PHILADELPHIA – The question of how prepared general surgery residents are to operate independently after their training is longstanding, but clear definitions of competency and readiness have been elusive. A consortium of general surgery residencies has developed a metric for assessing surgeon readiness, but what the metric revealed may be a cause for concern for the surgical profession.

Brian C. George, MD, of the University of Michigan, Ann Arbor, reported at the annual meeting of the American Surgical Association on results of a study designed to measure the autonomy and readiness for independent practice of residents at 14 general surgery programs.

•“Performance” scale to measure readiness for independent practice, with competence defined as practice-ready and exceptional performance.

• “Zwisch” scale, named after Jay Zwischenberger, MD, FACS, of the University of Kentucky, to assess the amount of autonomy granted to a resident by the supervising surgical attending.

• “Complexity” scale to measure the patient-related complexity of the case at hand.

The study used a smartphone-based app, SIMPL, to collect data from September 2015 through December 2016. In evaluating performance, 437 observers provided 8,526 different ratings of 522 residents.

In a subset analysis, the study authors focused on the 132 operations the Surgical Council on Resident Education considers the core procedures of general surgery and found that 77% of fifth-year residents were rated as competent. Further restricting the analysis to residents in their final 6 months of training performing the five most commonly rated core procedures – appendectomy, cholecystectomy, ventral hernia repair, inguinal/femoral hernia repair, and partial colectomy – the researchers found that competency ranged from a high of 96% for appendectomy to a low of 71% for partial colectomy.

“If you combine all five procedures into one category, on average the residents are rated competent 84% of the time during the last 6 months of training,” Dr. George said. “But what’s really interesting – and I think this is probably the most important result for this study – is that looking at just the less-frequently rated core procedures and excluding the top five, residents are deemed competent in the last 6 months of training for 74% of those observed procedures.”

According to the Zwisch” scale to measure autonomy, residents in their last 6 months of training displayed what Dr. George termed “meaningful autonomy” in 77% of their observed operations for the core procedures. “Interestingly,” he added, “they were observed to have maximum autonomy, which is the supervision-only level, for 33% of all observed procedures.”

The researchers did an adjusted analysis to account for confounding factors such as the stringency of individual raters and patient complexity. “Using this type of analysis, the likelihood that a typical trainee rated by a typical attendee would be deemed competent by the end of training for a relatively straightforward laparoscopy appendectomy is 97%,” Dr. George said. “For a difficult laparoscopic appendectomy, by the end of training, they’re likely to be deemed competent 92% of time.” In the adjusted analysis, for a straightforward partial colectomy the raters predicted trainees to be competent 91.8% of time, but only 81.8% of the time for a complicated partial colectomy. “For less-frequently performed core procedures, there are many for which residents are likely to be deemed competent at a much lower level,” Dr. George added.

In discussing the study, Ara Darzi, MD, of St. Mary’s Hospital, London, called the methodology “unique and commendable,” and asked “Would you make the case to say we should increase the number of years of trainees from PG5 to PG6 or at least make your fellowships compulsory?”

Dr. George answered that 80% of general surgery residents already go into fellowships. “Whether it’s required or not is above my pay grade,” he said. “I hope not. Five years is already a big ask for a lot of medical students who are considering this profession. If we increase the training requirements, we’re going to have a supply problem that we will then need to address. We will be trading one problem for another.” He later added “The 20,000 hours of surgical residency should be enough to train a general surgeon to competence – its up to us to figure out how.”

The following organizations supported the research: American Board of Surgery, Association for Surgical Education, Association for Program Directors in Surgery, Massachusetts General Hospital, Northwestern University, Indiana University, and the members of the Procedural Learning and Safety Collaborative.

Neither Dr. George nor Dr. Darzi had any relevant financial disclosures.

The complete manuscript of this study and its presentation at the American Surgical Association’s 137th Annual Meeting, April 2017, in Philadelphia, Pennsylvania, is to be published in Annals of Surgery pending editorial review.

PHILADELPHIA – The question of how prepared general surgery residents are to operate independently after their training is longstanding, but clear definitions of competency and readiness have been elusive. A consortium of general surgery residencies has developed a metric for assessing surgeon readiness, but what the metric revealed may be a cause for concern for the surgical profession.

Brian C. George, MD, of the University of Michigan, Ann Arbor, reported at the annual meeting of the American Surgical Association on results of a study designed to measure the autonomy and readiness for independent practice of residents at 14 general surgery programs.

•“Performance” scale to measure readiness for independent practice, with competence defined as practice-ready and exceptional performance.

• “Zwisch” scale, named after Jay Zwischenberger, MD, FACS, of the University of Kentucky, to assess the amount of autonomy granted to a resident by the supervising surgical attending.

• “Complexity” scale to measure the patient-related complexity of the case at hand.

The study used a smartphone-based app, SIMPL, to collect data from September 2015 through December 2016. In evaluating performance, 437 observers provided 8,526 different ratings of 522 residents.

In a subset analysis, the study authors focused on the 132 operations the Surgical Council on Resident Education considers the core procedures of general surgery and found that 77% of fifth-year residents were rated as competent. Further restricting the analysis to residents in their final 6 months of training performing the five most commonly rated core procedures – appendectomy, cholecystectomy, ventral hernia repair, inguinal/femoral hernia repair, and partial colectomy – the researchers found that competency ranged from a high of 96% for appendectomy to a low of 71% for partial colectomy.

“If you combine all five procedures into one category, on average the residents are rated competent 84% of the time during the last 6 months of training,” Dr. George said. “But what’s really interesting – and I think this is probably the most important result for this study – is that looking at just the less-frequently rated core procedures and excluding the top five, residents are deemed competent in the last 6 months of training for 74% of those observed procedures.”

According to the Zwisch” scale to measure autonomy, residents in their last 6 months of training displayed what Dr. George termed “meaningful autonomy” in 77% of their observed operations for the core procedures. “Interestingly,” he added, “they were observed to have maximum autonomy, which is the supervision-only level, for 33% of all observed procedures.”

The researchers did an adjusted analysis to account for confounding factors such as the stringency of individual raters and patient complexity. “Using this type of analysis, the likelihood that a typical trainee rated by a typical attendee would be deemed competent by the end of training for a relatively straightforward laparoscopy appendectomy is 97%,” Dr. George said. “For a difficult laparoscopic appendectomy, by the end of training, they’re likely to be deemed competent 92% of time.” In the adjusted analysis, for a straightforward partial colectomy the raters predicted trainees to be competent 91.8% of time, but only 81.8% of the time for a complicated partial colectomy. “For less-frequently performed core procedures, there are many for which residents are likely to be deemed competent at a much lower level,” Dr. George added.

In discussing the study, Ara Darzi, MD, of St. Mary’s Hospital, London, called the methodology “unique and commendable,” and asked “Would you make the case to say we should increase the number of years of trainees from PG5 to PG6 or at least make your fellowships compulsory?”

Dr. George answered that 80% of general surgery residents already go into fellowships. “Whether it’s required or not is above my pay grade,” he said. “I hope not. Five years is already a big ask for a lot of medical students who are considering this profession. If we increase the training requirements, we’re going to have a supply problem that we will then need to address. We will be trading one problem for another.” He later added “The 20,000 hours of surgical residency should be enough to train a general surgeon to competence – its up to us to figure out how.”

The following organizations supported the research: American Board of Surgery, Association for Surgical Education, Association for Program Directors in Surgery, Massachusetts General Hospital, Northwestern University, Indiana University, and the members of the Procedural Learning and Safety Collaborative.

Neither Dr. George nor Dr. Darzi had any relevant financial disclosures.

The complete manuscript of this study and its presentation at the American Surgical Association’s 137th Annual Meeting, April 2017, in Philadelphia, Pennsylvania, is to be published in Annals of Surgery pending editorial review.

PHILADELPHIA – The question of how prepared general surgery residents are to operate independently after their training is longstanding, but clear definitions of competency and readiness have been elusive. A consortium of general surgery residencies has developed a metric for assessing surgeon readiness, but what the metric revealed may be a cause for concern for the surgical profession.

Brian C. George, MD, of the University of Michigan, Ann Arbor, reported at the annual meeting of the American Surgical Association on results of a study designed to measure the autonomy and readiness for independent practice of residents at 14 general surgery programs.

•“Performance” scale to measure readiness for independent practice, with competence defined as practice-ready and exceptional performance.

• “Zwisch” scale, named after Jay Zwischenberger, MD, FACS, of the University of Kentucky, to assess the amount of autonomy granted to a resident by the supervising surgical attending.

• “Complexity” scale to measure the patient-related complexity of the case at hand.

The study used a smartphone-based app, SIMPL, to collect data from September 2015 through December 2016. In evaluating performance, 437 observers provided 8,526 different ratings of 522 residents.

In a subset analysis, the study authors focused on the 132 operations the Surgical Council on Resident Education considers the core procedures of general surgery and found that 77% of fifth-year residents were rated as competent. Further restricting the analysis to residents in their final 6 months of training performing the five most commonly rated core procedures – appendectomy, cholecystectomy, ventral hernia repair, inguinal/femoral hernia repair, and partial colectomy – the researchers found that competency ranged from a high of 96% for appendectomy to a low of 71% for partial colectomy.

“If you combine all five procedures into one category, on average the residents are rated competent 84% of the time during the last 6 months of training,” Dr. George said. “But what’s really interesting – and I think this is probably the most important result for this study – is that looking at just the less-frequently rated core procedures and excluding the top five, residents are deemed competent in the last 6 months of training for 74% of those observed procedures.”

According to the Zwisch” scale to measure autonomy, residents in their last 6 months of training displayed what Dr. George termed “meaningful autonomy” in 77% of their observed operations for the core procedures. “Interestingly,” he added, “they were observed to have maximum autonomy, which is the supervision-only level, for 33% of all observed procedures.”

The researchers did an adjusted analysis to account for confounding factors such as the stringency of individual raters and patient complexity. “Using this type of analysis, the likelihood that a typical trainee rated by a typical attendee would be deemed competent by the end of training for a relatively straightforward laparoscopy appendectomy is 97%,” Dr. George said. “For a difficult laparoscopic appendectomy, by the end of training, they’re likely to be deemed competent 92% of time.” In the adjusted analysis, for a straightforward partial colectomy the raters predicted trainees to be competent 91.8% of time, but only 81.8% of the time for a complicated partial colectomy. “For less-frequently performed core procedures, there are many for which residents are likely to be deemed competent at a much lower level,” Dr. George added.

In discussing the study, Ara Darzi, MD, of St. Mary’s Hospital, London, called the methodology “unique and commendable,” and asked “Would you make the case to say we should increase the number of years of trainees from PG5 to PG6 or at least make your fellowships compulsory?”

Dr. George answered that 80% of general surgery residents already go into fellowships. “Whether it’s required or not is above my pay grade,” he said. “I hope not. Five years is already a big ask for a lot of medical students who are considering this profession. If we increase the training requirements, we’re going to have a supply problem that we will then need to address. We will be trading one problem for another.” He later added “The 20,000 hours of surgical residency should be enough to train a general surgeon to competence – its up to us to figure out how.”

The following organizations supported the research: American Board of Surgery, Association for Surgical Education, Association for Program Directors in Surgery, Massachusetts General Hospital, Northwestern University, Indiana University, and the members of the Procedural Learning and Safety Collaborative.

Neither Dr. George nor Dr. Darzi had any relevant financial disclosures.

The complete manuscript of this study and its presentation at the American Surgical Association’s 137th Annual Meeting, April 2017, in Philadelphia, Pennsylvania, is to be published in Annals of Surgery pending editorial review.

BOSTON—Misdiagnosing optic neuritis may expose patients to risks associated with undergoing MRI with a contrast agent, lumbar puncture, and high-dose steroid treatment. It also costs patients and hospitals time and money. Leanne Stunkel, MD, a neurology resident at Washington University in St. Louis, and her colleagues observed a 60% misdiagnosis rate of optic neuritis among patients who were referred to their neuro-ophthalmology clinic, according to a study presented at the 69th Annual Meeting of the American Academy of Neurology.

“The most common [diagnostic] errors were overreliance on a single item of history and failure to consider alternative diagnoses,” said Dr. Stunkel.

Optic neuritis is an acute inflammatory demyelinating condition of the optic nerve. Presenting symptoms include acute or subacute vision loss, pain with eye movement, and changes in color vision, especially affecting the color red, said Dr. Stunkel. Many patients who were referred to their tertiary care clinic for optic neuritis turned out to have other conditions, which prompted the researchers to find out more about optic neuritis misdiagnosis.

Previous studies found a misdiagnosis rate of between 10% and 40%, but none of these studies examined which errors led to these misdiagnoses. To determine how often optic neuritis is misdiagnosed and which diagnostic errors play a role, and to identify diagnoses commonly mistaken for optic neuritis, Dr. Stunkel and colleagues performed a retrospective chart review.

The researchers reviewed new patient encounters between January 2014 and October 2016 to identify patients referred with a diagnosis of optic neuritis. Experienced neuro-ophthalmologists determined the final diagnosis. The researchers then applied the Diagnosis Error Evaluation and Research (DEER) taxonomy tool to identify diagnostic errors in cases in which the patient did not have optic neuritis.

A total of 122 patients were referred for optic neuritis during the study period. Only 40% of these patients were diagnosed with optic neuritis, and 60% of patients had alternative diagnoses. The most common alternative diagnoses were headache with eye pain and visual symptoms (22%), functional visual loss (19%), and other optic neuropathies (16%).

In addition, 15% of patients had retinal or macular problems rather than pathology of the optic nerve. Other diagnoses included neoplasms, congenital disk abnormalities, and inflammatory conditions that affected other parts of the eye.

The most common diagnostic errors were from problems eliciting or interpreting the history (33%). “We saw an overreliance on history of risk factors such as multiple sclerosis or other inflammatory disorders and some failure to elicit the fact that these were brief stereotyped episodes of vision loss, like in a migraine aura,” said Dr. Stunkel.

Twenty-one percent of diagnostic errors were due to errors interpreting physical exam findings, and 14% of errors were due to misinterpretation of diagnostic tests. Finally, 32% of diagnostic errors resulted from failure to consider alternative diagnoses. Of patients who did not have optic neuritis, 17% had already received a lumbar puncture, 17% had received a contrast MRI that turned out to be negative, and 11 patients had inappropriately received IV steroids, said Dr. Stunkel.

Some of the study limitations include that the DEER category assignments were subjective, and that not every referral for optic neuritis was included in the study due to limitations of the clinic’s electronic medical records system, said Dr. Stunkel.

—Erica Tricarico

BOSTON—Misdiagnosing optic neuritis may expose patients to risks associated with undergoing MRI with a contrast agent, lumbar puncture, and high-dose steroid treatment. It also costs patients and hospitals time and money. Leanne Stunkel, MD, a neurology resident at Washington University in St. Louis, and her colleagues observed a 60% misdiagnosis rate of optic neuritis among patients who were referred to their neuro-ophthalmology clinic, according to a study presented at the 69th Annual Meeting of the American Academy of Neurology.

“The most common [diagnostic] errors were overreliance on a single item of history and failure to consider alternative diagnoses,” said Dr. Stunkel.

Optic neuritis is an acute inflammatory demyelinating condition of the optic nerve. Presenting symptoms include acute or subacute vision loss, pain with eye movement, and changes in color vision, especially affecting the color red, said Dr. Stunkel. Many patients who were referred to their tertiary care clinic for optic neuritis turned out to have other conditions, which prompted the researchers to find out more about optic neuritis misdiagnosis.

Previous studies found a misdiagnosis rate of between 10% and 40%, but none of these studies examined which errors led to these misdiagnoses. To determine how often optic neuritis is misdiagnosed and which diagnostic errors play a role, and to identify diagnoses commonly mistaken for optic neuritis, Dr. Stunkel and colleagues performed a retrospective chart review.

The researchers reviewed new patient encounters between January 2014 and October 2016 to identify patients referred with a diagnosis of optic neuritis. Experienced neuro-ophthalmologists determined the final diagnosis. The researchers then applied the Diagnosis Error Evaluation and Research (DEER) taxonomy tool to identify diagnostic errors in cases in which the patient did not have optic neuritis.

