Nearly half of advanced Parkinson’s disease patients who receive treatment with subthalamic deep brain stimulation or levodopa-carbidopa intestinal gel infusion are affected by dysautonomia that has significant impacts on their daily lives, according to findings from a cross-sectional study.

“We suggest that identifying and managing autonomic targets, in addition to addressing motor disability, may enhance outcomes” of deep brain stimulation or levodopa-carbidopa intestinal gel therapies for advanced Parkinson’s disease, wrote the research team, led by Aristide Merola, MD, PhD, of the Gardner Family Center for Parkinson’s Disease and Movement Disorders at the University of Cincinnati.

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Nearly half of advanced Parkinson’s disease patients who receive treatment with subthalamic deep brain stimulation or levodopa-carbidopa intestinal gel infusion are affected by dysautonomia that has significant impacts on their daily lives, according to findings from a cross-sectional study.

“We suggest that identifying and managing autonomic targets, in addition to addressing motor disability, may enhance outcomes” of deep brain stimulation or levodopa-carbidopa intestinal gel therapies for advanced Parkinson’s disease, wrote the research team, led by Aristide Merola, MD, PhD, of the Gardner Family Center for Parkinson’s Disease and Movement Disorders at the University of Cincinnati.

designer491/Thinkstock

Nearly half of advanced Parkinson’s disease patients who receive treatment with subthalamic deep brain stimulation or levodopa-carbidopa intestinal gel infusion are affected by dysautonomia that has significant impacts on their daily lives, according to findings from a cross-sectional study.

“We suggest that identifying and managing autonomic targets, in addition to addressing motor disability, may enhance outcomes” of deep brain stimulation or levodopa-carbidopa intestinal gel therapies for advanced Parkinson’s disease, wrote the research team, led by Aristide Merola, MD, PhD, of the Gardner Family Center for Parkinson’s Disease and Movement Disorders at the University of Cincinnati.

designer491/Thinkstock

Oncology Practice will be on site this coming week at the annual meeting of the Society of Gynecologic Oncology in National Harbor, Md., reporting on the latest evidence for treating ovarian, cervical, and endometrial cancers. Key sessions include presentations on PARP inhibitors, novel radiation technologies, biomarker utilization in gynecologic oncology, rare tumors, and palliative care and survivorship.

The annual meeting begins Sunday, March 12, and our team will provide daily updates on the following presentations and more:

Rucaparib in patients with relapsed, primary platinum-sensitive high-grade ovarian carcinoma with germline or somatic BRCA mutations: Integrated summary of efficacy and safety from the phase II study ARIEL2.

Sentinel lymph node biopsy for early cervical cancer: Results of a randomized prospective, multicenter study (Senticol 2) comparing adding pelvic lymph node dissection vs. sentinel node biopsy only.

BRCA1 and RAD51C promoter hypermethylation confer sensitivity to the PARP inhibitor rucaparib in patients with relapsed, platinum-sensitive ovarian carcinoma in ARIEL2.

Cluster analysis of chemotherapy nonresponders for patients with serous epithelial ovarian cancer.

Oncologic outcomes of adjuvant chemotherapy in patients with risk factors after radical surgery in FIGO stage IB-IIA cervical cancer.

Combining whole pelvic radiation with chemotherapy in stage IVB cervical cancer: A novel treatment strategy.

Molecular response to neoadjuvant chemotherapy in high-grade serous ovarian carcinoma.

Clinical behavior of low-grade serous ovarian carcinoma: An analysis of 714 patients from the Ovarian Cancer Association Consortium (OCAC).

A randomized controlled trial comparing the efficacy of perioperative celecoxib versus ketorolac for perioperative pain control.

Combination therapy with IL-15 superagonist (ALT-803) and PD-1 blockade enhances human NK cell immunotherapy against ovarian cancer.

Reversal of obesity-driven aggressiveness of endometrial cancer by metformin.

A phase III trial of maintenance therapy in women with advanced ovarian/fallopian tube/peritoneal cancer after a complete clinical response to first-line therapy: An NRG oncology study.

Treatment with olaparib monotherapy in the maintenance setting significantly improves progression-free survival in patients with platinum-sensitive relapsed ovarian cancer: Results from the phase III SOLO2 study.

A prospective phase II trial of the listeria-based human papillomavirus immunotherpay axalimogene filolisbac in second- and third-line metastatic cervical cancer: A NRG oncology group trial.

Overall survival in BRCA1 or RAD51C methylated vs. mutated ovarian carcinoma following primary treatment with platinum chemotherapy.

Early palliative care is associated with improved quality of end-of-life care for women with high-risk gynecologic malignancies.

Contemporary recurrence and survival outcomes for stage IB squamous cell carcinoma of the vulva: Time to raise the bar.

Oncology Practice will be on site this coming week at the annual meeting of the Society of Gynecologic Oncology in National Harbor, Md., reporting on the latest evidence for treating ovarian, cervical, and endometrial cancers. Key sessions include presentations on PARP inhibitors, novel radiation technologies, biomarker utilization in gynecologic oncology, rare tumors, and palliative care and survivorship.

The annual meeting begins Sunday, March 12, and our team will provide daily updates on the following presentations and more:

Rucaparib in patients with relapsed, primary platinum-sensitive high-grade ovarian carcinoma with germline or somatic BRCA mutations: Integrated summary of efficacy and safety from the phase II study ARIEL2.

Sentinel lymph node biopsy for early cervical cancer: Results of a randomized prospective, multicenter study (Senticol 2) comparing adding pelvic lymph node dissection vs. sentinel node biopsy only.

BRCA1 and RAD51C promoter hypermethylation confer sensitivity to the PARP inhibitor rucaparib in patients with relapsed, platinum-sensitive ovarian carcinoma in ARIEL2.

Cluster analysis of chemotherapy nonresponders for patients with serous epithelial ovarian cancer.

Oncologic outcomes of adjuvant chemotherapy in patients with risk factors after radical surgery in FIGO stage IB-IIA cervical cancer.

Combining whole pelvic radiation with chemotherapy in stage IVB cervical cancer: A novel treatment strategy.

Molecular response to neoadjuvant chemotherapy in high-grade serous ovarian carcinoma.

Clinical behavior of low-grade serous ovarian carcinoma: An analysis of 714 patients from the Ovarian Cancer Association Consortium (OCAC).

A randomized controlled trial comparing the efficacy of perioperative celecoxib versus ketorolac for perioperative pain control.

Combination therapy with IL-15 superagonist (ALT-803) and PD-1 blockade enhances human NK cell immunotherapy against ovarian cancer.

Reversal of obesity-driven aggressiveness of endometrial cancer by metformin.

A phase III trial of maintenance therapy in women with advanced ovarian/fallopian tube/peritoneal cancer after a complete clinical response to first-line therapy: An NRG oncology study.

Treatment with olaparib monotherapy in the maintenance setting significantly improves progression-free survival in patients with platinum-sensitive relapsed ovarian cancer: Results from the phase III SOLO2 study.

A prospective phase II trial of the listeria-based human papillomavirus immunotherpay axalimogene filolisbac in second- and third-line metastatic cervical cancer: A NRG oncology group trial.

Overall survival in BRCA1 or RAD51C methylated vs. mutated ovarian carcinoma following primary treatment with platinum chemotherapy.

Early palliative care is associated with improved quality of end-of-life care for women with high-risk gynecologic malignancies.

Contemporary recurrence and survival outcomes for stage IB squamous cell carcinoma of the vulva: Time to raise the bar.

Oncology Practice will be on site this coming week at the annual meeting of the Society of Gynecologic Oncology in National Harbor, Md., reporting on the latest evidence for treating ovarian, cervical, and endometrial cancers. Key sessions include presentations on PARP inhibitors, novel radiation technologies, biomarker utilization in gynecologic oncology, rare tumors, and palliative care and survivorship.

The annual meeting begins Sunday, March 12, and our team will provide daily updates on the following presentations and more:

Rucaparib in patients with relapsed, primary platinum-sensitive high-grade ovarian carcinoma with germline or somatic BRCA mutations: Integrated summary of efficacy and safety from the phase II study ARIEL2.

Sentinel lymph node biopsy for early cervical cancer: Results of a randomized prospective, multicenter study (Senticol 2) comparing adding pelvic lymph node dissection vs. sentinel node biopsy only.

BRCA1 and RAD51C promoter hypermethylation confer sensitivity to the PARP inhibitor rucaparib in patients with relapsed, platinum-sensitive ovarian carcinoma in ARIEL2.

Cluster analysis of chemotherapy nonresponders for patients with serous epithelial ovarian cancer.

Oncologic outcomes of adjuvant chemotherapy in patients with risk factors after radical surgery in FIGO stage IB-IIA cervical cancer.

Combining whole pelvic radiation with chemotherapy in stage IVB cervical cancer: A novel treatment strategy.

Molecular response to neoadjuvant chemotherapy in high-grade serous ovarian carcinoma.

Clinical behavior of low-grade serous ovarian carcinoma: An analysis of 714 patients from the Ovarian Cancer Association Consortium (OCAC).

A randomized controlled trial comparing the efficacy of perioperative celecoxib versus ketorolac for perioperative pain control.

Combination therapy with IL-15 superagonist (ALT-803) and PD-1 blockade enhances human NK cell immunotherapy against ovarian cancer.

Reversal of obesity-driven aggressiveness of endometrial cancer by metformin.

A phase III trial of maintenance therapy in women with advanced ovarian/fallopian tube/peritoneal cancer after a complete clinical response to first-line therapy: An NRG oncology study.

Treatment with olaparib monotherapy in the maintenance setting significantly improves progression-free survival in patients with platinum-sensitive relapsed ovarian cancer: Results from the phase III SOLO2 study.

A prospective phase II trial of the listeria-based human papillomavirus immunotherpay axalimogene filolisbac in second- and third-line metastatic cervical cancer: A NRG oncology group trial.

Overall survival in BRCA1 or RAD51C methylated vs. mutated ovarian carcinoma following primary treatment with platinum chemotherapy.

Early palliative care is associated with improved quality of end-of-life care for women with high-risk gynecologic malignancies.

Contemporary recurrence and survival outcomes for stage IB squamous cell carcinoma of the vulva: Time to raise the bar.

Early elective delivery in the United States is at an all-time low of 1.9%, down from 17% in 2010, according to a report by a nonprofit group that monitors safety and care quality in hospitals.

Early elective delivery comprises Cesarean deliveries or inductions performed before 39 weeks without medical necessity, and higher rates are considered a barometer of poor labor management in hospitals. For its annual report on maternity practices, published Feb. 28, the Leapfrog Group, a Washington, D.C.–based nonprofit, collected voluntarily reported data from 1,859 hospitals, or about half of the nation’s hospitals, in 2016.

monkeybusinessimages/Thinkstock

Early elective delivery in the United States is at an all-time low of 1.9%, down from 17% in 2010, according to a report by a nonprofit group that monitors safety and care quality in hospitals.

Early elective delivery comprises Cesarean deliveries or inductions performed before 39 weeks without medical necessity, and higher rates are considered a barometer of poor labor management in hospitals. For its annual report on maternity practices, published Feb. 28, the Leapfrog Group, a Washington, D.C.–based nonprofit, collected voluntarily reported data from 1,859 hospitals, or about half of the nation’s hospitals, in 2016.

monkeybusinessimages/Thinkstock

Early elective delivery in the United States is at an all-time low of 1.9%, down from 17% in 2010, according to a report by a nonprofit group that monitors safety and care quality in hospitals.

Early elective delivery comprises Cesarean deliveries or inductions performed before 39 weeks without medical necessity, and higher rates are considered a barometer of poor labor management in hospitals. For its annual report on maternity practices, published Feb. 28, the Leapfrog Group, a Washington, D.C.–based nonprofit, collected voluntarily reported data from 1,859 hospitals, or about half of the nation’s hospitals, in 2016.

monkeybusinessimages/Thinkstock

Current evidence fails to support or reject routine screening pelvic exams for asymptomatic, low-risk, nonpregnant adult women, the U.S. Preventive Services Task Force concluded after reviewing the evidence on the accuracy, benefits, and potential harms.

The USPSTF issued an inconclusive “I” statement that was published online March 7 (JAMA. 2017;317[9]:947-53).

