is usually sufficient to make the diagnosis.6,8 However, magnetic resonance imaging (MRI) of the pelvis should be obtained in cases where the diagnosis is uncertain or the physical exam is more consistent with vaginal septum or agenesis.
Transverse vaginal septum
A reverse septum results from failure of the müllerian duct derivatives and UGS to fuse or canalize. This can occur in the lower, middle, or upper portion of the vagina, and septa may be thick or thin.6 Low transverse septa are more easily confused with imperforate hymen. Examination usually reveals a normal hymen with a short vagina posteriorly. In cases of extreme hematocolpos, vaginal septa also may present with a perineal bulge but, again, this will be posterior to a normal hymen.
Distal vaginal atresia
This condition occurs during embryonic development when the UGS fails to contribute to the lower portion of the vagina (FIGURE 2).5 In cases of distal vaginal atresia there is a lack of vaginal orifice, or only a vaginal dimple may be present.5,6 Rectovaginal examination will reveal a palpable mass if the upper vagina is distended with blood.6
Figure 2. Lower vaginal atresia
MRI is vital to firm diagnosis
In addition to pelvic ultrasonography, pelvic MRI is necessary to delineate the anatomy with both vaginal septum (FIGURE 3) and lower vaginal atresia (FIGURE 4), as preoperative evaluation of location and thickness of a vaginal septum as well as measurement of the total length of agenesis is imperative.6-8 Misdiagnosis of the vaginal septa or atresia as an imperforate hymen can lead to significant scarring and stenosis and can make corrective surgical procedures difficult or suboptimal.
| Figure 3. MRI of transverse vaginal septum |
Figure 4. MRI of lower vaginal atresia
Surgical management: hymenectomy
Imperforate hymen is managed surgically with hymenectomy. Repair is generally reserved for the newborn period or, ideally, in adolescence, as at puberty the presence of estrogen aids in surgical repair and healing.5 Simple aspiration of hematocolpos/ mucocolpos can lead to ascending infection, and pyocolpos and should be avoided.6
The goal of hymenectomy is to:
-
open the hymeneal membrane to allow egress of fluid and menstrual flow
-
allow for tampon use
The procedure is relatively straightforward and usually is performed under general anesthesia, although regional anesthesia also is an option.
Steps to the varying hymenectomy incisions
Cruciate incision
1. Incise the hymen at the 2-, 4-, 8-, and 10-o’clock positions into four quadrants.
2. Excise the quadrants along the lateral wall of the vagina.
Elliptical incision
1. Make a circumferential incision with the Bovie electrocautery, incising the hymenal membrane close to the hymenal ring.
U-incision
1. Similar to the elliptical incision, use the Bovie electrocautery to incise the tissue close to the hymenal ring posterior and laterally in a “u” shape.
2. Make a horizontal incision superiorly to remove the extra tissue.
Vertical incision
This incision has been described in cases where there is an attempt to spare the hymen for religious or cultural preference.
1. Make a midline vertical hymenotomy less than 1 cm. Drain the borders of the hymen.
2. Apply suture obliquely to form a circular opening.
References
1. Dominguez C, Rock J, Horowitz I. Surgical conditions of the vagina and urethra. In: TeLinde’s Operative Gynecology. 10th ed. Philadelphia, PA: Lippincott Williams and Wilkins; 1997.
2. Basaran M, Usal D, Aydemir C. Hymen sparing surgery for imperforate hymen: case reports and review of literature. J Pediatr Adolesc Gynecol. 2009;22(4):e61–e64.
Tips to a successful procedure
Ensure adequate suctioning. Before starting the procedure, insert a Foley catheter to completely drain the bladder and delineate the urethra. Making an initial incision into the hymen usually results in the expulsion of the old blood and mucus, which can be very thick and viscous; therefore, it is important to have adequate suction tubing.
Prevent scarring. After evacuating the old blood and mucus, excise the hymeneal membrane with a cruciate incision as is traditionally described. Alternatively, some experts use an elliptical incision or u-incision. (See “Steps to the varying hymenectomy incisions”.) Prevent excision of the hymenal tissue too close to the vaginal mucosa, as this can lead to scarring and stenosis and dyspareunia.3
Suturing the mucosal margins is likely unnecessary in adolescent patients. After excision of the hymenal tissue, one option is to suture the mucosal margins of the hymenal ring in an interrupted fashion with a fine, delayed-absorbable suture. Alternatively, at our institution, where we employ the u-incision (FIGURE 5), we assure hemostasis of the mucosal margins and do not suture the margins. Suturing the margins is believed to prevent adherence of the edges; however, in the pubertal girl, adherence is unlikely secondary to estrogen exposure.
Figure 5. Surgical correction with u-incision
Avoid infection; do not irrigate. We do not recommend that you irrigate the vagina and perform unnecessary uterine manipulation, as this may introduce bacteria into the dilated cervix and uterus.3,8
Septate/microperforate/cribiform hymen
These other hymeneal anomalies also may require surgical correction if they become clinically significant. Patients may present with difficulty inserting or removing a tampon, insertional dyspareunia, or incomplete drainage of menstrual blood.6
Imaging is usually not indicated to diagnose these hymenal anomalies, as physical examination will reveal a patent vaginal tract. A moistened Q-tip can be placed into the orifice or behind the septate hymen for confirmation (FIGURE 6).
Surgical correction of a microperforate or cribiform hymen is performed using the same principles as imperforate hymen.
Surgical correction of a septate hymen involves tying and suturing or clamping with a hemostat the upper and lower edges, with the excess hymenal tissue between the sutures then excised.8
Figure 6. Septate hymen
Postop care and follow up
Postoperative analgesia with lidocaine jelly or ice packs is usually sufficient for pain management. Reinforce proper hygienic care measures. At 2- to 3-week follow up, assess the patient for healing and evaluate the size of the hymenal orifice.
Key takeaways
-Differentiating imperforate hymen from low transverse vaginal septum or distal vaginal agenesis prior to surgery is of utmost importance because management is very different, and performing the wrong procedure can result in serious morbidity.
-With imperforate hymen, examination of the external genitalia reveals a perineal bulge secondary to hematocolpos.
-Pelvic MRI is essential to delineate the anatomy with both vaginal septum and agenesis, for preoperative evaluation of location and thickness of septum as well as measurement of total length of agenesis.
-Hymenectomy is relatively straightforward and may be performed using a cruciate, elliptical, or u-incision.
-Care should be taken to prevent excision of hymeneal tissue too close to the vaginal mucosa, as this can lead to scarring and stenosis, and later lead to dyspareunia.
Many gynecologists encounter imperforate hymen, a congenital vaginal anomaly, in general practice. As such, it is important to have a basic understanding of the condition and to be aware of appropriate screening, evaluation, and management. This knowledge will allow you to differentiate imperforate hymen from more complex anomalies—preventing significant morbidity that could result from performing the wrong surgical procedure on this condition—and to provide optimal surgical management.
How often and why does it occur?
Imperforate hymen occurs in approximately 1/1000 newborn girls. It is the most common obstructive anomaly of the female reproductive tract.1,2
The hymen consists of fibrous connective tissue attached to the vaginal wall. In the perinatal period, the hymen serves to separate the vaginal lumen from the urogenital sinus (UGS); this is usually perforated during embryonic life by canalization of the most caudal portion of the vaginal plate at the UGS. This establishes a connection between the lumen of the vaginal canal and the vaginal vestibule.3 Failure of the hymen to perforate completely in the perinatal period can result in varying anomalies, including imperforate (FIGURE 1), microperforate, cribiform, or septated hymen.
Figure 1. Imperforate hymen
How does it present?
Its presentation is variable and frequently asymptomatic in infants and children.4 As a result, the diagnosis is often delayed until puberty.3
In infancy. Newborns typically will present with a hymenal bulge from hydrocolpos or mucocolpos, which result from maternal estrogen secretion on the newborn’s vaginal epithelium.5 This is usually asymptomatic and self limited.
Rarely, large hydrocolpos/mucocolpos may become symptomatic and can lead to urinary obstruction, or they can present as an abdominal mass or intestinal obstruction.4
In adolescence. The majority of adolescents will present with cyclic or persistent pelvic pain and primary amenorrhea. If significant hematometra is present, an abdominal mass also may be palpated. In extreme cases, the patient may present with mass effect symptoms, including back pain, pain with defecation, constipation, nausea and vomiting, urinary retention, or hydronephrosis.6 Retrograde passage of blood into the fallopian tubes can cause hematosalpinx, which can lead to endometriosis and adhesion formation. Blood also may pass freely into the peritoneal cavity, forming hemoperitoneum.3
Related article: Your age-based guide to comprehensive well-woman care
Robert L. Barbieri, MD (October 2012)
Imperforate hymen, vaginal septum, or distal vaginal atresia?
When in doubt, refer. Imperforate hymen can be confused with distal vaginal atresia or low transverse vaginal septum. Often, the patient may present with similar signs and symptoms in all 3 cases. Accurately differentiating imperforate hymen from the former two more complex congenital anomalies prior to surgery is of utmost importance because management is very different, and performing the wrong procedure can result in serious morbidity. As such, it is important to appropriately define the anatomy and refer the complex cases to a specialist comfortable and skilled in managing congenital anomalies, usually a pediatric and adolescent gynecologist or reproductive endocrinologist.
Imperforate hymen
Examination of the external genitalia reveals a perineal bulge secondary to hematocolpos.7 This finding, coupled with a rectal examination and pelvic ultrasonography is usually sufficient to make the diagnosis.6,8 However, magnetic resonance imaging (MRI) of the pelvis should be obtained in cases where the diagnosis is uncertain or the physical exam is more consistent with vaginal septum or agenesis.
Transverse vaginal septum
A reverse septum results from failure of the müllerian duct derivatives and UGS to fuse or canalize. This can occur in the lower, middle, or upper portion of the vagina, and septa may be thick or thin.6 Low transverse septa are more easily confused with imperforate hymen. Examination usually reveals a normal hymen with a short vagina posteriorly. In cases of extreme hematocolpos, vaginal septa also may present with a perineal bulge but, again, this will be posterior to a normal hymen.
Distal vaginal atresia
This condition occurs during embryonic development when the UGS fails to contribute to the lower portion of the vagina (FIGURE 2).5 In cases of distal vaginal atresia there is a lack of vaginal orifice, or only a vaginal dimple may be present.5,6 Rectovaginal examination will reveal a palpable mass if the upper vagina is distended with blood.6
Figure 2. Lower vaginal atresia
MRI is vital to firm diagnosis
In addition to pelvic ultrasonography, pelvic MRI is necessary to delineate the anatomy with both vaginal septum (FIGURE 3) and lower vaginal atresia (FIGURE 4), as preoperative evaluation of location and thickness of a vaginal septum as well as measurement of the total length of agenesis is imperative.6-8 Misdiagnosis of the vaginal septa or atresia as an imperforate hymen can lead to significant scarring and stenosis and can make corrective surgical procedures difficult or suboptimal.
| Figure 3. MRI of transverse vaginal septum |
Figure 4. MRI of lower vaginal atresia
Surgical management: hymenectomy
Imperforate hymen is managed surgically with hymenectomy. Repair is generally reserved for the newborn period or, ideally, in adolescence, as at puberty the presence of estrogen aids in surgical repair and healing.5 Simple aspiration of hematocolpos/ mucocolpos can lead to ascending infection, and pyocolpos and should be avoided.6
The goal of hymenectomy is to:
-
open the hymeneal membrane to allow egress of fluid and menstrual flow
-
allow for tampon use
The procedure is relatively straightforward and usually is performed under general anesthesia, although regional anesthesia also is an option.
Steps to the varying hymenectomy incisions
Cruciate incision
1. Incise the hymen at the 2-, 4-, 8-, and 10-o’clock positions into four quadrants.
2. Excise the quadrants along the lateral wall of the vagina.
Elliptical incision
1. Make a circumferential incision with the Bovie electrocautery, incising the hymenal membrane close to the hymenal ring.
U-incision
1. Similar to the elliptical incision, use the Bovie electrocautery to incise the tissue close to the hymenal ring posterior and laterally in a “u” shape.