A total of 122 patients were referred for optic neuritis during the study period. Only 40% of these patients were diagnosed with optic neuritis, and 60% of patients had alternative diagnoses. The most common alternative diagnoses were headache with eye pain and visual symptoms (22%), functional visual loss (19%), and other optic neuropathies (16%).

In addition, 15% of patients had retinal or macular problems rather than pathology of the optic nerve. Other diagnoses included neoplasms, congenital disk abnormalities, and inflammatory conditions that affected other parts of the eye.

The most common diagnostic errors were from problems eliciting or interpreting the history (33%). “We saw an overreliance on history of risk factors such as multiple sclerosis or other inflammatory disorders and some failure to elicit the fact that these were brief stereotyped episodes of vision loss, like in a migraine aura,” said Dr. Stunkel.

Twenty-one percent of diagnostic errors were due to errors interpreting physical exam findings, and 14% of errors were due to misinterpretation of diagnostic tests. Finally, 32% of diagnostic errors resulted from failure to consider alternative diagnoses. Of patients who did not have optic neuritis, 17% had already received a lumbar puncture, 17% had received a contrast MRI that turned out to be negative, and 11 patients had inappropriately received IV steroids, said Dr. Stunkel.

Some of the study limitations include that the DEER category assignments were subjective, and that not every referral for optic neuritis was included in the study due to limitations of the clinic’s electronic medical records system, said Dr. Stunkel.

—Erica Tricarico

BOSTON—Misdiagnosing optic neuritis may expose patients to risks associated with undergoing MRI with a contrast agent, lumbar puncture, and high-dose steroid treatment. It also costs patients and hospitals time and money. Leanne Stunkel, MD, a neurology resident at Washington University in St. Louis, and her colleagues observed a 60% misdiagnosis rate of optic neuritis among patients who were referred to their neuro-ophthalmology clinic, according to a study presented at the 69th Annual Meeting of the American Academy of Neurology.

“The most common [diagnostic] errors were overreliance on a single item of history and failure to consider alternative diagnoses,” said Dr. Stunkel.

Optic neuritis is an acute inflammatory demyelinating condition of the optic nerve. Presenting symptoms include acute or subacute vision loss, pain with eye movement, and changes in color vision, especially affecting the color red, said Dr. Stunkel. Many patients who were referred to their tertiary care clinic for optic neuritis turned out to have other conditions, which prompted the researchers to find out more about optic neuritis misdiagnosis.

Previous studies found a misdiagnosis rate of between 10% and 40%, but none of these studies examined which errors led to these misdiagnoses. To determine how often optic neuritis is misdiagnosed and which diagnostic errors play a role, and to identify diagnoses commonly mistaken for optic neuritis, Dr. Stunkel and colleagues performed a retrospective chart review.

The researchers reviewed new patient encounters between January 2014 and October 2016 to identify patients referred with a diagnosis of optic neuritis. Experienced neuro-ophthalmologists determined the final diagnosis. The researchers then applied the Diagnosis Error Evaluation and Research (DEER) taxonomy tool to identify diagnostic errors in cases in which the patient did not have optic neuritis.

A total of 122 patients were referred for optic neuritis during the study period. Only 40% of these patients were diagnosed with optic neuritis, and 60% of patients had alternative diagnoses. The most common alternative diagnoses were headache with eye pain and visual symptoms (22%), functional visual loss (19%), and other optic neuropathies (16%).

In addition, 15% of patients had retinal or macular problems rather than pathology of the optic nerve. Other diagnoses included neoplasms, congenital disk abnormalities, and inflammatory conditions that affected other parts of the eye.

The most common diagnostic errors were from problems eliciting or interpreting the history (33%). “We saw an overreliance on history of risk factors such as multiple sclerosis or other inflammatory disorders and some failure to elicit the fact that these were brief stereotyped episodes of vision loss, like in a migraine aura,” said Dr. Stunkel.

Twenty-one percent of diagnostic errors were due to errors interpreting physical exam findings, and 14% of errors were due to misinterpretation of diagnostic tests. Finally, 32% of diagnostic errors resulted from failure to consider alternative diagnoses. Of patients who did not have optic neuritis, 17% had already received a lumbar puncture, 17% had received a contrast MRI that turned out to be negative, and 11 patients had inappropriately received IV steroids, said Dr. Stunkel.

Some of the study limitations include that the DEER category assignments were subjective, and that not every referral for optic neuritis was included in the study due to limitations of the clinic’s electronic medical records system, said Dr. Stunkel.

—Erica Tricarico

Here are the top discussion threads in ACS Communities just prior to press time (all of these threads are from the General Surgery community):

1. Potential Florida legislation prohibiting maintenance of certification requirements

2. My proposal for changing MOC

3. Surgical training and ethics in the ’50s/’60s

4. Timing of cholecystectomy in severe gallstone pancreatitis

5. GOO (Gastric Outlet Obstruction) – What would you do?

Here are the top discussion threads in ACS Communities just prior to press time (all of these threads are from the General Surgery community):

1. Potential Florida legislation prohibiting maintenance of certification requirements

2. My proposal for changing MOC

3. Surgical training and ethics in the ’50s/’60s

4. Timing of cholecystectomy in severe gallstone pancreatitis

5. GOO (Gastric Outlet Obstruction) – What would you do?

Here are the top discussion threads in ACS Communities just prior to press time (all of these threads are from the General Surgery community):

1. Potential Florida legislation prohibiting maintenance of certification requirements

2. My proposal for changing MOC

3. Surgical training and ethics in the ’50s/’60s

4. Timing of cholecystectomy in severe gallstone pancreatitis

5. GOO (Gastric Outlet Obstruction) – What would you do?

Hypertension awareness has improved significantly in adults since 2002, according to the National Center for Health Statistics.

The percentage of adults aged 18-39 years who had hypertension but reported not being told about it by a health care provider dropped 36% from 1999-2002, when it was 48.3%, to 2011-2014, when it was down to 30.8%. For adults aged 40-59 years, 26.6% were unaware of their hypertension in 1999-2002, compared with 17.4% in 2011-2014, a relative decrease of almost 35%. The decline was an even larger 55% for those aged 60 years and over – from 27.6% in 1999-2002 to 12.5% in 2011-2014, the NCHS reported.

[email protected]

Hypertension awareness has improved significantly in adults since 2002, according to the National Center for Health Statistics.

The percentage of adults aged 18-39 years who had hypertension but reported not being told about it by a health care provider dropped 36% from 1999-2002, when it was 48.3%, to 2011-2014, when it was down to 30.8%. For adults aged 40-59 years, 26.6% were unaware of their hypertension in 1999-2002, compared with 17.4% in 2011-2014, a relative decrease of almost 35%. The decline was an even larger 55% for those aged 60 years and over – from 27.6% in 1999-2002 to 12.5% in 2011-2014, the NCHS reported.

[email protected]

Hypertension awareness has improved significantly in adults since 2002, according to the National Center for Health Statistics.

The percentage of adults aged 18-39 years who had hypertension but reported not being told about it by a health care provider dropped 36% from 1999-2002, when it was 48.3%, to 2011-2014, when it was down to 30.8%. For adults aged 40-59 years, 26.6% were unaware of their hypertension in 1999-2002, compared with 17.4% in 2011-2014, a relative decrease of almost 35%. The decline was an even larger 55% for those aged 60 years and over – from 27.6% in 1999-2002 to 12.5% in 2011-2014, the NCHS reported.

[email protected]

The first Skin of Color column, "Diversity in Dermatology: A Society Devoted to Skin of Color," produced in collaboration with the Skin of Color Society appears on page 322. This column will be published quarterly and will serve to increase the knowledge available to dermatologists to help improve delivery of care to this underserved population.

Look for Skin of Color columns in upcoming issues of Cutis.

The first Skin of Color column, "Diversity in Dermatology: A Society Devoted to Skin of Color," produced in collaboration with the Skin of Color Society appears on page 322. This column will be published quarterly and will serve to increase the knowledge available to dermatologists to help improve delivery of care to this underserved population.

Look for Skin of Color columns in upcoming issues of Cutis.

The first Skin of Color column, "Diversity in Dermatology: A Society Devoted to Skin of Color," produced in collaboration with the Skin of Color Society appears on page 322. This column will be published quarterly and will serve to increase the knowledge available to dermatologists to help improve delivery of care to this underserved population.

Look for Skin of Color columns in upcoming issues of Cutis.

Skin cancers in patients with skin of color are less prevalent but have a higher morbidity and mortality compared to white patients. Challenges to early detection, including clinical differences in presentation, low public awareness, lower index of suspicion among health care providers, and access to specialty care, likely contribute to observed differences in prognosis between skin of color and white populations.

RELATED AUDIO: Why is skin cancer mortality higher in patients with skin of color? A peer-to-peer audiocast with Dr. Vincent A. DeLeo and Dr. Andrew F. Alexis.

Skin cancer is the most common malignancy in the United States, accounting for approximately 40% of all neoplasms in white patients but only 1% to 4% in Asian American and black patients.^1,2 Largely due to the photoprotective effects of increased constitutive epidermal melanin, melanoma is approximately 10 to 20 times less frequent in black patients and 3 to 7 times less common in Hispanics than age-matched whites.¹ Nonmelanoma skin cancers including squamous cell carcinoma (SCC) and basal cell carcinoma also are less prevalent in darker skin types.^3,4

In the United States, Hispanic, American Indian, and black patients have a 2- to 3-fold higher risk of mortality from malignant melanoma than white patients overall, even when diagnosed at the same stage.^2,5 The most recent Surveillance, Epidemiology, and End Results (SEER) Program cancer statistic review found that the 5-year relative survival of individuals with all stages of malignant melanoma from 2006 to 2012 was 91.1% for white patients and67.3% for black patients. Fortunately, the mortality rate for black patients decreased approximately 0.8% per year from 1975 to 2013.^5,6 No statistically significant change was seen in other ethnic groups, though research in East Asia suggests that age-standardized mortality rates from melanoma have increased by up to 7.4% per year over the last 30 years, with the greatest rise seen in Korean females.^5,7 Further epidemiologic research looking at the relative survival of Asian Americans and Pacific Islanders in the United States is needed.^8,9

Similar to melanoma, the mortality from SCC is disproportionately increased in skin of color populations, ranging from 18% to 29% in black patients.^3,10,11 There is a paucity of population-based studies in the United States looking at mortality rates of nonmelanoma skin cancers and their trends over time, but a 1993 study suggests that mortality rates are declining less consistently in black patients than white patients.¹¹

Factors that may contribute to higher mortality rates in patients with skin of color include a greater propensity for inherently aggressive skin cancers (eg, higher risk of SCC) and delays in diagnosis (eg, late-stage diagnosis of melanoma).^1,4 For melanoma, increased mortality has been attributed to a predominance of acral lentiginous melanomas, which are more frequently diagnosed at more advanced stages than other melanoma subtypes.^6,12,13 Black patients, Hispanics, Asians, and Pacific Islanders are all more likely to present with thicker tumors and metastases on initial presentation than their white counterparts (P<.001).^2,8,9,12-14 The higher risk of death from SCC results from the predominance of lesions on non–sun-exposed areas, particularly the legs and anogenital areas, and within sites of chronic scarring or inflammation.⁴ Unlike sun-induced SCC, the most commonly observed type of SCC in lighter skin types, SCCs that develop in association with chronic inflammatory or ulcerative processes are aggressive and invasive, and they metastasize to distant sites in 20% to 40% of cases (versus 1%–4% in sun-induced SCC).^1,3,4 For all skin cancers, poor access to medical care, patients’ unawareness of their skin cancer risk, lack of adequate skin examinations, and prevalence of lesions on uncommon sites that may be inconspicuous or overlooked have all been suggested to delay diagnosis.^1,15,16 Given that more advanced disease is associated with worse outcomes, the implications of this delay are enormous and remain a cause for concern.

RELATED AUDIO: Dr. Alexis discusses factors that contribute to the delayed diagnosis of melanoma in patients with skin of color and what physicians should know about the incidence and presentation of melanoma in this population to help educate their patients.

The alarming skin cancer mortality rates in patients with skin of color are a call to action for the medical community. The consistent use of full-body skin examinations including close inspection of mucosal, acral, and genital areas for all patients independent of skin type and racial/ethnic background is paramount. Advancing skin cancer education in skin of color populations, such as through distribution of patient-directed educational materials produced by organizations such as the American Academy of Dermatology, Skin Cancer Foundation, and Skin of Color Society, is an important step toward increased public awareness.¹⁶ Use of social and traditional media outlets as well as community-directed health outreach campaigns also are important strategies to change the common misconception that darker-skinned individuals do not get skin cancer. We hope that with a multipronged approach, disparities in skin cancer mortality will steadily be eliminated.

Skin cancers in patients with skin of color are less prevalent but have a higher morbidity and mortality compared to white patients. Challenges to early detection, including clinical differences in presentation, low public awareness, lower index of suspicion among health care providers, and access to specialty care, likely contribute to observed differences in prognosis between skin of color and white populations.

RELATED AUDIO: Why is skin cancer mortality higher in patients with skin of color? A peer-to-peer audiocast with Dr. Vincent A. DeLeo and Dr. Andrew F. Alexis.

Skin cancer is the most common malignancy in the United States, accounting for approximately 40% of all neoplasms in white patients but only 1% to 4% in Asian American and black patients.^1,2 Largely due to the photoprotective effects of increased constitutive epidermal melanin, melanoma is approximately 10 to 20 times less frequent in black patients and 3 to 7 times less common in Hispanics than age-matched whites.¹ Nonmelanoma skin cancers including squamous cell carcinoma (SCC) and basal cell carcinoma also are less prevalent in darker skin types.^3,4

In the United States, Hispanic, American Indian, and black patients have a 2- to 3-fold higher risk of mortality from malignant melanoma than white patients overall, even when diagnosed at the same stage.^2,5 The most recent Surveillance, Epidemiology, and End Results (SEER) Program cancer statistic review found that the 5-year relative survival of individuals with all stages of malignant melanoma from 2006 to 2012 was 91.1% for white patients and67.3% for black patients. Fortunately, the mortality rate for black patients decreased approximately 0.8% per year from 1975 to 2013.^5,6 No statistically significant change was seen in other ethnic groups, though research in East Asia suggests that age-standardized mortality rates from melanoma have increased by up to 7.4% per year over the last 30 years, with the greatest rise seen in Korean females.^5,7 Further epidemiologic research looking at the relative survival of Asian Americans and Pacific Islanders in the United States is needed.^8,9

Similar to melanoma, the mortality from SCC is disproportionately increased in skin of color populations, ranging from 18% to 29% in black patients.^3,10,11 There is a paucity of population-based studies in the United States looking at mortality rates of nonmelanoma skin cancers and their trends over time, but a 1993 study suggests that mortality rates are declining less consistently in black patients than white patients.¹¹

Factors that may contribute to higher mortality rates in patients with skin of color include a greater propensity for inherently aggressive skin cancers (eg, higher risk of SCC) and delays in diagnosis (eg, late-stage diagnosis of melanoma).^1,4 For melanoma, increased mortality has been attributed to a predominance of acral lentiginous melanomas, which are more frequently diagnosed at more advanced stages than other melanoma subtypes.^6,12,13 Black patients, Hispanics, Asians, and Pacific Islanders are all more likely to present with thicker tumors and metastases on initial presentation than their white counterparts (P<.001).^2,8,9,12-14 The higher risk of death from SCC results from the predominance of lesions on non–sun-exposed areas, particularly the legs and anogenital areas, and within sites of chronic scarring or inflammation.⁴ Unlike sun-induced SCC, the most commonly observed type of SCC in lighter skin types, SCCs that develop in association with chronic inflammatory or ulcerative processes are aggressive and invasive, and they metastasize to distant sites in 20% to 40% of cases (versus 1%–4% in sun-induced SCC).^1,3,4 For all skin cancers, poor access to medical care, patients’ unawareness of their skin cancer risk, lack of adequate skin examinations, and prevalence of lesions on uncommon sites that may be inconspicuous or overlooked have all been suggested to delay diagnosis.^1,15,16 Given that more advanced disease is associated with worse outcomes, the implications of this delay are enormous and remain a cause for concern.

RELATED AUDIO: Dr. Alexis discusses factors that contribute to the delayed diagnosis of melanoma in patients with skin of color and what physicians should know about the incidence and presentation of melanoma in this population to help educate their patients.