Researchers found no data comparing the impact of no screening versus screening pelvic examinations on patient health outcomes including reducing all-cause mortality, reducing cancer-specific and disease-specific morbidity and mortality, and improving quality of life.

“No direct evidence was identified for overall benefits and harms of the pelvic examination as a one-time or periodic screening test,” Janelle M. Guirguis-Blake, MD, of the University of Washington, Tacoma, and colleagues wrote in the accompanying evidence report (JAMA. 2017;317[9]:954-66). The review comprised nine studies: one addressing the harms of screening and eight addressing both harms and accuracy.

Although screening pelvic exams may identify serious conditions as well as benign ones, the potential remains for false-positive and false-negative results that might lead to invasive surgery and unnecessary testing and procedures, the researchers noted. However, the recommendations do not apply to certain conditions for which screening is already recommended, including cervical cancer (via Pap smear), gonorrhea, and chlamydia.

The recommendations are primarily a call for more research rather than a clear guide for clinicians, according to the USPSTF. The research gaps include studies on the physical and psychological harms of pelvic screening for asymptomatic women in primary care; the ability of screening to detect conditions beyond ovarian cancer, genital herpes, bacterial vaginosis, and trichomoniasis; and the impact of screening on a variety of health outcomes, including quality of life.

Given the inadequate evidence to recommend for or against screening, the USPSTF cited the recommendations of other organizations. Both the American College of Physicians and the American Academy of Family Physicians recommend against performing screening pelvic exams in asymptomatic, nonpregnant adult women. The American College of Obstetricians and Gynecologists recommends annual pelvic exams for women 21 years and older but acknowledges a lack of evidence and has said it should be a shared decision between the patient and clinician.

The USPSTF members reported having no relevant financial conflicts.

Current evidence fails to support or reject routine screening pelvic exams for asymptomatic, low-risk, nonpregnant adult women, the U.S. Preventive Services Task Force concluded after reviewing the evidence on the accuracy, benefits, and potential harms.

The USPSTF issued an inconclusive “I” statement that was published online March 7 (JAMA. 2017;317[9]:947-53).

Researchers found no data comparing the impact of no screening versus screening pelvic examinations on patient health outcomes including reducing all-cause mortality, reducing cancer-specific and disease-specific morbidity and mortality, and improving quality of life.

“No direct evidence was identified for overall benefits and harms of the pelvic examination as a one-time or periodic screening test,” Janelle M. Guirguis-Blake, MD, of the University of Washington, Tacoma, and colleagues wrote in the accompanying evidence report (JAMA. 2017;317[9]:954-66). The review comprised nine studies: one addressing the harms of screening and eight addressing both harms and accuracy.

Although screening pelvic exams may identify serious conditions as well as benign ones, the potential remains for false-positive and false-negative results that might lead to invasive surgery and unnecessary testing and procedures, the researchers noted. However, the recommendations do not apply to certain conditions for which screening is already recommended, including cervical cancer (via Pap smear), gonorrhea, and chlamydia.

The recommendations are primarily a call for more research rather than a clear guide for clinicians, according to the USPSTF. The research gaps include studies on the physical and psychological harms of pelvic screening for asymptomatic women in primary care; the ability of screening to detect conditions beyond ovarian cancer, genital herpes, bacterial vaginosis, and trichomoniasis; and the impact of screening on a variety of health outcomes, including quality of life.

Given the inadequate evidence to recommend for or against screening, the USPSTF cited the recommendations of other organizations. Both the American College of Physicians and the American Academy of Family Physicians recommend against performing screening pelvic exams in asymptomatic, nonpregnant adult women. The American College of Obstetricians and Gynecologists recommends annual pelvic exams for women 21 years and older but acknowledges a lack of evidence and has said it should be a shared decision between the patient and clinician.

The USPSTF members reported having no relevant financial conflicts.

Current evidence fails to support or reject routine screening pelvic exams for asymptomatic, low-risk, nonpregnant adult women, the U.S. Preventive Services Task Force concluded after reviewing the evidence on the accuracy, benefits, and potential harms.

The USPSTF issued an inconclusive “I” statement that was published online March 7 (JAMA. 2017;317[9]:947-53).

Researchers found no data comparing the impact of no screening versus screening pelvic examinations on patient health outcomes including reducing all-cause mortality, reducing cancer-specific and disease-specific morbidity and mortality, and improving quality of life.

“No direct evidence was identified for overall benefits and harms of the pelvic examination as a one-time or periodic screening test,” Janelle M. Guirguis-Blake, MD, of the University of Washington, Tacoma, and colleagues wrote in the accompanying evidence report (JAMA. 2017;317[9]:954-66). The review comprised nine studies: one addressing the harms of screening and eight addressing both harms and accuracy.

Although screening pelvic exams may identify serious conditions as well as benign ones, the potential remains for false-positive and false-negative results that might lead to invasive surgery and unnecessary testing and procedures, the researchers noted. However, the recommendations do not apply to certain conditions for which screening is already recommended, including cervical cancer (via Pap smear), gonorrhea, and chlamydia.

The recommendations are primarily a call for more research rather than a clear guide for clinicians, according to the USPSTF. The research gaps include studies on the physical and psychological harms of pelvic screening for asymptomatic women in primary care; the ability of screening to detect conditions beyond ovarian cancer, genital herpes, bacterial vaginosis, and trichomoniasis; and the impact of screening on a variety of health outcomes, including quality of life.

Given the inadequate evidence to recommend for or against screening, the USPSTF cited the recommendations of other organizations. Both the American College of Physicians and the American Academy of Family Physicians recommend against performing screening pelvic exams in asymptomatic, nonpregnant adult women. The American College of Obstetricians and Gynecologists recommends annual pelvic exams for women 21 years and older but acknowledges a lack of evidence and has said it should be a shared decision between the patient and clinician.

The USPSTF members reported having no relevant financial conflicts.

In this issue of Emergency Medicine, Greg Weingart, MD, and Shravan Kumar, MD, guide readers through the diagnosis, monitoring, and treatment of acute compartment syndrome, a relatively uncommon but devastating injury that may affect an extremity following a long bone fracture, deep vein thrombosis, or rhabdomyolysis from crush injuries or high-intensity exercising. Compartment syndrome occurs when increased pressure within a limited anatomic space compresses the circulation and tissue within that space until function becomes impossible. Even with heightened awareness of the disastrous sequelae, and with very early pressure monitoring of the injured compartment, physicians are at a loss to effectively intervene to prevent the continuing rise in pressure until a fasciotomy is required.

The disastrous consequences of rising pressure in a closed space suggests what can occur in the severely overcrowded EDs that now are common in every city in this country—EDs with too many patients waiting for treatment and inpatient beds.

Pressure on the nation’s ED capacity has been steadily increasing for the past three decades. Hospital/ED closings, demand for preadmission testing by managed care and primary care physicians, increasing numbers of documented and undocumented people seeking care, a rapidly aging population with more comorbidities, and increased numbers of patients seeking care under the Affordable Care Act have not been met with a commensurate increase in ED capacity. Between 1990 and 2010, the country’s urban and suburban areas lost one quarter of their hospital EDs (Hsia RY et al. JAMA. 2011;305[19]:1978-1985). In that same period, New York City lost 20 hospitals and about 5,000 inpatient beds; after 2010, when the state stopped bailing out financially failing hospitals, four more hospitals closed and were replaced by three freestanding EDs (FSEDs). Though FSEDs may partially fulfill the need for 24/7 emergency care at their former hospital sites, when patients in FSEDs require admission, they must compete with patients in hospital-based EDs for inpatient beds.

Despite the many and varied sources of increasing numbers of patients arriving in EDs, by all accounts this influx in and of itself is not the major driver of ED overcrowding. Trained, competent EPs, supported by skilled and highly motivated RNs, NPs, and PAs, are capable of efficiently managing even frequent surges in patient volume—as long as the “outflow” is not blocked. In many cases, this means having adequate, timely outpatient follow-up available to allow for safe discharge. But overwhelmingly, it means having adequate numbers of inpatient beds.

The discomfort and loss of privacy that patients experience from spending many hours or days on hallway stretchers are bad enough, but eventually patient safety also becomes a concern. With some creative approaches varying by location and circumstances, EPs have generally been able to successfully address the safety issues—so far. For example, many years ago, we began holding in reserve a small portion of our fee-for-service EM revenue available to supplement the hospital-provided base salaries. By frequently monitoring conditions throughout the day, taking into account rate of registration in the ED, day of the week, OR schedules, etc, we were able to decide before noon whether there was a need to offer 4, 6, or 8 evening/night hours at double the hourly sessional rate to the first EPs, PAs, and NPs in our group who responded to the e-mails. The hours worked did not earn these “first responders” any additional “RVU” credits as, for the most part, they were working closely with the inpatient services to monitor and supplement the care of admitted patients waiting in the ED. This arrangement provided an additional level of patient safety with no additional expense to the hospital. But flexible measures to provide patient comfort and ensure safety cannot solve the inflexible space issue, and instituting harsher regulations and core measures will only increase the pressures on ED staffs. What is required is a serious look at the national model for accruing ED costs, revenues, and third-party reimbursements, and then adjusting the formulas to address the current patient care realities before a “fasciotomy” is required. 

In this issue of Emergency Medicine, Greg Weingart, MD, and Shravan Kumar, MD, guide readers through the diagnosis, monitoring, and treatment of acute compartment syndrome, a relatively uncommon but devastating injury that may affect an extremity following a long bone fracture, deep vein thrombosis, or rhabdomyolysis from crush injuries or high-intensity exercising. Compartment syndrome occurs when increased pressure within a limited anatomic space compresses the circulation and tissue within that space until function becomes impossible. Even with heightened awareness of the disastrous sequelae, and with very early pressure monitoring of the injured compartment, physicians are at a loss to effectively intervene to prevent the continuing rise in pressure until a fasciotomy is required.

The disastrous consequences of rising pressure in a closed space suggests what can occur in the severely overcrowded EDs that now are common in every city in this country—EDs with too many patients waiting for treatment and inpatient beds.

Pressure on the nation’s ED capacity has been steadily increasing for the past three decades. Hospital/ED closings, demand for preadmission testing by managed care and primary care physicians, increasing numbers of documented and undocumented people seeking care, a rapidly aging population with more comorbidities, and increased numbers of patients seeking care under the Affordable Care Act have not been met with a commensurate increase in ED capacity. Between 1990 and 2010, the country’s urban and suburban areas lost one quarter of their hospital EDs (Hsia RY et al. JAMA. 2011;305[19]:1978-1985). In that same period, New York City lost 20 hospitals and about 5,000 inpatient beds; after 2010, when the state stopped bailing out financially failing hospitals, four more hospitals closed and were replaced by three freestanding EDs (FSEDs). Though FSEDs may partially fulfill the need for 24/7 emergency care at their former hospital sites, when patients in FSEDs require admission, they must compete with patients in hospital-based EDs for inpatient beds.

Despite the many and varied sources of increasing numbers of patients arriving in EDs, by all accounts this influx in and of itself is not the major driver of ED overcrowding. Trained, competent EPs, supported by skilled and highly motivated RNs, NPs, and PAs, are capable of efficiently managing even frequent surges in patient volume—as long as the “outflow” is not blocked. In many cases, this means having adequate, timely outpatient follow-up available to allow for safe discharge. But overwhelmingly, it means having adequate numbers of inpatient beds.

The discomfort and loss of privacy that patients experience from spending many hours or days on hallway stretchers are bad enough, but eventually patient safety also becomes a concern. With some creative approaches varying by location and circumstances, EPs have generally been able to successfully address the safety issues—so far. For example, many years ago, we began holding in reserve a small portion of our fee-for-service EM revenue available to supplement the hospital-provided base salaries. By frequently monitoring conditions throughout the day, taking into account rate of registration in the ED, day of the week, OR schedules, etc, we were able to decide before noon whether there was a need to offer 4, 6, or 8 evening/night hours at double the hourly sessional rate to the first EPs, PAs, and NPs in our group who responded to the e-mails. The hours worked did not earn these “first responders” any additional “RVU” credits as, for the most part, they were working closely with the inpatient services to monitor and supplement the care of admitted patients waiting in the ED. This arrangement provided an additional level of patient safety with no additional expense to the hospital. But flexible measures to provide patient comfort and ensure safety cannot solve the inflexible space issue, and instituting harsher regulations and core measures will only increase the pressures on ED staffs. What is required is a serious look at the national model for accruing ED costs, revenues, and third-party reimbursements, and then adjusting the formulas to address the current patient care realities before a “fasciotomy” is required. 