2. Make a horizontal incision superiorly to remove the extra tissue.
Vertical incision
This incision has been described in cases where there is an attempt to spare the hymen for religious or cultural preference.
1. Make a midline vertical hymenotomy less than 1 cm. Drain the borders of the hymen.
2. Apply suture obliquely to form a circular opening.
References
1. Dominguez C, Rock J, Horowitz I. Surgical conditions of the vagina and urethra. In: TeLinde’s Operative Gynecology. 10th ed. Philadelphia, PA: Lippincott Williams and Wilkins; 1997.
2. Basaran M, Usal D, Aydemir C. Hymen sparing surgery for imperforate hymen: case reports and review of literature. J Pediatr Adolesc Gynecol. 2009;22(4):e61–e64.
Tips to a successful procedure
Ensure adequate suctioning. Before starting the procedure, insert a Foley catheter to completely drain the bladder and delineate the urethra. Making an initial incision into the hymen usually results in the expulsion of the old blood and mucus, which can be very thick and viscous; therefore, it is important to have adequate suction tubing.
Prevent scarring. After evacuating the old blood and mucus, excise the hymeneal membrane with a cruciate incision as is traditionally described. Alternatively, some experts use an elliptical incision or u-incision. (See “Steps to the varying hymenectomy incisions”.) Prevent excision of the hymenal tissue too close to the vaginal mucosa, as this can lead to scarring and stenosis and dyspareunia.3
Suturing the mucosal margins is likely unnecessary in adolescent patients. After excision of the hymenal tissue, one option is to suture the mucosal margins of the hymenal ring in an interrupted fashion with a fine, delayed-absorbable suture. Alternatively, at our institution, where we employ the u-incision (FIGURE 5), we assure hemostasis of the mucosal margins and do not suture the margins. Suturing the margins is believed to prevent adherence of the edges; however, in the pubertal girl, adherence is unlikely secondary to estrogen exposure.
Figure 5. Surgical correction with u-incision
Avoid infection; do not irrigate. We do not recommend that you irrigate the vagina and perform unnecessary uterine manipulation, as this may introduce bacteria into the dilated cervix and uterus.3,8
Septate/microperforate/cribiform hymen
These other hymeneal anomalies also may require surgical correction if they become clinically significant. Patients may present with difficulty inserting or removing a tampon, insertional dyspareunia, or incomplete drainage of menstrual blood.6
Imaging is usually not indicated to diagnose these hymenal anomalies, as physical examination will reveal a patent vaginal tract. A moistened Q-tip can be placed into the orifice or behind the septate hymen for confirmation (FIGURE 6).
Surgical correction of a microperforate or cribiform hymen is performed using the same principles as imperforate hymen.
Surgical correction of a septate hymen involves tying and suturing or clamping with a hemostat the upper and lower edges, with the excess hymenal tissue between the sutures then excised.8
Figure 6. Septate hymen
Postop care and follow up
Postoperative analgesia with lidocaine jelly or ice packs is usually sufficient for pain management. Reinforce proper hygienic care measures. At 2- to 3-week follow up, assess the patient for healing and evaluate the size of the hymenal orifice.
Key takeaways
-Differentiating imperforate hymen from low transverse vaginal septum or distal vaginal agenesis prior to surgery is of utmost importance because management is very different, and performing the wrong procedure can result in serious morbidity.
-With imperforate hymen, examination of the external genitalia reveals a perineal bulge secondary to hematocolpos.
-Pelvic MRI is essential to delineate the anatomy with both vaginal septum and agenesis, for preoperative evaluation of location and thickness of septum as well as measurement of total length of agenesis.
-Hymenectomy is relatively straightforward and may be performed using a cruciate, elliptical, or u-incision.
-Care should be taken to prevent excision of hymeneal tissue too close to the vaginal mucosa, as this can lead to scarring and stenosis, and later lead to dyspareunia.
The Affordable Care Act and the drive for electronic health records: Are small practices being squeezed?
Two years ago, I zeroed in on the pressures straining small ObGyn practices in an article entitled, “Is private ObGyn practice on its way out?”1 The pressures haven’t eased in the interim. Today, small practices are still feeling squeezed to keep up with the many demands of modern specialty care. The push for electronic health records (EHRs), in particular, can profoundly affect physicians in private practice.
In this article, I outline some of the challenges facing small practices when they set out to implement EHRs, as well as the potential benefits they stand to gain a little farther down the road. Before we begin, however, let’s look at the latest trends in ObGyn practice, as they are related, in part, to the need to implement EHRs.
The exodus from private practice continues
A 2012 Accenture Physicians Alignment Survey shows an accelerating increase in physician employment. In 2000, 57% of all physicians were in independent practice; by the end of 2013, only 36% of physicians are projected to remain independent.2
The ObGyn specialty is a clear part of this trend, with both seasoned and incoming physicians finding hospital or other employment an attractive alternative to private practice. Fully one-third of ObGyn residents entering practice today sign hospital employment contracts. ObGyns who have made the switch from private to hospital practice, or who have become ObGyn hospitalists, often point to the difficulties of maintaining a solvent private practice, especially given the push toward EHRs and increasing regulatory and administrative burdens, as justification for their move.
The main reasons for the shift to employment. Top concerns influencing physicians’ decisions to opt for employment include:
- business expenses (87%)
- the dominance of managed care (61%)
- the requirement for EHRs (53%)
- the need to maintain and manage staff (53%)
- the increasing number of patients needed to break even (39%).2
A 2008 socioeconomic survey from ACOG revealed that 23.6% of ObGyn practices are solo practices, and 27.1% are single-specialty group practices. Many ObGyns—especially those in solo or small practices—are hesitant to make the large capital investment that is necessary to adopt EHRs.
EHRs offer benefits—and real costs
The system-wide benefits of health information technology (HIT), including EHRs, are many. Insurers stand to save money by reducing unnecessary tests, and patients will benefit from better coordination of their care and fewer medical errors. But these advantages don’t necessarily translate into savings or revenue for physician practices. Instead, physicians face payment cuts from Medicare and private insurance.
Although there’s wide agreement that HIT can improve quality of care and reduce health-care costs, fewer than one-quarter (22%) of office-based physicians had adopted EHRs by 2009. We know the main reasons why:
- upfront cost and maintenance expense
- uncertain return on investment
- fragmented business model in a high proportion of small and solo practices
- changing and inconsistent information technology (IT) systems.
What can a practice expect to fork over?
In 2011, the Agency for Healthcare Research and Quality (AHRQ) found that the “real-life” cost of implementing EHRs “in an average five-physician primary care practice, operating within a large physician network committed to network-wide implementation of electronic health records, is about $162,000, with an additional $85,500 in maintenance expenses during the first year.”3
These figures include an average of 134 hours needed per physician to prepare to use EHRs during patient visits.3
Fleming and colleagues investigated the cost associated with implementing EHRs within 26 primary care practices in Texas. They found the cost to be $32,409 per physician through the first 60 days after the EHR system was launched, with one-time costs for hardware of $25,000 per practice and an additional $7,000 per physician for personal computers, printers, and scanners. The annual cost of software and maintenance was approximately $17,100 per physician.4
Why physicians should hold out for the return on their investment
Despite these considerable expenses, EHRs hold promise over the long term. The Medical Group Management Association reported, through a 2009 survey of about 1,300 primary care and specialty practice members using EHRs, that efficiency gains from the elimination of paper charts, as well as transcription savings, better charge capturing, and reduced billing errors, resulted in a median revenue increase of $49,916 per full-time physician after operating costs.
After 5 years of EHR use, practices reported a median operating margin 10.1% higher than that of practices in the first year of EHR use.5
Trends in the adoption of EHRs
Private practice. An article in Health Affairs showed that, by 2011, only one in six office-based physicians was using an EHR system robust enough to approach “meaningful use”—that is, the use of EHRs to measurably improve the quality of health care.6 These robust systems offered physicians the ability to record information on patient demographics, view laboratory and imaging results, maintain patients’ problem lists, compile clinical notes, and manage prescription ordering. EHR adoption lagged among non−primary care physicians, physicians aged 55 and older, and physicians in small (1–2 providers) practices and physician-owned practices.6 (ObGyns were considered primary care providers in this survey.)
“Big” practice. By comparison, in 2011, 99% of physicians in health maintenance organizations, or HMOs, and 73% in academic health centers and other hospitals used EHR systems.6 The number of physicians in these practice settings is small but growing.
In 2011, only 17% of physicians were in large practices of 10 or more physicians; 40% were in practices of one or two physicians.6
Primary care. These practices lead others in the adoption of EHRs, in part because of federal assistance, including a nationwide system of regional HIT assistance centers established by the Health Information Technology for Economic and Clinical Health (HITECH) Act to help providers located in rural areas participate in the Centers for Medicare and Medicaid Services (CMS) programs in EHR. The goal of these programs is to provide HIT support to at least 100,000 primary care providers, including ObGyns, by 2014.
The numbers cited in the Health Affairs article largely mirror data developed by other research organizations, including the Deloitte Center for Health Solutions.6
The EHR incentive
The drive for EHRs started long before the Affordable Care Act (ACA) was passed in 2010. The US Congress took a first stab at encouraging the health-care community to embrace HIT in 1996, when it passed the Health Insurance Portability and Accountability Act (HIPAA). HIPAA created an electronic data interchange that health plans, health-care clearinghouses, and certain health-care providers, including pharmacists, are required to use for electronic transactions, including:
- claims and encounter information
- payment and remittance advice
- claims status
- eligibility
- enrollment and disenrollment
- referrals and authorizations
- coordination of benefits
- premium payment.
Congress stepped up its game in 2009, when it offered higher Medicare and Medicaid payments to physicians who adopt and “meaningfully use” EHRs. The HITECH Act included $30 billion in new Medicare and Medicaid incentive payments—as much as $44,000 under Medicare and $63,750 under Medicaid—as well as $500 million for states to develop health information exchanges.
The Act also established a government-led process for certification of electronic health records through a $35 billion appropriation for the Office of the National Coordinator for Health IT, housed in CMS.
Other programs designed to encourage use of EHRs
Other federal programs include the Physician Quality Reporting System (PQRS), which, when created in 2006, was a voluntary physician electronic reporting program. Under the ACA, however, it has become a mandate. Starting in 2015, Medicare payments will be reduced for nonparticipating physicians.
The Electronic Prescribing (eRx) Incentive Program, created in 2008 under the Medicare Improvements for Patients and Providers Act, provides incentives for eligible physicians who e-prescribe Medicare Part D medications through a qualified system. This program converted to a penalty program last year for physicians who don’t use eRx.
Grants were also provided under the HITECH Act to fund an HIT infrastructure and low-interest HIT loans. The AHRQ has awarded $300 million in federal grant money to more than 200 projects in 48 states to promote access to and encourage HIT adoption. Over $150 million in Medicaid transformation grants have been awarded to three states and territories for HIT in the Medicaid program under the 2005 Deficit Reduction Act.
The ACA carried these initiatives even further by establishing uniform standards that HIT systems must meet, including:
- automatic reconciliation of electronic fund transfers and HIPAA payment and remittance
- improved claims payment process
- consistent methods of health plan enrollment and claim edits
- simplified and improved routing of health-care transactions
- electronic claims attachments.
Clearly, a lot of effort and taxpayer dollars have been dedicated to drive efficient use of HIT and EHRs in the hopes that they can:
- help make sense of our increasingly fragmented health-care system
- improve patient safety
- increase efficiency
- reduce paperwork
- reduce unnecessary tests
- better coordinate patient care.
To see which providers are cashing in on the government’s incentives for EHRs, see “Some physicians are more likely to seek incentives for meaningful use of EHRs” on page 37.
The long view
HIT and EHRs are here to stay. Products are maturing and improving. Acceptance by large and small practices has gained traction. Are small practices being squeezed? No doubt.