The alarming skin cancer mortality rates in patients with skin of color are a call to action for the medical community. The consistent use of full-body skin examinations including close inspection of mucosal, acral, and genital areas for all patients independent of skin type and racial/ethnic background is paramount. Advancing skin cancer education in skin of color populations, such as through distribution of patient-directed educational materials produced by organizations such as the American Academy of Dermatology, Skin Cancer Foundation, and Skin of Color Society, is an important step toward increased public awareness.¹⁶ Use of social and traditional media outlets as well as community-directed health outreach campaigns also are important strategies to change the common misconception that darker-skinned individuals do not get skin cancer. We hope that with a multipronged approach, disparities in skin cancer mortality will steadily be eliminated.

Skin cancers in patients with skin of color are less prevalent but have a higher morbidity and mortality compared to white patients. Challenges to early detection, including clinical differences in presentation, low public awareness, lower index of suspicion among health care providers, and access to specialty care, likely contribute to observed differences in prognosis between skin of color and white populations.

RELATED AUDIO: Why is skin cancer mortality higher in patients with skin of color? A peer-to-peer audiocast with Dr. Vincent A. DeLeo and Dr. Andrew F. Alexis.

Skin cancer is the most common malignancy in the United States, accounting for approximately 40% of all neoplasms in white patients but only 1% to 4% in Asian American and black patients.^1,2 Largely due to the photoprotective effects of increased constitutive epidermal melanin, melanoma is approximately 10 to 20 times less frequent in black patients and 3 to 7 times less common in Hispanics than age-matched whites.¹ Nonmelanoma skin cancers including squamous cell carcinoma (SCC) and basal cell carcinoma also are less prevalent in darker skin types.^3,4

In the United States, Hispanic, American Indian, and black patients have a 2- to 3-fold higher risk of mortality from malignant melanoma than white patients overall, even when diagnosed at the same stage.^2,5 The most recent Surveillance, Epidemiology, and End Results (SEER) Program cancer statistic review found that the 5-year relative survival of individuals with all stages of malignant melanoma from 2006 to 2012 was 91.1% for white patients and67.3% for black patients. Fortunately, the mortality rate for black patients decreased approximately 0.8% per year from 1975 to 2013.^5,6 No statistically significant change was seen in other ethnic groups, though research in East Asia suggests that age-standardized mortality rates from melanoma have increased by up to 7.4% per year over the last 30 years, with the greatest rise seen in Korean females.^5,7 Further epidemiologic research looking at the relative survival of Asian Americans and Pacific Islanders in the United States is needed.^8,9

Similar to melanoma, the mortality from SCC is disproportionately increased in skin of color populations, ranging from 18% to 29% in black patients.^3,10,11 There is a paucity of population-based studies in the United States looking at mortality rates of nonmelanoma skin cancers and their trends over time, but a 1993 study suggests that mortality rates are declining less consistently in black patients than white patients.¹¹

Factors that may contribute to higher mortality rates in patients with skin of color include a greater propensity for inherently aggressive skin cancers (eg, higher risk of SCC) and delays in diagnosis (eg, late-stage diagnosis of melanoma).^1,4 For melanoma, increased mortality has been attributed to a predominance of acral lentiginous melanomas, which are more frequently diagnosed at more advanced stages than other melanoma subtypes.^6,12,13 Black patients, Hispanics, Asians, and Pacific Islanders are all more likely to present with thicker tumors and metastases on initial presentation than their white counterparts (P<.001).^2,8,9,12-14 The higher risk of death from SCC results from the predominance of lesions on non–sun-exposed areas, particularly the legs and anogenital areas, and within sites of chronic scarring or inflammation.⁴ Unlike sun-induced SCC, the most commonly observed type of SCC in lighter skin types, SCCs that develop in association with chronic inflammatory or ulcerative processes are aggressive and invasive, and they metastasize to distant sites in 20% to 40% of cases (versus 1%–4% in sun-induced SCC).^1,3,4 For all skin cancers, poor access to medical care, patients’ unawareness of their skin cancer risk, lack of adequate skin examinations, and prevalence of lesions on uncommon sites that may be inconspicuous or overlooked have all been suggested to delay diagnosis.^1,15,16 Given that more advanced disease is associated with worse outcomes, the implications of this delay are enormous and remain a cause for concern.

RELATED AUDIO: Dr. Alexis discusses factors that contribute to the delayed diagnosis of melanoma in patients with skin of color and what physicians should know about the incidence and presentation of melanoma in this population to help educate their patients.

The alarming skin cancer mortality rates in patients with skin of color are a call to action for the medical community. The consistent use of full-body skin examinations including close inspection of mucosal, acral, and genital areas for all patients independent of skin type and racial/ethnic background is paramount. Advancing skin cancer education in skin of color populations, such as through distribution of patient-directed educational materials produced by organizations such as the American Academy of Dermatology, Skin Cancer Foundation, and Skin of Color Society, is an important step toward increased public awareness.¹⁶ Use of social and traditional media outlets as well as community-directed health outreach campaigns also are important strategies to change the common misconception that darker-skinned individuals do not get skin cancer. We hope that with a multipronged approach, disparities in skin cancer mortality will steadily be eliminated.

Case

An 85-year-old right-handed woman who recently had been diagnosed with mild cognitive impairment arrived at the ED via emergency medical services (EMS) for evaluation of a reported fall. She was accompanied by her daughter, who resided with the patient and was her primary caregiver. The patient stated that she had tripped on a wet rug in the bathroom of her home, striking her head and face on the edge of the sink without losing consciousness. Her daughter reported that she was not assisting her mother when the fall occurred, but had witnessed the fall from the hallway and called EMS. At the patient’s home, EMS found the patient to be alert, oriented, and ambulatory with normal vital signs that remained stable throughout prehospital transport.

The remainder of the patient’s history was provided almost entirely by her daughter, who constantly interrupted her mother whenever she attempted to directly answer a question or provide information. On physical examination, the patient had bilateral tenderness, edema, and periorbital ecchymoses, and a left eye that was nearly swollen shut. Extraocular movements were normal, visual acuity was intact, and sclerae were noninjected. The patient had tenderness over both maxillary sinuses, and edema and ecchymosis of her left cheek. There was also tenderness, ecchymoses, and edema on the lateral aspects of both forearms, and decreased range of motion of her right lower arm and wrist. With the exception of the patient not knowing the date during the orientation part of the thorough neurological examination, the remainder of the physical examination was unremarkable.

Radiological evaluation found no evidence of traumatic brain injury, but did reveal an acute fracture of the left zygomatic arch, an acute displaced nasal bone fracture, an age-indeterminate fracture of the right zygomatic arch, and an acute right ulnar fracture. Considering all of these findings, particularly the pattern of acute injuries, the emergency physician (EP) considered elder abuse as the possible etiology of the patient’s acute and chronic injuries.

Although the patient had initially agreed with her daughter’s description of the events—including her claim that she had fallen—when the EP questioned the patient alone, she related a history of frequent verbal and less frequent physical abuse by her daughter. The patient further noted that immediately before sustaining the injuries that brought her to the ED, her daughter had been insisting that she sign documents to give her control of her banking and finances. After refusing to sign the papers, the patient said that she and her daughter got into an argument, which she noted “they tended to do frequently.” The patient admitted that during this argument, her daughter struck her in the face repeatedly with the cane that the daughter had grabbed with her right hand.

The EP admitted the patient to the hospital for management of her orthopedic injuries and related pain, and to formulate a safe discharge plan. During admission, additional diagnostic testing revealed multiple old rib fractures, anemia, and a low-serum albumin, which suggested poor nutritional status.

Epidemiology

The term elder abuse refers to harm or the risk of harm to an older adult from either action or negligence committed by someone in a relationship of trust, or when a victim has been targeted because of age or disability. Elder abuse encompasses physical, sexual, or psychological abuse, neglect, and financial exploitation.^1-5 Identified victims of elder abuse typically suffer from multiple forms of abuse.^1-5

At present, elder abuse annually affects 5% to 10% of community-dwelling older adults,^1-6 and nursing-home residents are at increased risk of abuse.^7-10 Poor medical outcomes, including depression and dementia,¹¹ and much higher mortality^6,12,13 have been linked to victims of elder abuse.

Etiology

When treating older adults, it is critically important for EPs and the ED staff to consider and identify elder abuse in the differential diagnosis.^14,15 Presently, only an estimated 1 in 24 cases of abuse is recognized and reported to the authorities,² and much of the subsequent morbidity and mortality of elder abuse results from poor detection. A visit to the ED for an acute injury or illness may be the only time socially isolated older adults leave their homes.^15-17 Additionally, the ED setting is uniquely suited to identify mistreatment, as a patient typically may be evaluated for several hours by providers from multiple disciplines who are able to observe, interact with, and examine the patient.¹⁵ The ED already exercises a similar essential role in the identification and initial intervention for both child abuse^18,19 and intimate partner violence among younger adults.^20,21

Recognition

Unfortunately, at present, ED providers rarely recognize and report elder abuse.^22-24 Though the reasons for this are not entirely understood, inadequate training, lack of time and space to conduct complete evaluations, reluctance to become involved with the legal system, and challenges to distinguishing intentional from unintentional injuries may be contributing factors.^24,25 A focus on improving EP and ED staff approaches to elder abuse is relevant and timely given the growing elderly population.

Risk Factors

When evaluating elderly patients, providers should consider research suggesting that some older adults may be at particularly high risk for abuse.^4,26-29 Notably, individuals who have cognitive impairment are more likely to be victims of abuse.^30-32 Health-related demographic characteristics such as poor physical and mental health, substance abuse, low income/socioeconomic status, and social isolation all may increase the potential for mistreatment.

Family History

Similar to situations resulting in intimate partner violence, a family history of abuse and exposure to traumatic events may increase risk, and those responsible for elder abuse often turn out to be spouses, romantic partners, or an adult child living with the elderly parent—though paid caregivers also can be abusive.

Suspicion of abuse should be increased when individuals in caregiving roles have a history or show signs of mental illness, substance abuse, financial dependence on the victim, or caregiver stress. Considering that a caregiver may be overwhelmed is particularly relevant when an elderly patient exhibits behavioral issues.

Medical History

Obtaining a clear and thorough medical history from the patient and caregiver, both together and alone, is paramount to assessing the potential for abuse. Many indicators from the history may suggest the possibility of mistreatment (Table 1)^33-37 and although challenging in a busy ED, a comprehensive head-to-toe examination is crucial to adequately assess abuse. Suspicious physical findings and injury patterns of physical abuse, sexual abuse, and neglect are listed in Table 2.^33-37 Ongoing research is aimed at improving ED providers’ ability to differentiate accidental injuries, such as fall injuries, from injuries caused by physical elder abuse.

Injury Patterns

Preliminary studies have indicated that physical abuse injuries most commonly occur on the head, neck, and upper extremities.^38,39 A study comparing abuse victims to accidental injury sufferers found that abuse victims often had large bruises (>5 cm) on the face, lateral right arm, or posterior torso.⁴⁰ Preliminary results from a study in progress suggest that injuries to the left periorbital area, neck, and ulnar forearm may be much more common in abuse than in accident.

Imaging Studies

Emergency radiologists are contributing additional concerning findings indicative of elder abuse,^38,41,42 such as the concomitant presence of old and new fractures, high-energy fractures inconsistent with the purported mechanism, and distal ulnar diaphyseal fractures.^41,42 The ultimate goal is to identify pathognomonic injury patterns similar to those found in child abuse cases, to assist ED providers.

Laboratory Studies

Although there are no laboratory tests to definitively identify abuse or neglect, specific findings that may indicate abuse include anemia, dehydration, malnutrition, hypothermia/hyperthermia, and rhabdomyolysis.⁴³ In addition, inappropriately high- or low-medication levels and the presence of illicit drugs, which are not often checked in elderly patients in the ED, may be a sign of abuse.⁴³

Laboratory studies that reveal undetectable levels of a patient’s prescription medications may indicate a caregiver’s intentional or neglectful withholding of such medications—especially diversion of opioid medications prescribed for painful conditions.⁴³ Likewise, elevated levels of prescribed drugs may point to intentional or unintentional overdose, whereas the presence of nonprescribed drugs or toxins may suggest poisoning.⁴³

Screening Tools

To improve identification of elder abuse in the ED, universal or targeted screening tools are under consideration. Though several screening tools for elder abuse are already available, none have been validated in the ED.^15,44,45 Research sponsored by the National Institute of Justice to identify an ED-specific screening tool is ongoing.¹⁵

Elder Abuse Suspicion Index

The Elder Abuse Suspicion Index (EASI) is a short screening tool that has been validated for cognitively intact patients being treated in family practice and ambulatory care settings, and may be used in EDs.⁴⁴ The tool comprises six questions: five for patient response, and a sixth question for clinician response. This tool is available at http://www.nicenet.ca/tools-easi-elder-abuse-suspicion-index.⁴⁶

Interventional Measures

When elder mistreatment is suspected or confirmed, health care providers must first address any acute medical, traumatic, or psychological issues. Bleeding, orthopedic injuries, metabolic abnormalities, infections, and agitation must be treated and/or stabilized, while neglected or inappropriately managed chronic medical conditions may require treatment.

Hospitalization should be considered for an older adult who needs extended treatment or observation and, in cases of immediate or continued danger of abuse, separation from contact with the suspected abuser. These measures present several challenges, particularly if the suspected abuser is the patient’s health care proxy, in which case early involvement of the hospital’s legal department, social services, and administration may be necessary—especially in navigating the guardianship process.

Engaging security also may be necessary if the patient requires one-to-one patient watch or when the perpetrator must be removed from the ED. Social workers, patient services representatives, and law enforcement officials should be informed when such intervention is necessary.

In instances when a patient is not at risk of immediate harm, interventions can be more individualized. Coordination with primary care physicians (PCPs) must also be facilitated prior to discharge, to ensure consistent longitudinal follow-up care, and social workers should provide any needed out-of-hospital resources to the patient—and caregiver—such as Meals-on-Wheels, medical transportation services, adult day care/senior center participation, and substance abuse treatment.

Patient Decision-Making Capacity

When a patient experiencing abuse declines interventions or services, the EP must evaluate the patient’s decision-making capacity. In unclear cases, a psychiatric evaluation can help to assess decision-making capacity. If the victim is deemed to have capacity with regard to care and/or discharge, the patient’s choice of returning to an unsafe environment must be respected, as is true in instances of intimate partner violence among younger adults—but not in child abuse cases. In such situations, the EP should nevertheless discuss safety planning, offer psychoeducation about violence and abuse, suggest appropriate community referrals, and encourage abused patients to return or call a contact person whenever they desire or feel the need to talk further. For a victim who is deemed not to possess capacity, providers should proceed with treatment considered to be in the best interest of the patient.

Reporting Abuse

Emergency department providers should notify the appropriate authorities when elder abuse is suspected or identified. A report may be made to the local Adult Protective Services (APS), but this agency operates much differently than Child Protective Services. Case workers with APS will not open a case while a patient is in the ED or hospital, as it is deemed a safe environment and any investigation they undertake will only commence upon discharge. Because of this, contacting the local police department prior to discharge should be considered.

Mandatory elder abuse-reporting laws vary from state to state. Health care providers should therefore contact their respective state or city department of health to obtain local legislation.

Multidisciplinary Approach

Ideally, a multidisciplinary, ED-based intervention team modeled on child abuse teams^18,19 would help to optimize treatment and ensure the safety and treatment of vulnerable older adults. These teams could conduct thorough medical, forensic, and social work assessments, allowing ED providers to attend to other patients. The team could also assist in arranging for appropriate and safe dispositions. An innovative Vulnerable Elder Protection Team was recently launched at New York-Presbyterian Weill Cornell Medical Center to provide these services, and its impact is currently being evaluated.

Case Conclusion

The EP who treated the patient realized that blows from a blunt object held by a right-handed person would tend to land on the left side of the victim’s face and upper torso, and that a right-handed victim who successfully blocked the blows intended for her face would instead sustain an isolated right ulna or radius midshaft fracture. These findings, together with the concomitant presence of both old and new fractures, led the EP to question the patient alone and, after obtaining a different history of the events that led to the injuries, admit her for further evaluation, treatment, and interventions to prevent continuing abuse.