In this issue of Emergency Medicine, Greg Weingart, MD, and Shravan Kumar, MD, guide readers through the diagnosis, monitoring, and treatment of acute compartment syndrome, a relatively uncommon but devastating injury that may affect an extremity following a long bone fracture, deep vein thrombosis, or rhabdomyolysis from crush injuries or high-intensity exercising. Compartment syndrome occurs when increased pressure within a limited anatomic space compresses the circulation and tissue within that space until function becomes impossible. Even with heightened awareness of the disastrous sequelae, and with very early pressure monitoring of the injured compartment, physicians are at a loss to effectively intervene to prevent the continuing rise in pressure until a fasciotomy is required.

The disastrous consequences of rising pressure in a closed space suggests what can occur in the severely overcrowded EDs that now are common in every city in this country—EDs with too many patients waiting for treatment and inpatient beds.

Pressure on the nation’s ED capacity has been steadily increasing for the past three decades. Hospital/ED closings, demand for preadmission testing by managed care and primary care physicians, increasing numbers of documented and undocumented people seeking care, a rapidly aging population with more comorbidities, and increased numbers of patients seeking care under the Affordable Care Act have not been met with a commensurate increase in ED capacity. Between 1990 and 2010, the country’s urban and suburban areas lost one quarter of their hospital EDs (Hsia RY et al. JAMA. 2011;305[19]:1978-1985). In that same period, New York City lost 20 hospitals and about 5,000 inpatient beds; after 2010, when the state stopped bailing out financially failing hospitals, four more hospitals closed and were replaced by three freestanding EDs (FSEDs). Though FSEDs may partially fulfill the need for 24/7 emergency care at their former hospital sites, when patients in FSEDs require admission, they must compete with patients in hospital-based EDs for inpatient beds.

Despite the many and varied sources of increasing numbers of patients arriving in EDs, by all accounts this influx in and of itself is not the major driver of ED overcrowding. Trained, competent EPs, supported by skilled and highly motivated RNs, NPs, and PAs, are capable of efficiently managing even frequent surges in patient volume—as long as the “outflow” is not blocked. In many cases, this means having adequate, timely outpatient follow-up available to allow for safe discharge. But overwhelmingly, it means having adequate numbers of inpatient beds.

The discomfort and loss of privacy that patients experience from spending many hours or days on hallway stretchers are bad enough, but eventually patient safety also becomes a concern. With some creative approaches varying by location and circumstances, EPs have generally been able to successfully address the safety issues—so far. For example, many years ago, we began holding in reserve a small portion of our fee-for-service EM revenue available to supplement the hospital-provided base salaries. By frequently monitoring conditions throughout the day, taking into account rate of registration in the ED, day of the week, OR schedules, etc, we were able to decide before noon whether there was a need to offer 4, 6, or 8 evening/night hours at double the hourly sessional rate to the first EPs, PAs, and NPs in our group who responded to the e-mails. The hours worked did not earn these “first responders” any additional “RVU” credits as, for the most part, they were working closely with the inpatient services to monitor and supplement the care of admitted patients waiting in the ED. This arrangement provided an additional level of patient safety with no additional expense to the hospital. But flexible measures to provide patient comfort and ensure safety cannot solve the inflexible space issue, and instituting harsher regulations and core measures will only increase the pressures on ED staffs. What is required is a serious look at the national model for accruing ED costs, revenues, and third-party reimbursements, and then adjusting the formulas to address the current patient care realities before a “fasciotomy” is required. 

Acute extremity pain is a common presentation seen daily in EDs. While most etiologies of extremity pain are benign, the complications of acute compartment syndrome are associated with significant morbidity. Moreover, acute compartment syndrome remains a difficult diagnosis that is often missed on initial presentation. Morbidity results from an increased pressure in an anatomically closed space, progressing to decreased perfusion and rapid tissue destruction.

Case

An obese 55-year-old man with a medical history of coronary artery disease, for which he was on aspirin therapy, presented for evaluation of right shin pain. The patient stated that he completed a 5-km race earlier that morning with his son. Immediately following the race, he experienced increasing right shin pain, which he attempted to initially manage with ice compresses and over-the-counter ibuprofen. He noted that neither the ice compresses nor the ibuprofen relieved his pain and that by 5:00 pm, the pain had worsened to the point where he had difficulty walking, prompting his visit to the ED.

Upon arrival at the ED, the patient was ambulatory but had significant pain at both rest and movement. His vital signs and his oxygen saturation on room air were normal. On physical examination, he had normal sensation to the entire right lower extremity and had equal pulses in both feet. The anterolateral aspect of the shin was exquisitely tender to light touch, and the patient was unable to dorsiflex or plantar flex without extreme pain. On passive dorsiflexion and plantar flexion of his right foot, he had exquisite pain. On palpation, the anterior shin was firm compared to the other muscle beds.

Epidemiology

Acute compartment syndrome—elevation of interstitial pressure in closed fascial compartment—affects 10 times as many men as women, at an average age of 32 years old and with an annual incidence of 7.3 per 100,000 men and 0.7 per 100,000 for women.¹ McQueen et al¹ found that the most common cause of acute compartment syndrome was fracture (69%), followed by soft tissue injury (23%). Younger patients are more likely to develop acute compartment syndrome from trauma because they typically have larger muscle beds with more tissue to become edematous compared to the older, hypotrophic muscles of elderly patients.

Pathophysiology

The fascia surrounds the major muscle groups and neurovascular bundles in the extremities to create distinct compartments. Since the fascia is not a compliant structure, it is typically not able to tolerate increases in volume or pressure in a given compartment. Compartment perfusion pressure is the mean arterial pressure minus the compartment pressure. Normal compartment pressure in adults is between 0 to 8 mm Hg.² When compartment perfusion pressures are below 70 to 80 mm Hg, there is an increased risk of compartment syndrome.

Although the exact pathophysiology of acute compartment syndrome is still debated,³ the most commonly accepted theory is the arteriovenous pressure gradient theory.⁴ In this theory, the rise in intracompartment pressure increases venous pressure, which in turn reduces the arteriovenous pressure gradient, reducing local tissue perfusion. The reduction in tissue perfusion, coupled with a reduction in venous drainage, causes significant tissue edema. This change in vascular pressure also causes a reduction in lymphatic drainage, further increasing pressure in the compartment. Finally, the edematous tissue compresses the arterioles leading to end-organ ischemia.⁵

Initially an absolute threshold compartment pressure was thought to cause irreversible tissue ischemia,⁶ but this theory has slowly lost favor after it was found that hypertension was actually protective in compartment syndrome.⁷ Current thinking is that the difference between the diastolic pressure and the compartment pressure leads to tissue ischemia (ie, acute compartment syndrome delta pressure = diastolic blood pressure [BP] – measured compartment pressure).^6,8

In 1996, McQueen and Court-Brown⁶ prospectively admitted all tibial diaphyseal fractures and continuously monitored their anterior compartment pressure. Using a delta pressure value of less than 30 mm Hg, only three patients were diagnosed with acute compartment syndrome and required fasciotomy. The patients’ absolute compartment pressures were 45 mm Hg, 65 mm Hg, and 75 mm Hg, while the delta pressures were 15 mm Hg, 10 mm Hg, and 15 mm Hg, respectively. Conversely, 53 patients had absolute compartment pressures over 30 mm Hg; 30 patients had pressure over 40 mm Hg; four patients had pressure over 50 mm Hg; and none required fasciotomy. This study highlights that the absolute compartment pressure is not helpful in making the diagnosis, and it is the elevated delta pressure that secures the diagnosis.

Etiology

Compartment syndrome is the end result of many different injury patterns. While fracture is the number one cause of compartment syndrome, many types of soft tissue injuries can also lead to compartment syndrome. Nonfracture etiologies of compartment syndrome are relatively uncommon, and as such can lead to a delay in diagnosis.

Fracture

Almost 70% of all cases of compartment syndrome are due to fracture.¹ Fractures of the tibia, distal radius, and ulna are the most common injuries that lead to acute compartment syndrome. Interestingly, acute compartment syndrome is caused by an equal distribution of high-energy and low-energy mechanisms of injuries.¹ Because the increase in compartment pressure is highest at the fracture site,⁹ it is imperative to measure pressures at the site of the fracture. Contrary to traditional teaching, an open fracture does not reduce the risk of compartment syndrome. McQueen and Court-Brown⁶ found there was no difference in the intracompartment pressure between open and closed fractures.

Fracture reduction and manipulation can actually increase the risk of compartment syndrome. In one case series, fracture manipulation increased compartment pressure by reducing the total volume in a stretched compartment.¹⁰ Dresing et al¹⁰ found the average pressure increased by 21 mm Hg during wrist reduction, warranting close observation after fracture reduction and close observation of the patient’s pain and neurovascular status.

McQueen et al¹¹ evaluated the risk factors for the development of acute compartment syndrome from tibial diaphyseal fractures and found that younger patients were at the highest risk. Patients between ages 10 to 19 years old had an odds ratio (OR) of 12.09; 20 to 29 years old had an OR of 9.84; and patients older than age 40 years had an OR of 1.¹¹ As previously stated, younger patients have larger muscle volumes compared to their older counterparts and therefore have less space for edema after the primary muscle injury.

Soft Tissue Injury

Direct soft tissue injury can lead to a rise in compartment pressures due to trauma, infections, and burns even in the absence of fractures. Unfortunately, under these circumstances, patients with direct soft tissue injury are at high risk for a delay in diagnosis.¹² The primary injury can be worsened by underlying coagulopathies.¹ A circumferential constrictive eschar from burns can also cause external compression to a compartment¹³ as well as edema, which decreases the compliance of the fascia, leading to a rise in compartment pressure.

Vascular Injuries and Unusual Causes

Arterial Vessel Damage. Injuries to single arterial vessels can also lend to the development of acute compartment syndrome. Arterial damage from high-energy trauma causes acute compartment syndromes due to the rapid development of a hematoma and pressure in affected compartments. Loss of the arterial blood flow from the traumatized artery also causes cell necrosis and edema to the muscle bed, further increasing the compartment pressure. The result of these injuries is the development of acute compartment syndrome in uncommon locations such as the thigh^{14 and foot.15}

Arterial damage from relatively low-energy ankle-inversion injuries have also been implicated in development of acute compartment syndrome of the foot.¹⁵ Conversely, damage to branches of an artery may cause symptoms in the compartments of the proximal extremity, but spare the blood flow and pulsations to the distal portion.¹³ This atypical mechanism of injury requires the physician to maintain a high index of suspicion and consider arteriography and direct pressure management in diagnosis and treatment of this condition.

Deep Vein Thrombosis. Deep vein thrombosis (DVT) can also be associated with acute compartment syndrome. A large clot burden, such as that observed in phlegmasia cerulea dolens, can lead to reduced venous flow and increased pressure, resulting in decreased arteriovenous gradient and tissue perfusion. Acute compartment syndrome caused by extensive DVT is often treated with anticoagulation therapy, thrombolysis or thrombectomy, but fasciotomy also has a role as an adjunct treatment to reduce compartment pressure sufficiently to return blood flow.¹⁶

Medication-Induced Compartment Syndrome

Injections of medications or illicit drugs can lead to increased compartment pressure through several independent mechanisms (Table).¹⁷ Local tissue vasotoxicity from direct injection of a caustic agent can cause direct muscle necrosis and edema. In addition, prolonged external compression while lying in a coma-like state induced by alcohol intoxication or central nervous system suppressant drugs, or a state of unconsciousness from any cause, can produce direct injury to the compartment (Table).

Diagnosis

Signs and Symptoms

Diagnosis of acute compartment syndrome is primarily clinical, using compartment pressure measurement as an adjunct in evaluation. Because the features of early acute compartment syndrome are nonspecific, a high clinical suspicion must be maintained for all at-risk populations.