In 2011, I urged all ObGyns—especially those in private practice—to read an article written by President Barack Obama’s health-reform deputies on how physicians can be successful under the ACA.1 It reads, in part:
To realize the full benefits of the Affordable Care Act, physicians will need to embrace rather than resist change. The economic forces put in motion by the Act are likely to lead to vertical organization of providers and accelerate physician employment by hospitals and aggregation into larger physician groups. The most successful physicians will be those who most effectively collaborate with other providers to improve outcomes, care productivity, and patient experience.7
1. DiVenere L, Yates J. Is private ObGyn practice on its way out? OBG Manage. 2011;23(10):42–54.
2. More US doctors leaving private practice due to rising costs and technology mandates, Accenture report finds [news release]. Arlington, Virginia: Accenture Newsroom; October 31, 2012. http://newsroom.accenture.com/news/more-us-doctors-leaving-private-practice-due-to-rising-costs-and-technology-mandates-accenture-report-finds.htm. Accessed June 5, 2013.
3. Study identifies costs of implementing electronic health records in network of physician practices: Research Activities October 2011, No. 374. Rockville, MD: Agency for Healthcare Research and Quality. http://www.ahrq.gov/news/newsletters/research-activities/oct11/1011RA15.html. Accessed June 5, 2013.
5. MGMA survey: Medical groups with EHRs report better financial performance than practices with paper medical records [news release]. New Orleans, Louisiana: Medical Group Management Association; October 25, 2010. http://www.mgma.com/press/default.aspx?id=39824. Accessed June 6, 2013.
8. US Government Accountability Office. Electronic Health Records: Number and Characteristics of Providers Awarded Medicaid Incentive Payments for 2011. GAO-13-146R. December 13, 2012. http://www.gao.gov/products/GAO-13-146R. Accessed June 6, 2013.
9. US Government Accountability Office. Electronic Health Records: Number and Characteristics of Providers Awarded Medicare Incentive Payments for 2011. GAO-12-778R. July 26, 2012. http://www.gao.gov/products/GAO-12-778R. Accessed June 6, 2013.
10. US Department of Health and Human Services. Doctors’ and hospitals’ use of health IT more than doubles since 2012 [news release]. Washington, DC: HHS.gov; May 22, 2013. http://www.hhs.gov/news/press/2013pres/05/20130522a.html. Accessed June 6, 2013.
Two years ago, I zeroed in on the pressures straining small ObGyn practices in an article entitled, “Is private ObGyn practice on its way out?”1 The pressures haven’t eased in the interim. Today, small practices are still feeling squeezed to keep up with the many demands of modern specialty care. The push for electronic health records (EHRs), in particular, can profoundly affect physicians in private practice.
In this article, I outline some of the challenges facing small practices when they set out to implement EHRs, as well as the potential benefits they stand to gain a little farther down the road. Before we begin, however, let’s look at the latest trends in ObGyn practice, as they are related, in part, to the need to implement EHRs.
The exodus from private practice continues
A 2012 Accenture Physicians Alignment Survey shows an accelerating increase in physician employment. In 2000, 57% of all physicians were in independent practice; by the end of 2013, only 36% of physicians are projected to remain independent.2
The ObGyn specialty is a clear part of this trend, with both seasoned and incoming physicians finding hospital or other employment an attractive alternative to private practice. Fully one-third of ObGyn residents entering practice today sign hospital employment contracts. ObGyns who have made the switch from private to hospital practice, or who have become ObGyn hospitalists, often point to the difficulties of maintaining a solvent private practice, especially given the push toward EHRs and increasing regulatory and administrative burdens, as justification for their move.
The main reasons for the shift to employment. Top concerns influencing physicians’ decisions to opt for employment include:
- business expenses (87%)
- the dominance of managed care (61%)
- the requirement for EHRs (53%)
- the need to maintain and manage staff (53%)
- the increasing number of patients needed to break even (39%).2
A 2008 socioeconomic survey from ACOG revealed that 23.6% of ObGyn practices are solo practices, and 27.1% are single-specialty group practices. Many ObGyns—especially those in solo or small practices—are hesitant to make the large capital investment that is necessary to adopt EHRs.
EHRs offer benefits—and real costs
The system-wide benefits of health information technology (HIT), including EHRs, are many. Insurers stand to save money by reducing unnecessary tests, and patients will benefit from better coordination of their care and fewer medical errors. But these advantages don’t necessarily translate into savings or revenue for physician practices. Instead, physicians face payment cuts from Medicare and private insurance.
Although there’s wide agreement that HIT can improve quality of care and reduce health-care costs, fewer than one-quarter (22%) of office-based physicians had adopted EHRs by 2009. We know the main reasons why:
- upfront cost and maintenance expense
- uncertain return on investment
- fragmented business model in a high proportion of small and solo practices
- changing and inconsistent information technology (IT) systems.
What can a practice expect to fork over?
In 2011, the Agency for Healthcare Research and Quality (AHRQ) found that the “real-life” cost of implementing EHRs “in an average five-physician primary care practice, operating within a large physician network committed to network-wide implementation of electronic health records, is about $162,000, with an additional $85,500 in maintenance expenses during the first year.”3
These figures include an average of 134 hours needed per physician to prepare to use EHRs during patient visits.3
Fleming and colleagues investigated the cost associated with implementing EHRs within 26 primary care practices in Texas. They found the cost to be $32,409 per physician through the first 60 days after the EHR system was launched, with one-time costs for hardware of $25,000 per practice and an additional $7,000 per physician for personal computers, printers, and scanners. The annual cost of software and maintenance was approximately $17,100 per physician.4
Why physicians should hold out for the return on their investment
Despite these considerable expenses, EHRs hold promise over the long term. The Medical Group Management Association reported, through a 2009 survey of about 1,300 primary care and specialty practice members using EHRs, that efficiency gains from the elimination of paper charts, as well as transcription savings, better charge capturing, and reduced billing errors, resulted in a median revenue increase of $49,916 per full-time physician after operating costs.
After 5 years of EHR use, practices reported a median operating margin 10.1% higher than that of practices in the first year of EHR use.5
Trends in the adoption of EHRs
Private practice. An article in Health Affairs showed that, by 2011, only one in six office-based physicians was using an EHR system robust enough to approach “meaningful use”—that is, the use of EHRs to measurably improve the quality of health care.6 These robust systems offered physicians the ability to record information on patient demographics, view laboratory and imaging results, maintain patients’ problem lists, compile clinical notes, and manage prescription ordering. EHR adoption lagged among non−primary care physicians, physicians aged 55 and older, and physicians in small (1–2 providers) practices and physician-owned practices.6 (ObGyns were considered primary care providers in this survey.)
“Big” practice. By comparison, in 2011, 99% of physicians in health maintenance organizations, or HMOs, and 73% in academic health centers and other hospitals used EHR systems.6 The number of physicians in these practice settings is small but growing.
In 2011, only 17% of physicians were in large practices of 10 or more physicians; 40% were in practices of one or two physicians.6
Primary care. These practices lead others in the adoption of EHRs, in part because of federal assistance, including a nationwide system of regional HIT assistance centers established by the Health Information Technology for Economic and Clinical Health (HITECH) Act to help providers located in rural areas participate in the Centers for Medicare and Medicaid Services (CMS) programs in EHR. The goal of these programs is to provide HIT support to at least 100,000 primary care providers, including ObGyns, by 2014.
The numbers cited in the Health Affairs article largely mirror data developed by other research organizations, including the Deloitte Center for Health Solutions.6
The EHR incentive
The drive for EHRs started long before the Affordable Care Act (ACA) was passed in 2010. The US Congress took a first stab at encouraging the health-care community to embrace HIT in 1996, when it passed the Health Insurance Portability and Accountability Act (HIPAA). HIPAA created an electronic data interchange that health plans, health-care clearinghouses, and certain health-care providers, including pharmacists, are required to use for electronic transactions, including:
- claims and encounter information
- payment and remittance advice
- claims status
- eligibility
- enrollment and disenrollment
- referrals and authorizations
- coordination of benefits
- premium payment.
Congress stepped up its game in 2009, when it offered higher Medicare and Medicaid payments to physicians who adopt and “meaningfully use” EHRs. The HITECH Act included $30 billion in new Medicare and Medicaid incentive payments—as much as $44,000 under Medicare and $63,750 under Medicaid—as well as $500 million for states to develop health information exchanges.
The Act also established a government-led process for certification of electronic health records through a $35 billion appropriation for the Office of the National Coordinator for Health IT, housed in CMS.
Other programs designed to encourage use of EHRs
Other federal programs include the Physician Quality Reporting System (PQRS), which, when created in 2006, was a voluntary physician electronic reporting program. Under the ACA, however, it has become a mandate. Starting in 2015, Medicare payments will be reduced for nonparticipating physicians.
The Electronic Prescribing (eRx) Incentive Program, created in 2008 under the Medicare Improvements for Patients and Providers Act, provides incentives for eligible physicians who e-prescribe Medicare Part D medications through a qualified system. This program converted to a penalty program last year for physicians who don’t use eRx.
Grants were also provided under the HITECH Act to fund an HIT infrastructure and low-interest HIT loans. The AHRQ has awarded $300 million in federal grant money to more than 200 projects in 48 states to promote access to and encourage HIT adoption. Over $150 million in Medicaid transformation grants have been awarded to three states and territories for HIT in the Medicaid program under the 2005 Deficit Reduction Act.
The ACA carried these initiatives even further by establishing uniform standards that HIT systems must meet, including:
- automatic reconciliation of electronic fund transfers and HIPAA payment and remittance
- improved claims payment process
- consistent methods of health plan enrollment and claim edits
- simplified and improved routing of health-care transactions
- electronic claims attachments.
Clearly, a lot of effort and taxpayer dollars have been dedicated to drive efficient use of HIT and EHRs in the hopes that they can:
- help make sense of our increasingly fragmented health-care system
- improve patient safety
- increase efficiency
- reduce paperwork
- reduce unnecessary tests
- better coordinate patient care.
To see which providers are cashing in on the government’s incentives for EHRs, see “Some physicians are more likely to seek incentives for meaningful use of EHRs” on page 37.
The long view
HIT and EHRs are here to stay. Products are maturing and improving. Acceptance by large and small practices has gained traction. Are small practices being squeezed? No doubt.
In 2011, I urged all ObGyns—especially those in private practice—to read an article written by President Barack Obama’s health-reform deputies on how physicians can be successful under the ACA.1 It reads, in part:
To realize the full benefits of the Affordable Care Act, physicians will need to embrace rather than resist change. The economic forces put in motion by the Act are likely to lead to vertical organization of providers and accelerate physician employment by hospitals and aggregation into larger physician groups. The most successful physicians will be those who most effectively collaborate with other providers to improve outcomes, care productivity, and patient experience.7
Two years ago, I zeroed in on the pressures straining small ObGyn practices in an article entitled, “Is private ObGyn practice on its way out?”1 The pressures haven’t eased in the interim. Today, small practices are still feeling squeezed to keep up with the many demands of modern specialty care. The push for electronic health records (EHRs), in particular, can profoundly affect physicians in private practice.
In this article, I outline some of the challenges facing small practices when they set out to implement EHRs, as well as the potential benefits they stand to gain a little farther down the road. Before we begin, however, let’s look at the latest trends in ObGyn practice, as they are related, in part, to the need to implement EHRs.
The exodus from private practice continues
A 2012 Accenture Physicians Alignment Survey shows an accelerating increase in physician employment. In 2000, 57% of all physicians were in independent practice; by the end of 2013, only 36% of physicians are projected to remain independent.2
The ObGyn specialty is a clear part of this trend, with both seasoned and incoming physicians finding hospital or other employment an attractive alternative to private practice. Fully one-third of ObGyn residents entering practice today sign hospital employment contracts. ObGyns who have made the switch from private to hospital practice, or who have become ObGyn hospitalists, often point to the difficulties of maintaining a solvent private practice, especially given the push toward EHRs and increasing regulatory and administrative burdens, as justification for their move.
The main reasons for the shift to employment. Top concerns influencing physicians’ decisions to opt for employment include:
- business expenses (87%)
- the dominance of managed care (61%)
- the requirement for EHRs (53%)
- the need to maintain and manage staff (53%)
- the increasing number of patients needed to break even (39%).2
A 2008 socioeconomic survey from ACOG revealed that 23.6% of ObGyn practices are solo practices, and 27.1% are single-specialty group practices. Many ObGyns—especially those in solo or small practices—are hesitant to make the large capital investment that is necessary to adopt EHRs.
