Myth: Itching is not a symptom of acne

Acne vulgaris typically is not considered to be a pruritic disease; however, many patients experience itching, which leads them to scratch their acne lesions, causing secondary bacterial infections and subsequent scarring, hypopigmentation, or hyperpigmentation of the involved skin. Although itching rarely is mentioned as a clinical feature of acne, pruritus can be an important contributory factor to the burden of disability and impaired quality of life in acne patients of all ages, and acne itching may be an important target for therapy.

In a descriptive study of 120 consecutive acne patients in Singapore, itch was found to be a common (70% of patients) and debilitating symptom of acne. The majority of patients (83%) reported itch at noon with severity that was comparable to a mosquito bite, and the most common physical descriptor was tickling (68%). Common aggravating factors included sweat (71%), heat (62%), and stress (31%). Fifty-five percent of patients said itching had a negative impact on their mood, and 52% reported that they had scratched or rubbed the affected area.

A study of 108 adolescents with acne limited to the face yielded half who reported itching within acne lesions. The presence of itching was unrelated to age, gender, where they lived, positive family history, or acne severity. In most patients, pruritus appeared relatively infrequently and for a short period of time: 7.4% reported itching every day, 24.1% on a weekly basis, 29.6% at least once a month, and 37.7% even less frequently. Itch episodes lasted less than 1 minute in most participants. However, 31.5% of participants sought medical treatment to reduce itching. The most important factors aggravating the intensity of itching were sweat, stress, physical effort, heat, fatigue, and dry air, respectively.

Regarding the impact of acne itching on quality of life, 29.6% of participants felt depressed and 1.8% were anxious because of their itching. Some participants also noted that itching caused difficulties in falling asleep and awakening from itching.

The pathogenesis of localized itching in acne could be connected with the change in pH of the microenvironment of the acne follicle, providing an optimal environment for the production of histamine or histaminelike products by Propionibacterium acnes. Pruritus also may be a complication of certain acne therapies. Increased awareness among patients of this potential side effect may be helpful in preventing the unnecessary discontinuation of an otherwise effective acne therapy. Understanding factors that may aggravate itching in acne lesions also may be helpful to patients.

Myth: Itching is not a symptom of acne

Acne vulgaris typically is not considered to be a pruritic disease; however, many patients experience itching, which leads them to scratch their acne lesions, causing secondary bacterial infections and subsequent scarring, hypopigmentation, or hyperpigmentation of the involved skin. Although itching rarely is mentioned as a clinical feature of acne, pruritus can be an important contributory factor to the burden of disability and impaired quality of life in acne patients of all ages, and acne itching may be an important target for therapy.

In a descriptive study of 120 consecutive acne patients in Singapore, itch was found to be a common (70% of patients) and debilitating symptom of acne. The majority of patients (83%) reported itch at noon with severity that was comparable to a mosquito bite, and the most common physical descriptor was tickling (68%). Common aggravating factors included sweat (71%), heat (62%), and stress (31%). Fifty-five percent of patients said itching had a negative impact on their mood, and 52% reported that they had scratched or rubbed the affected area.

A study of 108 adolescents with acne limited to the face yielded half who reported itching within acne lesions. The presence of itching was unrelated to age, gender, where they lived, positive family history, or acne severity. In most patients, pruritus appeared relatively infrequently and for a short period of time: 7.4% reported itching every day, 24.1% on a weekly basis, 29.6% at least once a month, and 37.7% even less frequently. Itch episodes lasted less than 1 minute in most participants. However, 31.5% of participants sought medical treatment to reduce itching. The most important factors aggravating the intensity of itching were sweat, stress, physical effort, heat, fatigue, and dry air, respectively.

Regarding the impact of acne itching on quality of life, 29.6% of participants felt depressed and 1.8% were anxious because of their itching. Some participants also noted that itching caused difficulties in falling asleep and awakening from itching.

The pathogenesis of localized itching in acne could be connected with the change in pH of the microenvironment of the acne follicle, providing an optimal environment for the production of histamine or histaminelike products by Propionibacterium acnes. Pruritus also may be a complication of certain acne therapies. Increased awareness among patients of this potential side effect may be helpful in preventing the unnecessary discontinuation of an otherwise effective acne therapy. Understanding factors that may aggravate itching in acne lesions also may be helpful to patients.

Myth: Itching is not a symptom of acne

Acne vulgaris typically is not considered to be a pruritic disease; however, many patients experience itching, which leads them to scratch their acne lesions, causing secondary bacterial infections and subsequent scarring, hypopigmentation, or hyperpigmentation of the involved skin. Although itching rarely is mentioned as a clinical feature of acne, pruritus can be an important contributory factor to the burden of disability and impaired quality of life in acne patients of all ages, and acne itching may be an important target for therapy.

In a descriptive study of 120 consecutive acne patients in Singapore, itch was found to be a common (70% of patients) and debilitating symptom of acne. The majority of patients (83%) reported itch at noon with severity that was comparable to a mosquito bite, and the most common physical descriptor was tickling (68%). Common aggravating factors included sweat (71%), heat (62%), and stress (31%). Fifty-five percent of patients said itching had a negative impact on their mood, and 52% reported that they had scratched or rubbed the affected area.

A study of 108 adolescents with acne limited to the face yielded half who reported itching within acne lesions. The presence of itching was unrelated to age, gender, where they lived, positive family history, or acne severity. In most patients, pruritus appeared relatively infrequently and for a short period of time: 7.4% reported itching every day, 24.1% on a weekly basis, 29.6% at least once a month, and 37.7% even less frequently. Itch episodes lasted less than 1 minute in most participants. However, 31.5% of participants sought medical treatment to reduce itching. The most important factors aggravating the intensity of itching were sweat, stress, physical effort, heat, fatigue, and dry air, respectively.

Regarding the impact of acne itching on quality of life, 29.6% of participants felt depressed and 1.8% were anxious because of their itching. Some participants also noted that itching caused difficulties in falling asleep and awakening from itching.

The pathogenesis of localized itching in acne could be connected with the change in pH of the microenvironment of the acne follicle, providing an optimal environment for the production of histamine or histaminelike products by Propionibacterium acnes. Pruritus also may be a complication of certain acne therapies. Increased awareness among patients of this potential side effect may be helpful in preventing the unnecessary discontinuation of an otherwise effective acne therapy. Understanding factors that may aggravate itching in acne lesions also may be helpful to patients.

Ankle effusions can be quite debilitating, causing band-like swelling and stiffness to the anterior aspect of ankle at the tibiotalar joint. Significant swelling can impair ankle dorsiflexion and plantar flexion. The differential diagnosis for joint effusions is wide, and includes traumatic effusion; gout; osteoarthritis; rheumatoid arthritis; and septic arthritis, which is one of the most important diagnoses for the emergency physician (EP) to identify and initiate prompt treatment to reduce the risk of serious morbidity and mortality. Differentiating these conditions requires joint aspiration and synovial fluid analysis. While a large effusion will be palpable and likely ballotable, smaller effusions are more challenging clinically. In such cases, point-of-care (POC) ultrasound can be a valuable tool in confirming a joint effusion.

Identifying Landmarks and Tibiotalar Joint

To access the tibiotalar joint space, it is important to identify useful landmarks.¹ This is best accomplished by having the patient in the supine position, with the affected knee flexed approximately 90° and plantar surface of the foot lying flat on the bed (Figure 1).

Performing the Arthrocentesis

The arthrocentesis is performed under sterile conditions using the high-frequency linear probe. A sterile probe cover is highly recommended if the operator will be using ultrasound to guide the procedure in real time.² Using the palpable landmarks as a guide, the clinician should align the probe just medial to the tibialis anterior tendon with the probe marker oriented cephalad; scanning should begin superior to the ankle joint. The tibia will appear as a hyperechoic stripe just under a thin soft tissue layer. When the tibia is visible, the clinician should then slide the probe distally. The joint space will demonstrated by visualization of the distal tibia and talus bone (Figure 3).

Pearls and Pitfalls

Point-of-care ultrasound is not only useful to guide arthrocentesis of joint effusions, but also to confirm the presence of an effusion prior to aspiration. At our institution, we have had many cases in which POC ultrasound demonstrated an absence of effusion, and we were able to avoid an unnecessary joint aspiration. Moreover, when an effusion is present, POC ultrasound-guided aspiration avoids complications. The use of POC ultrasound can also increase the confidence of the provider performing arthrocentesis of joints less commonly aspirated.

Summary

Joint aspiration is an important procedural tool for EPs, especially when used to rule out life-threatening conditions such as septic arthritis. Deeper joints and small fluid collections, however, can be difficult to access without image guidance. In the ED setting, POC ultrasound provides a widely available, easy-to-use, low-cost tool to increase the likelihood of success while minimizing damage to adjacent structures.

Ankle effusions can be quite debilitating, causing band-like swelling and stiffness to the anterior aspect of ankle at the tibiotalar joint. Significant swelling can impair ankle dorsiflexion and plantar flexion. The differential diagnosis for joint effusions is wide, and includes traumatic effusion; gout; osteoarthritis; rheumatoid arthritis; and septic arthritis, which is one of the most important diagnoses for the emergency physician (EP) to identify and initiate prompt treatment to reduce the risk of serious morbidity and mortality. Differentiating these conditions requires joint aspiration and synovial fluid analysis. While a large effusion will be palpable and likely ballotable, smaller effusions are more challenging clinically. In such cases, point-of-care (POC) ultrasound can be a valuable tool in confirming a joint effusion.