The classic features such as pain, pallor, paresthesias, paralysis, and pulselessness are all late findings of acute compartment syndrome and are associated with irreversible damage. However, pain out of proportion to injury and pain with passive stretch of muscles are early symptoms that require further attention and monitoring.⁸

The earliest objective finding on physical examination is compartment firmness.⁸ Unfortunately, the sensitivity of physical examination by orthopedic physicians is low (22%-26%) on cadaver models with elevated compartment pressures.¹⁸ Peripheral nerve tissue is very sensitive to ischemia and will stop functioning after 75 minutes.⁹ A review of clinical findings in acute compartment syndrome showed that the positive predictive values of these individual symptoms are low, but there is a high likelihood of compartment syndrome when at least three clinical findings are present simultaneously.¹⁹ In patients who are at high risk for developing acute compartment syndrome, but who may not be able to describe or who do not show clear symptoms (eg, patients who are obtunded, intubated, or very young/old), compartment pressure measurement can be a valuable aid in the diagnosis.

Compartment Pressure Measurement

There are several readily available methods to directly measure the compartment pressure. It is imperative to measure the compartment pressure closest to the fracture location (within 5 cm) because the pressure dissipates as distance increases from the fracture site.²⁰

Solid-State Transducer Intracompartmental Catheter. The Stryker Intra-Compartmental Pressure Monitor System (Stryker Surgical) is a commonly used solid-state transducer intracompartmental catheter (STIC) that allows measurement of compartment pressure.

The STIC system consists of a side-port needle, syringe of saline flush, and a digital read-out manometer. It has been validated against commonly used alternatives and found to be accurate^21,22 with a confidence interval between ± 5 to 6.23. This device uses a side port needle to allow for testing multiple compartments with the same needle as it is less likely to be occluded by tissue when compared to a standard needle.

The following technique should be employed to properly measure compartment pressure using the Stryker STIC device²³:

1. Place the side port needle on the tapered end of the diaphragm chamber.
2. Connect the prefilled syringe of normal saline to the diaphragm chamber.
3. Place the diaphragm chamber in the pressure monitor with the black side down and push until it is seated in the device.
4. Close the cover until it snaps.
5. Place the needle up and fill the system with normal saline from the syringe until there are no air bubbles in the system.
6. Turn the pressure monitor on.
7. Select an intended angle and press the “Zero” button and wait until it reads “00.”
8. Under sterile technique and appropriately anesthetized skin, insert the device into the compartment. Once in the compartment, slowly inject a small amount of saline into the compartment and record the provided number.

For details on needle-placement techniques, including depths, see Figures 1 to 4 for lower extremity compartments and Figures 5 to 7 for upper extremity compartments.²⁴

Laboratory Evaluation

Although the diagnosis of compartment syndrome is made by clinical findings and direct pressure measurement, laboratory tests can support the diagnosis.

Serum creatinine phosphokinase (CPK) is elevated with muscle necrosis. Both CPK and myoglobin proteins are glomerulotoxic, and acute kidney injury is a common complication of acute compartment syndrome. A CPK of greater than 1,000 IU/L has a sensitivity of 0.91 for acute compartment syndrome, but a specificity of only 0.52.2

In a multivariate model for predicting acute compartment syndrome, CPK greater than 4,000 IU/L, chloride greater than 104 mEq/L, and a blood urea nitrogen less than 10 mmol/L were found to be predictive of compartment syndrome during a patient’s hospital admission. No patient had compartment syndrome when all three variables were negative, and all patients with all three positive variables had acute compartment syndrome.²² This model was conducted on admitted patients during their inpatient hospital stay; therefore its application in the ED may not be valid, and the model has yet to be validated prospectively.

Treatment

Prompt surgical consultation for decompressive fasciotomy is paramount to the management of acute compartment syndrome in the ED. When acute compartment syndrome is suspected, elevation of the affected extremity is suggested in an attempt to decrease swelling.²⁷ The optimum height of elevation remains controversial; to prevent a decrease in arterial blood flow, it has been suggested not to raise the affected extremity above the level of the heart.⁸

A low systemic BP should be corrected to hopefully increase the compartment perfusion, and any applied external compressive forces (eg, casts, splints, dressings, eschars) should be removed.⁸ Removal of a cast can reduce the intracompartment pressure by 85%.⁵ Finally, applying cool compresses to the affected region can help reduce edema as a temporizing measure. Direct application of ice to the skin should be avoided to prevent cold-induced injury to the skin.

Appropriate medical resuscitation is imperative to good outcomes. Identifying and intervening when hypotension is present is necessary to improve tissue perfusion. Cellular derangement and death that can lead to hypocalcaemia, hyperkalemia, metabolic acidosis, and renal failure, require prompt recognition and correction.

At-Risk Populations

Pediatric Patients

Diagnosis of acute compartment syndrome in the general pediatric population is very difficult and therefore unfortunately associated with delays in diagnosis. The average time from injury to diagnosis can vary from 18.2to 31.1 hours.^28,29 In children younger than age 3 years, 60% of acute compartment syndrome cases are due to trauma; 27% are due to invasive infections; and 13% develop from intravenous (IV) infiltration.³⁰ Supracondylar humerus fractures are associated with increased risk of compartment syndrome. The volar compartment of the forearm is at risk after reduction of the fracture and when the elbow is flexed beyond 90°.³¹

Intubated and Obtunded Patients

Intubated and obtunded patients require special attention to prevent and/or identify the presence of acute compartment syndrome. Since clinical examination for compartment syndrome in these patients is unreliable, serial or continuous compartment pressure measurements are required to monitor for acute compartment syndrome.

Laboratory analysis, including monitoring of CPK levels, can also help identify developing compartment syndrome in intubated, sedated, or neurologically compromised patients.³² Onset of unexplained myoglobinuria or acute renal failure in an intubated patient should lead to consideration of compartment syndrome. In addition to laboratory studies, examination of atypical locations, such as the back or gluteal compartments, can also assist in identifying compartment syndrome in impaired patients.

Complications

The complications of compartment syndrome can be severe, and are typically organized as early and late stages of the disease.

Early Clinical Complications

Even with prompt diagnosis, acute compartment syndrome can lead to significant metabolic derangements. Patients with compartment syndrome are at significant risk for rhabdomyolysis and resultant renal failure from acute tubal necrosis. Likewise, both myocyte damage and death can cause extracellular electrolyte shifts, and hyperkalemia, metabolic acidosis, and hypocalcemia are frequently encountered under these circumstances.

Late Clinical Complications

Necrotic muscle is a significant risk factor for bacterial superinfection.³³ Necrotic muscle may quickly be seeded by bacteria, and lead to sepsis. Necrotic muscle may therefore require repeated debridement and even possible extremity amputation for infection control. Likewise, muscle necrosis can lead to muscle contractures and loss of function of the affected extremity.³

Medicolegal Complications

Delay in the diagnosis of acute compartment syndrome has become an increasing source of medicolegal liability. In a 2004 review by Bhattacharyya and Vrahas³⁴ of 23 years of claims from a medical malpractice insurer, only 19 claims were made for compartment syndrome. In this series, the following four risk factors were associated with an unsuccessful defense: (1) a linear association between the number of documented cardinal signs of compartment syndrome and an indemnity payment; (2) delays in fasciotomy; (3) poor communication with the patient and nursing staff; (4) and failure to intervene after documentation of an abnormal physical finding. All of the above were associated with a negative legal outcome.

Case Conclusion

The patient had a firm anterior compartment, CPK of 9,100 IU/L, normal renal function, compartment pressure of 60 mm Hg, and diastolic pressure of 80 mm Hg at the time of the procedure. Because the patient had a delta pressure of 20 mm Hg, orthopedic services were consulted, and the patient was taken to the operating room, where he underwent a bicompartment fasciotomy of the right lateral calf. The compartments were tense when opened and there was no evidence of myonecrosis. The patient was given continuous IV fluids and observed in the hospital for 2 days as his CPKs trended downward without subsequent renal injury.

Conclusion

Compartment syndrome requires high clinical suspicion for early diagnosis and treatment to prevent major disability. Early recognition of this condition is paramount, as the classical presentation of the five “Ps”—pain, pallor, pulselessness, paresthesias, and paralysis—are all late findings associated with irreversible consequences.

Given the difficulty in establishing the diagnosis by physical examination findings, the emergency physician (EP) should check and monitor compartment pressures when considering the diagnosis of acute compartment syndrome. In patients with acute compartment syndrome, delayed fasciotomies lead to poor outcomes and a 10-fold increase in surgical complications, such as infection and renal failure.³⁵

Although traumatic fractures are the most common cause of acute compartment syndrome, EPs must also recognize that obtundation, intubation, coagulopathies, and seemingly minor traumas all can potentially cause or lead to acute compartment syndrome.

Acute extremity pain is a common presentation seen daily in EDs. While most etiologies of extremity pain are benign, the complications of acute compartment syndrome are associated with significant morbidity. Moreover, acute compartment syndrome remains a difficult diagnosis that is often missed on initial presentation. Morbidity results from an increased pressure in an anatomically closed space, progressing to decreased perfusion and rapid tissue destruction.

Case

An obese 55-year-old man with a medical history of coronary artery disease, for which he was on aspirin therapy, presented for evaluation of right shin pain. The patient stated that he completed a 5-km race earlier that morning with his son. Immediately following the race, he experienced increasing right shin pain, which he attempted to initially manage with ice compresses and over-the-counter ibuprofen. He noted that neither the ice compresses nor the ibuprofen relieved his pain and that by 5:00 pm, the pain had worsened to the point where he had difficulty walking, prompting his visit to the ED.

Upon arrival at the ED, the patient was ambulatory but had significant pain at both rest and movement. His vital signs and his oxygen saturation on room air were normal. On physical examination, he had normal sensation to the entire right lower extremity and had equal pulses in both feet. The anterolateral aspect of the shin was exquisitely tender to light touch, and the patient was unable to dorsiflex or plantar flex without extreme pain. On passive dorsiflexion and plantar flexion of his right foot, he had exquisite pain. On palpation, the anterior shin was firm compared to the other muscle beds.

Epidemiology

Acute compartment syndrome—elevation of interstitial pressure in closed fascial compartment—affects 10 times as many men as women, at an average age of 32 years old and with an annual incidence of 7.3 per 100,000 men and 0.7 per 100,000 for women.¹ McQueen et al¹ found that the most common cause of acute compartment syndrome was fracture (69%), followed by soft tissue injury (23%). Younger patients are more likely to develop acute compartment syndrome from trauma because they typically have larger muscle beds with more tissue to become edematous compared to the older, hypotrophic muscles of elderly patients.

Pathophysiology

The fascia surrounds the major muscle groups and neurovascular bundles in the extremities to create distinct compartments. Since the fascia is not a compliant structure, it is typically not able to tolerate increases in volume or pressure in a given compartment. Compartment perfusion pressure is the mean arterial pressure minus the compartment pressure. Normal compartment pressure in adults is between 0 to 8 mm Hg.² When compartment perfusion pressures are below 70 to 80 mm Hg, there is an increased risk of compartment syndrome.

Although the exact pathophysiology of acute compartment syndrome is still debated,³ the most commonly accepted theory is the arteriovenous pressure gradient theory.⁴ In this theory, the rise in intracompartment pressure increases venous pressure, which in turn reduces the arteriovenous pressure gradient, reducing local tissue perfusion. The reduction in tissue perfusion, coupled with a reduction in venous drainage, causes significant tissue edema. This change in vascular pressure also causes a reduction in lymphatic drainage, further increasing pressure in the compartment. Finally, the edematous tissue compresses the arterioles leading to end-organ ischemia.⁵

Initially an absolute threshold compartment pressure was thought to cause irreversible tissue ischemia,⁶ but this theory has slowly lost favor after it was found that hypertension was actually protective in compartment syndrome.⁷ Current thinking is that the difference between the diastolic pressure and the compartment pressure leads to tissue ischemia (ie, acute compartment syndrome delta pressure = diastolic blood pressure [BP] – measured compartment pressure).^6,8

In 1996, McQueen and Court-Brown⁶ prospectively admitted all tibial diaphyseal fractures and continuously monitored their anterior compartment pressure. Using a delta pressure value of less than 30 mm Hg, only three patients were diagnosed with acute compartment syndrome and required fasciotomy. The patients’ absolute compartment pressures were 45 mm Hg, 65 mm Hg, and 75 mm Hg, while the delta pressures were 15 mm Hg, 10 mm Hg, and 15 mm Hg, respectively. Conversely, 53 patients had absolute compartment pressures over 30 mm Hg; 30 patients had pressure over 40 mm Hg; four patients had pressure over 50 mm Hg; and none required fasciotomy. This study highlights that the absolute compartment pressure is not helpful in making the diagnosis, and it is the elevated delta pressure that secures the diagnosis.