EHRs offer benefits—and real costs
The system-wide benefits of health information technology (HIT), including EHRs, are many. Insurers stand to save money by reducing unnecessary tests, and patients will benefit from better coordination of their care and fewer medical errors. But these advantages don’t necessarily translate into savings or revenue for physician practices. Instead, physicians face payment cuts from Medicare and private insurance.
Although there’s wide agreement that HIT can improve quality of care and reduce health-care costs, fewer than one-quarter (22%) of office-based physicians had adopted EHRs by 2009. We know the main reasons why:
- upfront cost and maintenance expense
- uncertain return on investment
- fragmented business model in a high proportion of small and solo practices
- changing and inconsistent information technology (IT) systems.
What can a practice expect to fork over?
In 2011, the Agency for Healthcare Research and Quality (AHRQ) found that the “real-life” cost of implementing EHRs “in an average five-physician primary care practice, operating within a large physician network committed to network-wide implementation of electronic health records, is about $162,000, with an additional $85,500 in maintenance expenses during the first year.”3
These figures include an average of 134 hours needed per physician to prepare to use EHRs during patient visits.3
Fleming and colleagues investigated the cost associated with implementing EHRs within 26 primary care practices in Texas. They found the cost to be $32,409 per physician through the first 60 days after the EHR system was launched, with one-time costs for hardware of $25,000 per practice and an additional $7,000 per physician for personal computers, printers, and scanners. The annual cost of software and maintenance was approximately $17,100 per physician.4
Why physicians should hold out for the return on their investment
Despite these considerable expenses, EHRs hold promise over the long term. The Medical Group Management Association reported, through a 2009 survey of about 1,300 primary care and specialty practice members using EHRs, that efficiency gains from the elimination of paper charts, as well as transcription savings, better charge capturing, and reduced billing errors, resulted in a median revenue increase of $49,916 per full-time physician after operating costs.
After 5 years of EHR use, practices reported a median operating margin 10.1% higher than that of practices in the first year of EHR use.5
Trends in the adoption of EHRs
Private practice. An article in Health Affairs showed that, by 2011, only one in six office-based physicians was using an EHR system robust enough to approach “meaningful use”—that is, the use of EHRs to measurably improve the quality of health care.6 These robust systems offered physicians the ability to record information on patient demographics, view laboratory and imaging results, maintain patients’ problem lists, compile clinical notes, and manage prescription ordering. EHR adoption lagged among non−primary care physicians, physicians aged 55 and older, and physicians in small (1–2 providers) practices and physician-owned practices.6 (ObGyns were considered primary care providers in this survey.)
“Big” practice. By comparison, in 2011, 99% of physicians in health maintenance organizations, or HMOs, and 73% in academic health centers and other hospitals used EHR systems.6 The number of physicians in these practice settings is small but growing.
In 2011, only 17% of physicians were in large practices of 10 or more physicians; 40% were in practices of one or two physicians.6
Primary care. These practices lead others in the adoption of EHRs, in part because of federal assistance, including a nationwide system of regional HIT assistance centers established by the Health Information Technology for Economic and Clinical Health (HITECH) Act to help providers located in rural areas participate in the Centers for Medicare and Medicaid Services (CMS) programs in EHR. The goal of these programs is to provide HIT support to at least 100,000 primary care providers, including ObGyns, by 2014.
The numbers cited in the Health Affairs article largely mirror data developed by other research organizations, including the Deloitte Center for Health Solutions.6
The EHR incentive
The drive for EHRs started long before the Affordable Care Act (ACA) was passed in 2010. The US Congress took a first stab at encouraging the health-care community to embrace HIT in 1996, when it passed the Health Insurance Portability and Accountability Act (HIPAA). HIPAA created an electronic data interchange that health plans, health-care clearinghouses, and certain health-care providers, including pharmacists, are required to use for electronic transactions, including:
- claims and encounter information
- payment and remittance advice
- claims status
- eligibility
- enrollment and disenrollment
- referrals and authorizations
- coordination of benefits
- premium payment.
Congress stepped up its game in 2009, when it offered higher Medicare and Medicaid payments to physicians who adopt and “meaningfully use” EHRs. The HITECH Act included $30 billion in new Medicare and Medicaid incentive payments—as much as $44,000 under Medicare and $63,750 under Medicaid—as well as $500 million for states to develop health information exchanges.
The Act also established a government-led process for certification of electronic health records through a $35 billion appropriation for the Office of the National Coordinator for Health IT, housed in CMS.
Other programs designed to encourage use of EHRs
Other federal programs include the Physician Quality Reporting System (PQRS), which, when created in 2006, was a voluntary physician electronic reporting program. Under the ACA, however, it has become a mandate. Starting in 2015, Medicare payments will be reduced for nonparticipating physicians.
The Electronic Prescribing (eRx) Incentive Program, created in 2008 under the Medicare Improvements for Patients and Providers Act, provides incentives for eligible physicians who e-prescribe Medicare Part D medications through a qualified system. This program converted to a penalty program last year for physicians who don’t use eRx.
Grants were also provided under the HITECH Act to fund an HIT infrastructure and low-interest HIT loans. The AHRQ has awarded $300 million in federal grant money to more than 200 projects in 48 states to promote access to and encourage HIT adoption. Over $150 million in Medicaid transformation grants have been awarded to three states and territories for HIT in the Medicaid program under the 2005 Deficit Reduction Act.
The ACA carried these initiatives even further by establishing uniform standards that HIT systems must meet, including:
- automatic reconciliation of electronic fund transfers and HIPAA payment and remittance
- improved claims payment process
- consistent methods of health plan enrollment and claim edits
- simplified and improved routing of health-care transactions
- electronic claims attachments.
Clearly, a lot of effort and taxpayer dollars have been dedicated to drive efficient use of HIT and EHRs in the hopes that they can:
- help make sense of our increasingly fragmented health-care system
- improve patient safety
- increase efficiency
- reduce paperwork
- reduce unnecessary tests
- better coordinate patient care.
To see which providers are cashing in on the government’s incentives for EHRs, see “Some physicians are more likely to seek incentives for meaningful use of EHRs” on page 37.
The long view
HIT and EHRs are here to stay. Products are maturing and improving. Acceptance by large and small practices has gained traction. Are small practices being squeezed? No doubt.
In 2011, I urged all ObGyns—especially those in private practice—to read an article written by President Barack Obama’s health-reform deputies on how physicians can be successful under the ACA.1 It reads, in part:
To realize the full benefits of the Affordable Care Act, physicians will need to embrace rather than resist change. The economic forces put in motion by the Act are likely to lead to vertical organization of providers and accelerate physician employment by hospitals and aggregation into larger physician groups. The most successful physicians will be those who most effectively collaborate with other providers to improve outcomes, care productivity, and patient experience.7
1. DiVenere L, Yates J. Is private ObGyn practice on its way out? OBG Manage. 2011;23(10):42–54.
2. More US doctors leaving private practice due to rising costs and technology mandates, Accenture report finds [news release]. Arlington, Virginia: Accenture Newsroom; October 31, 2012. http://newsroom.accenture.com/news/more-us-doctors-leaving-private-practice-due-to-rising-costs-and-technology-mandates-accenture-report-finds.htm. Accessed June 5, 2013.
3. Study identifies costs of implementing electronic health records in network of physician practices: Research Activities October 2011, No. 374. Rockville, MD: Agency for Healthcare Research and Quality. http://www.ahrq.gov/news/newsletters/research-activities/oct11/1011RA15.html. Accessed June 5, 2013.
5. MGMA survey: Medical groups with EHRs report better financial performance than practices with paper medical records [news release]. New Orleans, Louisiana: Medical Group Management Association; October 25, 2010. http://www.mgma.com/press/default.aspx?id=39824. Accessed June 6, 2013.
8. US Government Accountability Office. Electronic Health Records: Number and Characteristics of Providers Awarded Medicaid Incentive Payments for 2011. GAO-13-146R. December 13, 2012. http://www.gao.gov/products/GAO-13-146R. Accessed June 6, 2013.
9. US Government Accountability Office. Electronic Health Records: Number and Characteristics of Providers Awarded Medicare Incentive Payments for 2011. GAO-12-778R. July 26, 2012. http://www.gao.gov/products/GAO-12-778R. Accessed June 6, 2013.
10. US Department of Health and Human Services. Doctors’ and hospitals’ use of health IT more than doubles since 2012 [news release]. Washington, DC: HHS.gov; May 22, 2013. http://www.hhs.gov/news/press/2013pres/05/20130522a.html. Accessed June 6, 2013.
1. DiVenere L, Yates J. Is private ObGyn practice on its way out? OBG Manage. 2011;23(10):42–54.
2. More US doctors leaving private practice due to rising costs and technology mandates, Accenture report finds [news release]. Arlington, Virginia: Accenture Newsroom; October 31, 2012. http://newsroom.accenture.com/news/more-us-doctors-leaving-private-practice-due-to-rising-costs-and-technology-mandates-accenture-report-finds.htm. Accessed June 5, 2013.
3. Study identifies costs of implementing electronic health records in network of physician practices: Research Activities October 2011, No. 374. Rockville, MD: Agency for Healthcare Research and Quality. http://www.ahrq.gov/news/newsletters/research-activities/oct11/1011RA15.html. Accessed June 5, 2013.
5. MGMA survey: Medical groups with EHRs report better financial performance than practices with paper medical records [news release]. New Orleans, Louisiana: Medical Group Management Association; October 25, 2010. http://www.mgma.com/press/default.aspx?id=39824. Accessed June 6, 2013.
8. US Government Accountability Office. Electronic Health Records: Number and Characteristics of Providers Awarded Medicaid Incentive Payments for 2011. GAO-13-146R. December 13, 2012. http://www.gao.gov/products/GAO-13-146R. Accessed June 6, 2013.
9. US Government Accountability Office. Electronic Health Records: Number and Characteristics of Providers Awarded Medicare Incentive Payments for 2011. GAO-12-778R. July 26, 2012. http://www.gao.gov/products/GAO-12-778R. Accessed June 6, 2013.
10. US Department of Health and Human Services. Doctors’ and hospitals’ use of health IT more than doubles since 2012 [news release]. Washington, DC: HHS.gov; May 22, 2013. http://www.hhs.gov/news/press/2013pres/05/20130522a.html. Accessed June 6, 2013.
Wound Hematoma After Anterior Cervical Spine Surgery: in vitro Study of the Pathophysiology of Airway Obstruction
Preventing Surgical Site Infection: Preoperative Bathing
Letters
Addressing biceps rupture, at what price?
I was glad to see you publish “When is a conservative approach best for proximal biceps tendon rupture?” (J Fam Pract. 2013;62:134-136), as it addressed an injury commonly seen in sports medicine practice, but one not often written about. However, I believe the approach the authors presented—which included both an MRI and specialty referral—is expensive and unnecessary.
Biceps tendon rupture is primarily a clinical diagnosis, and the findings are so classic that imaging is usually unnecessary. Adding a $750 MRI to the cost of treatment is wasteful, and not done by any of the orthopedists I work with. If imaging is "necessary" due to patient desire or diagnostic confusion (hard to imagine), an ultrasound has very high sensitivity and specificity.
Since the lesion is almost totally cosmetic, there is little reason to consider fixing it. The biceps is not really used in many sports activities, and strength is not impaired. In fact, John Elway, a prominent football player in the National Football League, played most of his games with this injury.
In 40 years of practice, I’ve seen about 15 patients with biceps tendon rupture. Only one opted for surgery, and that was because he wanted to look good at the gym. Usually, a careful discussion is adequate to manage this problem. Yet the authors noted that 2 orthopedic surgeons examined their patient. My concern is not about the accuracy of the data they presented, but about turning a $200 problem into a $1500 expenditure.
James Kennedy, MD
Winter Park, Colo
Drs. Sofya Pugach and Isaac Pugach respond:
We thank Dr. Kennedy for his letter. We’re glad our article prompted a discussion of different approaches to proximal biceps tendon rupture, including the conservative management (no MRI) he discusses as well as surgical repair. Treatment of this condition is still a subject of debate in the medical literature, and there is no one correct "recipe."