Identifying Landmarks and Tibiotalar Joint

To access the tibiotalar joint space, it is important to identify useful landmarks.¹ This is best accomplished by having the patient in the supine position, with the affected knee flexed approximately 90° and plantar surface of the foot lying flat on the bed (Figure 1).

Performing the Arthrocentesis

The arthrocentesis is performed under sterile conditions using the high-frequency linear probe. A sterile probe cover is highly recommended if the operator will be using ultrasound to guide the procedure in real time.² Using the palpable landmarks as a guide, the clinician should align the probe just medial to the tibialis anterior tendon with the probe marker oriented cephalad; scanning should begin superior to the ankle joint. The tibia will appear as a hyperechoic stripe just under a thin soft tissue layer. When the tibia is visible, the clinician should then slide the probe distally. The joint space will demonstrated by visualization of the distal tibia and talus bone (Figure 3).

Pearls and Pitfalls

Point-of-care ultrasound is not only useful to guide arthrocentesis of joint effusions, but also to confirm the presence of an effusion prior to aspiration. At our institution, we have had many cases in which POC ultrasound demonstrated an absence of effusion, and we were able to avoid an unnecessary joint aspiration. Moreover, when an effusion is present, POC ultrasound-guided aspiration avoids complications. The use of POC ultrasound can also increase the confidence of the provider performing arthrocentesis of joints less commonly aspirated.

Summary

Joint aspiration is an important procedural tool for EPs, especially when used to rule out life-threatening conditions such as septic arthritis. Deeper joints and small fluid collections, however, can be difficult to access without image guidance. In the ED setting, POC ultrasound provides a widely available, easy-to-use, low-cost tool to increase the likelihood of success while minimizing damage to adjacent structures.

Ankle effusions can be quite debilitating, causing band-like swelling and stiffness to the anterior aspect of ankle at the tibiotalar joint. Significant swelling can impair ankle dorsiflexion and plantar flexion. The differential diagnosis for joint effusions is wide, and includes traumatic effusion; gout; osteoarthritis; rheumatoid arthritis; and septic arthritis, which is one of the most important diagnoses for the emergency physician (EP) to identify and initiate prompt treatment to reduce the risk of serious morbidity and mortality. Differentiating these conditions requires joint aspiration and synovial fluid analysis. While a large effusion will be palpable and likely ballotable, smaller effusions are more challenging clinically. In such cases, point-of-care (POC) ultrasound can be a valuable tool in confirming a joint effusion.

Identifying Landmarks and Tibiotalar Joint

To access the tibiotalar joint space, it is important to identify useful landmarks.¹ This is best accomplished by having the patient in the supine position, with the affected knee flexed approximately 90° and plantar surface of the foot lying flat on the bed (Figure 1).

Performing the Arthrocentesis

The arthrocentesis is performed under sterile conditions using the high-frequency linear probe. A sterile probe cover is highly recommended if the operator will be using ultrasound to guide the procedure in real time.² Using the palpable landmarks as a guide, the clinician should align the probe just medial to the tibialis anterior tendon with the probe marker oriented cephalad; scanning should begin superior to the ankle joint. The tibia will appear as a hyperechoic stripe just under a thin soft tissue layer. When the tibia is visible, the clinician should then slide the probe distally. The joint space will demonstrated by visualization of the distal tibia and talus bone (Figure 3).

Pearls and Pitfalls

Point-of-care ultrasound is not only useful to guide arthrocentesis of joint effusions, but also to confirm the presence of an effusion prior to aspiration. At our institution, we have had many cases in which POC ultrasound demonstrated an absence of effusion, and we were able to avoid an unnecessary joint aspiration. Moreover, when an effusion is present, POC ultrasound-guided aspiration avoids complications. The use of POC ultrasound can also increase the confidence of the provider performing arthrocentesis of joints less commonly aspirated.

Summary

Joint aspiration is an important procedural tool for EPs, especially when used to rule out life-threatening conditions such as septic arthritis. Deeper joints and small fluid collections, however, can be difficult to access without image guidance. In the ED setting, POC ultrasound provides a widely available, easy-to-use, low-cost tool to increase the likelihood of success while minimizing damage to adjacent structures.

Genetic factors accounted for about 40% of variability in the risk of colorectal cancer (CRC) in an analysis of monozygotic and same-sex dizygotic twins from the Nordic Twin Study of Cancer to reported in the August issue of Clinical Gastroenterology and Hepatology (2017 Jan. doi: 10.1016/j.cgh.2016.12.041).

Thus, CRC “has a substantial heritable component, and may be more heritable in women than men,” Rebecca E. Graff, ScD, of the Harvard T.H. Chan School of Public Health, Boston, and the University of California, San Francisco, and her colleagues wrote. “Siblings, and particularly monozygotic cotwins, of individuals with colon or rectal cancer should consider personalized screening,” they added.

©Christian Jasiuk/Thinkstock

Genetic factors accounted for about 40% of variability in the risk of colorectal cancer (CRC) in an analysis of monozygotic and same-sex dizygotic twins from the Nordic Twin Study of Cancer to reported in the August issue of Clinical Gastroenterology and Hepatology (2017 Jan. doi: 10.1016/j.cgh.2016.12.041).

Thus, CRC “has a substantial heritable component, and may be more heritable in women than men,” Rebecca E. Graff, ScD, of the Harvard T.H. Chan School of Public Health, Boston, and the University of California, San Francisco, and her colleagues wrote. “Siblings, and particularly monozygotic cotwins, of individuals with colon or rectal cancer should consider personalized screening,” they added.

©Christian Jasiuk/Thinkstock

Genetic factors accounted for about 40% of variability in the risk of colorectal cancer (CRC) in an analysis of monozygotic and same-sex dizygotic twins from the Nordic Twin Study of Cancer to reported in the August issue of Clinical Gastroenterology and Hepatology (2017 Jan. doi: 10.1016/j.cgh.2016.12.041).

Thus, CRC “has a substantial heritable component, and may be more heritable in women than men,” Rebecca E. Graff, ScD, of the Harvard T.H. Chan School of Public Health, Boston, and the University of California, San Francisco, and her colleagues wrote. “Siblings, and particularly monozygotic cotwins, of individuals with colon or rectal cancer should consider personalized screening,” they added.

©Christian Jasiuk/Thinkstock

Endoscopists who took about a minute longer during screening esophagogastroduodenoscopy (EGD) detected significantly more upper gastrointestinal neoplasms than their quicker colleagues, in a retrospective study reported in the August issue of Gastroenterology (doi: 10.1053/j.gastro.2017.05.009).

Detection rates were 0.28% and 0.20%, respectively (P = .005), and this difference remained statistically significant after the investigators controlled for numerous factors that also can affect the chances of detecting gastric neoplasms during upper endoscopy, reported Jae Myung Park, MD, and his colleagues at Seoul (Korea) St. Mary’s Hospital.

Gastric cancer is the second leading cause of cancer mortality worldwide, they noted. Although EGD has been practiced globally for decades, there is no consensus on which performance metrics optimize diagnostic yield. Both Korea and Japan have adopted screening EGD to help diagnose gastric cancer, but interval cancers and false-positive results remain concerns, and the field lacks rigorous analyses comparing EGD time with gastric cancer detection rates. Therefore, the researchers studied 111,962 consecutive patients who underwent EGD at one hospital in Seoul from 2009 through 2015. Fourteen board-certified endoscopists performed these procedures at a single endoscopy unit.A total of 262 patients (0.23%) were diagnosed with gastric neoplasia or dysplasia, duodenal neoplasia, or esophageal carcinoma. This finding closely resembled a prior report from Korea, the investigators noted. Detection rates among individual endoscopists ranged from 0.14% to 0.32%, and longer EGD time was associated with a higher detection rate with an R value of 0.54 (P = .046). During the first year of the study, EGDs without biopsies averaged 2 minutes, 53 seconds. Based on this finding, the researchers set a cutoff time of 3 minutes and classified eight endoscopists as fast (mean EGD duration, 2 minutes and 38 seconds; standard deviation, 21 seconds) and six endoscopists as slow (mean duration, 3 minutes and 25 seconds; SD, 19 seconds). Slower endoscopists were significantly more likely to detect gastric adenomas or carcinomas, even after the investigators controlled for the biopsy rates and experience level of these endoscopists and patients’ age, sex, smoking status, alcohol use, and family history of cancer (odds ratio, 1.52; 95% confidence interval, 1.17-1.97; P = .0018).

Older age, male sex, and smoking also were significant correlates of cancer detection in the multivariable model. Biopsy rates among endoscopists ranged from 7% to 28%, and taking a biopsy was an even stronger predictor of detecting an upper GI neoplasm than was EGD duration, with an R value of 0.76 (P = .002). Although this study was observational and retrospective and lacked data on prior EGD examinations, surveillance intervals, and rates of false-negative results, it “supports the hypothesis that examination duration affects the diagnostic accuracy of EGD,” Dr. Park and his coinvestigators reported. “Prolonging the examination time will allow more careful examination by the endoscopist, which will enable the detection of more subtle lesions. Based on our data, we believe that these indicators can improve the quality of EGD.”

Funders included the Ministry of Education, Science, and Technology; the Ministry of Science, ICT, and Future Planning; and the Ministry of Health & Welfare, Republic of Korea. The investigators reported having no conflicts of interest.

Endoscopists who took about a minute longer during screening esophagogastroduodenoscopy (EGD) detected significantly more upper gastrointestinal neoplasms than their quicker colleagues, in a retrospective study reported in the August issue of Gastroenterology (doi: 10.1053/j.gastro.2017.05.009).