Etiology

Compartment syndrome is the end result of many different injury patterns. While fracture is the number one cause of compartment syndrome, many types of soft tissue injuries can also lead to compartment syndrome. Nonfracture etiologies of compartment syndrome are relatively uncommon, and as such can lead to a delay in diagnosis.

Fracture

Almost 70% of all cases of compartment syndrome are due to fracture.¹ Fractures of the tibia, distal radius, and ulna are the most common injuries that lead to acute compartment syndrome. Interestingly, acute compartment syndrome is caused by an equal distribution of high-energy and low-energy mechanisms of injuries.¹ Because the increase in compartment pressure is highest at the fracture site,⁹ it is imperative to measure pressures at the site of the fracture. Contrary to traditional teaching, an open fracture does not reduce the risk of compartment syndrome. McQueen and Court-Brown⁶ found there was no difference in the intracompartment pressure between open and closed fractures.

Fracture reduction and manipulation can actually increase the risk of compartment syndrome. In one case series, fracture manipulation increased compartment pressure by reducing the total volume in a stretched compartment.¹⁰ Dresing et al¹⁰ found the average pressure increased by 21 mm Hg during wrist reduction, warranting close observation after fracture reduction and close observation of the patient’s pain and neurovascular status.

McQueen et al¹¹ evaluated the risk factors for the development of acute compartment syndrome from tibial diaphyseal fractures and found that younger patients were at the highest risk. Patients between ages 10 to 19 years old had an odds ratio (OR) of 12.09; 20 to 29 years old had an OR of 9.84; and patients older than age 40 years had an OR of 1.¹¹ As previously stated, younger patients have larger muscle volumes compared to their older counterparts and therefore have less space for edema after the primary muscle injury.

Soft Tissue Injury

Direct soft tissue injury can lead to a rise in compartment pressures due to trauma, infections, and burns even in the absence of fractures. Unfortunately, under these circumstances, patients with direct soft tissue injury are at high risk for a delay in diagnosis.¹² The primary injury can be worsened by underlying coagulopathies.¹ A circumferential constrictive eschar from burns can also cause external compression to a compartment¹³ as well as edema, which decreases the compliance of the fascia, leading to a rise in compartment pressure.

Vascular Injuries and Unusual Causes

Arterial Vessel Damage. Injuries to single arterial vessels can also lend to the development of acute compartment syndrome. Arterial damage from high-energy trauma causes acute compartment syndromes due to the rapid development of a hematoma and pressure in affected compartments. Loss of the arterial blood flow from the traumatized artery also causes cell necrosis and edema to the muscle bed, further increasing the compartment pressure. The result of these injuries is the development of acute compartment syndrome in uncommon locations such as the thigh^{14 and foot.15}

Arterial damage from relatively low-energy ankle-inversion injuries have also been implicated in development of acute compartment syndrome of the foot.¹⁵ Conversely, damage to branches of an artery may cause symptoms in the compartments of the proximal extremity, but spare the blood flow and pulsations to the distal portion.¹³ This atypical mechanism of injury requires the physician to maintain a high index of suspicion and consider arteriography and direct pressure management in diagnosis and treatment of this condition.

Deep Vein Thrombosis. Deep vein thrombosis (DVT) can also be associated with acute compartment syndrome. A large clot burden, such as that observed in phlegmasia cerulea dolens, can lead to reduced venous flow and increased pressure, resulting in decreased arteriovenous gradient and tissue perfusion. Acute compartment syndrome caused by extensive DVT is often treated with anticoagulation therapy, thrombolysis or thrombectomy, but fasciotomy also has a role as an adjunct treatment to reduce compartment pressure sufficiently to return blood flow.¹⁶

Medication-Induced Compartment Syndrome

Injections of medications or illicit drugs can lead to increased compartment pressure through several independent mechanisms (Table).¹⁷ Local tissue vasotoxicity from direct injection of a caustic agent can cause direct muscle necrosis and edema. In addition, prolonged external compression while lying in a coma-like state induced by alcohol intoxication or central nervous system suppressant drugs, or a state of unconsciousness from any cause, can produce direct injury to the compartment (Table).

Diagnosis

Signs and Symptoms

Diagnosis of acute compartment syndrome is primarily clinical, using compartment pressure measurement as an adjunct in evaluation. Because the features of early acute compartment syndrome are nonspecific, a high clinical suspicion must be maintained for all at-risk populations.

The classic features such as pain, pallor, paresthesias, paralysis, and pulselessness are all late findings of acute compartment syndrome and are associated with irreversible damage. However, pain out of proportion to injury and pain with passive stretch of muscles are early symptoms that require further attention and monitoring.⁸

The earliest objective finding on physical examination is compartment firmness.⁸ Unfortunately, the sensitivity of physical examination by orthopedic physicians is low (22%-26%) on cadaver models with elevated compartment pressures.¹⁸ Peripheral nerve tissue is very sensitive to ischemia and will stop functioning after 75 minutes.⁹ A review of clinical findings in acute compartment syndrome showed that the positive predictive values of these individual symptoms are low, but there is a high likelihood of compartment syndrome when at least three clinical findings are present simultaneously.¹⁹ In patients who are at high risk for developing acute compartment syndrome, but who may not be able to describe or who do not show clear symptoms (eg, patients who are obtunded, intubated, or very young/old), compartment pressure measurement can be a valuable aid in the diagnosis.

Compartment Pressure Measurement

There are several readily available methods to directly measure the compartment pressure. It is imperative to measure the compartment pressure closest to the fracture location (within 5 cm) because the pressure dissipates as distance increases from the fracture site.²⁰

Solid-State Transducer Intracompartmental Catheter. The Stryker Intra-Compartmental Pressure Monitor System (Stryker Surgical) is a commonly used solid-state transducer intracompartmental catheter (STIC) that allows measurement of compartment pressure.

The STIC system consists of a side-port needle, syringe of saline flush, and a digital read-out manometer. It has been validated against commonly used alternatives and found to be accurate^21,22 with a confidence interval between ± 5 to 6.23. This device uses a side port needle to allow for testing multiple compartments with the same needle as it is less likely to be occluded by tissue when compared to a standard needle.

The following technique should be employed to properly measure compartment pressure using the Stryker STIC device²³:

1. Place the side port needle on the tapered end of the diaphragm chamber.
2. Connect the prefilled syringe of normal saline to the diaphragm chamber.
3. Place the diaphragm chamber in the pressure monitor with the black side down and push until it is seated in the device.
4. Close the cover until it snaps.
5. Place the needle up and fill the system with normal saline from the syringe until there are no air bubbles in the system.
6. Turn the pressure monitor on.
7. Select an intended angle and press the “Zero” button and wait until it reads “00.”
8. Under sterile technique and appropriately anesthetized skin, insert the device into the compartment. Once in the compartment, slowly inject a small amount of saline into the compartment and record the provided number.

For details on needle-placement techniques, including depths, see Figures 1 to 4 for lower extremity compartments and Figures 5 to 7 for upper extremity compartments.²⁴

Laboratory Evaluation

Although the diagnosis of compartment syndrome is made by clinical findings and direct pressure measurement, laboratory tests can support the diagnosis.

Serum creatinine phosphokinase (CPK) is elevated with muscle necrosis. Both CPK and myoglobin proteins are glomerulotoxic, and acute kidney injury is a common complication of acute compartment syndrome. A CPK of greater than 1,000 IU/L has a sensitivity of 0.91 for acute compartment syndrome, but a specificity of only 0.52.2

In a multivariate model for predicting acute compartment syndrome, CPK greater than 4,000 IU/L, chloride greater than 104 mEq/L, and a blood urea nitrogen less than 10 mmol/L were found to be predictive of compartment syndrome during a patient’s hospital admission. No patient had compartment syndrome when all three variables were negative, and all patients with all three positive variables had acute compartment syndrome.²² This model was conducted on admitted patients during their inpatient hospital stay; therefore its application in the ED may not be valid, and the model has yet to be validated prospectively.

Treatment

Prompt surgical consultation for decompressive fasciotomy is paramount to the management of acute compartment syndrome in the ED. When acute compartment syndrome is suspected, elevation of the affected extremity is suggested in an attempt to decrease swelling.²⁷ The optimum height of elevation remains controversial; to prevent a decrease in arterial blood flow, it has been suggested not to raise the affected extremity above the level of the heart.⁸

A low systemic BP should be corrected to hopefully increase the compartment perfusion, and any applied external compressive forces (eg, casts, splints, dressings, eschars) should be removed.⁸ Removal of a cast can reduce the intracompartment pressure by 85%.⁵ Finally, applying cool compresses to the affected region can help reduce edema as a temporizing measure. Direct application of ice to the skin should be avoided to prevent cold-induced injury to the skin.

Appropriate medical resuscitation is imperative to good outcomes. Identifying and intervening when hypotension is present is necessary to improve tissue perfusion. Cellular derangement and death that can lead to hypocalcaemia, hyperkalemia, metabolic acidosis, and renal failure, require prompt recognition and correction.

At-Risk Populations

Pediatric Patients

Diagnosis of acute compartment syndrome in the general pediatric population is very difficult and therefore unfortunately associated with delays in diagnosis. The average time from injury to diagnosis can vary from 18.2to 31.1 hours.^28,29 In children younger than age 3 years, 60% of acute compartment syndrome cases are due to trauma; 27% are due to invasive infections; and 13% develop from intravenous (IV) infiltration.³⁰ Supracondylar humerus fractures are associated with increased risk of compartment syndrome. The volar compartment of the forearm is at risk after reduction of the fracture and when the elbow is flexed beyond 90°.³¹

Intubated and Obtunded Patients

Intubated and obtunded patients require special attention to prevent and/or identify the presence of acute compartment syndrome. Since clinical examination for compartment syndrome in these patients is unreliable, serial or continuous compartment pressure measurements are required to monitor for acute compartment syndrome.

Laboratory analysis, including monitoring of CPK levels, can also help identify developing compartment syndrome in intubated, sedated, or neurologically compromised patients.³² Onset of unexplained myoglobinuria or acute renal failure in an intubated patient should lead to consideration of compartment syndrome. In addition to laboratory studies, examination of atypical locations, such as the back or gluteal compartments, can also assist in identifying compartment syndrome in impaired patients.

Complications

The complications of compartment syndrome can be severe, and are typically organized as early and late stages of the disease.

Early Clinical Complications

Even with prompt diagnosis, acute compartment syndrome can lead to significant metabolic derangements. Patients with compartment syndrome are at significant risk for rhabdomyolysis and resultant renal failure from acute tubal necrosis. Likewise, both myocyte damage and death can cause extracellular electrolyte shifts, and hyperkalemia, metabolic acidosis, and hypocalcemia are frequently encountered under these circumstances.

Late Clinical Complications

Necrotic muscle is a significant risk factor for bacterial superinfection.³³ Necrotic muscle may quickly be seeded by bacteria, and lead to sepsis. Necrotic muscle may therefore require repeated debridement and even possible extremity amputation for infection control. Likewise, muscle necrosis can lead to muscle contractures and loss of function of the affected extremity.³

Medicolegal Complications

Delay in the diagnosis of acute compartment syndrome has become an increasing source of medicolegal liability. In a 2004 review by Bhattacharyya and Vrahas³⁴ of 23 years of claims from a medical malpractice insurer, only 19 claims were made for compartment syndrome. In this series, the following four risk factors were associated with an unsuccessful defense: (1) a linear association between the number of documented cardinal signs of compartment syndrome and an indemnity payment; (2) delays in fasciotomy; (3) poor communication with the patient and nursing staff; (4) and failure to intervene after documentation of an abnormal physical finding. All of the above were associated with a negative legal outcome.