Sofya Pugach, MD, PhD, MPH
Isaac Z. Pugach, MD
Dallas, Tex
Saying No to EMRs
"End EMR tyranny!" (Editorial, J Fam Pract. 2013;62:173) reminded me of my own experience. As a solo practitioner, I began trying to implement my own EMR 13 years ago. I kept switching to bigger screens and newer computer system, but things just got worse.
Finally, I bought a top-rated pen-based tablet, but even then, voice and handwriting recognition didn’t work. I had to stay in the office until 9:30 pm just to type my notes. My children were asleep by the time I got home.
So I revolted. I went back to paper and pen and opted out of Medicare. Now I’m home at 5:30 every evening, seeing my children and enjoying my life—all because I got rid of this bureaucratic burden. I regret that I have only one practice to give to paper and pen!
Farid Taie, DO
Plano, Tex
… and saying Yes
For the past 2 years, our large multispecialty group has been in the throes of transitioning 250 doctors from the inadequate but familiar paper charts to the daunting EMR system.
I’ve been in practice for 36 years. Most of my colleagues are in my age group, and don’t take easily to change—or to computers. Three colleagues opted to retire rather than accommodate the changes, while others of us would never want to return to paper.
To be sure, it requires an investment of time to assimilate quick texts, problem lists, and myriad other details, but once that’s done, the EMR is a far superior system.
In a very few years, those of us who paved the way to EMRs will be retired, proud that we were the pioneers who brought about this important transition.
Cherry Brandstater, MD
Redlands, Calif
Addressing biceps rupture, at what price?
I was glad to see you publish “When is a conservative approach best for proximal biceps tendon rupture?” (J Fam Pract. 2013;62:134-136), as it addressed an injury commonly seen in sports medicine practice, but one not often written about. However, I believe the approach the authors presented—which included both an MRI and specialty referral—is expensive and unnecessary.
Biceps tendon rupture is primarily a clinical diagnosis, and the findings are so classic that imaging is usually unnecessary. Adding a $750 MRI to the cost of treatment is wasteful, and not done by any of the orthopedists I work with. If imaging is "necessary" due to patient desire or diagnostic confusion (hard to imagine), an ultrasound has very high sensitivity and specificity.
Since the lesion is almost totally cosmetic, there is little reason to consider fixing it. The biceps is not really used in many sports activities, and strength is not impaired. In fact, John Elway, a prominent football player in the National Football League, played most of his games with this injury.
In 40 years of practice, I’ve seen about 15 patients with biceps tendon rupture. Only one opted for surgery, and that was because he wanted to look good at the gym. Usually, a careful discussion is adequate to manage this problem. Yet the authors noted that 2 orthopedic surgeons examined their patient. My concern is not about the accuracy of the data they presented, but about turning a $200 problem into a $1500 expenditure.
James Kennedy, MD
Winter Park, Colo
Drs. Sofya Pugach and Isaac Pugach respond:
We thank Dr. Kennedy for his letter. We’re glad our article prompted a discussion of different approaches to proximal biceps tendon rupture, including the conservative management (no MRI) he discusses as well as surgical repair. Treatment of this condition is still a subject of debate in the medical literature, and there is no one correct "recipe."
Sofya Pugach, MD, PhD, MPH
Isaac Z. Pugach, MD
Dallas, Tex
Saying No to EMRs
"End EMR tyranny!" (Editorial, J Fam Pract. 2013;62:173) reminded me of my own experience. As a solo practitioner, I began trying to implement my own EMR 13 years ago. I kept switching to bigger screens and newer computer system, but things just got worse.
Finally, I bought a top-rated pen-based tablet, but even then, voice and handwriting recognition didn’t work. I had to stay in the office until 9:30 pm just to type my notes. My children were asleep by the time I got home.
So I revolted. I went back to paper and pen and opted out of Medicare. Now I’m home at 5:30 every evening, seeing my children and enjoying my life—all because I got rid of this bureaucratic burden. I regret that I have only one practice to give to paper and pen!
Farid Taie, DO
Plano, Tex
… and saying Yes
For the past 2 years, our large multispecialty group has been in the throes of transitioning 250 doctors from the inadequate but familiar paper charts to the daunting EMR system.
I’ve been in practice for 36 years. Most of my colleagues are in my age group, and don’t take easily to change—or to computers. Three colleagues opted to retire rather than accommodate the changes, while others of us would never want to return to paper.
To be sure, it requires an investment of time to assimilate quick texts, problem lists, and myriad other details, but once that’s done, the EMR is a far superior system.
In a very few years, those of us who paved the way to EMRs will be retired, proud that we were the pioneers who brought about this important transition.
Cherry Brandstater, MD
Redlands, Calif
Addressing biceps rupture, at what price?
I was glad to see you publish “When is a conservative approach best for proximal biceps tendon rupture?” (J Fam Pract. 2013;62:134-136), as it addressed an injury commonly seen in sports medicine practice, but one not often written about. However, I believe the approach the authors presented—which included both an MRI and specialty referral—is expensive and unnecessary.
Biceps tendon rupture is primarily a clinical diagnosis, and the findings are so classic that imaging is usually unnecessary. Adding a $750 MRI to the cost of treatment is wasteful, and not done by any of the orthopedists I work with. If imaging is "necessary" due to patient desire or diagnostic confusion (hard to imagine), an ultrasound has very high sensitivity and specificity.
Since the lesion is almost totally cosmetic, there is little reason to consider fixing it. The biceps is not really used in many sports activities, and strength is not impaired. In fact, John Elway, a prominent football player in the National Football League, played most of his games with this injury.
In 40 years of practice, I’ve seen about 15 patients with biceps tendon rupture. Only one opted for surgery, and that was because he wanted to look good at the gym. Usually, a careful discussion is adequate to manage this problem. Yet the authors noted that 2 orthopedic surgeons examined their patient. My concern is not about the accuracy of the data they presented, but about turning a $200 problem into a $1500 expenditure.
James Kennedy, MD
Winter Park, Colo
Drs. Sofya Pugach and Isaac Pugach respond:
We thank Dr. Kennedy for his letter. We’re glad our article prompted a discussion of different approaches to proximal biceps tendon rupture, including the conservative management (no MRI) he discusses as well as surgical repair. Treatment of this condition is still a subject of debate in the medical literature, and there is no one correct "recipe."
Sofya Pugach, MD, PhD, MPH
Isaac Z. Pugach, MD
Dallas, Tex
Saying No to EMRs
"End EMR tyranny!" (Editorial, J Fam Pract. 2013;62:173) reminded me of my own experience. As a solo practitioner, I began trying to implement my own EMR 13 years ago. I kept switching to bigger screens and newer computer system, but things just got worse.
Finally, I bought a top-rated pen-based tablet, but even then, voice and handwriting recognition didn’t work. I had to stay in the office until 9:30 pm just to type my notes. My children were asleep by the time I got home.
So I revolted. I went back to paper and pen and opted out of Medicare. Now I’m home at 5:30 every evening, seeing my children and enjoying my life—all because I got rid of this bureaucratic burden. I regret that I have only one practice to give to paper and pen!
Farid Taie, DO
Plano, Tex
… and saying Yes
For the past 2 years, our large multispecialty group has been in the throes of transitioning 250 doctors from the inadequate but familiar paper charts to the daunting EMR system.
I’ve been in practice for 36 years. Most of my colleagues are in my age group, and don’t take easily to change—or to computers. Three colleagues opted to retire rather than accommodate the changes, while others of us would never want to return to paper.
To be sure, it requires an investment of time to assimilate quick texts, problem lists, and myriad other details, but once that’s done, the EMR is a far superior system.
In a very few years, those of us who paved the way to EMRs will be retired, proud that we were the pioneers who brought about this important transition.
Cherry Brandstater, MD
Redlands, Calif
Words—not scores—inspire me
Being a physician does not seem as rewarding today as it did 30 years ago.
Under constant pressure to focus on production, meaningful use, and compliance with myriad regulations, it’s easy to lose sight of the most rewarding part of our work—caring for our patients. And most are highly satisfied with our care.
The modern rendition of patient satisfaction is the “patient experience” score, with the data tracked and disseminated by firms specializing in such reports. I do see some value in these reports, as they can help us pinpoint areas of our office operations or personal interactions that could be improved. But on an emotional level, they just don’t cut it. Patient experience scores, and the form in which they’re presented, are too much like report cards. They don’t inspire me.
What inspires me is receiving a heartfelt “thank you” from a grateful patient, and I’m reasonably sure the same is true for you. Which is why I offer the following excerpts from a truly inspiring “thank you” speech delivered by Sam Miller, an emeritus trustee of the Cleveland Clinic, at the clinic’s 2012 Professional Excellence Awards:
“You mean a lot to me personally and you mean a lot to each other, for you are, as far as I’m concerned, the veritable guardians of this community.
“Someday after enough DNA tests, they will discover the gene in doctors making you walking hearts, perennial consciences, and empathetic human beings. And when they do, they will look for this gene in all humanity, and we will have found the answer to wars and to peace and to love. Love means reaching towards neighbors and the world with the same care, regard, generosity and empathy we normally reserve for ourselves and those closest to us,” he said. “This is the gene that a doctor has inherited.”
“You will not have to wait for your reward in heaven,” Miller said. “Every day when you see the smiles of the sick, the poor, the look of hope and momentary happiness of that particular unfortunate that you’ve been able to help, that is heaven by itself. That is the magnificent gene that you possess.”
I offer heartfelt thanks to Mr. Miller for his deeply moving words, and I invite you, my fellow family physicians, to share your stories of patients whose expressions of appreciation have truly inspired you.
Being a physician does not seem as rewarding today as it did 30 years ago.
Under constant pressure to focus on production, meaningful use, and compliance with myriad regulations, it’s easy to lose sight of the most rewarding part of our work—caring for our patients. And most are highly satisfied with our care.
The modern rendition of patient satisfaction is the “patient experience” score, with the data tracked and disseminated by firms specializing in such reports. I do see some value in these reports, as they can help us pinpoint areas of our office operations or personal interactions that could be improved. But on an emotional level, they just don’t cut it. Patient experience scores, and the form in which they’re presented, are too much like report cards. They don’t inspire me.
What inspires me is receiving a heartfelt “thank you” from a grateful patient, and I’m reasonably sure the same is true for you. Which is why I offer the following excerpts from a truly inspiring “thank you” speech delivered by Sam Miller, an emeritus trustee of the Cleveland Clinic, at the clinic’s 2012 Professional Excellence Awards:
“You mean a lot to me personally and you mean a lot to each other, for you are, as far as I’m concerned, the veritable guardians of this community.
“Someday after enough DNA tests, they will discover the gene in doctors making you walking hearts, perennial consciences, and empathetic human beings. And when they do, they will look for this gene in all humanity, and we will have found the answer to wars and to peace and to love. Love means reaching towards neighbors and the world with the same care, regard, generosity and empathy we normally reserve for ourselves and those closest to us,” he said. “This is the gene that a doctor has inherited.”
“You will not have to wait for your reward in heaven,” Miller said. “Every day when you see the smiles of the sick, the poor, the look of hope and momentary happiness of that particular unfortunate that you’ve been able to help, that is heaven by itself. That is the magnificent gene that you possess.”
I offer heartfelt thanks to Mr. Miller for his deeply moving words, and I invite you, my fellow family physicians, to share your stories of patients whose expressions of appreciation have truly inspired you.
Being a physician does not seem as rewarding today as it did 30 years ago.
Under constant pressure to focus on production, meaningful use, and compliance with myriad regulations, it’s easy to lose sight of the most rewarding part of our work—caring for our patients. And most are highly satisfied with our care.
The modern rendition of patient satisfaction is the “patient experience” score, with the data tracked and disseminated by firms specializing in such reports. I do see some value in these reports, as they can help us pinpoint areas of our office operations or personal interactions that could be improved. But on an emotional level, they just don’t cut it. Patient experience scores, and the form in which they’re presented, are too much like report cards. They don’t inspire me.