Detection rates were 0.28% and 0.20%, respectively (P = .005), and this difference remained statistically significant after the investigators controlled for numerous factors that also can affect the chances of detecting gastric neoplasms during upper endoscopy, reported Jae Myung Park, MD, and his colleagues at Seoul (Korea) St. Mary’s Hospital.

Gastric cancer is the second leading cause of cancer mortality worldwide, they noted. Although EGD has been practiced globally for decades, there is no consensus on which performance metrics optimize diagnostic yield. Both Korea and Japan have adopted screening EGD to help diagnose gastric cancer, but interval cancers and false-positive results remain concerns, and the field lacks rigorous analyses comparing EGD time with gastric cancer detection rates. Therefore, the researchers studied 111,962 consecutive patients who underwent EGD at one hospital in Seoul from 2009 through 2015. Fourteen board-certified endoscopists performed these procedures at a single endoscopy unit.A total of 262 patients (0.23%) were diagnosed with gastric neoplasia or dysplasia, duodenal neoplasia, or esophageal carcinoma. This finding closely resembled a prior report from Korea, the investigators noted. Detection rates among individual endoscopists ranged from 0.14% to 0.32%, and longer EGD time was associated with a higher detection rate with an R value of 0.54 (P = .046). During the first year of the study, EGDs without biopsies averaged 2 minutes, 53 seconds. Based on this finding, the researchers set a cutoff time of 3 minutes and classified eight endoscopists as fast (mean EGD duration, 2 minutes and 38 seconds; standard deviation, 21 seconds) and six endoscopists as slow (mean duration, 3 minutes and 25 seconds; SD, 19 seconds). Slower endoscopists were significantly more likely to detect gastric adenomas or carcinomas, even after the investigators controlled for the biopsy rates and experience level of these endoscopists and patients’ age, sex, smoking status, alcohol use, and family history of cancer (odds ratio, 1.52; 95% confidence interval, 1.17-1.97; P = .0018).

Older age, male sex, and smoking also were significant correlates of cancer detection in the multivariable model. Biopsy rates among endoscopists ranged from 7% to 28%, and taking a biopsy was an even stronger predictor of detecting an upper GI neoplasm than was EGD duration, with an R value of 0.76 (P = .002). Although this study was observational and retrospective and lacked data on prior EGD examinations, surveillance intervals, and rates of false-negative results, it “supports the hypothesis that examination duration affects the diagnostic accuracy of EGD,” Dr. Park and his coinvestigators reported. “Prolonging the examination time will allow more careful examination by the endoscopist, which will enable the detection of more subtle lesions. Based on our data, we believe that these indicators can improve the quality of EGD.”

Funders included the Ministry of Education, Science, and Technology; the Ministry of Science, ICT, and Future Planning; and the Ministry of Health & Welfare, Republic of Korea. The investigators reported having no conflicts of interest.

Endoscopists who took about a minute longer during screening esophagogastroduodenoscopy (EGD) detected significantly more upper gastrointestinal neoplasms than their quicker colleagues, in a retrospective study reported in the August issue of Gastroenterology (doi: 10.1053/j.gastro.2017.05.009).

Detection rates were 0.28% and 0.20%, respectively (P = .005), and this difference remained statistically significant after the investigators controlled for numerous factors that also can affect the chances of detecting gastric neoplasms during upper endoscopy, reported Jae Myung Park, MD, and his colleagues at Seoul (Korea) St. Mary’s Hospital.

Gastric cancer is the second leading cause of cancer mortality worldwide, they noted. Although EGD has been practiced globally for decades, there is no consensus on which performance metrics optimize diagnostic yield. Both Korea and Japan have adopted screening EGD to help diagnose gastric cancer, but interval cancers and false-positive results remain concerns, and the field lacks rigorous analyses comparing EGD time with gastric cancer detection rates. Therefore, the researchers studied 111,962 consecutive patients who underwent EGD at one hospital in Seoul from 2009 through 2015. Fourteen board-certified endoscopists performed these procedures at a single endoscopy unit.A total of 262 patients (0.23%) were diagnosed with gastric neoplasia or dysplasia, duodenal neoplasia, or esophageal carcinoma. This finding closely resembled a prior report from Korea, the investigators noted. Detection rates among individual endoscopists ranged from 0.14% to 0.32%, and longer EGD time was associated with a higher detection rate with an R value of 0.54 (P = .046). During the first year of the study, EGDs without biopsies averaged 2 minutes, 53 seconds. Based on this finding, the researchers set a cutoff time of 3 minutes and classified eight endoscopists as fast (mean EGD duration, 2 minutes and 38 seconds; standard deviation, 21 seconds) and six endoscopists as slow (mean duration, 3 minutes and 25 seconds; SD, 19 seconds). Slower endoscopists were significantly more likely to detect gastric adenomas or carcinomas, even after the investigators controlled for the biopsy rates and experience level of these endoscopists and patients’ age, sex, smoking status, alcohol use, and family history of cancer (odds ratio, 1.52; 95% confidence interval, 1.17-1.97; P = .0018).

Older age, male sex, and smoking also were significant correlates of cancer detection in the multivariable model. Biopsy rates among endoscopists ranged from 7% to 28%, and taking a biopsy was an even stronger predictor of detecting an upper GI neoplasm than was EGD duration, with an R value of 0.76 (P = .002). Although this study was observational and retrospective and lacked data on prior EGD examinations, surveillance intervals, and rates of false-negative results, it “supports the hypothesis that examination duration affects the diagnostic accuracy of EGD,” Dr. Park and his coinvestigators reported. “Prolonging the examination time will allow more careful examination by the endoscopist, which will enable the detection of more subtle lesions. Based on our data, we believe that these indicators can improve the quality of EGD.”

Funders included the Ministry of Education, Science, and Technology; the Ministry of Science, ICT, and Future Planning; and the Ministry of Health & Welfare, Republic of Korea. The investigators reported having no conflicts of interest.

SAN FRANCISCO – Teens who answered “no response” for one or more questions during a standard suicide screening in the ED typically have a risk of suicide nearly on par with those who answered “yes” to at least one question, results of a study showed.

“Risk for suicidality was substantial among both groups,” Tricia Hengehold of the University of Cincinnati reported at the Pediatric Academic Societies meeting. “About half of each group fit the medium-risk category, although the yes group had more teens in the high-risk category comparatively.”

Devonyu/Thinkstock

[email protected]

SAN FRANCISCO – Teens who answered “no response” for one or more questions during a standard suicide screening in the ED typically have a risk of suicide nearly on par with those who answered “yes” to at least one question, results of a study showed.

“Risk for suicidality was substantial among both groups,” Tricia Hengehold of the University of Cincinnati reported at the Pediatric Academic Societies meeting. “About half of each group fit the medium-risk category, although the yes group had more teens in the high-risk category comparatively.”

Devonyu/Thinkstock

[email protected]

SAN FRANCISCO – Teens who answered “no response” for one or more questions during a standard suicide screening in the ED typically have a risk of suicide nearly on par with those who answered “yes” to at least one question, results of a study showed.

“Risk for suicidality was substantial among both groups,” Tricia Hengehold of the University of Cincinnati reported at the Pediatric Academic Societies meeting. “About half of each group fit the medium-risk category, although the yes group had more teens in the high-risk category comparatively.”

Devonyu/Thinkstock

[email protected]

Case

An Asian man in his third decade, with a medical history of hypertension and hyperlipidemia, and who had recently been involved in a motor vehicle collision (MVC), presented to the ED with a chief complaint of severe bilateral upper and lower extremity weakness. The patient noted that the weakness had begun the previous evening and became progressively worse throughout the night, to the point that he was unable to move any of his extremities on the morning of presentation.

Upon arrival at the ED, the patient was awake, alert, and oriented to self, time, and place; he also spoke in full sentences without distress. He denied fever, chills, difficulty breathing, or preceding viral illness. The patient stated that he was not taking any medications and denied a history of alcohol, tobacco, or drug abuse.

Initial vital signs at presentation were: blood pressure, 141/50 mm Hg; heart rate, 90 beats/min; respiratory rate, 16 breaths/min; and temperature, 97.4°F. Oxygen saturation was 100% on room air. On physical examination, the patient was in no acute distress and had a normal mental status. His pupils were normally reactive and his other cranial nerves were normal. Muscle strength in the upper and lower extremities was 1/5 with 1+ reflexes bilaterally, and there was no sensory deficit. The patient was placed on continuous cardiac monitoring with pulse oximetry.

What is the differential diagnosis for acute extremity weakness or paralysis?

The differential diagnosis for acute symmetrical extremity weakness or paralysis is broad and includes conditions of neurological, inflammatory, and toxic/metabolic etiologies.¹ Neurological diagnoses to consider include acute stroke, specifically of the anterior cerebral or middle cerebral artery territories; Guillain-Barré syndrome; myasthenia gravis; spinal cord compression; and tick paralysis. Acute ischemic or hemorrhagic stroke most frequently presents with unilateral upper or lower extremity weakness accompanied by garbled speech and sensory deficits. Patients who have suffered a brainstem or cerebellar stroke commonly present with alterations of consciousness, visual changes, and ataxia. Posterior circulation strokes are also characterized by crossed neurological deficits, such as motor deficits on one side of the body and sensory deficits on the other.

Spinal Cord Pathology. Signs and symptoms of spinal cord compression or inflammation vary widely depending on the level affected. Motor and sensory findings of spinal cord pathology include muscle weakness, spasticity, hyper- or hyporeflexia, and a discrete level below which sensation is absent or reduced.