Summary

Elder abuse has the potential to affect an increasing number of older adults in this growing population, and an ED visit may offer the only opportunity to identify victims and provide intervention, in turn reducing morbidity and mortality. The results of ongoing research will improve the ability of EPs and ED staff to accurately assess the presence or risk of elder abuse and respond more effectively. It is essential that EPs always consider elder abuse and neglect as a possible etiology when evaluating injuries in this population. Moreover, when identified, addressing elder mistreatment may dramatically improve quality of life or save the lives of these vulnerable patients.


Case

An 85-year-old right-handed woman who recently had been diagnosed with mild cognitive impairment arrived at the ED via emergency medical services (EMS) for evaluation of a reported fall. She was accompanied by her daughter, who resided with the patient and was her primary caregiver. The patient stated that she had tripped on a wet rug in the bathroom of her home, striking her head and face on the edge of the sink without losing consciousness. Her daughter reported that she was not assisting her mother when the fall occurred, but had witnessed the fall from the hallway and called EMS. At the patient’s home, EMS found the patient to be alert, oriented, and ambulatory with normal vital signs that remained stable throughout prehospital transport.

The remainder of the patient’s history was provided almost entirely by her daughter, who constantly interrupted her mother whenever she attempted to directly answer a question or provide information. On physical examination, the patient had bilateral tenderness, edema, and periorbital ecchymoses, and a left eye that was nearly swollen shut. Extraocular movements were normal, visual acuity was intact, and sclerae were noninjected. The patient had tenderness over both maxillary sinuses, and edema and ecchymosis of her left cheek. There was also tenderness, ecchymoses, and edema on the lateral aspects of both forearms, and decreased range of motion of her right lower arm and wrist. With the exception of the patient not knowing the date during the orientation part of the thorough neurological examination, the remainder of the physical examination was unremarkable.

Radiological evaluation found no evidence of traumatic brain injury, but did reveal an acute fracture of the left zygomatic arch, an acute displaced nasal bone fracture, an age-indeterminate fracture of the right zygomatic arch, and an acute right ulnar fracture. Considering all of these findings, particularly the pattern of acute injuries, the emergency physician (EP) considered elder abuse as the possible etiology of the patient’s acute and chronic injuries.

Although the patient had initially agreed with her daughter’s description of the events—including her claim that she had fallen—when the EP questioned the patient alone, she related a history of frequent verbal and less frequent physical abuse by her daughter. The patient further noted that immediately before sustaining the injuries that brought her to the ED, her daughter had been insisting that she sign documents to give her control of her banking and finances. After refusing to sign the papers, the patient said that she and her daughter got into an argument, which she noted “they tended to do frequently.” The patient admitted that during this argument, her daughter struck her in the face repeatedly with the cane that the daughter had grabbed with her right hand.

The EP admitted the patient to the hospital for management of her orthopedic injuries and related pain, and to formulate a safe discharge plan. During admission, additional diagnostic testing revealed multiple old rib fractures, anemia, and a low-serum albumin, which suggested poor nutritional status.

Epidemiology

The term elder abuse refers to harm or the risk of harm to an older adult from either action or negligence committed by someone in a relationship of trust, or when a victim has been targeted because of age or disability. Elder abuse encompasses physical, sexual, or psychological abuse, neglect, and financial exploitation.^1-5 Identified victims of elder abuse typically suffer from multiple forms of abuse.^1-5

At present, elder abuse annually affects 5% to 10% of community-dwelling older adults,^1-6 and nursing-home residents are at increased risk of abuse.^7-10 Poor medical outcomes, including depression and dementia,¹¹ and much higher mortality^6,12,13 have been linked to victims of elder abuse.

Etiology

When treating older adults, it is critically important for EPs and the ED staff to consider and identify elder abuse in the differential diagnosis.^14,15 Presently, only an estimated 1 in 24 cases of abuse is recognized and reported to the authorities,² and much of the subsequent morbidity and mortality of elder abuse results from poor detection. A visit to the ED for an acute injury or illness may be the only time socially isolated older adults leave their homes.^15-17 Additionally, the ED setting is uniquely suited to identify mistreatment, as a patient typically may be evaluated for several hours by providers from multiple disciplines who are able to observe, interact with, and examine the patient.¹⁵ The ED already exercises a similar essential role in the identification and initial intervention for both child abuse^18,19 and intimate partner violence among younger adults.^20,21

Recognition

Unfortunately, at present, ED providers rarely recognize and report elder abuse.^22-24 Though the reasons for this are not entirely understood, inadequate training, lack of time and space to conduct complete evaluations, reluctance to become involved with the legal system, and challenges to distinguishing intentional from unintentional injuries may be contributing factors.^24,25 A focus on improving EP and ED staff approaches to elder abuse is relevant and timely given the growing elderly population.

Risk Factors

When evaluating elderly patients, providers should consider research suggesting that some older adults may be at particularly high risk for abuse.^4,26-29 Notably, individuals who have cognitive impairment are more likely to be victims of abuse.^30-32 Health-related demographic characteristics such as poor physical and mental health, substance abuse, low income/socioeconomic status, and social isolation all may increase the potential for mistreatment.

Family History

Similar to situations resulting in intimate partner violence, a family history of abuse and exposure to traumatic events may increase risk, and those responsible for elder abuse often turn out to be spouses, romantic partners, or an adult child living with the elderly parent—though paid caregivers also can be abusive.

Suspicion of abuse should be increased when individuals in caregiving roles have a history or show signs of mental illness, substance abuse, financial dependence on the victim, or caregiver stress. Considering that a caregiver may be overwhelmed is particularly relevant when an elderly patient exhibits behavioral issues.

Medical History

Obtaining a clear and thorough medical history from the patient and caregiver, both together and alone, is paramount to assessing the potential for abuse. Many indicators from the history may suggest the possibility of mistreatment (Table 1)^33-37 and although challenging in a busy ED, a comprehensive head-to-toe examination is crucial to adequately assess abuse. Suspicious physical findings and injury patterns of physical abuse, sexual abuse, and neglect are listed in Table 2.^33-37 Ongoing research is aimed at improving ED providers’ ability to differentiate accidental injuries, such as fall injuries, from injuries caused by physical elder abuse.

Injury Patterns

Preliminary studies have indicated that physical abuse injuries most commonly occur on the head, neck, and upper extremities.^38,39 A study comparing abuse victims to accidental injury sufferers found that abuse victims often had large bruises (>5 cm) on the face, lateral right arm, or posterior torso.⁴⁰ Preliminary results from a study in progress suggest that injuries to the left periorbital area, neck, and ulnar forearm may be much more common in abuse than in accident.

Imaging Studies

Emergency radiologists are contributing additional concerning findings indicative of elder abuse,^38,41,42 such as the concomitant presence of old and new fractures, high-energy fractures inconsistent with the purported mechanism, and distal ulnar diaphyseal fractures.^41,42 The ultimate goal is to identify pathognomonic injury patterns similar to those found in child abuse cases, to assist ED providers.

Laboratory Studies

Although there are no laboratory tests to definitively identify abuse or neglect, specific findings that may indicate abuse include anemia, dehydration, malnutrition, hypothermia/hyperthermia, and rhabdomyolysis.⁴³ In addition, inappropriately high- or low-medication levels and the presence of illicit drugs, which are not often checked in elderly patients in the ED, may be a sign of abuse.⁴³

Laboratory studies that reveal undetectable levels of a patient’s prescription medications may indicate a caregiver’s intentional or neglectful withholding of such medications—especially diversion of opioid medications prescribed for painful conditions.⁴³ Likewise, elevated levels of prescribed drugs may point to intentional or unintentional overdose, whereas the presence of nonprescribed drugs or toxins may suggest poisoning.⁴³

Screening Tools

To improve identification of elder abuse in the ED, universal or targeted screening tools are under consideration. Though several screening tools for elder abuse are already available, none have been validated in the ED.^15,44,45 Research sponsored by the National Institute of Justice to identify an ED-specific screening tool is ongoing.¹⁵

Elder Abuse Suspicion Index

The Elder Abuse Suspicion Index (EASI) is a short screening tool that has been validated for cognitively intact patients being treated in family practice and ambulatory care settings, and may be used in EDs.⁴⁴ The tool comprises six questions: five for patient response, and a sixth question for clinician response. This tool is available at http://www.nicenet.ca/tools-easi-elder-abuse-suspicion-index.⁴⁶

Interventional Measures

When elder mistreatment is suspected or confirmed, health care providers must first address any acute medical, traumatic, or psychological issues. Bleeding, orthopedic injuries, metabolic abnormalities, infections, and agitation must be treated and/or stabilized, while neglected or inappropriately managed chronic medical conditions may require treatment.

Hospitalization should be considered for an older adult who needs extended treatment or observation and, in cases of immediate or continued danger of abuse, separation from contact with the suspected abuser. These measures present several challenges, particularly if the suspected abuser is the patient’s health care proxy, in which case early involvement of the hospital’s legal department, social services, and administration may be necessary—especially in navigating the guardianship process.

Engaging security also may be necessary if the patient requires one-to-one patient watch or when the perpetrator must be removed from the ED. Social workers, patient services representatives, and law enforcement officials should be informed when such intervention is necessary.

In instances when a patient is not at risk of immediate harm, interventions can be more individualized. Coordination with primary care physicians (PCPs) must also be facilitated prior to discharge, to ensure consistent longitudinal follow-up care, and social workers should provide any needed out-of-hospital resources to the patient—and caregiver—such as Meals-on-Wheels, medical transportation services, adult day care/senior center participation, and substance abuse treatment.

Patient Decision-Making Capacity

When a patient experiencing abuse declines interventions or services, the EP must evaluate the patient’s decision-making capacity. In unclear cases, a psychiatric evaluation can help to assess decision-making capacity. If the victim is deemed to have capacity with regard to care and/or discharge, the patient’s choice of returning to an unsafe environment must be respected, as is true in instances of intimate partner violence among younger adults—but not in child abuse cases. In such situations, the EP should nevertheless discuss safety planning, offer psychoeducation about violence and abuse, suggest appropriate community referrals, and encourage abused patients to return or call a contact person whenever they desire or feel the need to talk further. For a victim who is deemed not to possess capacity, providers should proceed with treatment considered to be in the best interest of the patient.

Reporting Abuse

Emergency department providers should notify the appropriate authorities when elder abuse is suspected or identified. A report may be made to the local Adult Protective Services (APS), but this agency operates much differently than Child Protective Services. Case workers with APS will not open a case while a patient is in the ED or hospital, as it is deemed a safe environment and any investigation they undertake will only commence upon discharge. Because of this, contacting the local police department prior to discharge should be considered.

Mandatory elder abuse-reporting laws vary from state to state. Health care providers should therefore contact their respective state or city department of health to obtain local legislation.

Multidisciplinary Approach

Ideally, a multidisciplinary, ED-based intervention team modeled on child abuse teams^18,19 would help to optimize treatment and ensure the safety and treatment of vulnerable older adults. These teams could conduct thorough medical, forensic, and social work assessments, allowing ED providers to attend to other patients. The team could also assist in arranging for appropriate and safe dispositions. An innovative Vulnerable Elder Protection Team was recently launched at New York-Presbyterian Weill Cornell Medical Center to provide these services, and its impact is currently being evaluated.

Case Conclusion

The EP who treated the patient realized that blows from a blunt object held by a right-handed person would tend to land on the left side of the victim’s face and upper torso, and that a right-handed victim who successfully blocked the blows intended for her face would instead sustain an isolated right ulna or radius midshaft fracture. These findings, together with the concomitant presence of both old and new fractures, led the EP to question the patient alone and, after obtaining a different history of the events that led to the injuries, admit her for further evaluation, treatment, and interventions to prevent continuing abuse.

Summary

Elder abuse has the potential to affect an increasing number of older adults in this growing population, and an ED visit may offer the only opportunity to identify victims and provide intervention, in turn reducing morbidity and mortality. The results of ongoing research will improve the ability of EPs and ED staff to accurately assess the presence or risk of elder abuse and respond more effectively. It is essential that EPs always consider elder abuse and neglect as a possible etiology when evaluating injuries in this population. Moreover, when identified, addressing elder mistreatment may dramatically improve quality of life or save the lives of these vulnerable patients.


Case

An 85-year-old right-handed woman who recently had been diagnosed with mild cognitive impairment arrived at the ED via emergency medical services (EMS) for evaluation of a reported fall. She was accompanied by her daughter, who resided with the patient and was her primary caregiver. The patient stated that she had tripped on a wet rug in the bathroom of her home, striking her head and face on the edge of the sink without losing consciousness. Her daughter reported that she was not assisting her mother when the fall occurred, but had witnessed the fall from the hallway and called EMS. At the patient’s home, EMS found the patient to be alert, oriented, and ambulatory with normal vital signs that remained stable throughout prehospital transport.

The remainder of the patient’s history was provided almost entirely by her daughter, who constantly interrupted her mother whenever she attempted to directly answer a question or provide information. On physical examination, the patient had bilateral tenderness, edema, and periorbital ecchymoses, and a left eye that was nearly swollen shut. Extraocular movements were normal, visual acuity was intact, and sclerae were noninjected. The patient had tenderness over both maxillary sinuses, and edema and ecchymosis of her left cheek. There was also tenderness, ecchymoses, and edema on the lateral aspects of both forearms, and decreased range of motion of her right lower arm and wrist. With the exception of the patient not knowing the date during the orientation part of the thorough neurological examination, the remainder of the physical examination was unremarkable.

Radiological evaluation found no evidence of traumatic brain injury, but did reveal an acute fracture of the left zygomatic arch, an acute displaced nasal bone fracture, an age-indeterminate fracture of the right zygomatic arch, and an acute right ulnar fracture. Considering all of these findings, particularly the pattern of acute injuries, the emergency physician (EP) considered elder abuse as the possible etiology of the patient’s acute and chronic injuries.

Although the patient had initially agreed with her daughter’s description of the events—including her claim that she had fallen—when the EP questioned the patient alone, she related a history of frequent verbal and less frequent physical abuse by her daughter. The patient further noted that immediately before sustaining the injuries that brought her to the ED, her daughter had been insisting that she sign documents to give her control of her banking and finances. After refusing to sign the papers, the patient said that she and her daughter got into an argument, which she noted “they tended to do frequently.” The patient admitted that during this argument, her daughter struck her in the face repeatedly with the cane that the daughter had grabbed with her right hand.

The EP admitted the patient to the hospital for management of her orthopedic injuries and related pain, and to formulate a safe discharge plan. During admission, additional diagnostic testing revealed multiple old rib fractures, anemia, and a low-serum albumin, which suggested poor nutritional status.

Epidemiology

The term elder abuse refers to harm or the risk of harm to an older adult from either action or negligence committed by someone in a relationship of trust, or when a victim has been targeted because of age or disability. Elder abuse encompasses physical, sexual, or psychological abuse, neglect, and financial exploitation.^1-5 Identified victims of elder abuse typically suffer from multiple forms of abuse.^1-5

At present, elder abuse annually affects 5% to 10% of community-dwelling older adults,^1-6 and nursing-home residents are at increased risk of abuse.^7-10 Poor medical outcomes, including depression and dementia,¹¹ and much higher mortality^6,12,13 have been linked to victims of elder abuse.

Etiology

When treating older adults, it is critically important for EPs and the ED staff to consider and identify elder abuse in the differential diagnosis.^14,15 Presently, only an estimated 1 in 24 cases of abuse is recognized and reported to the authorities,² and much of the subsequent morbidity and mortality of elder abuse results from poor detection. A visit to the ED for an acute injury or illness may be the only time socially isolated older adults leave their homes.^15-17 Additionally, the ED setting is uniquely suited to identify mistreatment, as a patient typically may be evaluated for several hours by providers from multiple disciplines who are able to observe, interact with, and examine the patient.¹⁵ The ED already exercises a similar essential role in the identification and initial intervention for both child abuse^18,19 and intimate partner violence among younger adults.^20,21

Recognition

Unfortunately, at present, ED providers rarely recognize and report elder abuse.^22-24 Though the reasons for this are not entirely understood, inadequate training, lack of time and space to conduct complete evaluations, reluctance to become involved with the legal system, and challenges to distinguishing intentional from unintentional injuries may be contributing factors.^24,25 A focus on improving EP and ED staff approaches to elder abuse is relevant and timely given the growing elderly population.