What inspires me is receiving a heartfelt “thank you” from a grateful patient, and I’m reasonably sure the same is true for you. Which is why I offer the following excerpts from a truly inspiring “thank you” speech delivered by Sam Miller, an emeritus trustee of the Cleveland Clinic, at the clinic’s 2012 Professional Excellence Awards:
“You mean a lot to me personally and you mean a lot to each other, for you are, as far as I’m concerned, the veritable guardians of this community.
“Someday after enough DNA tests, they will discover the gene in doctors making you walking hearts, perennial consciences, and empathetic human beings. And when they do, they will look for this gene in all humanity, and we will have found the answer to wars and to peace and to love. Love means reaching towards neighbors and the world with the same care, regard, generosity and empathy we normally reserve for ourselves and those closest to us,” he said. “This is the gene that a doctor has inherited.”
“You will not have to wait for your reward in heaven,” Miller said. “Every day when you see the smiles of the sick, the poor, the look of hope and momentary happiness of that particular unfortunate that you’ve been able to help, that is heaven by itself. That is the magnificent gene that you possess.”
I offer heartfelt thanks to Mr. Miller for his deeply moving words, and I invite you, my fellow family physicians, to share your stories of patients whose expressions of appreciation have truly inspired you.
Finger injuries: 5 cases to test your skills
Some finger injuries require little more than icing; others are more serious, often emergent, conditions with outcomes that are dependent on an accurate diagnosis and rapid initiation of treatment.
The 5 cases that follow describe injuries with varying degrees of severity. Read each case and select the multiple-choice answer you think is most appropriate. Then read on to find out if you were right—and to learn more about the clinical presentation, diagnosis, and treatment for each type of injury.
CASE 1 A 45-year-old auto body worker walks into your office at 5:30 pm, just as your staff is closing up for the day. A few hours ago, he reports, he was spray-painting a car with a paint gun when he felt a sudden pain in his right index finger. His immediate thought was that he had torn something, but the pain quickly subsided. So he continued to work—until about 45 minutes ago, when the pain became so intense that he knew he needed medical care right away.
Examination reveals redness and increased skin temperature on the radial palmar side of the proximal interphalangeal (PIP) joint of the index finger. Two-point discrimination is decreased to 10 mm, vs 5 mm on the same finger of the opposite hand. The patient can flex his PIP and distal interphalangeal (DIP) joints but complains of pain and stiffness. You obtain x-rays of the injured
finger (FIGURE 1).
WHAT'S YOUR NEXT STEP?
B. Update the patient’s tetanus immunization and start him on a broad-spectrum antibiotic.
C. Put a dorsal splint on the injured finger in the “safe hand” position and schedule a return visit in one week.
D. “Buddy tape” the index and long fingers and refer the patient to a hand surgeon.
Answer: Send the auto-body worker to the nearest ED and call ahead (A).
This patient sustained a high-pressure injection injury to the PIP joint of his right index finger. The patient’s description of how the injury occurred suggested this, and the radiograph confirmed it by showing some paint under the skin (See arrow, FIGURE 1). Such injuries occur when a high pressure (typically from a hose) forces air or a substance—eg, diesel fuel, paint, or solvent—through the skin into the finger.
Although high-pressure injection injury often has a benign presentation, it is actually a medical emergency. If aggressive surgical debridement does not occur within a 6-hour window, the patient runs a high risk for amputation of the digit.1 A hand surgeon should be contacted as soon as possible.
The severity of the injury varies, depending on the amount of pressure (amputation rates are as high as 43% when the pressure per square inch >1000), the type of material injected (diesel fuel is the most toxic), and the location.1,2
Instruct the patient to remove any jewelry, such as a wedding band or watch, on the affected hand or wrist, and to keep the hand elevated. Broad-spectrum antibiotics should be started right away, and a tetanus booster given, if needed. Do not apply heat or use local anesthesia, as both can increase the swelling.2
CASE 2 A 17-year-old cheerleader comes to see you on Monday afternoon, after injuring her left pinky during a Friday night game. The patient, who is right-handed, points to the left PIP joint when you ask where it hurts, and tells you that the finger is stiff. She has been icing it since the injury occurred, to make sure she is ready to cheer by next weekend.
The injury occurred when she was spotting another cheerleader during a routine, the patient reports, adding that the pinky was “dislocated.” The coach “popped” it back in place and buddy-taped the injured finger to her ring finger.
The patient is able to flex and extend the DIP joint on the pinky when the PIP joint is stabilized. She can also flex the PIP joint unassisted, but has difficulty extending it. The digit demonstrates slight flexion of the PIP joint. You note tenderness over both collateral ligaments and the dorsum of the PIP joint, but not over the volar aspect of the injured finger, and order x-rays (FIGURE 2).
WHAT'S YOUR NEXT STEP?
B. Refer the patient to a hand surgeon.
C. Apply an extension block splint so the patient can flex the finger but not extend it, and schedule a follow-up appointment in one to 2 weeks.
D. Apply an aluminum dorsal splint, allowing the DIP joint to be flexed and keeping the PIP joint in full extension for 4 weeks.
Answer: Refer the cheerleader to a hand surgeon (B).
This patient has a rupture of the central extensor tendon of the pinky finger at the PIP joint. The mechanism of injury and her inability to completely extend the injured finger at the PIP joint alert you to this type of injury. An x-ray may sometimes be normal but in this case, it shows the flexion of the PIP joint. Surgical repair of the rupture should be scheduled without delay.3
Most injuries at this joint occur from forced extension, not flexion, and result in a volar plate rupture.4 If swelling and pain make evaluation of an acute dislocation injury difficult, splinting in the “safe hand” position for 72 hours while icing the injured finger will make it possible to do a more detailed follow-up exam.3
Extended periods of splinting can make the PIP joint very stiff, however—and harder to treat than the original injury.5 If the rupture of the central extensor tendon is undetected or simply not treated, a Boutonniere deformity, in which the PIP joint is flexed and the DIP joint is hyperextended, is the likely result.3
CASE 3 A 24-year-old man “jammed” his right ring finger while trying to catch a ball that was passed to him during a pick-up basketball game. He has rested and iced the finger for a couple of days, but it’s still painful and hard to move. He has no significant medical history and has been taking only acetaminophen for the pain.
Examination reveals that the injured finger has good capillary refill, 2-point discrimination is intact at 5 mm, and the other fingers on his right hand have no deformities and a normal range of motion. On the injured finger, however, the DIP joint is swollen and tender; it cannot be fully extended (FiGURE 3).
WHAT'S YOUR DIAGNOSIS?
B. Distal tuft fracture.
C. Mallet finger.
D. Finger sprain.
E. Trigger finger.
Answer: The basketball player has mallet finger (C).
Mallet finger typically occurs on the dominant hand. The key physical finding is that the joint is “stuck” in flexion, which is evident during an exam and on x-ray. Although the DIP joint may be passively fully extended, the patient with mallet finger is unable to actively extend it.
Mallet injuries, which are common in sports and associated with minor trauma, are typically caused by sudden forced flexion of the DIP joint during active extension of the finger. This can either stretch or tear the extensor tendon or lead to avulsion of the tendon insertion from the dorsum of the distal phalanx, with or without a fragment of bone. The injury is called a “soft” mallet finger when there is no bone involvement and a “bony” mallet finger when an avulsion is present, like the one that is evident on the FIGURE 3 x-ray (see arrow).
On clinical examination, the finger may or may not have an obvious deformity; similarly, you won’t always see bruising, swelling, or tenderness over the DIP joint.6 The work-up should include posterior/anterior, oblique, and lateral x-rays, followed by an examination of the soft tissue and a range-of-motion evaluation of the metacarpophalangeal and PIP joints. In acute injuries, tenderness is elicited with palpation over the dorsal aspect of the DIP joint. Although most patients develop an extensor lag at the DIP joint immediately after injury, the deformity may be delayed by a few hours or even days.6,7
Nonsurgical management is the standard of care for most mallet injuries, including mallet fractures involving less than one-third of the articular surface with no associated DIP joint subluxation.7
If there is no displacement, round-the-clock splinting to keep the joint in extension for a minimum of 6 weeks is indicated, followed by 2 to 3 weeks of nighttime splinting. It is important that the splinting allow for complete extension of the DIP joint but flexion of the PIP joint. Keeping the PIP in extension for prolonged periods can lead to permanent stiffness of the joint, while failure to provide any immobilization may lead to permanent deformity.
Surgery is indicated for a fracture fragment involving >30% of the joint surface (as demonstrated in the radiograph), volar subluxation, or a swan neck deformity—and when conservative therapy fails.7
CASE 4 An 18-year-old high school football player presents with pain and swelling at the tip of his right ring finger from an injury that occurred a week ago. When the player he was trying to tackle broke away, the patient says, he immediately felt pain and a “pop” in the finger.
The DIP joint of his right ring finger is swollen (FIGURE 4), but appears normal otherwise. When you isolate the joint, however, the patient is unable to flex it. You can palpate a stump on the volar surface of the finger.
What’s your next step?
B. Treat with splinting, RICE (rest, ice, compression, and elevation), and nonsteroidal anti-inflammatory drugs.
C. Order an ultrasound of the finger and palm.
D. Order magnetic resonance imaging (MRI) of the hand.
Answer: Order an ultrasound of the football player’s finger and palm (C).
This patient has Jersey finger, caused by a traumatic avulsion of the flexor digitorum profundus (FDP) from the distal phalanx and diagnosed based on the mechanism of injury and the patient’s inability to flex the DIP joint. The injury often does not show on x-rays, and the diagnosis may be missed for several weeks.
Jersey finger usually happens in sports like football or rugby, where players tackle each other, and involves forced, passive extension of the DIP joint at a time of active flexion. Management of Jersey finger starts with splinting, with both the DIP and PIP in slight flexion. Surgical reattachment of the flexor tendon is needed, with best results when it is done within 7 to 10 days of injury.4
You may be able to palpate the tendon stump in the palm or along the digit; bony avulsions can be trapped at the flexor sheath. Soft tissue swelling can be misleading, however, and the point of maximal tenderness is not an accurate means of identifying the avulsed tendon stump.8
Ultrasound is effective in differentiating between a partial and full thickness rupture and in localizing the distal tendon stump.8 MRI is usually reserved for precise evaluation of the tendon edges, to aid in operative planning. If the tendon is retracted to the palm, scarring may be irreversible because of the lack of blood supply.
Athletes typically return to play 12 weeks after injury, starting with protected activity and progressing to full gripping/grasping. Physical therapy and/or occupational therapy will be needed after the surgical wound has healed.
CASE 5 A 40-year-old construction worker who smashed his left index finger with a hammer one day ago presents with severe pain in his fingertip, which he is unable to move. On examination, you find that the distal finger is swollen and there is extensive ecchymosis and swelling underneath the nail. The finger has normal sensation, but you are unable to see capillary refill due to a large hematoma.
X-rays (FIGURE 5) reveal a distal tuft fracture. The patient’s main concern is the pain, and he asks what you can do to relieve it.
What’s your next step?
B. Perform fenestration of the nail.
C. Refer the patient to a hand surgeon.
D. Order computed tomography of the hand.
Answer: Perform fenestration of the construction worker’s nail (B).
This patient has a closed fracture of the distal phalanx, called a tuft fracture, and a sub-ungual hematoma, evident from the x-ray and the physical presentation.
Subungual hematoma requires fenestration with a needle to create small holes in the nail. If the nail bed is lacerated, the nail is removed and the injured nail bed repaired with sutures.
Tuft fractures sometimes require reduction. More often, they are stable and minimally displaced and can be managed conservatively, with splinting with a padded aluminum splint or a fingertip guard (Stax splint) for 3 to 4 weeks. Antibiotics are not indicated unless there is suspicion of an overlying or secondary infection. Referral to a hand surgeon is required for severe crush injuries, avulsion of the nail matrix, and open fractures of the distal phalanx.5,6
1. Hogan CJ, Ruland RT. High-pressure injection injuries to the upper extremity: a review of the literature. J Orthop Trauma. 2006;20:503-511.