Guillain-Barré Syndrome. Patients who have Guillain-Barré syndrome (a disease of the myelin sheaths of the peripheral nerves) often present with complaints of numbness or paresthesias in the extremities.² The condition is characterized by progressive symmetric muscle weakness accompanied by absent or depressed deep tendon reflexes and is typically associated with a recent exposure to an infectious agent such as a viral upper respiratory infection, bacterial infection, or vaccine.

Myasthenia Gravis. Myasthenia gravis is a disease of the neuromuscular junction. It presents with weakness in any muscle group, and the muscles are easily fatigued by repetitive use.

Toxic Exposures. Toxins, such as botulinum, ixovotoxin, nicotine, succinylcholine, and tetrodotoxin, are prominent, though less common, causes of muscular weakness or paralysis. Botulinum toxin acts at the neuromuscular junction. Patients with botulism typically present with a gastrointestinal prodrome of nausea, vomiting, and diarrhea followed by cranial nerve dysfunction and descending muscle weakness.³

Tetrodotoxin, nicotine, and curare-like paralytics act at the motor end plate of the neuromuscular junction to produce neuromuscular blockade with subsequent muscular weakness or paralysis. Similarly, ixovotoxin, the toxin responsible for tick paralysis, causes ascending flaccid paralysis by decreasing the release of acetylcholine at the neuromuscular junction.³

Metabolic and Endocrine Disorders. Conditions such as hypokalemia, hypomagnesemia, and periodic paralysis can also present with neurological complaints such as generalized weakness and paresthesias. Of note, it is important to differentiate true neuromuscular weakness from weakness secondary to limited effort.

Case Continuation

Because of the patient’s history of an MVC, cervical cord compression was considered concerning enough to require exclusion through magnetic resonance imaging (MRI) of the cervical spine. However, upon arrival at the MRI suite, the patient became severely tachypneic and tachycardic, and was unable to tolerate lying flat. He was intubated for impending respiratory failure. Laboratory results from blood drawn prior to transport to MRI were reported immediately after the resuscitation and were notable for the following: potassium, <1.5 mEq/L; bicarbonate, 20 mEq/L; creatine kinase, 889 U/L; ethanol, not detected.

What is hypokalemic periodic paralysis?

Hypokalemic periodic paralysis (HypoKPP) is a syndrome of episodic muscle weakness with concomitant hypokalemia. Familial forms of HypoKPP have been attributed to mutations in genes coding for either calcium or sodium channels.

The nonfamilial form of HypoKPP is attributed to hyperthyroidism and is most often seen in Asian men in the second and third decades of life. The disorder is characterized by acute onset hypokalemia and extremity paralysis with simultaneous hyperthyroid state. It is believed that hypokalemia occurs as a result of intracellular shift of potassium from thyroid-induced hormone sensitization of the Na⁺/K⁺-ATPase rather than a depletion of total body potassium. Acute episodes of paralysis are triggered by high-carbohydrate meals, alcohol consumption, emotional stress, and infection. Paralysis can last from 3 to 96 hours and is accompanied by decreased or absent deep tendon reflexes with normal sensation and mental status.

In the nonfamilial form of HypoKPP, signs of thyrotoxicosis are often present and include tachycardia, moist skin, and hyperthermia, but it may be difficult to specifically recognize this etiology given the patient’s grave clinical condition.⁴ Similar to many significant metabolic and electrolyte disturbances, complications of HypoKPP include dysrhythmia, respiratory failure, and sometimes death.⁵

How should HypoKPP be managed in the ED?

Management of HypoKPP begins with careful assessment of the patient’s airway, breathing, and circulation. Once the patient is stabilized, management of consequential effects of hypokalemia, such as respiratory distress and muscular paralysis, should focus on correcting the electrolyte and endocrine derangements.

Propranolol. If the patient exhibits signs of thyrotoxicosis, initial treatment includes propranolol, a nonselective beta-blocker, which both prevents the intracellular shift of potassium and assists in correcting the underlying hyperthyroid and hypermetabolic state. Although there is no standard propranolol dosing protocol for HypoKPP, some authors suggest that an aggressive dose of 2 mg intravenously (IV) every 10 minutes can shorten the patient’s episode of paralysis to 6 hours.⁶

Potassium Chloride. Administration of potassium chloride to raise the serum potassium to life-sustaining concentrations should be done cautiously through IV infusion of standard doses.⁷ In correcting hypokalemia with potassium, care should be taken to avoid overcorrection, which may subsequently result in rebound hyperkalemia as the total body potassium redistributes. Lower doses of potassium (ie, <50 mEq per dose), are preferred to achieve adequate repletion while avoiding rebound hyperkalemia.⁸

Case Conclusion

The results of thyroid studies that had been added on to the original set of laboratory studies revealed profound hyperthyroidism, with an essentially absent concentration of thyroid-stimulating hormone.

Case

An Asian man in his third decade, with a medical history of hypertension and hyperlipidemia, and who had recently been involved in a motor vehicle collision (MVC), presented to the ED with a chief complaint of severe bilateral upper and lower extremity weakness. The patient noted that the weakness had begun the previous evening and became progressively worse throughout the night, to the point that he was unable to move any of his extremities on the morning of presentation.

Upon arrival at the ED, the patient was awake, alert, and oriented to self, time, and place; he also spoke in full sentences without distress. He denied fever, chills, difficulty breathing, or preceding viral illness. The patient stated that he was not taking any medications and denied a history of alcohol, tobacco, or drug abuse.

Initial vital signs at presentation were: blood pressure, 141/50 mm Hg; heart rate, 90 beats/min; respiratory rate, 16 breaths/min; and temperature, 97.4°F. Oxygen saturation was 100% on room air. On physical examination, the patient was in no acute distress and had a normal mental status. His pupils were normally reactive and his other cranial nerves were normal. Muscle strength in the upper and lower extremities was 1/5 with 1+ reflexes bilaterally, and there was no sensory deficit. The patient was placed on continuous cardiac monitoring with pulse oximetry.

What is the differential diagnosis for acute extremity weakness or paralysis?

The differential diagnosis for acute symmetrical extremity weakness or paralysis is broad and includes conditions of neurological, inflammatory, and toxic/metabolic etiologies.¹ Neurological diagnoses to consider include acute stroke, specifically of the anterior cerebral or middle cerebral artery territories; Guillain-Barré syndrome; myasthenia gravis; spinal cord compression; and tick paralysis. Acute ischemic or hemorrhagic stroke most frequently presents with unilateral upper or lower extremity weakness accompanied by garbled speech and sensory deficits. Patients who have suffered a brainstem or cerebellar stroke commonly present with alterations of consciousness, visual changes, and ataxia. Posterior circulation strokes are also characterized by crossed neurological deficits, such as motor deficits on one side of the body and sensory deficits on the other.

Spinal Cord Pathology. Signs and symptoms of spinal cord compression or inflammation vary widely depending on the level affected. Motor and sensory findings of spinal cord pathology include muscle weakness, spasticity, hyper- or hyporeflexia, and a discrete level below which sensation is absent or reduced.

Guillain-Barré Syndrome. Patients who have Guillain-Barré syndrome (a disease of the myelin sheaths of the peripheral nerves) often present with complaints of numbness or paresthesias in the extremities.² The condition is characterized by progressive symmetric muscle weakness accompanied by absent or depressed deep tendon reflexes and is typically associated with a recent exposure to an infectious agent such as a viral upper respiratory infection, bacterial infection, or vaccine.

Myasthenia Gravis. Myasthenia gravis is a disease of the neuromuscular junction. It presents with weakness in any muscle group, and the muscles are easily fatigued by repetitive use.

Toxic Exposures. Toxins, such as botulinum, ixovotoxin, nicotine, succinylcholine, and tetrodotoxin, are prominent, though less common, causes of muscular weakness or paralysis. Botulinum toxin acts at the neuromuscular junction. Patients with botulism typically present with a gastrointestinal prodrome of nausea, vomiting, and diarrhea followed by cranial nerve dysfunction and descending muscle weakness.³

Tetrodotoxin, nicotine, and curare-like paralytics act at the motor end plate of the neuromuscular junction to produce neuromuscular blockade with subsequent muscular weakness or paralysis. Similarly, ixovotoxin, the toxin responsible for tick paralysis, causes ascending flaccid paralysis by decreasing the release of acetylcholine at the neuromuscular junction.³

Metabolic and Endocrine Disorders. Conditions such as hypokalemia, hypomagnesemia, and periodic paralysis can also present with neurological complaints such as generalized weakness and paresthesias. Of note, it is important to differentiate true neuromuscular weakness from weakness secondary to limited effort.

Case Continuation

Because of the patient’s history of an MVC, cervical cord compression was considered concerning enough to require exclusion through magnetic resonance imaging (MRI) of the cervical spine. However, upon arrival at the MRI suite, the patient became severely tachypneic and tachycardic, and was unable to tolerate lying flat. He was intubated for impending respiratory failure. Laboratory results from blood drawn prior to transport to MRI were reported immediately after the resuscitation and were notable for the following: potassium, <1.5 mEq/L; bicarbonate, 20 mEq/L; creatine kinase, 889 U/L; ethanol, not detected.

What is hypokalemic periodic paralysis?

Hypokalemic periodic paralysis (HypoKPP) is a syndrome of episodic muscle weakness with concomitant hypokalemia. Familial forms of HypoKPP have been attributed to mutations in genes coding for either calcium or sodium channels.