Risk Factors

When evaluating elderly patients, providers should consider research suggesting that some older adults may be at particularly high risk for abuse.^4,26-29 Notably, individuals who have cognitive impairment are more likely to be victims of abuse.^30-32 Health-related demographic characteristics such as poor physical and mental health, substance abuse, low income/socioeconomic status, and social isolation all may increase the potential for mistreatment.

Family History

Similar to situations resulting in intimate partner violence, a family history of abuse and exposure to traumatic events may increase risk, and those responsible for elder abuse often turn out to be spouses, romantic partners, or an adult child living with the elderly parent—though paid caregivers also can be abusive.

Suspicion of abuse should be increased when individuals in caregiving roles have a history or show signs of mental illness, substance abuse, financial dependence on the victim, or caregiver stress. Considering that a caregiver may be overwhelmed is particularly relevant when an elderly patient exhibits behavioral issues.

Medical History

Obtaining a clear and thorough medical history from the patient and caregiver, both together and alone, is paramount to assessing the potential for abuse. Many indicators from the history may suggest the possibility of mistreatment (Table 1)^33-37 and although challenging in a busy ED, a comprehensive head-to-toe examination is crucial to adequately assess abuse. Suspicious physical findings and injury patterns of physical abuse, sexual abuse, and neglect are listed in Table 2.^33-37 Ongoing research is aimed at improving ED providers’ ability to differentiate accidental injuries, such as fall injuries, from injuries caused by physical elder abuse.

Injury Patterns

Preliminary studies have indicated that physical abuse injuries most commonly occur on the head, neck, and upper extremities.^38,39 A study comparing abuse victims to accidental injury sufferers found that abuse victims often had large bruises (>5 cm) on the face, lateral right arm, or posterior torso.⁴⁰ Preliminary results from a study in progress suggest that injuries to the left periorbital area, neck, and ulnar forearm may be much more common in abuse than in accident.

Imaging Studies

Emergency radiologists are contributing additional concerning findings indicative of elder abuse,^38,41,42 such as the concomitant presence of old and new fractures, high-energy fractures inconsistent with the purported mechanism, and distal ulnar diaphyseal fractures.^41,42 The ultimate goal is to identify pathognomonic injury patterns similar to those found in child abuse cases, to assist ED providers.

Laboratory Studies

Although there are no laboratory tests to definitively identify abuse or neglect, specific findings that may indicate abuse include anemia, dehydration, malnutrition, hypothermia/hyperthermia, and rhabdomyolysis.⁴³ In addition, inappropriately high- or low-medication levels and the presence of illicit drugs, which are not often checked in elderly patients in the ED, may be a sign of abuse.⁴³

Laboratory studies that reveal undetectable levels of a patient’s prescription medications may indicate a caregiver’s intentional or neglectful withholding of such medications—especially diversion of opioid medications prescribed for painful conditions.⁴³ Likewise, elevated levels of prescribed drugs may point to intentional or unintentional overdose, whereas the presence of nonprescribed drugs or toxins may suggest poisoning.⁴³

Screening Tools

To improve identification of elder abuse in the ED, universal or targeted screening tools are under consideration. Though several screening tools for elder abuse are already available, none have been validated in the ED.^15,44,45 Research sponsored by the National Institute of Justice to identify an ED-specific screening tool is ongoing.¹⁵

Elder Abuse Suspicion Index

The Elder Abuse Suspicion Index (EASI) is a short screening tool that has been validated for cognitively intact patients being treated in family practice and ambulatory care settings, and may be used in EDs.⁴⁴ The tool comprises six questions: five for patient response, and a sixth question for clinician response. This tool is available at http://www.nicenet.ca/tools-easi-elder-abuse-suspicion-index.⁴⁶

Interventional Measures

When elder mistreatment is suspected or confirmed, health care providers must first address any acute medical, traumatic, or psychological issues. Bleeding, orthopedic injuries, metabolic abnormalities, infections, and agitation must be treated and/or stabilized, while neglected or inappropriately managed chronic medical conditions may require treatment.

Hospitalization should be considered for an older adult who needs extended treatment or observation and, in cases of immediate or continued danger of abuse, separation from contact with the suspected abuser. These measures present several challenges, particularly if the suspected abuser is the patient’s health care proxy, in which case early involvement of the hospital’s legal department, social services, and administration may be necessary—especially in navigating the guardianship process.

Engaging security also may be necessary if the patient requires one-to-one patient watch or when the perpetrator must be removed from the ED. Social workers, patient services representatives, and law enforcement officials should be informed when such intervention is necessary.

In instances when a patient is not at risk of immediate harm, interventions can be more individualized. Coordination with primary care physicians (PCPs) must also be facilitated prior to discharge, to ensure consistent longitudinal follow-up care, and social workers should provide any needed out-of-hospital resources to the patient—and caregiver—such as Meals-on-Wheels, medical transportation services, adult day care/senior center participation, and substance abuse treatment.

Patient Decision-Making Capacity

When a patient experiencing abuse declines interventions or services, the EP must evaluate the patient’s decision-making capacity. In unclear cases, a psychiatric evaluation can help to assess decision-making capacity. If the victim is deemed to have capacity with regard to care and/or discharge, the patient’s choice of returning to an unsafe environment must be respected, as is true in instances of intimate partner violence among younger adults—but not in child abuse cases. In such situations, the EP should nevertheless discuss safety planning, offer psychoeducation about violence and abuse, suggest appropriate community referrals, and encourage abused patients to return or call a contact person whenever they desire or feel the need to talk further. For a victim who is deemed not to possess capacity, providers should proceed with treatment considered to be in the best interest of the patient.

Reporting Abuse

Emergency department providers should notify the appropriate authorities when elder abuse is suspected or identified. A report may be made to the local Adult Protective Services (APS), but this agency operates much differently than Child Protective Services. Case workers with APS will not open a case while a patient is in the ED or hospital, as it is deemed a safe environment and any investigation they undertake will only commence upon discharge. Because of this, contacting the local police department prior to discharge should be considered.

Mandatory elder abuse-reporting laws vary from state to state. Health care providers should therefore contact their respective state or city department of health to obtain local legislation.

Multidisciplinary Approach

Ideally, a multidisciplinary, ED-based intervention team modeled on child abuse teams^18,19 would help to optimize treatment and ensure the safety and treatment of vulnerable older adults. These teams could conduct thorough medical, forensic, and social work assessments, allowing ED providers to attend to other patients. The team could also assist in arranging for appropriate and safe dispositions. An innovative Vulnerable Elder Protection Team was recently launched at New York-Presbyterian Weill Cornell Medical Center to provide these services, and its impact is currently being evaluated.

Case Conclusion

The EP who treated the patient realized that blows from a blunt object held by a right-handed person would tend to land on the left side of the victim’s face and upper torso, and that a right-handed victim who successfully blocked the blows intended for her face would instead sustain an isolated right ulna or radius midshaft fracture. These findings, together with the concomitant presence of both old and new fractures, led the EP to question the patient alone and, after obtaining a different history of the events that led to the injuries, admit her for further evaluation, treatment, and interventions to prevent continuing abuse.

Summary

Elder abuse has the potential to affect an increasing number of older adults in this growing population, and an ED visit may offer the only opportunity to identify victims and provide intervention, in turn reducing morbidity and mortality. The results of ongoing research will improve the ability of EPs and ED staff to accurately assess the presence or risk of elder abuse and respond more effectively. It is essential that EPs always consider elder abuse and neglect as a possible etiology when evaluating injuries in this population. Moreover, when identified, addressing elder mistreatment may dramatically improve quality of life or save the lives of these vulnerable patients.


Case

A 49-year-old man with a history of hypertension, for which he was taking aspirin, carvedilol, hydralazine, and nifedipine, presented to the ED with complaints of left-sided weakness that started 3 hours before he came to the ED. Initial vital signs were: blood pressure, 158/90 mm Hg; heart rate, 74 beats/min; respiratory rate, 18 breaths/min; and temperature, 98°F. Oxygen saturation was 100% on room air, and a finger-stick glucose test was 106 mg/dL.

Physical examination revealed slowed speech with mild dysarthria, mild left facial droop, 2/5 strength in all muscle groups in the left upper and lower extremities, and decreased sensation to light touch on the left side. The patient also had left-sided sensory neglect and an abnormal gait, and dragged his left foot on the floor when walking. The rest of his examination was normal.

The stroke team was activated, and the patient was immediately transferred to the ED radiology department for imaging studies. A noncontrast head computed tomography (CT) was negative for any acute intracranial hemorrhage or cerebral edema. A CT angiogram (CTA) also was performed, which revealed atherosclerosis but no arterial occlusion. Based on these findings and the existing protocol, the patient received an intravenous (IV) bolus of tissue plasminogen activator (tPA). Approximately 17 minutes after tPA administration, the patient developed left-sided upper and lower lip swelling. There was no voice change, tongue swelling, or uvular deviation.

What is the differential diagnosis of swelling of the lip?

The differential diagnoses for lip swelling includes trauma, allergic reaction, and angioedema (hereditary, or angiotensin converting enzyme inhibitor [ACEI]-induced). The patient in this case denied any trauma to the lip, and no bleeding was noted from the lip; however, his entire left lip (upper and lower) was swollen. He was not taking any ACEIs or angiotensin-receptor blockers (ARBs). He also denied a family history of angioedema or any prior similar episodes. The patient further denied exposure to any new medications, foods, or other substances and had no respiratory distress, urticaria, or other findings consistent with an allergy.

What are the common adverse effects of tPA?

The only US Food and Drug-approved pharmacological treatment for ischemic stroke is tPA (also known as IV rtPA). Tissue plasminogen activator hydrolyzes plasminogen to plasmin, which exerts a fibrinolytic effect. Based on the ability of tPA to lyse thrombus, it is also a standard therapy for hemodynamically unstable patients with confirmed pulmonary embolism, as well as for patients with myocardial infarction in whom percutaneous intervention is contraindicated or unavailable. Despite the beneficial effects of tPA, significant adverse effects are associated with the drug. For example, thrombolysis may result in conversion of an ischemic stroke into a hemorrhagic event, resulting in generalized bleeding from mucosal surfaces.

The increase in plasmin may play a role in the development of angioedema by activating the kinin pathway, leading to the formation of the vasodilator bradykinin (Figure). Plasmin also activates the complement system and leads to the production of anaphylatoxins C₃a, C₄a, and C₅a, which also cause mast cell degranulation and histamine release.¹

When does post-tPA angioedema occur?

In the few published case reports available, tPA-induced angioedema was shown to typically occur in the stroke distribution (which was attributed to the left-sided swelling in this patient).² Following tPA administration, the onset of angioedema reportedly varies from as early as 10 to 15 minutes from initiation until about 1 hour postinfusion. The short half-life of tPA (approximately 7 minutes)² limits the outer- time window for the initial development of angioedema, but progression can continue well beyond this timeframe.

What is the treatment for tPA-induced angioedema?

The first priority of acute management of angioedema is discontinuation of the inciting substance, if possible—in this case, the tPA infusion.³ Assessment and maintenance of a patent airway are of utmost concern. Patients with posterior oropharyngeal effects or who are progressing should be admitted to an intensive care unit (ICU) for observation.^4-6

Endotracheal Intubation. Providers should have a low threshold for endotracheal intubation, which should ideally be performed in any patient at risk for airway compromise.⁴ Due to the extensive airway swelling that can occur in the setting of angioedema, airway intervention should optimally be performed by an available clinician with the most skill and experience in this area. It is wise to be prepared to utilize advanced airway techniques, if available, including fiberoptic laryngoscopy or potentially cricothyrotomy.

Histamine Agonists. Standard therapy for patients who develop angioedema should include histamine antagonists, such as diphenhydramine (H₁ antagonist) and famotidine (H₂ antagonist) along with corticosteroids. Although these therapies are unlikely to be helpful in the treatment of tPA-induced angioedema, the difficulty in excluding allergic angioedema and the low risk of adverse effects associated with these medications support their use.

Fresh Frozen Plasma. Fresh frozen plasma (FFP) should be considered for patients who have a history of hereditary angioedema. Fresh frozen plasma contains enzymes that degrade bradykinin. Although FFP has been used successfully in the treatment of ACEI-induced angioedema, its use (or benefit) in tPA-related cases is not clear.

Icatibant. A selective bradykinin B₂-receptor antagonist, icatibant has been used to treat patients with ACEI-induced angioedema because of its effects on bradykinin receptors. Comparison of the efficacy of icatibant to the prevailing treatment strategy of diphenhydramine, famotidine, and methylprednisolone found a shorter time to symptom relief with icatibant.⁷ However, icatibant is extremely expensive ($23,000/30 mg). As previously mentioned, based on its similar mechanism of action, lower cost, and safety profile, FFP can be given (off label) in this situation.

Case Conclusion

The patient was given diphenhydramine, famotidine, and methylprednisolone, but did not show any improvement. His upper/lower lip swelling continued to worsen, and 30 minutes after the onset of angioedema, he was unable to open his mouth more than 1 cm.

Multiple attempts to perform awake fiberoptic intubation failed due to inadequate sedation; however, intubation was successfully performed following light sedation. The patient self-extubated in the ICU on hospital day 3, and the angioedema had progressively decreased. Angioedema and weakness completely resolved by hospital day 4, and he was discharged home on hospital day 7.

Case

A 49-year-old man with a history of hypertension, for which he was taking aspirin, carvedilol, hydralazine, and nifedipine, presented to the ED with complaints of left-sided weakness that started 3 hours before he came to the ED. Initial vital signs were: blood pressure, 158/90 mm Hg; heart rate, 74 beats/min; respiratory rate, 18 breaths/min; and temperature, 98°F. Oxygen saturation was 100% on room air, and a finger-stick glucose test was 106 mg/dL.

Physical examination revealed slowed speech with mild dysarthria, mild left facial droop, 2/5 strength in all muscle groups in the left upper and lower extremities, and decreased sensation to light touch on the left side. The patient also had left-sided sensory neglect and an abnormal gait, and dragged his left foot on the floor when walking. The rest of his examination was normal.

The stroke team was activated, and the patient was immediately transferred to the ED radiology department for imaging studies. A noncontrast head computed tomography (CT) was negative for any acute intracranial hemorrhage or cerebral edema. A CT angiogram (CTA) also was performed, which revealed atherosclerosis but no arterial occlusion. Based on these findings and the existing protocol, the patient received an intravenous (IV) bolus of tissue plasminogen activator (tPA). Approximately 17 minutes after tPA administration, the patient developed left-sided upper and lower lip swelling. There was no voice change, tongue swelling, or uvular deviation.

What is the differential diagnosis of swelling of the lip?

The differential diagnoses for lip swelling includes trauma, allergic reaction, and angioedema (hereditary, or angiotensin converting enzyme inhibitor [ACEI]-induced). The patient in this case denied any trauma to the lip, and no bleeding was noted from the lip; however, his entire left lip (upper and lower) was swollen. He was not taking any ACEIs or angiotensin-receptor blockers (ARBs). He also denied a family history of angioedema or any prior similar episodes. The patient further denied exposure to any new medications, foods, or other substances and had no respiratory distress, urticaria, or other findings consistent with an allergy.

What are the common adverse effects of tPA?

The only US Food and Drug-approved pharmacological treatment for ischemic stroke is tPA (also known as IV rtPA). Tissue plasminogen activator hydrolyzes plasminogen to plasmin, which exerts a fibrinolytic effect. Based on the ability of tPA to lyse thrombus, it is also a standard therapy for hemodynamically unstable patients with confirmed pulmonary embolism, as well as for patients with myocardial infarction in whom percutaneous intervention is contraindicated or unavailable. Despite the beneficial effects of tPA, significant adverse effects are associated with the drug. For example, thrombolysis may result in conversion of an ischemic stroke into a hemorrhagic event, resulting in generalized bleeding from mucosal surfaces.

The increase in plasmin may play a role in the development of angioedema by activating the kinin pathway, leading to the formation of the vasodilator bradykinin (Figure). Plasmin also activates the complement system and leads to the production of anaphylatoxins C₃a, C₄a, and C₅a, which also cause mast cell degranulation and histamine release.¹

When does post-tPA angioedema occur?