2. Gonzalez R, Kasdan ML. High pressure injection injuries of the hand. Clin Occup Environ Med. 2006;5:407-411.
3. Freiberg A. Management of proximal interphalangeal joint injuries. Can J Plast Surg. 2007;15:199-203.
4. Perron AD, Brady WJ, Keats TE, et al. Orthopedic pitfalls in the emergency department: closed tendon injuries of the hand. Am J Emerg Med. 2001;19:76-80.
5. Oetgen ME, Dodds SD. Non-operative treatment of common finger injuries. Curr Rev Musculoskel Med. 2008;1:97-102.
6. Anderson D. Mallet finger. Aust Fam Physician. 2011;40:91-92.
7. Smit JM, Beets MR. Treatment options for mallet finger: a review. Plast Reconstr Surg. 2010;126:1624-1629.
8. Goodson A, Morgan M. Current management of Jersey finger in rugby players: cases series and literature review. Hand Surg. 2010;15:103-107.
Some finger injuries require little more than icing; others are more serious, often emergent, conditions with outcomes that are dependent on an accurate diagnosis and rapid initiation of treatment.
The 5 cases that follow describe injuries with varying degrees of severity. Read each case and select the multiple-choice answer you think is most appropriate. Then read on to find out if you were right—and to learn more about the clinical presentation, diagnosis, and treatment for each type of injury.
CASE 1 A 45-year-old auto body worker walks into your office at 5:30 pm, just as your staff is closing up for the day. A few hours ago, he reports, he was spray-painting a car with a paint gun when he felt a sudden pain in his right index finger. His immediate thought was that he had torn something, but the pain quickly subsided. So he continued to work—until about 45 minutes ago, when the pain became so intense that he knew he needed medical care right away.
Examination reveals redness and increased skin temperature on the radial palmar side of the proximal interphalangeal (PIP) joint of the index finger. Two-point discrimination is decreased to 10 mm, vs 5 mm on the same finger of the opposite hand. The patient can flex his PIP and distal interphalangeal (DIP) joints but complains of pain and stiffness. You obtain x-rays of the injured
finger (FIGURE 1).
WHAT'S YOUR NEXT STEP?
B. Update the patient’s tetanus immunization and start him on a broad-spectrum antibiotic.
C. Put a dorsal splint on the injured finger in the “safe hand” position and schedule a return visit in one week.
D. “Buddy tape” the index and long fingers and refer the patient to a hand surgeon.
Answer: Send the auto-body worker to the nearest ED and call ahead (A).
This patient sustained a high-pressure injection injury to the PIP joint of his right index finger. The patient’s description of how the injury occurred suggested this, and the radiograph confirmed it by showing some paint under the skin (See arrow, FIGURE 1). Such injuries occur when a high pressure (typically from a hose) forces air or a substance—eg, diesel fuel, paint, or solvent—through the skin into the finger.
Although high-pressure injection injury often has a benign presentation, it is actually a medical emergency. If aggressive surgical debridement does not occur within a 6-hour window, the patient runs a high risk for amputation of the digit.1 A hand surgeon should be contacted as soon as possible.
The severity of the injury varies, depending on the amount of pressure (amputation rates are as high as 43% when the pressure per square inch >1000), the type of material injected (diesel fuel is the most toxic), and the location.1,2
Instruct the patient to remove any jewelry, such as a wedding band or watch, on the affected hand or wrist, and to keep the hand elevated. Broad-spectrum antibiotics should be started right away, and a tetanus booster given, if needed. Do not apply heat or use local anesthesia, as both can increase the swelling.2
CASE 2 A 17-year-old cheerleader comes to see you on Monday afternoon, after injuring her left pinky during a Friday night game. The patient, who is right-handed, points to the left PIP joint when you ask where it hurts, and tells you that the finger is stiff. She has been icing it since the injury occurred, to make sure she is ready to cheer by next weekend.
The injury occurred when she was spotting another cheerleader during a routine, the patient reports, adding that the pinky was “dislocated.” The coach “popped” it back in place and buddy-taped the injured finger to her ring finger.
The patient is able to flex and extend the DIP joint on the pinky when the PIP joint is stabilized. She can also flex the PIP joint unassisted, but has difficulty extending it. The digit demonstrates slight flexion of the PIP joint. You note tenderness over both collateral ligaments and the dorsum of the PIP joint, but not over the volar aspect of the injured finger, and order x-rays (FIGURE 2).
WHAT'S YOUR NEXT STEP?
B. Refer the patient to a hand surgeon.
C. Apply an extension block splint so the patient can flex the finger but not extend it, and schedule a follow-up appointment in one to 2 weeks.
D. Apply an aluminum dorsal splint, allowing the DIP joint to be flexed and keeping the PIP joint in full extension for 4 weeks.
Answer: Refer the cheerleader to a hand surgeon (B).
This patient has a rupture of the central extensor tendon of the pinky finger at the PIP joint. The mechanism of injury and her inability to completely extend the injured finger at the PIP joint alert you to this type of injury. An x-ray may sometimes be normal but in this case, it shows the flexion of the PIP joint. Surgical repair of the rupture should be scheduled without delay.3
Most injuries at this joint occur from forced extension, not flexion, and result in a volar plate rupture.4 If swelling and pain make evaluation of an acute dislocation injury difficult, splinting in the “safe hand” position for 72 hours while icing the injured finger will make it possible to do a more detailed follow-up exam.3
Extended periods of splinting can make the PIP joint very stiff, however—and harder to treat than the original injury.5 If the rupture of the central extensor tendon is undetected or simply not treated, a Boutonniere deformity, in which the PIP joint is flexed and the DIP joint is hyperextended, is the likely result.3
CASE 3 A 24-year-old man “jammed” his right ring finger while trying to catch a ball that was passed to him during a pick-up basketball game. He has rested and iced the finger for a couple of days, but it’s still painful and hard to move. He has no significant medical history and has been taking only acetaminophen for the pain.
Examination reveals that the injured finger has good capillary refill, 2-point discrimination is intact at 5 mm, and the other fingers on his right hand have no deformities and a normal range of motion. On the injured finger, however, the DIP joint is swollen and tender; it cannot be fully extended (FiGURE 3).
WHAT'S YOUR DIAGNOSIS?
B. Distal tuft fracture.
C. Mallet finger.
D. Finger sprain.
E. Trigger finger.
Answer: The basketball player has mallet finger (C).
Mallet finger typically occurs on the dominant hand. The key physical finding is that the joint is “stuck” in flexion, which is evident during an exam and on x-ray. Although the DIP joint may be passively fully extended, the patient with mallet finger is unable to actively extend it.
Mallet injuries, which are common in sports and associated with minor trauma, are typically caused by sudden forced flexion of the DIP joint during active extension of the finger. This can either stretch or tear the extensor tendon or lead to avulsion of the tendon insertion from the dorsum of the distal phalanx, with or without a fragment of bone. The injury is called a “soft” mallet finger when there is no bone involvement and a “bony” mallet finger when an avulsion is present, like the one that is evident on the FIGURE 3 x-ray (see arrow).
On clinical examination, the finger may or may not have an obvious deformity; similarly, you won’t always see bruising, swelling, or tenderness over the DIP joint.6 The work-up should include posterior/anterior, oblique, and lateral x-rays, followed by an examination of the soft tissue and a range-of-motion evaluation of the metacarpophalangeal and PIP joints. In acute injuries, tenderness is elicited with palpation over the dorsal aspect of the DIP joint. Although most patients develop an extensor lag at the DIP joint immediately after injury, the deformity may be delayed by a few hours or even days.6,7
Nonsurgical management is the standard of care for most mallet injuries, including mallet fractures involving less than one-third of the articular surface with no associated DIP joint subluxation.7
If there is no displacement, round-the-clock splinting to keep the joint in extension for a minimum of 6 weeks is indicated, followed by 2 to 3 weeks of nighttime splinting. It is important that the splinting allow for complete extension of the DIP joint but flexion of the PIP joint. Keeping the PIP in extension for prolonged periods can lead to permanent stiffness of the joint, while failure to provide any immobilization may lead to permanent deformity.
Surgery is indicated for a fracture fragment involving >30% of the joint surface (as demonstrated in the radiograph), volar subluxation, or a swan neck deformity—and when conservative therapy fails.7
CASE 4 An 18-year-old high school football player presents with pain and swelling at the tip of his right ring finger from an injury that occurred a week ago. When the player he was trying to tackle broke away, the patient says, he immediately felt pain and a “pop” in the finger.
The DIP joint of his right ring finger is swollen (FIGURE 4), but appears normal otherwise. When you isolate the joint, however, the patient is unable to flex it. You can palpate a stump on the volar surface of the finger.
What’s your next step?
B. Treat with splinting, RICE (rest, ice, compression, and elevation), and nonsteroidal anti-inflammatory drugs.
C. Order an ultrasound of the finger and palm.
D. Order magnetic resonance imaging (MRI) of the hand.
Answer: Order an ultrasound of the football player’s finger and palm (C).
This patient has Jersey finger, caused by a traumatic avulsion of the flexor digitorum profundus (FDP) from the distal phalanx and diagnosed based on the mechanism of injury and the patient’s inability to flex the DIP joint. The injury often does not show on x-rays, and the diagnosis may be missed for several weeks.
Jersey finger usually happens in sports like football or rugby, where players tackle each other, and involves forced, passive extension of the DIP joint at a time of active flexion. Management of Jersey finger starts with splinting, with both the DIP and PIP in slight flexion. Surgical reattachment of the flexor tendon is needed, with best results when it is done within 7 to 10 days of injury.4
You may be able to palpate the tendon stump in the palm or along the digit; bony avulsions can be trapped at the flexor sheath. Soft tissue swelling can be misleading, however, and the point of maximal tenderness is not an accurate means of identifying the avulsed tendon stump.8
Ultrasound is effective in differentiating between a partial and full thickness rupture and in localizing the distal tendon stump.8 MRI is usually reserved for precise evaluation of the tendon edges, to aid in operative planning. If the tendon is retracted to the palm, scarring may be irreversible because of the lack of blood supply.
Athletes typically return to play 12 weeks after injury, starting with protected activity and progressing to full gripping/grasping. Physical therapy and/or occupational therapy will be needed after the surgical wound has healed.
CASE 5 A 40-year-old construction worker who smashed his left index finger with a hammer one day ago presents with severe pain in his fingertip, which he is unable to move. On examination, you find that the distal finger is swollen and there is extensive ecchymosis and swelling underneath the nail. The finger has normal sensation, but you are unable to see capillary refill due to a large hematoma.
X-rays (FIGURE 5) reveal a distal tuft fracture. The patient’s main concern is the pain, and he asks what you can do to relieve it.
What’s your next step?
B. Perform fenestration of the nail.
C. Refer the patient to a hand surgeon.
D. Order computed tomography of the hand.
Answer: Perform fenestration of the construction worker’s nail (B).
This patient has a closed fracture of the distal phalanx, called a tuft fracture, and a sub-ungual hematoma, evident from the x-ray and the physical presentation.
Subungual hematoma requires fenestration with a needle to create small holes in the nail. If the nail bed is lacerated, the nail is removed and the injured nail bed repaired with sutures.
Tuft fractures sometimes require reduction. More often, they are stable and minimally displaced and can be managed conservatively, with splinting with a padded aluminum splint or a fingertip guard (Stax splint) for 3 to 4 weeks. Antibiotics are not indicated unless there is suspicion of an overlying or secondary infection. Referral to a hand surgeon is required for severe crush injuries, avulsion of the nail matrix, and open fractures of the distal phalanx.5,6
Some finger injuries require little more than icing; others are more serious, often emergent, conditions with outcomes that are dependent on an accurate diagnosis and rapid initiation of treatment.
The 5 cases that follow describe injuries with varying degrees of severity. Read each case and select the multiple-choice answer you think is most appropriate. Then read on to find out if you were right—and to learn more about the clinical presentation, diagnosis, and treatment for each type of injury.
CASE 1 A 45-year-old auto body worker walks into your office at 5:30 pm, just as your staff is closing up for the day. A few hours ago, he reports, he was spray-painting a car with a paint gun when he felt a sudden pain in his right index finger. His immediate thought was that he had torn something, but the pain quickly subsided. So he continued to work—until about 45 minutes ago, when the pain became so intense that he knew he needed medical care right away.