The nonfamilial form of HypoKPP is attributed to hyperthyroidism and is most often seen in Asian men in the second and third decades of life. The disorder is characterized by acute onset hypokalemia and extremity paralysis with simultaneous hyperthyroid state. It is believed that hypokalemia occurs as a result of intracellular shift of potassium from thyroid-induced hormone sensitization of the Na⁺/K⁺-ATPase rather than a depletion of total body potassium. Acute episodes of paralysis are triggered by high-carbohydrate meals, alcohol consumption, emotional stress, and infection. Paralysis can last from 3 to 96 hours and is accompanied by decreased or absent deep tendon reflexes with normal sensation and mental status.

In the nonfamilial form of HypoKPP, signs of thyrotoxicosis are often present and include tachycardia, moist skin, and hyperthermia, but it may be difficult to specifically recognize this etiology given the patient’s grave clinical condition.⁴ Similar to many significant metabolic and electrolyte disturbances, complications of HypoKPP include dysrhythmia, respiratory failure, and sometimes death.⁵

How should HypoKPP be managed in the ED?

Management of HypoKPP begins with careful assessment of the patient’s airway, breathing, and circulation. Once the patient is stabilized, management of consequential effects of hypokalemia, such as respiratory distress and muscular paralysis, should focus on correcting the electrolyte and endocrine derangements.

Propranolol. If the patient exhibits signs of thyrotoxicosis, initial treatment includes propranolol, a nonselective beta-blocker, which both prevents the intracellular shift of potassium and assists in correcting the underlying hyperthyroid and hypermetabolic state. Although there is no standard propranolol dosing protocol for HypoKPP, some authors suggest that an aggressive dose of 2 mg intravenously (IV) every 10 minutes can shorten the patient’s episode of paralysis to 6 hours.⁶

Potassium Chloride. Administration of potassium chloride to raise the serum potassium to life-sustaining concentrations should be done cautiously through IV infusion of standard doses.⁷ In correcting hypokalemia with potassium, care should be taken to avoid overcorrection, which may subsequently result in rebound hyperkalemia as the total body potassium redistributes. Lower doses of potassium (ie, <50 mEq per dose), are preferred to achieve adequate repletion while avoiding rebound hyperkalemia.⁸

Case Conclusion

The results of thyroid studies that had been added on to the original set of laboratory studies revealed profound hyperthyroidism, with an essentially absent concentration of thyroid-stimulating hormone.

Case

An Asian man in his third decade, with a medical history of hypertension and hyperlipidemia, and who had recently been involved in a motor vehicle collision (MVC), presented to the ED with a chief complaint of severe bilateral upper and lower extremity weakness. The patient noted that the weakness had begun the previous evening and became progressively worse throughout the night, to the point that he was unable to move any of his extremities on the morning of presentation.

Upon arrival at the ED, the patient was awake, alert, and oriented to self, time, and place; he also spoke in full sentences without distress. He denied fever, chills, difficulty breathing, or preceding viral illness. The patient stated that he was not taking any medications and denied a history of alcohol, tobacco, or drug abuse.

Initial vital signs at presentation were: blood pressure, 141/50 mm Hg; heart rate, 90 beats/min; respiratory rate, 16 breaths/min; and temperature, 97.4°F. Oxygen saturation was 100% on room air. On physical examination, the patient was in no acute distress and had a normal mental status. His pupils were normally reactive and his other cranial nerves were normal. Muscle strength in the upper and lower extremities was 1/5 with 1+ reflexes bilaterally, and there was no sensory deficit. The patient was placed on continuous cardiac monitoring with pulse oximetry.

What is the differential diagnosis for acute extremity weakness or paralysis?

The differential diagnosis for acute symmetrical extremity weakness or paralysis is broad and includes conditions of neurological, inflammatory, and toxic/metabolic etiologies.¹ Neurological diagnoses to consider include acute stroke, specifically of the anterior cerebral or middle cerebral artery territories; Guillain-Barré syndrome; myasthenia gravis; spinal cord compression; and tick paralysis. Acute ischemic or hemorrhagic stroke most frequently presents with unilateral upper or lower extremity weakness accompanied by garbled speech and sensory deficits. Patients who have suffered a brainstem or cerebellar stroke commonly present with alterations of consciousness, visual changes, and ataxia. Posterior circulation strokes are also characterized by crossed neurological deficits, such as motor deficits on one side of the body and sensory deficits on the other.

Spinal Cord Pathology. Signs and symptoms of spinal cord compression or inflammation vary widely depending on the level affected. Motor and sensory findings of spinal cord pathology include muscle weakness, spasticity, hyper- or hyporeflexia, and a discrete level below which sensation is absent or reduced.

Guillain-Barré Syndrome. Patients who have Guillain-Barré syndrome (a disease of the myelin sheaths of the peripheral nerves) often present with complaints of numbness or paresthesias in the extremities.² The condition is characterized by progressive symmetric muscle weakness accompanied by absent or depressed deep tendon reflexes and is typically associated with a recent exposure to an infectious agent such as a viral upper respiratory infection, bacterial infection, or vaccine.

Myasthenia Gravis. Myasthenia gravis is a disease of the neuromuscular junction. It presents with weakness in any muscle group, and the muscles are easily fatigued by repetitive use.

Toxic Exposures. Toxins, such as botulinum, ixovotoxin, nicotine, succinylcholine, and tetrodotoxin, are prominent, though less common, causes of muscular weakness or paralysis. Botulinum toxin acts at the neuromuscular junction. Patients with botulism typically present with a gastrointestinal prodrome of nausea, vomiting, and diarrhea followed by cranial nerve dysfunction and descending muscle weakness.³

Tetrodotoxin, nicotine, and curare-like paralytics act at the motor end plate of the neuromuscular junction to produce neuromuscular blockade with subsequent muscular weakness or paralysis. Similarly, ixovotoxin, the toxin responsible for tick paralysis, causes ascending flaccid paralysis by decreasing the release of acetylcholine at the neuromuscular junction.³

Metabolic and Endocrine Disorders. Conditions such as hypokalemia, hypomagnesemia, and periodic paralysis can also present with neurological complaints such as generalized weakness and paresthesias. Of note, it is important to differentiate true neuromuscular weakness from weakness secondary to limited effort.

Case Continuation

Because of the patient’s history of an MVC, cervical cord compression was considered concerning enough to require exclusion through magnetic resonance imaging (MRI) of the cervical spine. However, upon arrival at the MRI suite, the patient became severely tachypneic and tachycardic, and was unable to tolerate lying flat. He was intubated for impending respiratory failure. Laboratory results from blood drawn prior to transport to MRI were reported immediately after the resuscitation and were notable for the following: potassium, <1.5 mEq/L; bicarbonate, 20 mEq/L; creatine kinase, 889 U/L; ethanol, not detected.

What is hypokalemic periodic paralysis?

Hypokalemic periodic paralysis (HypoKPP) is a syndrome of episodic muscle weakness with concomitant hypokalemia. Familial forms of HypoKPP have been attributed to mutations in genes coding for either calcium or sodium channels.

The nonfamilial form of HypoKPP is attributed to hyperthyroidism and is most often seen in Asian men in the second and third decades of life. The disorder is characterized by acute onset hypokalemia and extremity paralysis with simultaneous hyperthyroid state. It is believed that hypokalemia occurs as a result of intracellular shift of potassium from thyroid-induced hormone sensitization of the Na⁺/K⁺-ATPase rather than a depletion of total body potassium. Acute episodes of paralysis are triggered by high-carbohydrate meals, alcohol consumption, emotional stress, and infection. Paralysis can last from 3 to 96 hours and is accompanied by decreased or absent deep tendon reflexes with normal sensation and mental status.

In the nonfamilial form of HypoKPP, signs of thyrotoxicosis are often present and include tachycardia, moist skin, and hyperthermia, but it may be difficult to specifically recognize this etiology given the patient’s grave clinical condition.⁴ Similar to many significant metabolic and electrolyte disturbances, complications of HypoKPP include dysrhythmia, respiratory failure, and sometimes death.⁵

How should HypoKPP be managed in the ED?

Management of HypoKPP begins with careful assessment of the patient’s airway, breathing, and circulation. Once the patient is stabilized, management of consequential effects of hypokalemia, such as respiratory distress and muscular paralysis, should focus on correcting the electrolyte and endocrine derangements.

Propranolol. If the patient exhibits signs of thyrotoxicosis, initial treatment includes propranolol, a nonselective beta-blocker, which both prevents the intracellular shift of potassium and assists in correcting the underlying hyperthyroid and hypermetabolic state. Although there is no standard propranolol dosing protocol for HypoKPP, some authors suggest that an aggressive dose of 2 mg intravenously (IV) every 10 minutes can shorten the patient’s episode of paralysis to 6 hours.⁶

Potassium Chloride. Administration of potassium chloride to raise the serum potassium to life-sustaining concentrations should be done cautiously through IV infusion of standard doses.⁷ In correcting hypokalemia with potassium, care should be taken to avoid overcorrection, which may subsequently result in rebound hyperkalemia as the total body potassium redistributes. Lower doses of potassium (ie, <50 mEq per dose), are preferred to achieve adequate repletion while avoiding rebound hyperkalemia.⁸

Case Conclusion

The results of thyroid studies that had been added on to the original set of laboratory studies revealed profound hyperthyroidism, with an essentially absent concentration of thyroid-stimulating hormone.

WASHINGTON – If patients have sleep disordered breathing with obstructive sleep apnea, will its treatment have cardiovascular disease benefits, especially in terms of the incidence or severity of atrial fibrillation?

Observational evidence suggests that apnea interventions may help these patients, but no clear case yet exists to prove that a breathing intervention works, experts say, and, as a result, U.S. practice is mixed when it comes to using treatment for obstructive sleep apnea (OSA), specifically continuous positive airway pressure (CPAP), to prevent or treat atrial fibrillation.