Case Conclusion

The patient had a firm anterior compartment, CPK of 9,100 IU/L, normal renal function, compartment pressure of 60 mm Hg, and diastolic pressure of 80 mm Hg at the time of the procedure. Because the patient had a delta pressure of 20 mm Hg, orthopedic services were consulted, and the patient was taken to the operating room, where he underwent a bicompartment fasciotomy of the right lateral calf. The compartments were tense when opened and there was no evidence of myonecrosis. The patient was given continuous IV fluids and observed in the hospital for 2 days as his CPKs trended downward without subsequent renal injury.

Conclusion

Compartment syndrome requires high clinical suspicion for early diagnosis and treatment to prevent major disability. Early recognition of this condition is paramount, as the classical presentation of the five “Ps”—pain, pallor, pulselessness, paresthesias, and paralysis—are all late findings associated with irreversible consequences.

Given the difficulty in establishing the diagnosis by physical examination findings, the emergency physician (EP) should check and monitor compartment pressures when considering the diagnosis of acute compartment syndrome. In patients with acute compartment syndrome, delayed fasciotomies lead to poor outcomes and a 10-fold increase in surgical complications, such as infection and renal failure.³⁵

Although traumatic fractures are the most common cause of acute compartment syndrome, EPs must also recognize that obtundation, intubation, coagulopathies, and seemingly minor traumas all can potentially cause or lead to acute compartment syndrome.

Acute extremity pain is a common presentation seen daily in EDs. While most etiologies of extremity pain are benign, the complications of acute compartment syndrome are associated with significant morbidity. Moreover, acute compartment syndrome remains a difficult diagnosis that is often missed on initial presentation. Morbidity results from an increased pressure in an anatomically closed space, progressing to decreased perfusion and rapid tissue destruction.

Case

An obese 55-year-old man with a medical history of coronary artery disease, for which he was on aspirin therapy, presented for evaluation of right shin pain. The patient stated that he completed a 5-km race earlier that morning with his son. Immediately following the race, he experienced increasing right shin pain, which he attempted to initially manage with ice compresses and over-the-counter ibuprofen. He noted that neither the ice compresses nor the ibuprofen relieved his pain and that by 5:00 pm, the pain had worsened to the point where he had difficulty walking, prompting his visit to the ED.

Upon arrival at the ED, the patient was ambulatory but had significant pain at both rest and movement. His vital signs and his oxygen saturation on room air were normal. On physical examination, he had normal sensation to the entire right lower extremity and had equal pulses in both feet. The anterolateral aspect of the shin was exquisitely tender to light touch, and the patient was unable to dorsiflex or plantar flex without extreme pain. On passive dorsiflexion and plantar flexion of his right foot, he had exquisite pain. On palpation, the anterior shin was firm compared to the other muscle beds.

Epidemiology

Acute compartment syndrome—elevation of interstitial pressure in closed fascial compartment—affects 10 times as many men as women, at an average age of 32 years old and with an annual incidence of 7.3 per 100,000 men and 0.7 per 100,000 for women.¹ McQueen et al¹ found that the most common cause of acute compartment syndrome was fracture (69%), followed by soft tissue injury (23%). Younger patients are more likely to develop acute compartment syndrome from trauma because they typically have larger muscle beds with more tissue to become edematous compared to the older, hypotrophic muscles of elderly patients.

Pathophysiology

The fascia surrounds the major muscle groups and neurovascular bundles in the extremities to create distinct compartments. Since the fascia is not a compliant structure, it is typically not able to tolerate increases in volume or pressure in a given compartment. Compartment perfusion pressure is the mean arterial pressure minus the compartment pressure. Normal compartment pressure in adults is between 0 to 8 mm Hg.² When compartment perfusion pressures are below 70 to 80 mm Hg, there is an increased risk of compartment syndrome.

Although the exact pathophysiology of acute compartment syndrome is still debated,³ the most commonly accepted theory is the arteriovenous pressure gradient theory.⁴ In this theory, the rise in intracompartment pressure increases venous pressure, which in turn reduces the arteriovenous pressure gradient, reducing local tissue perfusion. The reduction in tissue perfusion, coupled with a reduction in venous drainage, causes significant tissue edema. This change in vascular pressure also causes a reduction in lymphatic drainage, further increasing pressure in the compartment. Finally, the edematous tissue compresses the arterioles leading to end-organ ischemia.⁵

Initially an absolute threshold compartment pressure was thought to cause irreversible tissue ischemia,⁶ but this theory has slowly lost favor after it was found that hypertension was actually protective in compartment syndrome.⁷ Current thinking is that the difference between the diastolic pressure and the compartment pressure leads to tissue ischemia (ie, acute compartment syndrome delta pressure = diastolic blood pressure [BP] – measured compartment pressure).^6,8

In 1996, McQueen and Court-Brown⁶ prospectively admitted all tibial diaphyseal fractures and continuously monitored their anterior compartment pressure. Using a delta pressure value of less than 30 mm Hg, only three patients were diagnosed with acute compartment syndrome and required fasciotomy. The patients’ absolute compartment pressures were 45 mm Hg, 65 mm Hg, and 75 mm Hg, while the delta pressures were 15 mm Hg, 10 mm Hg, and 15 mm Hg, respectively. Conversely, 53 patients had absolute compartment pressures over 30 mm Hg; 30 patients had pressure over 40 mm Hg; four patients had pressure over 50 mm Hg; and none required fasciotomy. This study highlights that the absolute compartment pressure is not helpful in making the diagnosis, and it is the elevated delta pressure that secures the diagnosis.

Etiology

Compartment syndrome is the end result of many different injury patterns. While fracture is the number one cause of compartment syndrome, many types of soft tissue injuries can also lead to compartment syndrome. Nonfracture etiologies of compartment syndrome are relatively uncommon, and as such can lead to a delay in diagnosis.

Fracture

Almost 70% of all cases of compartment syndrome are due to fracture.¹ Fractures of the tibia, distal radius, and ulna are the most common injuries that lead to acute compartment syndrome. Interestingly, acute compartment syndrome is caused by an equal distribution of high-energy and low-energy mechanisms of injuries.¹ Because the increase in compartment pressure is highest at the fracture site,⁹ it is imperative to measure pressures at the site of the fracture. Contrary to traditional teaching, an open fracture does not reduce the risk of compartment syndrome. McQueen and Court-Brown⁶ found there was no difference in the intracompartment pressure between open and closed fractures.

Fracture reduction and manipulation can actually increase the risk of compartment syndrome. In one case series, fracture manipulation increased compartment pressure by reducing the total volume in a stretched compartment.¹⁰ Dresing et al¹⁰ found the average pressure increased by 21 mm Hg during wrist reduction, warranting close observation after fracture reduction and close observation of the patient’s pain and neurovascular status.

McQueen et al¹¹ evaluated the risk factors for the development of acute compartment syndrome from tibial diaphyseal fractures and found that younger patients were at the highest risk. Patients between ages 10 to 19 years old had an odds ratio (OR) of 12.09; 20 to 29 years old had an OR of 9.84; and patients older than age 40 years had an OR of 1.¹¹ As previously stated, younger patients have larger muscle volumes compared to their older counterparts and therefore have less space for edema after the primary muscle injury.

Soft Tissue Injury

Direct soft tissue injury can lead to a rise in compartment pressures due to trauma, infections, and burns even in the absence of fractures. Unfortunately, under these circumstances, patients with direct soft tissue injury are at high risk for a delay in diagnosis.¹² The primary injury can be worsened by underlying coagulopathies.¹ A circumferential constrictive eschar from burns can also cause external compression to a compartment¹³ as well as edema, which decreases the compliance of the fascia, leading to a rise in compartment pressure.

Vascular Injuries and Unusual Causes

Arterial Vessel Damage. Injuries to single arterial vessels can also lend to the development of acute compartment syndrome. Arterial damage from high-energy trauma causes acute compartment syndromes due to the rapid development of a hematoma and pressure in affected compartments. Loss of the arterial blood flow from the traumatized artery also causes cell necrosis and edema to the muscle bed, further increasing the compartment pressure. The result of these injuries is the development of acute compartment syndrome in uncommon locations such as the thigh^{14 and foot.15}

Arterial damage from relatively low-energy ankle-inversion injuries have also been implicated in development of acute compartment syndrome of the foot.¹⁵ Conversely, damage to branches of an artery may cause symptoms in the compartments of the proximal extremity, but spare the blood flow and pulsations to the distal portion.¹³ This atypical mechanism of injury requires the physician to maintain a high index of suspicion and consider arteriography and direct pressure management in diagnosis and treatment of this condition.

Deep Vein Thrombosis. Deep vein thrombosis (DVT) can also be associated with acute compartment syndrome. A large clot burden, such as that observed in phlegmasia cerulea dolens, can lead to reduced venous flow and increased pressure, resulting in decreased arteriovenous gradient and tissue perfusion. Acute compartment syndrome caused by extensive DVT is often treated with anticoagulation therapy, thrombolysis or thrombectomy, but fasciotomy also has a role as an adjunct treatment to reduce compartment pressure sufficiently to return blood flow.¹⁶

Medication-Induced Compartment Syndrome

Injections of medications or illicit drugs can lead to increased compartment pressure through several independent mechanisms (Table).¹⁷ Local tissue vasotoxicity from direct injection of a caustic agent can cause direct muscle necrosis and edema. In addition, prolonged external compression while lying in a coma-like state induced by alcohol intoxication or central nervous system suppressant drugs, or a state of unconsciousness from any cause, can produce direct injury to the compartment (Table).

Diagnosis

Signs and Symptoms

Diagnosis of acute compartment syndrome is primarily clinical, using compartment pressure measurement as an adjunct in evaluation. Because the features of early acute compartment syndrome are nonspecific, a high clinical suspicion must be maintained for all at-risk populations.

The classic features such as pain, pallor, paresthesias, paralysis, and pulselessness are all late findings of acute compartment syndrome and are associated with irreversible damage. However, pain out of proportion to injury and pain with passive stretch of muscles are early symptoms that require further attention and monitoring.⁸

The earliest objective finding on physical examination is compartment firmness.⁸ Unfortunately, the sensitivity of physical examination by orthopedic physicians is low (22%-26%) on cadaver models with elevated compartment pressures.¹⁸ Peripheral nerve tissue is very sensitive to ischemia and will stop functioning after 75 minutes.⁹ A review of clinical findings in acute compartment syndrome showed that the positive predictive values of these individual symptoms are low, but there is a high likelihood of compartment syndrome when at least three clinical findings are present simultaneously.¹⁹ In patients who are at high risk for developing acute compartment syndrome, but who may not be able to describe or who do not show clear symptoms (eg, patients who are obtunded, intubated, or very young/old), compartment pressure measurement can be a valuable aid in the diagnosis.

Compartment Pressure Measurement

There are several readily available methods to directly measure the compartment pressure. It is imperative to measure the compartment pressure closest to the fracture location (within 5 cm) because the pressure dissipates as distance increases from the fracture site.²⁰

Solid-State Transducer Intracompartmental Catheter. The Stryker Intra-Compartmental Pressure Monitor System (Stryker Surgical) is a commonly used solid-state transducer intracompartmental catheter (STIC) that allows measurement of compartment pressure.

The STIC system consists of a side-port needle, syringe of saline flush, and a digital read-out manometer. It has been validated against commonly used alternatives and found to be accurate^21,22 with a confidence interval between ± 5 to 6.23. This device uses a side port needle to allow for testing multiple compartments with the same needle as it is less likely to be occluded by tissue when compared to a standard needle.

The following technique should be employed to properly measure compartment pressure using the Stryker STIC device²³:

1. Place the side port needle on the tapered end of the diaphragm chamber.
2. Connect the prefilled syringe of normal saline to the diaphragm chamber.
3. Place the diaphragm chamber in the pressure monitor with the black side down and push until it is seated in the device.
4. Close the cover until it snaps.
5. Place the needle up and fill the system with normal saline from the syringe until there are no air bubbles in the system.
6. Turn the pressure monitor on.
7. Select an intended angle and press the “Zero” button and wait until it reads “00.”
8. Under sterile technique and appropriately anesthetized skin, insert the device into the compartment. Once in the compartment, slowly inject a small amount of saline into the compartment and record the provided number.

For details on needle-placement techniques, including depths, see Figures 1 to 4 for lower extremity compartments and Figures 5 to 7 for upper extremity compartments.²⁴

Laboratory Evaluation

Although the diagnosis of compartment syndrome is made by clinical findings and direct pressure measurement, laboratory tests can support the diagnosis.