In the few published case reports available, tPA-induced angioedema was shown to typically occur in the stroke distribution (which was attributed to the left-sided swelling in this patient).² Following tPA administration, the onset of angioedema reportedly varies from as early as 10 to 15 minutes from initiation until about 1 hour postinfusion. The short half-life of tPA (approximately 7 minutes)² limits the outer- time window for the initial development of angioedema, but progression can continue well beyond this timeframe.

What is the treatment for tPA-induced angioedema?

The first priority of acute management of angioedema is discontinuation of the inciting substance, if possible—in this case, the tPA infusion.³ Assessment and maintenance of a patent airway are of utmost concern. Patients with posterior oropharyngeal effects or who are progressing should be admitted to an intensive care unit (ICU) for observation.^4-6

Endotracheal Intubation. Providers should have a low threshold for endotracheal intubation, which should ideally be performed in any patient at risk for airway compromise.⁴ Due to the extensive airway swelling that can occur in the setting of angioedema, airway intervention should optimally be performed by an available clinician with the most skill and experience in this area. It is wise to be prepared to utilize advanced airway techniques, if available, including fiberoptic laryngoscopy or potentially cricothyrotomy.

Histamine Agonists. Standard therapy for patients who develop angioedema should include histamine antagonists, such as diphenhydramine (H₁ antagonist) and famotidine (H₂ antagonist) along with corticosteroids. Although these therapies are unlikely to be helpful in the treatment of tPA-induced angioedema, the difficulty in excluding allergic angioedema and the low risk of adverse effects associated with these medications support their use.

Fresh Frozen Plasma. Fresh frozen plasma (FFP) should be considered for patients who have a history of hereditary angioedema. Fresh frozen plasma contains enzymes that degrade bradykinin. Although FFP has been used successfully in the treatment of ACEI-induced angioedema, its use (or benefit) in tPA-related cases is not clear.

Icatibant. A selective bradykinin B₂-receptor antagonist, icatibant has been used to treat patients with ACEI-induced angioedema because of its effects on bradykinin receptors. Comparison of the efficacy of icatibant to the prevailing treatment strategy of diphenhydramine, famotidine, and methylprednisolone found a shorter time to symptom relief with icatibant.⁷ However, icatibant is extremely expensive ($23,000/30 mg). As previously mentioned, based on its similar mechanism of action, lower cost, and safety profile, FFP can be given (off label) in this situation.

Case Conclusion

The patient was given diphenhydramine, famotidine, and methylprednisolone, but did not show any improvement. His upper/lower lip swelling continued to worsen, and 30 minutes after the onset of angioedema, he was unable to open his mouth more than 1 cm.

Multiple attempts to perform awake fiberoptic intubation failed due to inadequate sedation; however, intubation was successfully performed following light sedation. The patient self-extubated in the ICU on hospital day 3, and the angioedema had progressively decreased. Angioedema and weakness completely resolved by hospital day 4, and he was discharged home on hospital day 7.

Case

A 49-year-old man with a history of hypertension, for which he was taking aspirin, carvedilol, hydralazine, and nifedipine, presented to the ED with complaints of left-sided weakness that started 3 hours before he came to the ED. Initial vital signs were: blood pressure, 158/90 mm Hg; heart rate, 74 beats/min; respiratory rate, 18 breaths/min; and temperature, 98°F. Oxygen saturation was 100% on room air, and a finger-stick glucose test was 106 mg/dL.

Physical examination revealed slowed speech with mild dysarthria, mild left facial droop, 2/5 strength in all muscle groups in the left upper and lower extremities, and decreased sensation to light touch on the left side. The patient also had left-sided sensory neglect and an abnormal gait, and dragged his left foot on the floor when walking. The rest of his examination was normal.

The stroke team was activated, and the patient was immediately transferred to the ED radiology department for imaging studies. A noncontrast head computed tomography (CT) was negative for any acute intracranial hemorrhage or cerebral edema. A CT angiogram (CTA) also was performed, which revealed atherosclerosis but no arterial occlusion. Based on these findings and the existing protocol, the patient received an intravenous (IV) bolus of tissue plasminogen activator (tPA). Approximately 17 minutes after tPA administration, the patient developed left-sided upper and lower lip swelling. There was no voice change, tongue swelling, or uvular deviation.

What is the differential diagnosis of swelling of the lip?

The differential diagnoses for lip swelling includes trauma, allergic reaction, and angioedema (hereditary, or angiotensin converting enzyme inhibitor [ACEI]-induced). The patient in this case denied any trauma to the lip, and no bleeding was noted from the lip; however, his entire left lip (upper and lower) was swollen. He was not taking any ACEIs or angiotensin-receptor blockers (ARBs). He also denied a family history of angioedema or any prior similar episodes. The patient further denied exposure to any new medications, foods, or other substances and had no respiratory distress, urticaria, or other findings consistent with an allergy.

What are the common adverse effects of tPA?

The only US Food and Drug-approved pharmacological treatment for ischemic stroke is tPA (also known as IV rtPA). Tissue plasminogen activator hydrolyzes plasminogen to plasmin, which exerts a fibrinolytic effect. Based on the ability of tPA to lyse thrombus, it is also a standard therapy for hemodynamically unstable patients with confirmed pulmonary embolism, as well as for patients with myocardial infarction in whom percutaneous intervention is contraindicated or unavailable. Despite the beneficial effects of tPA, significant adverse effects are associated with the drug. For example, thrombolysis may result in conversion of an ischemic stroke into a hemorrhagic event, resulting in generalized bleeding from mucosal surfaces.

The increase in plasmin may play a role in the development of angioedema by activating the kinin pathway, leading to the formation of the vasodilator bradykinin (Figure). Plasmin also activates the complement system and leads to the production of anaphylatoxins C₃a, C₄a, and C₅a, which also cause mast cell degranulation and histamine release.¹

When does post-tPA angioedema occur?

In the few published case reports available, tPA-induced angioedema was shown to typically occur in the stroke distribution (which was attributed to the left-sided swelling in this patient).² Following tPA administration, the onset of angioedema reportedly varies from as early as 10 to 15 minutes from initiation until about 1 hour postinfusion. The short half-life of tPA (approximately 7 minutes)² limits the outer- time window for the initial development of angioedema, but progression can continue well beyond this timeframe.

What is the treatment for tPA-induced angioedema?

The first priority of acute management of angioedema is discontinuation of the inciting substance, if possible—in this case, the tPA infusion.³ Assessment and maintenance of a patent airway are of utmost concern. Patients with posterior oropharyngeal effects or who are progressing should be admitted to an intensive care unit (ICU) for observation.^4-6

Endotracheal Intubation. Providers should have a low threshold for endotracheal intubation, which should ideally be performed in any patient at risk for airway compromise.⁴ Due to the extensive airway swelling that can occur in the setting of angioedema, airway intervention should optimally be performed by an available clinician with the most skill and experience in this area. It is wise to be prepared to utilize advanced airway techniques, if available, including fiberoptic laryngoscopy or potentially cricothyrotomy.

Histamine Agonists. Standard therapy for patients who develop angioedema should include histamine antagonists, such as diphenhydramine (H₁ antagonist) and famotidine (H₂ antagonist) along with corticosteroids. Although these therapies are unlikely to be helpful in the treatment of tPA-induced angioedema, the difficulty in excluding allergic angioedema and the low risk of adverse effects associated with these medications support their use.

Fresh Frozen Plasma. Fresh frozen plasma (FFP) should be considered for patients who have a history of hereditary angioedema. Fresh frozen plasma contains enzymes that degrade bradykinin. Although FFP has been used successfully in the treatment of ACEI-induced angioedema, its use (or benefit) in tPA-related cases is not clear.

Icatibant. A selective bradykinin B₂-receptor antagonist, icatibant has been used to treat patients with ACEI-induced angioedema because of its effects on bradykinin receptors. Comparison of the efficacy of icatibant to the prevailing treatment strategy of diphenhydramine, famotidine, and methylprednisolone found a shorter time to symptom relief with icatibant.⁷ However, icatibant is extremely expensive ($23,000/30 mg). As previously mentioned, based on its similar mechanism of action, lower cost, and safety profile, FFP can be given (off label) in this situation.

Case Conclusion

The patient was given diphenhydramine, famotidine, and methylprednisolone, but did not show any improvement. His upper/lower lip swelling continued to worsen, and 30 minutes after the onset of angioedema, he was unable to open his mouth more than 1 cm.

Multiple attempts to perform awake fiberoptic intubation failed due to inadequate sedation; however, intubation was successfully performed following light sedation. The patient self-extubated in the ICU on hospital day 3, and the angioedema had progressively decreased. Angioedema and weakness completely resolved by hospital day 4, and he was discharged home on hospital day 7.

Artificial dermal fillers and autologous fat grafting have become increasingly popular in recent years, primarily because they augment existing soft tissue volumes, thus producing aesthetic improvements at a lower cost than traditional plastic surgery (ie, facelift), and with nearly no recovery time. According to the American Society for Aesthetic Plastic Surgery, more than 2 million hyaluronic acid (HA) dermal filler procedures were performed in 2016, an increase of 3% from 2015.¹ In addition, 80,000 autologous fat grafting procedures were performed in 2016, an increase of 13% from 2015. In total, there were 2.6 million soft tissue filler procedures in 2016, an increase of 2% from 2015.¹

With the increased demand and access to both artificial dermal fillers and autologous fat grafting, there has been a plethora of reported adverse events, ranging from expected erythema to acute blindness and stroke. Emergency physicians should have a thorough understanding of facial vascular anatomy, as well as the effects of available facial volumization products, including potential complications and treatment options. Through our review of two patient cases, we propose a simplified protocol for the treatment of patients with acute arterial occlusion secondary to facial volumization procedures.

Case 1

A 38-year-old white woman presented to the ED for evaluation of transient blurred vision and blanching of the left cheek and upper lip, which began approximately 40 minutes prior to presentation, immediately after her primary care physician (PCP) injected her left nasolabial fold with calcium hydroxyapatite (CaHA). The patient stated that her vision became blurry and her eyes began to tear within 1 minute of receiving the injection. She further noted that these visual changes were painless and lasted for approximately 30 seconds.

The patient’s PCP believed these symptoms were due to pain at the injection site. While the patient was at her PCP’s office, the reception clerk noticed the blanching of the patient’s left cheek and informed the PCP, who referred the patient to our ED for evaluation.

Workup

The patient’s vital signs at presentation were normal. Her medical history was unremarkable and negative for smoking, alcohol, or drug use. She was not taking any medications and had no known drug allergies. The patient’s history was negative for any prior cosmetic procedures, and she confirmed this was the first and only time had a facial revolumization.

Facial examination revealed a Fitzpatrick scale (FS; a numerical scoring system used to assess a patient’s reaction to ultraviolet radiation) score of type 3. She also had left-sided blanching that extended from the midpoint of the nose diagonally to the lateral midbuccal cheek to the level of the oral commissure, including the cutaneous upper lip, alar, and nasal side wall. There was minimal capillary refill with compression at the affected site, and sensation was diminished to fine touch and pinprick. The facial muscles were intact, and, with the exception of puncture marks along both nasolabial folds, the remainder of the facial examination was normal.

The ophthalmic examination revealed a reactive pupil at 2 mm, white sclera, pink conjunctiva, red reflex, and normal fundoscopic vessels. The patient’s bedside Snellen visual acuity and visual field assessments were normal. The neurological examination was likewise normal, and no other physical findings were noted.

Laboratory evaluation included complete blood count (CBC), Chem 7 panel (creatinine, blood urea nitrogen [BUN], carbon dioxide, chloride, glucose, sodium, and potassium), and international normalized ratio (INR), which were all within normal limits.

Diagnosis and Treatment

The patient was diagnosed with acute angular arterial occlusion and transient retinal artery embolism secondary to facial volumization with CaHA. She was treated with oral acetylsalicylic acid aspirin (ASA) 325 mg, prednisone 40 mg, and sildenafil 50 mg; and subcutaneous (SC) enoxaparin 60 mg (1 mg/kg). Topical nitroglycerin paste 2% was applied to the affected area.

Ophthalmology and plastic surgery services were contacted for consultation. Based on no acute findings on examination, the ophthalmologist provided no additional treatment recommendations. The patient was observed in the ED for 4 hours, during which time the facial blanching resolved and her capillary refill time returned to normal at 2 seconds.

After evaluating the patient, the plastic surgeon recommended discharge home with instructions to continue taking the oral ASA and sildenafil, as well as a methylprednisolone dose pack for 6 days. He also recommended the patient begin hyperbaric oxygen (HBO) therapy the day after discharge, since there was no HBO chamber available during her hospital stay.

The patient complied with all discharge instructions, including HBO therapy. At plastic surgery follow-up, the patient had no long-term adverse effects from the CaHA injection.

Case 2

A 54-year-old Asian woman presented to the ED for evaluation of a 24-hour history of progressive and persistent pain, swelling, and discoloration of the nasolabial and upper lip region. She stated her symptoms began within 1 hour of receiving a fat graft injection into the affected area by her cosmetic surgeon. After examining the patient, the cosmetic surgeon referred her to the ED for further evaluation. The patient stated that she had undergone six prior facial revolumization procedures, but noted the recent procedure was her first autologous fat graft.

Workup

The patient’s medical history was unremarkable. Her social history was positive for one glass of wine per day and negative for smoking. The patient was not taking any medications and had no known drug allergies.

The patient’s vital signs at presentation were normal. She was evaluated approximately 30 hours after the fat graft procedure. Facial examination revealed an FS of type 4 with right-sided ischemia along the cutaneous upper lip, alar, and cheek (Figure 1).

Capillary refill time with compression was 0 in the affected area. Sensation to fine touch and pinprick was 0. The facial muscles were intact and, with the exception of puncture marks along both nasolabial folds, the remainder of the facial examination was normal. The neurological examination was likewise normal, and no other physical findings were noted. Laboratory evaluation included CBC, Chem 7 panel, and INR, which were all within normal limits.

Diagnosis and Treatment

The patient was diagnosed with acute angular arterial occlusion with soft tissue ischemia secondary to facial revolumization with autologous fat grafting. She was given oral acyclovir 800 mg, ASA 325 mg, cephalexin 500 mg, prednisone 40 mg, and sildenafil 50 mg; and SC enoxaparin 60 mg (1 mg/kg). Topical nitroglycerin paste 2% was applied to the affected area.

Plastic surgery services were contacted for consultation. After evaluating the patient, the plastic surgeon recommended discharge home with instructions to continue taking the oral acyclovir, ASA, cephalexin, prednisone, and sildenafil for 6 days. He also recommended the patient start HBO therapy the day after discharge home.

The patient refused HBO therapy, but did visit a plastic surgeon for a follow-up examination 3 days after discharge from the ED. A photograph of the patient’s nasolabial and upper lip region taken during this visit is presented in Figure 2.

Five days after discharge from the ED, the patient presented to a plastic surgery clinic for evaluation; a photograph was also obtained at this visit (Figure 3). The plastic surgeon at this clinic referred the patient to a tertiary center for a second opinion regarding the need for HBO therapy. The plastic surgeon at the tertiary center affirmed the initial plastic surgeon’s diagnosis and recommendation for HBO therapy. Although the patient did not return for further evaluation, she underwent 10 HBO treatments at the tertiary center with an acceptable aesthetic result.

Noninvasive Injectable Cosmetic Facial Augmentation

Facial augmentation procedures include the use of autologous adipose bovine collagen, HA gels, CaHA, and plastic compounds to fill wrinkles, folds, or soft tissue defects due to normal aging or trauma. Plastic surgeons traditionally use adipose and manufactured products for scar revision, midfacial restoration of volume loss from aging or trauma, cheek and chin augmentation, tear-trough correction (the diagonal crease running from the inner eye canthus to the maxilla resulting in a groove that creates a tired appearance), nose reshaping, lip enhancement, and correction of facial asymmetry.

Today the use of manufactured soft tissue revolumization products (ie, fillers) is no longer solely in the purview of plastic surgeons, but rather has become ubiquitous with nonsurgeons and allied health care professionals. As the overall number of revolumization procedures increases, so too does the risk for local and distant vascular complications.