[email protected]

On Twitter @mitchelzoler

This article was updated on 7/10/17.

WASHINGTON – If patients have sleep disordered breathing with obstructive sleep apnea, will its treatment have cardiovascular disease benefits, especially in terms of the incidence or severity of atrial fibrillation?

Observational evidence suggests that apnea interventions may help these patients, but no clear case yet exists to prove that a breathing intervention works, experts say, and, as a result, U.S. practice is mixed when it comes to using treatment for obstructive sleep apnea (OSA), specifically continuous positive airway pressure (CPAP), to prevent or treat atrial fibrillation.

[email protected]

On Twitter @mitchelzoler

This article was updated on 7/10/17.

WASHINGTON – If patients have sleep disordered breathing with obstructive sleep apnea, will its treatment have cardiovascular disease benefits, especially in terms of the incidence or severity of atrial fibrillation?

Observational evidence suggests that apnea interventions may help these patients, but no clear case yet exists to prove that a breathing intervention works, experts say, and, as a result, U.S. practice is mixed when it comes to using treatment for obstructive sleep apnea (OSA), specifically continuous positive airway pressure (CPAP), to prevent or treat atrial fibrillation.

[email protected]

On Twitter @mitchelzoler

This article was updated on 7/10/17.

A 46-year-old man with a remote history of general tonic-clonic seizures, for which he was taking phenytoin, presented to the ED 30 minutes after sustaining a witnessed mechanical fall. The patient had fallen onto his nondominant left hand, which resulted in an injury to his elbow. He reported neither losing consciousness nor experiencing any seizures following the incident. He denied dislocating the joint or sustaining any other injuries from the fall. He also denied a history of past left elbow injury.

The patient was alert, oriented, and provided a full history of the incident. Regarding medical history, he stated that his last seizure had occurred 10 years prior. Except for the left elbow pain, a review of his systems was negative. The patient appeared in no acute distress, and supported his left upper extremity with a bandana and his right hand.

The patient’s vital signs were normal. The physical examination was negative except for the left elbow, which had significant swelling and limited range of motion without skin break, leading to suspicion for a prehospital dislocation with self-reduction. The joints above, below, and at the injury site were assessed for neurovascular injury.

Discussion

There is a paucity of information on vascular injury from elbow dislocation in the emergency medicine literature. A recent literature search referenced orthopedic pitfalls in the ED,¹ but most data appear in the orthopedic and vascular literature. A case report from the orthopedic literature in Brazil cites a vascular injury after ED relocation of a dislocated elbow following an assault.²

The elbow is the second most commonly dislocated joint (not including the patella) after the shoulder.³ Posterior dislocations make up the majority of these injuries. Simple versus complex injuries can be differentiated by the presence or absence of fracture.⁴ Simple complications include stiffness; loss of mobility, especially with full extension; neurovascular injuries; and compartment syndrome. Complex injuries involve fractures and potential neurovascular injuries, stiffness, pain, and loss of mobility.

Soft tissue injuries, fractures, and neurovascular complaints represent the majority of ED encounters, and are commonly related to falls. The elbow is the articulation of the humerus, ulna, and radius bones. Range of motion includes, but is not limited to, flexion, extension, supination, and pronation. Tears in the lateral ulnar ligament, joint capsule, and medial collateral ligament lead to instability of the joint and increase risk of dislocation.

Fractures make up to 20% of injuries to the elbow. These include fractures of the radial head and neck (most common), olecranon, and distal humerus.⁵ Open elbow fractures are rare, as are vascular injuries (5%-13% of cases).⁶ When present, vascular elbow injuries usually involve the brachial artery, and display abnormal palpable and Doppler assessment of the brachial and radial arteries.⁶

Nerve injuries may include injury to the radial nerve. Manifestations of radial nerve injury include abnormal sensation to the dorsum of the hand, trouble straightening the arm, and wrist-drop. Ulnar nerve injury typically presents with abnormal sensation to the fourth and fifth digits and decreased grip strength.

Conclusion

Vascular abnormalities are rare complications following elbow injuries. Our patient sustained a lacerated brachial artery, which was repaired via saphenous graft; brachial and basilic vein lacerations, which were ligated; and an avulsion fracture with an unstable joint, which was stabilized with external fixation and stabilization. He was discharged the following day with full neurovascular function.

A methodical approach to assessing patients presenting with elbow injury is essential to making the correct diagnosis. This should include a careful evaluation of the joints above and below the area of injury, as well as attention to the neurovascular examination, with a heightened suspicion for a vascular abnormality in complex injuries. Doppler and ultrasound evaluation with multiple rechecks can assist with the diagnosis. Our patient was rapidly assessed with a concern for a vascular injury, and was emergently referred to vascular surgery for repair of the brachial artery and stabilization of the joint.

A 46-year-old man with a remote history of general tonic-clonic seizures, for which he was taking phenytoin, presented to the ED 30 minutes after sustaining a witnessed mechanical fall. The patient had fallen onto his nondominant left hand, which resulted in an injury to his elbow. He reported neither losing consciousness nor experiencing any seizures following the incident. He denied dislocating the joint or sustaining any other injuries from the fall. He also denied a history of past left elbow injury.

The patient was alert, oriented, and provided a full history of the incident. Regarding medical history, he stated that his last seizure had occurred 10 years prior. Except for the left elbow pain, a review of his systems was negative. The patient appeared in no acute distress, and supported his left upper extremity with a bandana and his right hand.

The patient’s vital signs were normal. The physical examination was negative except for the left elbow, which had significant swelling and limited range of motion without skin break, leading to suspicion for a prehospital dislocation with self-reduction. The joints above, below, and at the injury site were assessed for neurovascular injury.

Discussion

There is a paucity of information on vascular injury from elbow dislocation in the emergency medicine literature. A recent literature search referenced orthopedic pitfalls in the ED,¹ but most data appear in the orthopedic and vascular literature. A case report from the orthopedic literature in Brazil cites a vascular injury after ED relocation of a dislocated elbow following an assault.²

The elbow is the second most commonly dislocated joint (not including the patella) after the shoulder.³ Posterior dislocations make up the majority of these injuries. Simple versus complex injuries can be differentiated by the presence or absence of fracture.⁴ Simple complications include stiffness; loss of mobility, especially with full extension; neurovascular injuries; and compartment syndrome. Complex injuries involve fractures and potential neurovascular injuries, stiffness, pain, and loss of mobility.

Soft tissue injuries, fractures, and neurovascular complaints represent the majority of ED encounters, and are commonly related to falls. The elbow is the articulation of the humerus, ulna, and radius bones. Range of motion includes, but is not limited to, flexion, extension, supination, and pronation. Tears in the lateral ulnar ligament, joint capsule, and medial collateral ligament lead to instability of the joint and increase risk of dislocation.

Fractures make up to 20% of injuries to the elbow. These include fractures of the radial head and neck (most common), olecranon, and distal humerus.⁵ Open elbow fractures are rare, as are vascular injuries (5%-13% of cases).⁶ When present, vascular elbow injuries usually involve the brachial artery, and display abnormal palpable and Doppler assessment of the brachial and radial arteries.⁶

Nerve injuries may include injury to the radial nerve. Manifestations of radial nerve injury include abnormal sensation to the dorsum of the hand, trouble straightening the arm, and wrist-drop. Ulnar nerve injury typically presents with abnormal sensation to the fourth and fifth digits and decreased grip strength.

Conclusion

Vascular abnormalities are rare complications following elbow injuries. Our patient sustained a lacerated brachial artery, which was repaired via saphenous graft; brachial and basilic vein lacerations, which were ligated; and an avulsion fracture with an unstable joint, which was stabilized with external fixation and stabilization. He was discharged the following day with full neurovascular function.

A methodical approach to assessing patients presenting with elbow injury is essential to making the correct diagnosis. This should include a careful evaluation of the joints above and below the area of injury, as well as attention to the neurovascular examination, with a heightened suspicion for a vascular abnormality in complex injuries. Doppler and ultrasound evaluation with multiple rechecks can assist with the diagnosis. Our patient was rapidly assessed with a concern for a vascular injury, and was emergently referred to vascular surgery for repair of the brachial artery and stabilization of the joint.

A 46-year-old man with a remote history of general tonic-clonic seizures, for which he was taking phenytoin, presented to the ED 30 minutes after sustaining a witnessed mechanical fall. The patient had fallen onto his nondominant left hand, which resulted in an injury to his elbow. He reported neither losing consciousness nor experiencing any seizures following the incident. He denied dislocating the joint or sustaining any other injuries from the fall. He also denied a history of past left elbow injury.

The patient was alert, oriented, and provided a full history of the incident. Regarding medical history, he stated that his last seizure had occurred 10 years prior. Except for the left elbow pain, a review of his systems was negative. The patient appeared in no acute distress, and supported his left upper extremity with a bandana and his right hand.

The patient’s vital signs were normal. The physical examination was negative except for the left elbow, which had significant swelling and limited range of motion without skin break, leading to suspicion for a prehospital dislocation with self-reduction. The joints above, below, and at the injury site were assessed for neurovascular injury.

Discussion

There is a paucity of information on vascular injury from elbow dislocation in the emergency medicine literature. A recent literature search referenced orthopedic pitfalls in the ED,¹ but most data appear in the orthopedic and vascular literature. A case report from the orthopedic literature in Brazil cites a vascular injury after ED relocation of a dislocated elbow following an assault.²

The elbow is the second most commonly dislocated joint (not including the patella) after the shoulder.³ Posterior dislocations make up the majority of these injuries. Simple versus complex injuries can be differentiated by the presence or absence of fracture.⁴ Simple complications include stiffness; loss of mobility, especially with full extension; neurovascular injuries; and compartment syndrome. Complex injuries involve fractures and potential neurovascular injuries, stiffness, pain, and loss of mobility.