Serum creatinine phosphokinase (CPK) is elevated with muscle necrosis. Both CPK and myoglobin proteins are glomerulotoxic, and acute kidney injury is a common complication of acute compartment syndrome. A CPK of greater than 1,000 IU/L has a sensitivity of 0.91 for acute compartment syndrome, but a specificity of only 0.52.2

In a multivariate model for predicting acute compartment syndrome, CPK greater than 4,000 IU/L, chloride greater than 104 mEq/L, and a blood urea nitrogen less than 10 mmol/L were found to be predictive of compartment syndrome during a patient’s hospital admission. No patient had compartment syndrome when all three variables were negative, and all patients with all three positive variables had acute compartment syndrome.²² This model was conducted on admitted patients during their inpatient hospital stay; therefore its application in the ED may not be valid, and the model has yet to be validated prospectively.

Treatment

Prompt surgical consultation for decompressive fasciotomy is paramount to the management of acute compartment syndrome in the ED. When acute compartment syndrome is suspected, elevation of the affected extremity is suggested in an attempt to decrease swelling.²⁷ The optimum height of elevation remains controversial; to prevent a decrease in arterial blood flow, it has been suggested not to raise the affected extremity above the level of the heart.⁸

A low systemic BP should be corrected to hopefully increase the compartment perfusion, and any applied external compressive forces (eg, casts, splints, dressings, eschars) should be removed.⁸ Removal of a cast can reduce the intracompartment pressure by 85%.⁵ Finally, applying cool compresses to the affected region can help reduce edema as a temporizing measure. Direct application of ice to the skin should be avoided to prevent cold-induced injury to the skin.

Appropriate medical resuscitation is imperative to good outcomes. Identifying and intervening when hypotension is present is necessary to improve tissue perfusion. Cellular derangement and death that can lead to hypocalcaemia, hyperkalemia, metabolic acidosis, and renal failure, require prompt recognition and correction.

At-Risk Populations

Pediatric Patients

Diagnosis of acute compartment syndrome in the general pediatric population is very difficult and therefore unfortunately associated with delays in diagnosis. The average time from injury to diagnosis can vary from 18.2to 31.1 hours.^28,29 In children younger than age 3 years, 60% of acute compartment syndrome cases are due to trauma; 27% are due to invasive infections; and 13% develop from intravenous (IV) infiltration.³⁰ Supracondylar humerus fractures are associated with increased risk of compartment syndrome. The volar compartment of the forearm is at risk after reduction of the fracture and when the elbow is flexed beyond 90°.³¹

Intubated and Obtunded Patients

Intubated and obtunded patients require special attention to prevent and/or identify the presence of acute compartment syndrome. Since clinical examination for compartment syndrome in these patients is unreliable, serial or continuous compartment pressure measurements are required to monitor for acute compartment syndrome.

Laboratory analysis, including monitoring of CPK levels, can also help identify developing compartment syndrome in intubated, sedated, or neurologically compromised patients.³² Onset of unexplained myoglobinuria or acute renal failure in an intubated patient should lead to consideration of compartment syndrome. In addition to laboratory studies, examination of atypical locations, such as the back or gluteal compartments, can also assist in identifying compartment syndrome in impaired patients.

Complications

The complications of compartment syndrome can be severe, and are typically organized as early and late stages of the disease.

Early Clinical Complications

Even with prompt diagnosis, acute compartment syndrome can lead to significant metabolic derangements. Patients with compartment syndrome are at significant risk for rhabdomyolysis and resultant renal failure from acute tubal necrosis. Likewise, both myocyte damage and death can cause extracellular electrolyte shifts, and hyperkalemia, metabolic acidosis, and hypocalcemia are frequently encountered under these circumstances.

Late Clinical Complications

Necrotic muscle is a significant risk factor for bacterial superinfection.³³ Necrotic muscle may quickly be seeded by bacteria, and lead to sepsis. Necrotic muscle may therefore require repeated debridement and even possible extremity amputation for infection control. Likewise, muscle necrosis can lead to muscle contractures and loss of function of the affected extremity.³

Medicolegal Complications

Delay in the diagnosis of acute compartment syndrome has become an increasing source of medicolegal liability. In a 2004 review by Bhattacharyya and Vrahas³⁴ of 23 years of claims from a medical malpractice insurer, only 19 claims were made for compartment syndrome. In this series, the following four risk factors were associated with an unsuccessful defense: (1) a linear association between the number of documented cardinal signs of compartment syndrome and an indemnity payment; (2) delays in fasciotomy; (3) poor communication with the patient and nursing staff; (4) and failure to intervene after documentation of an abnormal physical finding. All of the above were associated with a negative legal outcome.

Case Conclusion

The patient had a firm anterior compartment, CPK of 9,100 IU/L, normal renal function, compartment pressure of 60 mm Hg, and diastolic pressure of 80 mm Hg at the time of the procedure. Because the patient had a delta pressure of 20 mm Hg, orthopedic services were consulted, and the patient was taken to the operating room, where he underwent a bicompartment fasciotomy of the right lateral calf. The compartments were tense when opened and there was no evidence of myonecrosis. The patient was given continuous IV fluids and observed in the hospital for 2 days as his CPKs trended downward without subsequent renal injury.

Conclusion

Compartment syndrome requires high clinical suspicion for early diagnosis and treatment to prevent major disability. Early recognition of this condition is paramount, as the classical presentation of the five “Ps”—pain, pallor, pulselessness, paresthesias, and paralysis—are all late findings associated with irreversible consequences.

Given the difficulty in establishing the diagnosis by physical examination findings, the emergency physician (EP) should check and monitor compartment pressures when considering the diagnosis of acute compartment syndrome. In patients with acute compartment syndrome, delayed fasciotomies lead to poor outcomes and a 10-fold increase in surgical complications, such as infection and renal failure.³⁵

Although traumatic fractures are the most common cause of acute compartment syndrome, EPs must also recognize that obtundation, intubation, coagulopathies, and seemingly minor traumas all can potentially cause or lead to acute compartment syndrome.

Editor’s Note: This article has been adapted from an article originally published in Federal Practitioner (Clement C, Stock C. Who overdoses at a VA emergency department? Fed Prac. 2016;33[11]:14-19. http://www.fedprac.com).

Overdose deaths remain epidemic throughout the United States. The rates of unintentional overdose deaths, increasing by 137% between 2000 and 2014, have been driven by a 4-fold increase in prescription opioid overdoses during that period.^1-3

Veterans died of accidental overdose at a rate of 19.85 deaths/100,000 people compared with a rate of 10.49 deaths in the general population, based on 2005 data.⁴ There is wide state-by-state variation, with the lowest age-adjusted opioid overdose death rate of 1.9 deaths/100,000 person-years among veterans in Mississippi and the highest rate in Utah of 33.9 deaths/100,000 person-years, using 2001 to 2009 data.⁵ These data can be compared with a crude general population overdose death rate of 10.6 deaths per 100,000 person-years in Mississippi and 18.4 deaths per 100,000 person-years in the general Utah population during that same period.⁶

Overdose deaths in the United States occur most often in persons aged 25 to 54 years.⁷ Older age has been associated with iatrogenic opioid overdose in hospitalized patients.⁸ Pulmonary disease, cardiovascular disease (CVD), and psychiatric disorders, including past or present substance use, have been associated with an increased risk of opioid overdose.⁹ However, veterans with substance use disorders are less likely to be prescribed opioids than are nonveterans with substance use disorders.¹⁰ Also, concomitant use of sedating medications, such as benzodiazepines (BZDs), can increase mortality from opioid overdose.¹¹ Patients prescribed opioids for chronic pain conditions often take BZDs for various reasons.¹² Veterans seem more likely to receive opioids to treat chronic pain but at lower average daily doses than doses prescribed to nonveterans.¹⁰

Emergency management of life-threatening opioid overdose includes prompt administration of naloxone.¹³ Naloxone is approved by the US Food and Drug Administration for complete or partial reversal of opioid-induced clinical effects, most critically respiratory depression.^14,15 Naloxone administration in the ED may serve as a surrogate for an overdose event. During the study period, naloxone take-home kits were not available in the Veterans Affairs (VA) setting.

A 2010 ED study described demographic information and comorbidities in opioid overdose, but the study did not include veterans.¹⁶ The clinical characteristics of veterans treated for opioid overdose have not been published. Because identifying characteristics of veterans who overdose may help tailor overdose-prevention efforts, the objective of this study is to describe clinical characteristics of veterans treated for opioid overdose.

Methods

A retrospective chart review and archived data study was approved by the University of Utah and VA Institutional Review Boards, and conducted at the George E. Wahlen Veterans Affairs Medical Center (VAMC) in Salt Lake City, Utah. This chart review included veterans who were admitted to the ED and treated with naloxone between January 1, 2009 and January 1, 2013. 

The authors used the Pharmacy Benefits Management Data Manager to extract data from the VA Data Warehouse and verified the data by open chart review (Table). The following data were collected: ED visit date (overdose date); demographic information, including age, gender, and race; evidence of next of kin or other contact at the same address as the veteran; diagnoses based on International Classification of Diseases, 9th Revision (ICD-9) codes, including sleep apnea, obesity, cardiac disease, pulmonary disease, mental health diagnoses (ICD-9 codes 290-302 [wild card characters (*) included many subdiagnoses]), cancer, and substance use disorders and/or dependencies (SUDD); tobacco use; VA-issued prescription opioid and BZD availability, including dose, fill dates, quantities dispensed, and day supplies; specialty of opioid prescriber; urine-drug screening (UDS) results; and outcome of the overdose. 

No standardized research criteria identify overdose in medical chart review.¹⁷ For each identified patient, the authors reviewed provider and nursing notes charted during an ED visit that included naloxone administration. The event was included as an opioid overdose when notes indicated that the veteran was unresponsive and given naloxone, which resulted in increased respirations or increased responsiveness. Cases were excluded if the reason for naloxone administration was anything other than opioid overdose.

Medical, mental health, and SUDD diagnoses were included only if the veteran had more than three patient-care encounters (PCE) with ICD-9 codes for a specific diagnosis entered by providers. A PCE used in the electronic medical record (EMR) helps collect, manage, and display outpatient encounter data, including providers, procedure codes, and diagnostic codes. Tobacco use was extracted from health factors documented during primary care visit screenings. (Health factors help capture data entered in note templates in the EMR and can be used to query trends.) A diagnosis of obesity was based on a calculated body mass index of at or greater than 30 kg/m² on the day of the ED visit date or the most recently charted height and weight. The type of SUDD was stratified into opioids (ICD-9 codes 304.0*), sedatives (ICD-9 codes 304.1*), alcohol (ICD-9 codes 303.*), and other (ICD-9 codes 304.2-305.9).

The dosage of opioids and BZDs available to a veteran was determined by using methods similar to those described by Gomes et al¹⁸: the dose of opioids and BZDs available based on prescriptions dispensed during the 120 days prior to the ED visit date and the dose available on the day of the ED visit date if prescription instructions were being followed. Prescription opioids and BZDs were converted to daily morphineequivalent dose (MED) and daily lorazepam equivalent dose (LED), using established methods.^19,20

Veterans were stratified into four groups based on prescribed medication availability: opioids only, BZDs only, opioids and BZDs, and neither opioids nor BZDs. The specialty of the opioid prescribers was categorized as primary care, pain specialist, surgeon, emergency specialist, or hospitalist (discharge prescription). Veteran EMRs contain a list of medications obtained outside the VA facility, referred to as non-VA prescriptions. These medications were not included in the analysis because accuracy could not be verified.

A study author reviewed the results of any UDS performed up to 120 days before the ED visit date to determine whether the result reflected the currently prescribed prescription medications. If the UDS was positive for the prescribed opioids and/or BZDs and for any nonprescribed drug, including alcohol, the UDS was classified as not reflective. If the prescribed BZD was alprazolam, clonazepam, or lorazepam, a BZD-positive UDS was not required for the UDS to be considered reflective because of the sensitivity of the UDS BZD immunoassay used at the George E. Wahlen VAMC clinical laboratory.²¹

Outcomes of the overdose were categorized as discharged, hospitalized, or deceased. Descriptive statistical analyses were performed using Microsoft Excel. Group comparisons were performed using Pearson chi-square or Student t test.