Dermal Fillers

Dermal fillers vary widely in their respective properties, solubility, injection-technique flow requirements, and inherent complication risks. Regardless of type, all dermal fillers have the potential to cause serious complications. Most adverse events are related to substance type, volume, and injection technique. Bruising and trauma-related edema following dermal filler procedures are considered normal.

Though complications from dermal filler injections are rarely lethal, serious adverse events can result in permanent functional and aesthetic deficits. With proper physician training, planning, and injection technique, most adverse events can be avoided.

Hyaluronic Acid. Hyaluronic acid (HA)-containing injectable gel fillers (eg, Belotero, Juvederm, Perlane, and Restylane) are one of the most commonly used volumization products—especially by nonplastic surgeons. These gel fillers, which vary in viscosity and elasticity, may be injected from the superficial dermis to the periosteum. Dilution, dispersion, and degradation may be achieved in vivo either by high arterial flow or hyaluronidase.

Calcium Hydroxylapatite. Calcium hydroxylapatite (Radiesse) microsphere fillers consist of a very viscous paste that is mixed with lidocaine prior to injection to increase its flowability. The CaHA solution is injected at the deep dermis to periosteum level. Since CaHA is not easily diluted, dispersed, or degraded by high arterial flow, it tends to retain its consistency. When this procedure is performed by a novice, it can result in complete occlusion at the injection site or through embolization via antegrade or retrograde flow.

Poly-L-lactic Acid. Poly-L-lactic acid (PLLA; Sculptra) is a low-viscosity fluid comprised of synthetic polymer beads. The PLLA microparticles are not dissolvable or degradable by high arterial flow, and are designed to induce an inflammatory response with neocollagenesis.

Polymethyl Methacrylate. Polymethyl methacrylate (PMMA; Bellafil) consists of a combination of microscopic synthetic polymer beads suspended in a variety of substances. For facial enhancement, PMMA is usually suspended in HA or bovine collagen. Off-label use of silicon oils and gels such as PMMA are gaining in popularity—often with disastrous consequences such as acute arterial occlusion, bone erosion, and skin ulcerations.^2,3

Autologous Adipose Tissue. Plastic surgeons primarily use autologous adipose tissue to volumize the face, breasts, buttocks, and scars. Autologous fat grafts are typically placed in fat, superficial and deep muscles, and deep fat pads through a 2- to 2.5-mm facial fat grafting cannula using a multichannel technique that leaves minute amounts of fat in each channel. Fat embolization may occur when a nonfacial fat graft cannula or needle used to transplant the fat graft enters an artery either through direct sharp puncture or traumatic tear cannulation.^4-9

Adverse Events

The first recorded manufactured adverse event from an injectable dermal filler was in 1991. At that time, the US Food and Drug Administration warned of adverse events secondary to collagen injections, including open sores, abscess formation associated with delayed healing of the skin, and partial blindness.¹⁰

Arterial Embolization and Cannulation. The most serious complications from dermal fillers are accidental injection and/or embolization of the filler into the arterial system. Since 1991, an increased number of cases of soft tissue necrosis, blindness, and stroke have been reported as a result of injection of fillers in the glabella, forehead creases, temple, crow’s feet, nose, cheeks, nasolabial folds, and lower lip.^11-15

Accidental cannulation and inadvertent injection of fillers into the arterial vessels can have catastrophic complications. The potential of such inadvertent complications occurs despite skill level of the practitioner or surgeon. Therefore, recognition and treatment of a vascular occlusion must be immediate and aggressive to avoid devastating and potentially irreversible complications including blindness, stroke, and death.^11-15

Acute Blindness and Stroke. The issues and concerns associated with local intra-arterial dermal filler injection and distal embolism are well described in the literature. However, the mechanism of retinal artery occlusion is much more complex given the need for deep placement of products and the force necessary to cause distention and elevation of the dermis. Hence, higher g-forces are applied via the plunger, forcing the intra-arterial filler proximally past the origin of the retinal artery. When the clinician stops the injection, the arterial systolic pressure immediately embolizes the filler into the distal branches of the ophthalmic artery. This causes acute pain and blindness (Figure 5). Depending on the g-force applied, filler can enter into the internal carotid artery and embolize resulting in cerebral ischemia. Signs of cerebral ischemia may be mild or overt.^4-9

Management

Patients with intra-arterial dermal filler injection constitute a medical emergency requiring immediate intervention. We recommend clinicians initiate the treatment protocols outlined in the Box and Table 1.

Hyaluronidase. Injection of hyaluronidase may assist in degrading the HA around the arterial puncture site, relieving compression, which may increase blood flow. There is a risk of distal embolization from a dislodged HA emboli.

Fat Graft Injections. There are no known degradation products for fat, CaHA, PLLA, or PMMA products. The use of normal saline or hyaluronidase has no proven efficacy and may increase the compression pressure in the artery and surrounding tissue, causing further ischemia.

Long-term Sequelae

Despite aggressive intervention, permanent complications of cerebral ischemia, blindness, and severe soft tissue necrosis may occur. In six cases in the literature, patients treated with ocular massage therapy,^7,14 carbon dioxide rebreathing,¹⁴ HBO therapy,^7,14 oral and IV corticosteroids,^6-9 antiplatelet drugs,⁶ and fibrinolytic agents,^7,16 or mechanical thrombolysis¹⁶ showed no clinical effects. Neither the treated nor the untreated patients in any of these case studies had any return of vision.^4-7,9,20-27

Conclusion

Although artificial dermal fillers such as HA, CaHA, PLLA, and PMMA, and autologous adipose tissue grafts offer a minimally invasive alternative to plastic surgical procedures, they are not without complication or adverse effects, such as the acute arterial occlusion experienced by both of our patients. Patients presenting to the ED with adverse effects from such procedures must be managed promptly, employing the suggested management and treatment protocol, including consultation with ophthalmology, plastic surgery, and neurological services as indicated, to avoid permanent sequela and damage.

Artificial dermal fillers and autologous fat grafting have become increasingly popular in recent years, primarily because they augment existing soft tissue volumes, thus producing aesthetic improvements at a lower cost than traditional plastic surgery (ie, facelift), and with nearly no recovery time. According to the American Society for Aesthetic Plastic Surgery, more than 2 million hyaluronic acid (HA) dermal filler procedures were performed in 2016, an increase of 3% from 2015.¹ In addition, 80,000 autologous fat grafting procedures were performed in 2016, an increase of 13% from 2015. In total, there were 2.6 million soft tissue filler procedures in 2016, an increase of 2% from 2015.¹

With the increased demand and access to both artificial dermal fillers and autologous fat grafting, there has been a plethora of reported adverse events, ranging from expected erythema to acute blindness and stroke. Emergency physicians should have a thorough understanding of facial vascular anatomy, as well as the effects of available facial volumization products, including potential complications and treatment options. Through our review of two patient cases, we propose a simplified protocol for the treatment of patients with acute arterial occlusion secondary to facial volumization procedures.

Case 1

A 38-year-old white woman presented to the ED for evaluation of transient blurred vision and blanching of the left cheek and upper lip, which began approximately 40 minutes prior to presentation, immediately after her primary care physician (PCP) injected her left nasolabial fold with calcium hydroxyapatite (CaHA). The patient stated that her vision became blurry and her eyes began to tear within 1 minute of receiving the injection. She further noted that these visual changes were painless and lasted for approximately 30 seconds.

The patient’s PCP believed these symptoms were due to pain at the injection site. While the patient was at her PCP’s office, the reception clerk noticed the blanching of the patient’s left cheek and informed the PCP, who referred the patient to our ED for evaluation.

Workup

The patient’s vital signs at presentation were normal. Her medical history was unremarkable and negative for smoking, alcohol, or drug use. She was not taking any medications and had no known drug allergies. The patient’s history was negative for any prior cosmetic procedures, and she confirmed this was the first and only time had a facial revolumization.

Facial examination revealed a Fitzpatrick scale (FS; a numerical scoring system used to assess a patient’s reaction to ultraviolet radiation) score of type 3. She also had left-sided blanching that extended from the midpoint of the nose diagonally to the lateral midbuccal cheek to the level of the oral commissure, including the cutaneous upper lip, alar, and nasal side wall. There was minimal capillary refill with compression at the affected site, and sensation was diminished to fine touch and pinprick. The facial muscles were intact, and, with the exception of puncture marks along both nasolabial folds, the remainder of the facial examination was normal.

The ophthalmic examination revealed a reactive pupil at 2 mm, white sclera, pink conjunctiva, red reflex, and normal fundoscopic vessels. The patient’s bedside Snellen visual acuity and visual field assessments were normal. The neurological examination was likewise normal, and no other physical findings were noted.

Laboratory evaluation included complete blood count (CBC), Chem 7 panel (creatinine, blood urea nitrogen [BUN], carbon dioxide, chloride, glucose, sodium, and potassium), and international normalized ratio (INR), which were all within normal limits.

Diagnosis and Treatment

The patient was diagnosed with acute angular arterial occlusion and transient retinal artery embolism secondary to facial volumization with CaHA. She was treated with oral acetylsalicylic acid aspirin (ASA) 325 mg, prednisone 40 mg, and sildenafil 50 mg; and subcutaneous (SC) enoxaparin 60 mg (1 mg/kg). Topical nitroglycerin paste 2% was applied to the affected area.

Ophthalmology and plastic surgery services were contacted for consultation. Based on no acute findings on examination, the ophthalmologist provided no additional treatment recommendations. The patient was observed in the ED for 4 hours, during which time the facial blanching resolved and her capillary refill time returned to normal at 2 seconds.

After evaluating the patient, the plastic surgeon recommended discharge home with instructions to continue taking the oral ASA and sildenafil, as well as a methylprednisolone dose pack for 6 days. He also recommended the patient begin hyperbaric oxygen (HBO) therapy the day after discharge, since there was no HBO chamber available during her hospital stay.

The patient complied with all discharge instructions, including HBO therapy. At plastic surgery follow-up, the patient had no long-term adverse effects from the CaHA injection.

Case 2

A 54-year-old Asian woman presented to the ED for evaluation of a 24-hour history of progressive and persistent pain, swelling, and discoloration of the nasolabial and upper lip region. She stated her symptoms began within 1 hour of receiving a fat graft injection into the affected area by her cosmetic surgeon. After examining the patient, the cosmetic surgeon referred her to the ED for further evaluation. The patient stated that she had undergone six prior facial revolumization procedures, but noted the recent procedure was her first autologous fat graft.

Workup

The patient’s medical history was unremarkable. Her social history was positive for one glass of wine per day and negative for smoking. The patient was not taking any medications and had no known drug allergies.

The patient’s vital signs at presentation were normal. She was evaluated approximately 30 hours after the fat graft procedure. Facial examination revealed an FS of type 4 with right-sided ischemia along the cutaneous upper lip, alar, and cheek (Figure 1).

Capillary refill time with compression was 0 in the affected area. Sensation to fine touch and pinprick was 0. The facial muscles were intact and, with the exception of puncture marks along both nasolabial folds, the remainder of the facial examination was normal. The neurological examination was likewise normal, and no other physical findings were noted. Laboratory evaluation included CBC, Chem 7 panel, and INR, which were all within normal limits.

Diagnosis and Treatment

The patient was diagnosed with acute angular arterial occlusion with soft tissue ischemia secondary to facial revolumization with autologous fat grafting. She was given oral acyclovir 800 mg, ASA 325 mg, cephalexin 500 mg, prednisone 40 mg, and sildenafil 50 mg; and SC enoxaparin 60 mg (1 mg/kg). Topical nitroglycerin paste 2% was applied to the affected area.

Plastic surgery services were contacted for consultation. After evaluating the patient, the plastic surgeon recommended discharge home with instructions to continue taking the oral acyclovir, ASA, cephalexin, prednisone, and sildenafil for 6 days. He also recommended the patient start HBO therapy the day after discharge home.

The patient refused HBO therapy, but did visit a plastic surgeon for a follow-up examination 3 days after discharge from the ED. A photograph of the patient’s nasolabial and upper lip region taken during this visit is presented in Figure 2.

Five days after discharge from the ED, the patient presented to a plastic surgery clinic for evaluation; a photograph was also obtained at this visit (Figure 3). The plastic surgeon at this clinic referred the patient to a tertiary center for a second opinion regarding the need for HBO therapy. The plastic surgeon at the tertiary center affirmed the initial plastic surgeon’s diagnosis and recommendation for HBO therapy. Although the patient did not return for further evaluation, she underwent 10 HBO treatments at the tertiary center with an acceptable aesthetic result.

Noninvasive Injectable Cosmetic Facial Augmentation

Facial augmentation procedures include the use of autologous adipose bovine collagen, HA gels, CaHA, and plastic compounds to fill wrinkles, folds, or soft tissue defects due to normal aging or trauma. Plastic surgeons traditionally use adipose and manufactured products for scar revision, midfacial restoration of volume loss from aging or trauma, cheek and chin augmentation, tear-trough correction (the diagonal crease running from the inner eye canthus to the maxilla resulting in a groove that creates a tired appearance), nose reshaping, lip enhancement, and correction of facial asymmetry.

Today the use of manufactured soft tissue revolumization products (ie, fillers) is no longer solely in the purview of plastic surgeons, but rather has become ubiquitous with nonsurgeons and allied health care professionals. As the overall number of revolumization procedures increases, so too does the risk for local and distant vascular complications.

Dermal Fillers

Dermal fillers vary widely in their respective properties, solubility, injection-technique flow requirements, and inherent complication risks. Regardless of type, all dermal fillers have the potential to cause serious complications. Most adverse events are related to substance type, volume, and injection technique. Bruising and trauma-related edema following dermal filler procedures are considered normal.

Though complications from dermal filler injections are rarely lethal, serious adverse events can result in permanent functional and aesthetic deficits. With proper physician training, planning, and injection technique, most adverse events can be avoided.

Hyaluronic Acid. Hyaluronic acid (HA)-containing injectable gel fillers (eg, Belotero, Juvederm, Perlane, and Restylane) are one of the most commonly used volumization products—especially by nonplastic surgeons. These gel fillers, which vary in viscosity and elasticity, may be injected from the superficial dermis to the periosteum. Dilution, dispersion, and degradation may be achieved in vivo either by high arterial flow or hyaluronidase.

Calcium Hydroxylapatite. Calcium hydroxylapatite (Radiesse) microsphere fillers consist of a very viscous paste that is mixed with lidocaine prior to injection to increase its flowability. The CaHA solution is injected at the deep dermis to periosteum level. Since CaHA is not easily diluted, dispersed, or degraded by high arterial flow, it tends to retain its consistency. When this procedure is performed by a novice, it can result in complete occlusion at the injection site or through embolization via antegrade or retrograde flow.

Poly-L-lactic Acid. Poly-L-lactic acid (PLLA; Sculptra) is a low-viscosity fluid comprised of synthetic polymer beads. The PLLA microparticles are not dissolvable or degradable by high arterial flow, and are designed to induce an inflammatory response with neocollagenesis.