Soft tissue injuries, fractures, and neurovascular complaints represent the majority of ED encounters, and are commonly related to falls. The elbow is the articulation of the humerus, ulna, and radius bones. Range of motion includes, but is not limited to, flexion, extension, supination, and pronation. Tears in the lateral ulnar ligament, joint capsule, and medial collateral ligament lead to instability of the joint and increase risk of dislocation.

Fractures make up to 20% of injuries to the elbow. These include fractures of the radial head and neck (most common), olecranon, and distal humerus.⁵ Open elbow fractures are rare, as are vascular injuries (5%-13% of cases).⁶ When present, vascular elbow injuries usually involve the brachial artery, and display abnormal palpable and Doppler assessment of the brachial and radial arteries.⁶

Nerve injuries may include injury to the radial nerve. Manifestations of radial nerve injury include abnormal sensation to the dorsum of the hand, trouble straightening the arm, and wrist-drop. Ulnar nerve injury typically presents with abnormal sensation to the fourth and fifth digits and decreased grip strength.

Conclusion

Vascular abnormalities are rare complications following elbow injuries. Our patient sustained a lacerated brachial artery, which was repaired via saphenous graft; brachial and basilic vein lacerations, which were ligated; and an avulsion fracture with an unstable joint, which was stabilized with external fixation and stabilization. He was discharged the following day with full neurovascular function.

A methodical approach to assessing patients presenting with elbow injury is essential to making the correct diagnosis. This should include a careful evaluation of the joints above and below the area of injury, as well as attention to the neurovascular examination, with a heightened suspicion for a vascular abnormality in complex injuries. Doppler and ultrasound evaluation with multiple rechecks can assist with the diagnosis. Our patient was rapidly assessed with a concern for a vascular injury, and was emergently referred to vascular surgery for repair of the brachial artery and stabilization of the joint.

Identifying Characteristics

The sticktight flea (Echidnophaga gallinacea) earns its name by embedding its head in the host's skin using broad and serrated laciniae and can feed at one site for up to 19 days.¹ It differs in morphology from dog (Ctenocephalides canis) and cat (Ctenocephalides felis) fleas, lacking genal (mustache area) and promotal (back of the head) ctenidia (combs), and is half the size of the cat flea. It has 2 pairs of setae (hairs) behind the antennae with an anteriorly flattened head (Figure). 

Disease Transmission

Although its primary host is poultry and it also is known as the stickfast or chicken flea, the sticktight flea has been found in many species of birds and mammals, including humans. It is becoming more common in dogs in many parts of the world, including the United States,^2-5 and has been found to be the most common flea on dogs in areas of South Africa.⁶ Other noted hosts of E gallinacea are rodents, cottontail rabbits, cats, ground squirrels, and pigs.^7-14 Human infestation occurs from exposure to affected animals.¹⁵ As blood feeders, fleas have long been known to serve as vectors for many diseases, including bubonic plague, typhus, and tularemia, as well as an intermediate host of the dog tapeworm (Dipylidium caninum).⁵ Rickettsia felis, belonging to the spotted fever group, is an emerging infectious disease in humans commonly found in the cat flea (C felis) but also has been detected in E gallinacea.⁷ Echidnophaga gallinacea is found worldwide in the tropics, subtropics, and temperate zones, and it is the only representative of the genus found in the United States.¹ Given the wide range of wild and domestic animal hosts and wide geographic distribution for E gallinacea, it represents an increasing risk for humans.

Echidnophaga gallinacea favors feeding from fleshy areas without thick fur or plumage. In birds, the area around the eyes, comb, and wattles is included; in dogs, it can be the eyes, in between the toes, and in the genital area.¹ Flea bites cause irritation and itching for hosts including humans, typically resulting in clusters of firm, pruritic, erythematous papules with a central punctum.¹⁵ Severe bites also may lead to bullous lesions. In birds, symptoms can be extreme, with infestation around the eyes leading to swelling and blindness, a decline in egg production, weight loss, and death in young birds.¹ Similar to other fleas, E gallinacea is wingless and depends on jumping onto a host for transmission, which can be from the ground, carpeting and flooring, furniture, or another host. Fleas are champion jumpers (relative to body size) and can jump 100 times their length.¹⁶

Management

Treating sticktight fleas can be tricky, as they embed tightly into the host's skin. Animals should be treated by a qualified veterinarian. Removal of attached fleas in humans requires grasping the flea firmly with tweezers and pulling from the skin. If the infestation is considerable, malathion 5% liquid or gel can be applied. Patients can treat itching with topical steroids and antipruritic creams, and oral antihistamines can be used to relieve symptoms and reduce the likelihood of damaged skin as well as the potential for secondary infection. The flea-infested environment should be treated with insecticides. For treatment of hard surfaces, dichlorvos and propetamphos are effective. Organophosphates work well on fabric and carpeting. Domestic pets and livestock may be treated by a veterinarian with agents such as fipronil, selamectin, imidacloprid, metaflumizone, nitenpyram, lufenuron, methoprene, and pyriproxyfen.
 

Identifying Characteristics

The sticktight flea (Echidnophaga gallinacea) earns its name by embedding its head in the host's skin using broad and serrated laciniae and can feed at one site for up to 19 days.¹ It differs in morphology from dog (Ctenocephalides canis) and cat (Ctenocephalides felis) fleas, lacking genal (mustache area) and promotal (back of the head) ctenidia (combs), and is half the size of the cat flea. It has 2 pairs of setae (hairs) behind the antennae with an anteriorly flattened head (Figure). 

Disease Transmission

Although its primary host is poultry and it also is known as the stickfast or chicken flea, the sticktight flea has been found in many species of birds and mammals, including humans. It is becoming more common in dogs in many parts of the world, including the United States,^2-5 and has been found to be the most common flea on dogs in areas of South Africa.⁶ Other noted hosts of E gallinacea are rodents, cottontail rabbits, cats, ground squirrels, and pigs.^7-14 Human infestation occurs from exposure to affected animals.¹⁵ As blood feeders, fleas have long been known to serve as vectors for many diseases, including bubonic plague, typhus, and tularemia, as well as an intermediate host of the dog tapeworm (Dipylidium caninum).⁵ Rickettsia felis, belonging to the spotted fever group, is an emerging infectious disease in humans commonly found in the cat flea (C felis) but also has been detected in E gallinacea.⁷ Echidnophaga gallinacea is found worldwide in the tropics, subtropics, and temperate zones, and it is the only representative of the genus found in the United States.¹ Given the wide range of wild and domestic animal hosts and wide geographic distribution for E gallinacea, it represents an increasing risk for humans.

Echidnophaga gallinacea favors feeding from fleshy areas without thick fur or plumage. In birds, the area around the eyes, comb, and wattles is included; in dogs, it can be the eyes, in between the toes, and in the genital area.¹ Flea bites cause irritation and itching for hosts including humans, typically resulting in clusters of firm, pruritic, erythematous papules with a central punctum.¹⁵ Severe bites also may lead to bullous lesions. In birds, symptoms can be extreme, with infestation around the eyes leading to swelling and blindness, a decline in egg production, weight loss, and death in young birds.¹ Similar to other fleas, E gallinacea is wingless and depends on jumping onto a host for transmission, which can be from the ground, carpeting and flooring, furniture, or another host. Fleas are champion jumpers (relative to body size) and can jump 100 times their length.¹⁶

Management

Treating sticktight fleas can be tricky, as they embed tightly into the host's skin. Animals should be treated by a qualified veterinarian. Removal of attached fleas in humans requires grasping the flea firmly with tweezers and pulling from the skin. If the infestation is considerable, malathion 5% liquid or gel can be applied. Patients can treat itching with topical steroids and antipruritic creams, and oral antihistamines can be used to relieve symptoms and reduce the likelihood of damaged skin as well as the potential for secondary infection. The flea-infested environment should be treated with insecticides. For treatment of hard surfaces, dichlorvos and propetamphos are effective. Organophosphates work well on fabric and carpeting. Domestic pets and livestock may be treated by a veterinarian with agents such as fipronil, selamectin, imidacloprid, metaflumizone, nitenpyram, lufenuron, methoprene, and pyriproxyfen.
 

Identifying Characteristics

The sticktight flea (Echidnophaga gallinacea) earns its name by embedding its head in the host's skin using broad and serrated laciniae and can feed at one site for up to 19 days.¹ It differs in morphology from dog (Ctenocephalides canis) and cat (Ctenocephalides felis) fleas, lacking genal (mustache area) and promotal (back of the head) ctenidia (combs), and is half the size of the cat flea. It has 2 pairs of setae (hairs) behind the antennae with an anteriorly flattened head (Figure). 

Disease Transmission

Although its primary host is poultry and it also is known as the stickfast or chicken flea, the sticktight flea has been found in many species of birds and mammals, including humans. It is becoming more common in dogs in many parts of the world, including the United States,^2-5 and has been found to be the most common flea on dogs in areas of South Africa.⁶ Other noted hosts of E gallinacea are rodents, cottontail rabbits, cats, ground squirrels, and pigs.^7-14 Human infestation occurs from exposure to affected animals.¹⁵ As blood feeders, fleas have long been known to serve as vectors for many diseases, including bubonic plague, typhus, and tularemia, as well as an intermediate host of the dog tapeworm (Dipylidium caninum).⁵ Rickettsia felis, belonging to the spotted fever group, is an emerging infectious disease in humans commonly found in the cat flea (C felis) but also has been detected in E gallinacea.⁷ Echidnophaga gallinacea is found worldwide in the tropics, subtropics, and temperate zones, and it is the only representative of the genus found in the United States.¹ Given the wide range of wild and domestic animal hosts and wide geographic distribution for E gallinacea, it represents an increasing risk for humans.