Examination reveals redness and increased skin temperature on the radial palmar side of the proximal interphalangeal (PIP) joint of the index finger. Two-point discrimination is decreased to 10 mm, vs 5 mm on the same finger of the opposite hand. The patient can flex his PIP and distal interphalangeal (DIP) joints but complains of pain and stiffness. You obtain x-rays of the injured
finger (FIGURE 1).
WHAT'S YOUR NEXT STEP?
B. Update the patient’s tetanus immunization and start him on a broad-spectrum antibiotic.
C. Put a dorsal splint on the injured finger in the “safe hand” position and schedule a return visit in one week.
D. “Buddy tape” the index and long fingers and refer the patient to a hand surgeon.
Answer: Send the auto-body worker to the nearest ED and call ahead (A).
This patient sustained a high-pressure injection injury to the PIP joint of his right index finger. The patient’s description of how the injury occurred suggested this, and the radiograph confirmed it by showing some paint under the skin (See arrow, FIGURE 1). Such injuries occur when a high pressure (typically from a hose) forces air or a substance—eg, diesel fuel, paint, or solvent—through the skin into the finger.
Although high-pressure injection injury often has a benign presentation, it is actually a medical emergency. If aggressive surgical debridement does not occur within a 6-hour window, the patient runs a high risk for amputation of the digit.1 A hand surgeon should be contacted as soon as possible.
The severity of the injury varies, depending on the amount of pressure (amputation rates are as high as 43% when the pressure per square inch >1000), the type of material injected (diesel fuel is the most toxic), and the location.1,2
Instruct the patient to remove any jewelry, such as a wedding band or watch, on the affected hand or wrist, and to keep the hand elevated. Broad-spectrum antibiotics should be started right away, and a tetanus booster given, if needed. Do not apply heat or use local anesthesia, as both can increase the swelling.2
CASE 2 A 17-year-old cheerleader comes to see you on Monday afternoon, after injuring her left pinky during a Friday night game. The patient, who is right-handed, points to the left PIP joint when you ask where it hurts, and tells you that the finger is stiff. She has been icing it since the injury occurred, to make sure she is ready to cheer by next weekend.
The injury occurred when she was spotting another cheerleader during a routine, the patient reports, adding that the pinky was “dislocated.” The coach “popped” it back in place and buddy-taped the injured finger to her ring finger.
The patient is able to flex and extend the DIP joint on the pinky when the PIP joint is stabilized. She can also flex the PIP joint unassisted, but has difficulty extending it. The digit demonstrates slight flexion of the PIP joint. You note tenderness over both collateral ligaments and the dorsum of the PIP joint, but not over the volar aspect of the injured finger, and order x-rays (FIGURE 2).
WHAT'S YOUR NEXT STEP?
B. Refer the patient to a hand surgeon.
C. Apply an extension block splint so the patient can flex the finger but not extend it, and schedule a follow-up appointment in one to 2 weeks.
D. Apply an aluminum dorsal splint, allowing the DIP joint to be flexed and keeping the PIP joint in full extension for 4 weeks.
Answer: Refer the cheerleader to a hand surgeon (B).
This patient has a rupture of the central extensor tendon of the pinky finger at the PIP joint. The mechanism of injury and her inability to completely extend the injured finger at the PIP joint alert you to this type of injury. An x-ray may sometimes be normal but in this case, it shows the flexion of the PIP joint. Surgical repair of the rupture should be scheduled without delay.3
Most injuries at this joint occur from forced extension, not flexion, and result in a volar plate rupture.4 If swelling and pain make evaluation of an acute dislocation injury difficult, splinting in the “safe hand” position for 72 hours while icing the injured finger will make it possible to do a more detailed follow-up exam.3
Extended periods of splinting can make the PIP joint very stiff, however—and harder to treat than the original injury.5 If the rupture of the central extensor tendon is undetected or simply not treated, a Boutonniere deformity, in which the PIP joint is flexed and the DIP joint is hyperextended, is the likely result.3
CASE 3 A 24-year-old man “jammed” his right ring finger while trying to catch a ball that was passed to him during a pick-up basketball game. He has rested and iced the finger for a couple of days, but it’s still painful and hard to move. He has no significant medical history and has been taking only acetaminophen for the pain.
Examination reveals that the injured finger has good capillary refill, 2-point discrimination is intact at 5 mm, and the other fingers on his right hand have no deformities and a normal range of motion. On the injured finger, however, the DIP joint is swollen and tender; it cannot be fully extended (FiGURE 3).
WHAT'S YOUR DIAGNOSIS?
B. Distal tuft fracture.
C. Mallet finger.
D. Finger sprain.
E. Trigger finger.
Answer: The basketball player has mallet finger (C).
Mallet finger typically occurs on the dominant hand. The key physical finding is that the joint is “stuck” in flexion, which is evident during an exam and on x-ray. Although the DIP joint may be passively fully extended, the patient with mallet finger is unable to actively extend it.
Mallet injuries, which are common in sports and associated with minor trauma, are typically caused by sudden forced flexion of the DIP joint during active extension of the finger. This can either stretch or tear the extensor tendon or lead to avulsion of the tendon insertion from the dorsum of the distal phalanx, with or without a fragment of bone. The injury is called a “soft” mallet finger when there is no bone involvement and a “bony” mallet finger when an avulsion is present, like the one that is evident on the FIGURE 3 x-ray (see arrow).
On clinical examination, the finger may or may not have an obvious deformity; similarly, you won’t always see bruising, swelling, or tenderness over the DIP joint.6 The work-up should include posterior/anterior, oblique, and lateral x-rays, followed by an examination of the soft tissue and a range-of-motion evaluation of the metacarpophalangeal and PIP joints. In acute injuries, tenderness is elicited with palpation over the dorsal aspect of the DIP joint. Although most patients develop an extensor lag at the DIP joint immediately after injury, the deformity may be delayed by a few hours or even days.6,7
Nonsurgical management is the standard of care for most mallet injuries, including mallet fractures involving less than one-third of the articular surface with no associated DIP joint subluxation.7
If there is no displacement, round-the-clock splinting to keep the joint in extension for a minimum of 6 weeks is indicated, followed by 2 to 3 weeks of nighttime splinting. It is important that the splinting allow for complete extension of the DIP joint but flexion of the PIP joint. Keeping the PIP in extension for prolonged periods can lead to permanent stiffness of the joint, while failure to provide any immobilization may lead to permanent deformity.
Surgery is indicated for a fracture fragment involving >30% of the joint surface (as demonstrated in the radiograph), volar subluxation, or a swan neck deformity—and when conservative therapy fails.7
CASE 4 An 18-year-old high school football player presents with pain and swelling at the tip of his right ring finger from an injury that occurred a week ago. When the player he was trying to tackle broke away, the patient says, he immediately felt pain and a “pop” in the finger.
The DIP joint of his right ring finger is swollen (FIGURE 4), but appears normal otherwise. When you isolate the joint, however, the patient is unable to flex it. You can palpate a stump on the volar surface of the finger.
What’s your next step?
B. Treat with splinting, RICE (rest, ice, compression, and elevation), and nonsteroidal anti-inflammatory drugs.
C. Order an ultrasound of the finger and palm.
D. Order magnetic resonance imaging (MRI) of the hand.
Answer: Order an ultrasound of the football player’s finger and palm (C).
This patient has Jersey finger, caused by a traumatic avulsion of the flexor digitorum profundus (FDP) from the distal phalanx and diagnosed based on the mechanism of injury and the patient’s inability to flex the DIP joint. The injury often does not show on x-rays, and the diagnosis may be missed for several weeks.
Jersey finger usually happens in sports like football or rugby, where players tackle each other, and involves forced, passive extension of the DIP joint at a time of active flexion. Management of Jersey finger starts with splinting, with both the DIP and PIP in slight flexion. Surgical reattachment of the flexor tendon is needed, with best results when it is done within 7 to 10 days of injury.4
You may be able to palpate the tendon stump in the palm or along the digit; bony avulsions can be trapped at the flexor sheath. Soft tissue swelling can be misleading, however, and the point of maximal tenderness is not an accurate means of identifying the avulsed tendon stump.8
Ultrasound is effective in differentiating between a partial and full thickness rupture and in localizing the distal tendon stump.8 MRI is usually reserved for precise evaluation of the tendon edges, to aid in operative planning. If the tendon is retracted to the palm, scarring may be irreversible because of the lack of blood supply.
Athletes typically return to play 12 weeks after injury, starting with protected activity and progressing to full gripping/grasping. Physical therapy and/or occupational therapy will be needed after the surgical wound has healed.
CASE 5 A 40-year-old construction worker who smashed his left index finger with a hammer one day ago presents with severe pain in his fingertip, which he is unable to move. On examination, you find that the distal finger is swollen and there is extensive ecchymosis and swelling underneath the nail. The finger has normal sensation, but you are unable to see capillary refill due to a large hematoma.
X-rays (FIGURE 5) reveal a distal tuft fracture. The patient’s main concern is the pain, and he asks what you can do to relieve it.
What’s your next step?
B. Perform fenestration of the nail.
C. Refer the patient to a hand surgeon.
D. Order computed tomography of the hand.
Answer: Perform fenestration of the construction worker’s nail (B).
This patient has a closed fracture of the distal phalanx, called a tuft fracture, and a sub-ungual hematoma, evident from the x-ray and the physical presentation.
Subungual hematoma requires fenestration with a needle to create small holes in the nail. If the nail bed is lacerated, the nail is removed and the injured nail bed repaired with sutures.
Tuft fractures sometimes require reduction. More often, they are stable and minimally displaced and can be managed conservatively, with splinting with a padded aluminum splint or a fingertip guard (Stax splint) for 3 to 4 weeks. Antibiotics are not indicated unless there is suspicion of an overlying or secondary infection. Referral to a hand surgeon is required for severe crush injuries, avulsion of the nail matrix, and open fractures of the distal phalanx.5,6
1. Hogan CJ, Ruland RT. High-pressure injection injuries to the upper extremity: a review of the literature. J Orthop Trauma. 2006;20:503-511.
2. Gonzalez R, Kasdan ML. High pressure injection injuries of the hand. Clin Occup Environ Med. 2006;5:407-411.
3. Freiberg A. Management of proximal interphalangeal joint injuries. Can J Plast Surg. 2007;15:199-203.
4. Perron AD, Brady WJ, Keats TE, et al. Orthopedic pitfalls in the emergency department: closed tendon injuries of the hand. Am J Emerg Med. 2001;19:76-80.
5. Oetgen ME, Dodds SD. Non-operative treatment of common finger injuries. Curr Rev Musculoskel Med. 2008;1:97-102.
6. Anderson D. Mallet finger. Aust Fam Physician. 2011;40:91-92.
7. Smit JM, Beets MR. Treatment options for mallet finger: a review. Plast Reconstr Surg. 2010;126:1624-1629.
8. Goodson A, Morgan M. Current management of Jersey finger in rugby players: cases series and literature review. Hand Surg. 2010;15:103-107.
1. Hogan CJ, Ruland RT. High-pressure injection injuries to the upper extremity: a review of the literature. J Orthop Trauma. 2006;20:503-511.
2. Gonzalez R, Kasdan ML. High pressure injection injuries of the hand. Clin Occup Environ Med. 2006;5:407-411.
3. Freiberg A. Management of proximal interphalangeal joint injuries. Can J Plast Surg. 2007;15:199-203.
4. Perron AD, Brady WJ, Keats TE, et al. Orthopedic pitfalls in the emergency department: closed tendon injuries of the hand. Am J Emerg Med. 2001;19:76-80.
5. Oetgen ME, Dodds SD. Non-operative treatment of common finger injuries. Curr Rev Musculoskel Med. 2008;1:97-102.
6. Anderson D. Mallet finger. Aust Fam Physician. 2011;40:91-92.
7. Smit JM, Beets MR. Treatment options for mallet finger: a review. Plast Reconstr Surg. 2010;126:1624-1629.
8. Goodson A, Morgan M. Current management of Jersey finger in rugby players: cases series and literature review. Hand Surg. 2010;15:103-107.