Polymethyl Methacrylate. Polymethyl methacrylate (PMMA; Bellafil) consists of a combination of microscopic synthetic polymer beads suspended in a variety of substances. For facial enhancement, PMMA is usually suspended in HA or bovine collagen. Off-label use of silicon oils and gels such as PMMA are gaining in popularity—often with disastrous consequences such as acute arterial occlusion, bone erosion, and skin ulcerations.^2,3

Autologous Adipose Tissue. Plastic surgeons primarily use autologous adipose tissue to volumize the face, breasts, buttocks, and scars. Autologous fat grafts are typically placed in fat, superficial and deep muscles, and deep fat pads through a 2- to 2.5-mm facial fat grafting cannula using a multichannel technique that leaves minute amounts of fat in each channel. Fat embolization may occur when a nonfacial fat graft cannula or needle used to transplant the fat graft enters an artery either through direct sharp puncture or traumatic tear cannulation.^4-9

Adverse Events

The first recorded manufactured adverse event from an injectable dermal filler was in 1991. At that time, the US Food and Drug Administration warned of adverse events secondary to collagen injections, including open sores, abscess formation associated with delayed healing of the skin, and partial blindness.¹⁰

Arterial Embolization and Cannulation. The most serious complications from dermal fillers are accidental injection and/or embolization of the filler into the arterial system. Since 1991, an increased number of cases of soft tissue necrosis, blindness, and stroke have been reported as a result of injection of fillers in the glabella, forehead creases, temple, crow’s feet, nose, cheeks, nasolabial folds, and lower lip.^11-15

Accidental cannulation and inadvertent injection of fillers into the arterial vessels can have catastrophic complications. The potential of such inadvertent complications occurs despite skill level of the practitioner or surgeon. Therefore, recognition and treatment of a vascular occlusion must be immediate and aggressive to avoid devastating and potentially irreversible complications including blindness, stroke, and death.^11-15

Acute Blindness and Stroke. The issues and concerns associated with local intra-arterial dermal filler injection and distal embolism are well described in the literature. However, the mechanism of retinal artery occlusion is much more complex given the need for deep placement of products and the force necessary to cause distention and elevation of the dermis. Hence, higher g-forces are applied via the plunger, forcing the intra-arterial filler proximally past the origin of the retinal artery. When the clinician stops the injection, the arterial systolic pressure immediately embolizes the filler into the distal branches of the ophthalmic artery. This causes acute pain and blindness (Figure 5). Depending on the g-force applied, filler can enter into the internal carotid artery and embolize resulting in cerebral ischemia. Signs of cerebral ischemia may be mild or overt.^4-9

Management

Patients with intra-arterial dermal filler injection constitute a medical emergency requiring immediate intervention. We recommend clinicians initiate the treatment protocols outlined in the Box and Table 1.

Hyaluronidase. Injection of hyaluronidase may assist in degrading the HA around the arterial puncture site, relieving compression, which may increase blood flow. There is a risk of distal embolization from a dislodged HA emboli.

Fat Graft Injections. There are no known degradation products for fat, CaHA, PLLA, or PMMA products. The use of normal saline or hyaluronidase has no proven efficacy and may increase the compression pressure in the artery and surrounding tissue, causing further ischemia.

Long-term Sequelae

Despite aggressive intervention, permanent complications of cerebral ischemia, blindness, and severe soft tissue necrosis may occur. In six cases in the literature, patients treated with ocular massage therapy,^7,14 carbon dioxide rebreathing,¹⁴ HBO therapy,^7,14 oral and IV corticosteroids,^6-9 antiplatelet drugs,⁶ and fibrinolytic agents,^7,16 or mechanical thrombolysis¹⁶ showed no clinical effects. Neither the treated nor the untreated patients in any of these case studies had any return of vision.^4-7,9,20-27

Conclusion

Although artificial dermal fillers such as HA, CaHA, PLLA, and PMMA, and autologous adipose tissue grafts offer a minimally invasive alternative to plastic surgical procedures, they are not without complication or adverse effects, such as the acute arterial occlusion experienced by both of our patients. Patients presenting to the ED with adverse effects from such procedures must be managed promptly, employing the suggested management and treatment protocol, including consultation with ophthalmology, plastic surgery, and neurological services as indicated, to avoid permanent sequela and damage.

Artificial dermal fillers and autologous fat grafting have become increasingly popular in recent years, primarily because they augment existing soft tissue volumes, thus producing aesthetic improvements at a lower cost than traditional plastic surgery (ie, facelift), and with nearly no recovery time. According to the American Society for Aesthetic Plastic Surgery, more than 2 million hyaluronic acid (HA) dermal filler procedures were performed in 2016, an increase of 3% from 2015.¹ In addition, 80,000 autologous fat grafting procedures were performed in 2016, an increase of 13% from 2015. In total, there were 2.6 million soft tissue filler procedures in 2016, an increase of 2% from 2015.¹

With the increased demand and access to both artificial dermal fillers and autologous fat grafting, there has been a plethora of reported adverse events, ranging from expected erythema to acute blindness and stroke. Emergency physicians should have a thorough understanding of facial vascular anatomy, as well as the effects of available facial volumization products, including potential complications and treatment options. Through our review of two patient cases, we propose a simplified protocol for the treatment of patients with acute arterial occlusion secondary to facial volumization procedures.

Case 1

A 38-year-old white woman presented to the ED for evaluation of transient blurred vision and blanching of the left cheek and upper lip, which began approximately 40 minutes prior to presentation, immediately after her primary care physician (PCP) injected her left nasolabial fold with calcium hydroxyapatite (CaHA). The patient stated that her vision became blurry and her eyes began to tear within 1 minute of receiving the injection. She further noted that these visual changes were painless and lasted for approximately 30 seconds.

The patient’s PCP believed these symptoms were due to pain at the injection site. While the patient was at her PCP’s office, the reception clerk noticed the blanching of the patient’s left cheek and informed the PCP, who referred the patient to our ED for evaluation.

Workup

The patient’s vital signs at presentation were normal. Her medical history was unremarkable and negative for smoking, alcohol, or drug use. She was not taking any medications and had no known drug allergies. The patient’s history was negative for any prior cosmetic procedures, and she confirmed this was the first and only time had a facial revolumization.

Facial examination revealed a Fitzpatrick scale (FS; a numerical scoring system used to assess a patient’s reaction to ultraviolet radiation) score of type 3. She also had left-sided blanching that extended from the midpoint of the nose diagonally to the lateral midbuccal cheek to the level of the oral commissure, including the cutaneous upper lip, alar, and nasal side wall. There was minimal capillary refill with compression at the affected site, and sensation was diminished to fine touch and pinprick. The facial muscles were intact, and, with the exception of puncture marks along both nasolabial folds, the remainder of the facial examination was normal.

The ophthalmic examination revealed a reactive pupil at 2 mm, white sclera, pink conjunctiva, red reflex, and normal fundoscopic vessels. The patient’s bedside Snellen visual acuity and visual field assessments were normal. The neurological examination was likewise normal, and no other physical findings were noted.

Laboratory evaluation included complete blood count (CBC), Chem 7 panel (creatinine, blood urea nitrogen [BUN], carbon dioxide, chloride, glucose, sodium, and potassium), and international normalized ratio (INR), which were all within normal limits.

Diagnosis and Treatment

The patient was diagnosed with acute angular arterial occlusion and transient retinal artery embolism secondary to facial volumization with CaHA. She was treated with oral acetylsalicylic acid aspirin (ASA) 325 mg, prednisone 40 mg, and sildenafil 50 mg; and subcutaneous (SC) enoxaparin 60 mg (1 mg/kg). Topical nitroglycerin paste 2% was applied to the affected area.

Ophthalmology and plastic surgery services were contacted for consultation. Based on no acute findings on examination, the ophthalmologist provided no additional treatment recommendations. The patient was observed in the ED for 4 hours, during which time the facial blanching resolved and her capillary refill time returned to normal at 2 seconds.

After evaluating the patient, the plastic surgeon recommended discharge home with instructions to continue taking the oral ASA and sildenafil, as well as a methylprednisolone dose pack for 6 days. He also recommended the patient begin hyperbaric oxygen (HBO) therapy the day after discharge, since there was no HBO chamber available during her hospital stay.

The patient complied with all discharge instructions, including HBO therapy. At plastic surgery follow-up, the patient had no long-term adverse effects from the CaHA injection.

Case 2

A 54-year-old Asian woman presented to the ED for evaluation of a 24-hour history of progressive and persistent pain, swelling, and discoloration of the nasolabial and upper lip region. She stated her symptoms began within 1 hour of receiving a fat graft injection into the affected area by her cosmetic surgeon. After examining the patient, the cosmetic surgeon referred her to the ED for further evaluation. The patient stated that she had undergone six prior facial revolumization procedures, but noted the recent procedure was her first autologous fat graft.

Workup

The patient’s medical history was unremarkable. Her social history was positive for one glass of wine per day and negative for smoking. The patient was not taking any medications and had no known drug allergies.

The patient’s vital signs at presentation were normal. She was evaluated approximately 30 hours after the fat graft procedure. Facial examination revealed an FS of type 4 with right-sided ischemia along the cutaneous upper lip, alar, and cheek (Figure 1).

Capillary refill time with compression was 0 in the affected area. Sensation to fine touch and pinprick was 0. The facial muscles were intact and, with the exception of puncture marks along both nasolabial folds, the remainder of the facial examination was normal. The neurological examination was likewise normal, and no other physical findings were noted. Laboratory evaluation included CBC, Chem 7 panel, and INR, which were all within normal limits.

Diagnosis and Treatment

The patient was diagnosed with acute angular arterial occlusion with soft tissue ischemia secondary to facial revolumization with autologous fat grafting. She was given oral acyclovir 800 mg, ASA 325 mg, cephalexin 500 mg, prednisone 40 mg, and sildenafil 50 mg; and SC enoxaparin 60 mg (1 mg/kg). Topical nitroglycerin paste 2% was applied to the affected area.

Plastic surgery services were contacted for consultation. After evaluating the patient, the plastic surgeon recommended discharge home with instructions to continue taking the oral acyclovir, ASA, cephalexin, prednisone, and sildenafil for 6 days. He also recommended the patient start HBO therapy the day after discharge home.

The patient refused HBO therapy, but did visit a plastic surgeon for a follow-up examination 3 days after discharge from the ED. A photograph of the patient’s nasolabial and upper lip region taken during this visit is presented in Figure 2.

Five days after discharge from the ED, the patient presented to a plastic surgery clinic for evaluation; a photograph was also obtained at this visit (Figure 3). The plastic surgeon at this clinic referred the patient to a tertiary center for a second opinion regarding the need for HBO therapy. The plastic surgeon at the tertiary center affirmed the initial plastic surgeon’s diagnosis and recommendation for HBO therapy. Although the patient did not return for further evaluation, she underwent 10 HBO treatments at the tertiary center with an acceptable aesthetic result.

Noninvasive Injectable Cosmetic Facial Augmentation

Facial augmentation procedures include the use of autologous adipose bovine collagen, HA gels, CaHA, and plastic compounds to fill wrinkles, folds, or soft tissue defects due to normal aging or trauma. Plastic surgeons traditionally use adipose and manufactured products for scar revision, midfacial restoration of volume loss from aging or trauma, cheek and chin augmentation, tear-trough correction (the diagonal crease running from the inner eye canthus to the maxilla resulting in a groove that creates a tired appearance), nose reshaping, lip enhancement, and correction of facial asymmetry.

Today the use of manufactured soft tissue revolumization products (ie, fillers) is no longer solely in the purview of plastic surgeons, but rather has become ubiquitous with nonsurgeons and allied health care professionals. As the overall number of revolumization procedures increases, so too does the risk for local and distant vascular complications.

Dermal Fillers

Dermal fillers vary widely in their respective properties, solubility, injection-technique flow requirements, and inherent complication risks. Regardless of type, all dermal fillers have the potential to cause serious complications. Most adverse events are related to substance type, volume, and injection technique. Bruising and trauma-related edema following dermal filler procedures are considered normal.

Though complications from dermal filler injections are rarely lethal, serious adverse events can result in permanent functional and aesthetic deficits. With proper physician training, planning, and injection technique, most adverse events can be avoided.

Hyaluronic Acid. Hyaluronic acid (HA)-containing injectable gel fillers (eg, Belotero, Juvederm, Perlane, and Restylane) are one of the most commonly used volumization products—especially by nonplastic surgeons. These gel fillers, which vary in viscosity and elasticity, may be injected from the superficial dermis to the periosteum. Dilution, dispersion, and degradation may be achieved in vivo either by high arterial flow or hyaluronidase.

Calcium Hydroxylapatite. Calcium hydroxylapatite (Radiesse) microsphere fillers consist of a very viscous paste that is mixed with lidocaine prior to injection to increase its flowability. The CaHA solution is injected at the deep dermis to periosteum level. Since CaHA is not easily diluted, dispersed, or degraded by high arterial flow, it tends to retain its consistency. When this procedure is performed by a novice, it can result in complete occlusion at the injection site or through embolization via antegrade or retrograde flow.

Poly-L-lactic Acid. Poly-L-lactic acid (PLLA; Sculptra) is a low-viscosity fluid comprised of synthetic polymer beads. The PLLA microparticles are not dissolvable or degradable by high arterial flow, and are designed to induce an inflammatory response with neocollagenesis.

Polymethyl Methacrylate. Polymethyl methacrylate (PMMA; Bellafil) consists of a combination of microscopic synthetic polymer beads suspended in a variety of substances. For facial enhancement, PMMA is usually suspended in HA or bovine collagen. Off-label use of silicon oils and gels such as PMMA are gaining in popularity—often with disastrous consequences such as acute arterial occlusion, bone erosion, and skin ulcerations.^2,3

Autologous Adipose Tissue. Plastic surgeons primarily use autologous adipose tissue to volumize the face, breasts, buttocks, and scars. Autologous fat grafts are typically placed in fat, superficial and deep muscles, and deep fat pads through a 2- to 2.5-mm facial fat grafting cannula using a multichannel technique that leaves minute amounts of fat in each channel. Fat embolization may occur when a nonfacial fat graft cannula or needle used to transplant the fat graft enters an artery either through direct sharp puncture or traumatic tear cannulation.^4-9

Adverse Events

The first recorded manufactured adverse event from an injectable dermal filler was in 1991. At that time, the US Food and Drug Administration warned of adverse events secondary to collagen injections, including open sores, abscess formation associated with delayed healing of the skin, and partial blindness.¹⁰

Arterial Embolization and Cannulation. The most serious complications from dermal fillers are accidental injection and/or embolization of the filler into the arterial system. Since 1991, an increased number of cases of soft tissue necrosis, blindness, and stroke have been reported as a result of injection of fillers in the glabella, forehead creases, temple, crow’s feet, nose, cheeks, nasolabial folds, and lower lip.^11-15

Accidental cannulation and inadvertent injection of fillers into the arterial vessels can have catastrophic complications. The potential of such inadvertent complications occurs despite skill level of the practitioner or surgeon. Therefore, recognition and treatment of a vascular occlusion must be immediate and aggressive to avoid devastating and potentially irreversible complications including blindness, stroke, and death.^11-15

Acute Blindness and Stroke. The issues and concerns associated with local intra-arterial dermal filler injection and distal embolism are well described in the literature. However, the mechanism of retinal artery occlusion is much more complex given the need for deep placement of products and the force necessary to cause distention and elevation of the dermis. Hence, higher g-forces are applied via the plunger, forcing the intra-arterial filler proximally past the origin of the retinal artery. When the clinician stops the injection, the arterial systolic pressure immediately embolizes the filler into the distal branches of the ophthalmic artery. This causes acute pain and blindness (Figure 5). Depending on the g-force applied, filler can enter into the internal carotid artery and embolize resulting in cerebral ischemia. Signs of cerebral ischemia may be mild or overt.^4-9

Management

Patients with intra-arterial dermal filler injection constitute a medical emergency requiring immediate intervention. We recommend clinicians initiate the treatment protocols outlined in the Box and Table 1.

Hyaluronidase. Injection of hyaluronidase may assist in degrading the HA around the arterial puncture site, relieving compression, which may increase blood flow. There is a risk of distal embolization from a dislodged HA emboli.

Fat Graft Injections. There are no known degradation products for fat, CaHA, PLLA, or PMMA products. The use of normal saline or hyaluronidase has no proven efficacy and may increase the compression pressure in the artery and surrounding tissue, causing further ischemia.

Long-term Sequelae

Despite aggressive intervention, permanent complications of cerebral ischemia, blindness, and severe soft tissue necrosis may occur. In six cases in the literature, patients treated with ocular massage therapy,^7,14 carbon dioxide rebreathing,¹⁴ HBO therapy,^7,14 oral and IV corticosteroids,^6-9 antiplatelet drugs,⁶ and fibrinolytic agents,^7,16 or mechanical thrombolysis¹⁶ showed no clinical effects. Neither the treated nor the untreated patients in any of these case studies had any return of vision.^4-7,9,20-27

Conclusion

Although artificial dermal fillers such as HA, CaHA, PLLA, and PMMA, and autologous adipose tissue grafts offer a minimally invasive alternative to plastic surgical procedures, they are not without complication or adverse effects, such as the acute arterial occlusion experienced by both of our patients. Patients presenting to the ED with adverse effects from such procedures must be managed promptly, employing the suggested management and treatment protocol, including consultation with ophthalmology, plastic surgery, and neurological services as indicated, to avoid permanent sequela and damage.