Echidnophaga gallinacea favors feeding from fleshy areas without thick fur or plumage. In birds, the area around the eyes, comb, and wattles is included; in dogs, it can be the eyes, in between the toes, and in the genital area.¹ Flea bites cause irritation and itching for hosts including humans, typically resulting in clusters of firm, pruritic, erythematous papules with a central punctum.¹⁵ Severe bites also may lead to bullous lesions. In birds, symptoms can be extreme, with infestation around the eyes leading to swelling and blindness, a decline in egg production, weight loss, and death in young birds.¹ Similar to other fleas, E gallinacea is wingless and depends on jumping onto a host for transmission, which can be from the ground, carpeting and flooring, furniture, or another host. Fleas are champion jumpers (relative to body size) and can jump 100 times their length.¹⁶

Management

Treating sticktight fleas can be tricky, as they embed tightly into the host's skin. Animals should be treated by a qualified veterinarian. Removal of attached fleas in humans requires grasping the flea firmly with tweezers and pulling from the skin. If the infestation is considerable, malathion 5% liquid or gel can be applied. Patients can treat itching with topical steroids and antipruritic creams, and oral antihistamines can be used to relieve symptoms and reduce the likelihood of damaged skin as well as the potential for secondary infection. The flea-infested environment should be treated with insecticides. For treatment of hard surfaces, dichlorvos and propetamphos are effective. Organophosphates work well on fabric and carpeting. Domestic pets and livestock may be treated by a veterinarian with agents such as fipronil, selamectin, imidacloprid, metaflumizone, nitenpyram, lufenuron, methoprene, and pyriproxyfen.
 

Young women treated for early hormone receptor–positive, HER2-negative breast cancer fare better if their adjuvant endocrine therapy includes ovarian function suppression (OFS), according to a new analysis published online.

Senior author Gini F. Fleming, MD, director of the medical oncology breast program at the University of Chicago Medical Center, and her colleagues analyzed data from a pair of international phase III randomized adjuvant trials: the Suppression of Ovarian Function Trial (SOFT) and the Tamoxifen and Exemestane Trial (TEXT).

Main analyses were based on a respective 240 and 145 women younger than 35 years who had undergone surgery for early hormone receptor–positive, HER2-negative early breast cancer, received chemotherapy, and were randomly assigned to 5 years of various adjuvant endocrine therapies.

In SOFT, the 5-year breast cancer–free interval was 67.1% (95% CI, 54.6%-76.9%) with tamoxifen (Nolvadex) alone, 75.9% (64.0%-84.4%) with tamoxifen plus OFS, and 83.2% (72.7%-90.0%) with exemestane (Aromasin) plus OFS (J Clin Oncol. 2017 June 27 doi: 10.1200/JCO.2016.72.0946). In TEXT, it was 79.2% (66.2%-87.7%) with tamoxifen plus OFS and 81.6% (69.8%-89.2%) with exemestane plus OFS.

In a quality of life analysis among women receiving OFS, vasomotor symptoms (hot flushes and sweats) showed greatest increase from baseline (roughly 30-40 points) in the first 6 months of therapy. Loss of sexual interest and difficulties in becoming aroused were also noteworthy (8 points or greater). However, scores for global quality of life (physical well-being, mood, coping effort, and health perception) showed little change from baseline and were essentially the same as those seen among premenopausal women aged 35 or older in the same trials.

Overall, 19.8% of the young women in SOFT and TEXT stopped all protocol-assigned endocrine therapy early. The proportion rose with time and was higher than that among the older premenopausal group.

“There was a meaningful clinical benefit in breast cancer outcomes with the addition of OFS to tamoxifen and some additional benefit from use of an aromatase inhibitor with OFS. Longer follow-up is critical to clarify potential survival benefits,” the investigators wrote. “There were substantial adverse effects from these combined endocrine treatments, but they were not different in the younger and older than 35 years populations. Despite this, rates of nonadherence were slightly higher in women younger than 35 years.

“Availability of these age-specific data regarding risks and benefits of combined endocrine therapy will support shared decision making regarding OFS among young women at high risk for recurrence and death from breast cancer and, it is hoped, improve adherence among those who select OFS,” they concluded.

Young women treated for early hormone receptor–positive, HER2-negative breast cancer fare better if their adjuvant endocrine therapy includes ovarian function suppression (OFS), according to a new analysis published online.

Senior author Gini F. Fleming, MD, director of the medical oncology breast program at the University of Chicago Medical Center, and her colleagues analyzed data from a pair of international phase III randomized adjuvant trials: the Suppression of Ovarian Function Trial (SOFT) and the Tamoxifen and Exemestane Trial (TEXT).

Main analyses were based on a respective 240 and 145 women younger than 35 years who had undergone surgery for early hormone receptor–positive, HER2-negative early breast cancer, received chemotherapy, and were randomly assigned to 5 years of various adjuvant endocrine therapies.

In SOFT, the 5-year breast cancer–free interval was 67.1% (95% CI, 54.6%-76.9%) with tamoxifen (Nolvadex) alone, 75.9% (64.0%-84.4%) with tamoxifen plus OFS, and 83.2% (72.7%-90.0%) with exemestane (Aromasin) plus OFS (J Clin Oncol. 2017 June 27 doi: 10.1200/JCO.2016.72.0946). In TEXT, it was 79.2% (66.2%-87.7%) with tamoxifen plus OFS and 81.6% (69.8%-89.2%) with exemestane plus OFS.

In a quality of life analysis among women receiving OFS, vasomotor symptoms (hot flushes and sweats) showed greatest increase from baseline (roughly 30-40 points) in the first 6 months of therapy. Loss of sexual interest and difficulties in becoming aroused were also noteworthy (8 points or greater). However, scores for global quality of life (physical well-being, mood, coping effort, and health perception) showed little change from baseline and were essentially the same as those seen among premenopausal women aged 35 or older in the same trials.

Overall, 19.8% of the young women in SOFT and TEXT stopped all protocol-assigned endocrine therapy early. The proportion rose with time and was higher than that among the older premenopausal group.

“There was a meaningful clinical benefit in breast cancer outcomes with the addition of OFS to tamoxifen and some additional benefit from use of an aromatase inhibitor with OFS. Longer follow-up is critical to clarify potential survival benefits,” the investigators wrote. “There were substantial adverse effects from these combined endocrine treatments, but they were not different in the younger and older than 35 years populations. Despite this, rates of nonadherence were slightly higher in women younger than 35 years.

“Availability of these age-specific data regarding risks and benefits of combined endocrine therapy will support shared decision making regarding OFS among young women at high risk for recurrence and death from breast cancer and, it is hoped, improve adherence among those who select OFS,” they concluded.

Young women treated for early hormone receptor–positive, HER2-negative breast cancer fare better if their adjuvant endocrine therapy includes ovarian function suppression (OFS), according to a new analysis published online.

Senior author Gini F. Fleming, MD, director of the medical oncology breast program at the University of Chicago Medical Center, and her colleagues analyzed data from a pair of international phase III randomized adjuvant trials: the Suppression of Ovarian Function Trial (SOFT) and the Tamoxifen and Exemestane Trial (TEXT).

Main analyses were based on a respective 240 and 145 women younger than 35 years who had undergone surgery for early hormone receptor–positive, HER2-negative early breast cancer, received chemotherapy, and were randomly assigned to 5 years of various adjuvant endocrine therapies.

In SOFT, the 5-year breast cancer–free interval was 67.1% (95% CI, 54.6%-76.9%) with tamoxifen (Nolvadex) alone, 75.9% (64.0%-84.4%) with tamoxifen plus OFS, and 83.2% (72.7%-90.0%) with exemestane (Aromasin) plus OFS (J Clin Oncol. 2017 June 27 doi: 10.1200/JCO.2016.72.0946). In TEXT, it was 79.2% (66.2%-87.7%) with tamoxifen plus OFS and 81.6% (69.8%-89.2%) with exemestane plus OFS.

In a quality of life analysis among women receiving OFS, vasomotor symptoms (hot flushes and sweats) showed greatest increase from baseline (roughly 30-40 points) in the first 6 months of therapy. Loss of sexual interest and difficulties in becoming aroused were also noteworthy (8 points or greater). However, scores for global quality of life (physical well-being, mood, coping effort, and health perception) showed little change from baseline and were essentially the same as those seen among premenopausal women aged 35 or older in the same trials.

Overall, 19.8% of the young women in SOFT and TEXT stopped all protocol-assigned endocrine therapy early. The proportion rose with time and was higher than that among the older premenopausal group.

“There was a meaningful clinical benefit in breast cancer outcomes with the addition of OFS to tamoxifen and some additional benefit from use of an aromatase inhibitor with OFS. Longer follow-up is critical to clarify potential survival benefits,” the investigators wrote. “There were substantial adverse effects from these combined endocrine treatments, but they were not different in the younger and older than 35 years populations. Despite this, rates of nonadherence were slightly higher in women younger than 35 years.

“Availability of these age-specific data regarding risks and benefits of combined endocrine therapy will support shared decision making regarding OFS among young women at high risk for recurrence and death from breast cancer and, it is hoped, improve adherence among those who select OFS,” they concluded.