Results

The ED at the George E. Wahlen VAMC averages 64 visits per day, almost 94,000 visits within the study period. One hundred seventy ED visits between January 1, 2009 and January 1, 2013, involved naloxone administration. Ninety-two visits met the inclusion criteria of opioid overdose, representing about 0.002% of all ED visits at this facility (Figure 1). Six veterans had multiple ED visits within the study period, including four veterans who were in the opioid-only group.

The majority of veterans in this study were non-Hispanic white (n = 83, 90%), male (n = 88, 96%), with a mean age of 63 years. Less than 40% listed a next of kin or contact person living at their address.

Based on prescriptions available within 120 days before the overdose, 67 veterans (73%) possessed opioid and/or BZD prescriptions. In this group, the MED available on the day of the ED visit ranged from 7.5 mg to 830 mg. The MED was less than or equal to 200 mg in 71.6% and less than or equal to 50 mg in 34.3% of these cases. Veterans prescribed both opioids and BZDs had higher MED (average, 259 mg) available within 120 days of the ED visit than did those prescribed opioids only (average, 118 mg) (P = .015; standard deviation [SD], 132.9). The LED ranged from 1 mg to 12 mg for veterans with available BZDs.

Based on prescriptions available on the day of opioid overdose, 53 veterans (58%) had opioid prescriptions. The ranges of MED and LED available on the day of overdose were the same as the 120-day availability period. The average MED was 183 mg in veterans prescribed both opioids and BZDs and 126 mg in those prescribed opioids only (P = .283; SD, 168.65; Figure 2). The time between the last opioid fill date and the overdose visit date averaged 20 days (range, 0 to 28 days) in veterans prescribed opioids.

Discussion

This retrospective review identified 92 veterans who were treated with naloxone in the ED for opioid overdose during a 4-year period at the George E. Wahlen VAMC. Seventy-eight cases were excluded because the reason entered in charts for naloxone administration was itching, constipation, altered mental status, or unclear documentation.

Veterans in this study were, on average, older than the overdose fatalities in the United States. Opioid-overdose deaths in all US states and in Utah alone occur most frequently in non-Hispanic white men aged between 35 and 54 years.^7,22,23 In the 2010 Nationwide Emergency Department Sample of 136,000 opioid overdoses, of which 98% survived, most were aged 18 to 54 years.¹⁶ The older age in this study most likely reflects the age range of veterans served in the Veterans Health Administration (VHA); however, as more young veterans enter the VHA, the age range of overdose victims may more closely resemble the age ranges found in previous studies. Post hoc analysis showed eight veterans (9%) with probable intentional opioid overdose based on chart review, whereas the incidence of intentional prescription drug overdose in the United States is 17.1%.²⁴

In Utah, almost 93% of fatal overdoses occur at a residential location.²² Less than half of the veterans in this study had a contact or next of kin listed as living at the same address. Although veterans may not have identified someone living with them, in many cases, it is likely another person witnessed the overdose. Relying on EMRs to identify who should receive prevention education in addition to the veteran, may result in missed opportunities to include another person likely to witness an overdose.²⁵ Prescribers should make a conscious effort to ask veterans to identify someone who may be able to assist with rescue efforts in the event of an overdose.

Diagnoses associated with increased risk of opioid-overdose death include sleep apnea, morbid obesity, pulmonary disease or CVD, and/or a history of psychiatric disorders and SUDD.^8,9,16 In a large sample of older veterans, only 64% had at least one medical or psychiatric diagnosis.²⁶ Less than half of the 18,000 VA primary care patients in five VA centers had any psychiatric condition, and less than 65% had CVD, pulmonary disease, or cancer.²⁷ All veterans in this study had medical and psychiatric comorbidity.

In contrast, a large ED sample described by Yokell et al¹⁶ found chronic mental conditions in 33.9%, circulatory disorders in 29.1%, and respiratory conditions in 25.6% of their sample. Bohnert et al⁹ found a significantly elevated hazard ratio (HR) for any psychiatric disorder in a sample of nearly 4,500 veterans. There was variation in the HR when individual psychiatric diagnoses were broken out, with bipolar disorder having the largest HR and schizophrenia having the lowest but still elevated HR.⁹ In this study, individual diagnoses were not broken out because the smaller sample size could diminish the clinical significance of any apparent differences.

Edlund et al¹⁰ found that less than 8% of veterans treated with opioids for chronic noncancer pain had nonopioid SUDD. Bohnert et al⁹ found an HR of 21.95 for overdose death among those with opioid-use disorders. The sample in this study had a much higher incidence of nonopioid SUDD compared with that of the study by Edlund et al,¹⁰ but none of the veterans in this study had a documented history of opioid-use disorder. The absence of opioid-use disorders in this sample is unexpected and points to a need for providers to screen for opioid-use disorder whenever opioids are prescribed or renewed. If prevention practices were directed only to those with opioid SUDDs, none of the veterans in this study would have been included in those efforts. Non-SUDD providers should address the risks of opioid overdose in veterans with sleep apnea, morbid obesity, pulmonary disease or CVD, and/or a history of psychiatric disorders.

Gomes et al¹⁸ found that greater than 100 mg MED available on the day of overdose doubled the risk of opioid-related mortality. The VA/Department of Defense Clinical Practice Guideline for Management of Opioid Therapy for Chronic Pain identifies 200 mg MED as a threshold to define high-dose opioid therapy.²⁸ Fulton-Kehoe et al²⁹ found that 28% of overdose victims were prescribed less than 50 mg MED. In this study, the average dose available to veterans was greater than 100 mg MED; however, one-third of all study veterans had less than 50 mg MED available. Using a threshold dose of 50 mg MED to target prevention efforts would capture only two-thirds of those who experienced overdose; a 200-mg MED threshold would exclude the majority, based on the average MED in each group in this study. Overdose education should be provided to veterans with access to opioids, regardless of dose.

Use of BZDs with opioids may result in greater central nervous system (CNS) depression, pharmacokinetic interactions, or pharmacodynamic interactions at the µ- opioid receptor.^30-32 About one-third of veterans in this study were prescribed opioids and BZDs concurrently, a combination noted in about 33% of opioid overdose deaths reported by the Centers for Disease Control and Prevention.²⁴ Individuals taking methadone combined with BZDs have been found to have severe medical outcomes.³³ If preventive efforts are targeted to those receiving opioids and other CNS depressants, such as BZDs, about half (42%) of the veterans in this study would not receive a potentially life-saving message about preventing overdoses. All veterans with opioids should be educated about the additional risk of overdose posed by drug interactions with other CNS depressants.

The time since the last fill of an opioid prescription ranged from 0 to 28 days. This time frame indicates that some overdoses may have occurred on the day an opioid was filled but most occurred near the end of the expected days’ supply. Because information about adherence or use of the opioid was not studied, it cannot be assumed that medication misuse is the primary reason for the overdose. Providing prevention efforts only at the time of medication dispensing would be insufficient. Clinicians should review local and remote prescription data, including via their states’ prescription drug monitoring program, when discussing the risk of overdose with veterans.

Most veterans had at least one UDS result in the chart. Although half the UDSs obtained reflected prescribed medications, the possibility of aberrant behaviors, which increases the risk of overdose, cannot be ruled out with the methods used in this study.³⁴ Medication management agreements that require UDSs for veterans with chronic pain were not mandatory at the George E. Wahlen VAMC during the study period, and those used did not mandate discontinuation of opioid therapy if suspected aberrant behaviors were present.

A Utah study based on interviews of overdose victims’ next of kin found that 76% were concerned about victims’ aberrant behaviors, such as medication misuse, prior to the death.²² In contrast, a study of commercial and Medicaid recipients estimated medication misuse rates in at or less than 30% of the sample.³⁵ Urine-drug screening results not reflective of the prescribed regimens have been found in up to 50% of patients receiving chronic opioid therapy.

The UDS findings in this study were determined by the authors and did not capture clinical decisions or interpretations made after results were available or whether these decisions resulted in overdose-prevention strategies, such as targeted education or changes in prescription availability. Targeting preventive efforts toward veterans only with UDS results suggesting medication misuse would have missed more than half the veterans in this study. Urine-drug screening should be used as a clinical monitoring tool whenever opioids, BZDs, or other substances are used or prescribed.

The VA now has a nationwide program, Opioid Overdose Education and Naloxone Distribution (OEND), promoting overdose education and take-home naloxone distribution for providers and patients to prevent opioid-related overdose deaths. A national SharePoint site has been created within the VA that lists resources to support this effort.

Almost all veterans in this review survived the overdose and were hospitalized following the ED visit. Other investigators also have found that the majority (51% to 98%) of overdose victims reaching the ED survived, but fewer patients (3% to 51%) in those studies were hospitalized.^16,36 It is unknown whether there are differences in risk factors associated with survived or fatal overdoses.

Limitations

Although Utah ranked third for drug-overdose death rates in 2008 and had the highest death rate among veterans from 2001 to 2009, this review captured only overdoses among veterans treated during the study period at the George E. Wahlen VAMC ED.^5,6 The number and characteristics of veterans during this same period who were treated for overdose in other community EDs or urgent care centers throughout Utah is unknown.

The definition of opioid and BZD dose available in this study may not represent actual use of opioids or BZDs because it was based on chart review of prescription dispensing information and UDS procedures at the George E. Wahlen VAMC, and medication misuse cannot be ruled out. This study did not evaluate specific aberrant behaviors.

Conclusion

Current overdose-prevention screening efforts primarily identify patients on high-dose opioids and those with SUDD. Many veterans in this study were older than the average US victims’ age, did not have SUDD, were prescribed opioid doses not considered high risk by current guidelines, were nearer the end of their medication supply, and had UDS reflective of prescribed medications. This study suggests that any veteran with access to opioids, whether prescribed or not, is at risk for an opioid overdose. Established risk factors may aid in developing overdose-prevention programs, but prevention should not be limited to veterans with prescribed opioids and known risk factors. Clinicians should screen patients for opioid-use disorder whenever opioids are prescribed and continue to screen them throughout therapy. Broader screening for overdose risk is needed to avoid missing important opportunities for overdose prevention.

Acknowledgments

Gale Anderson, VISN 19 PBM Data Manager, performed initial data query for the study.

Editor’s Note: This article has been adapted from an article originally published in Federal Practitioner (Clement C, Stock C. Who overdoses at a VA emergency department? Fed Prac. 2016;33[11]:14-19. http://www.fedprac.com).

Overdose deaths remain epidemic throughout the United States. The rates of unintentional overdose deaths, increasing by 137% between 2000 and 2014, have been driven by a 4-fold increase in prescription opioid overdoses during that period.^1-3

Veterans died of accidental overdose at a rate of 19.85 deaths/100,000 people compared with a rate of 10.49 deaths in the general population, based on 2005 data.⁴ There is wide state-by-state variation, with the lowest age-adjusted opioid overdose death rate of 1.9 deaths/100,000 person-years among veterans in Mississippi and the highest rate in Utah of 33.9 deaths/100,000 person-years, using 2001 to 2009 data.⁵ These data can be compared with a crude general population overdose death rate of 10.6 deaths per 100,000 person-years in Mississippi and 18.4 deaths per 100,000 person-years in the general Utah population during that same period.⁶

Overdose deaths in the United States occur most often in persons aged 25 to 54 years.⁷ Older age has been associated with iatrogenic opioid overdose in hospitalized patients.⁸ Pulmonary disease, cardiovascular disease (CVD), and psychiatric disorders, including past or present substance use, have been associated with an increased risk of opioid overdose.⁹ However, veterans with substance use disorders are less likely to be prescribed opioids than are nonveterans with substance use disorders.¹⁰ Also, concomitant use of sedating medications, such as benzodiazepines (BZDs), can increase mortality from opioid overdose.¹¹ Patients prescribed opioids for chronic pain conditions often take BZDs for various reasons.¹² Veterans seem more likely to receive opioids to treat chronic pain but at lower average daily doses than doses prescribed to nonveterans.¹⁰

Emergency management of life-threatening opioid overdose includes prompt administration of naloxone.¹³ Naloxone is approved by the US Food and Drug Administration for complete or partial reversal of opioid-induced clinical effects, most critically respiratory depression.^14,15 Naloxone administration in the ED may serve as a surrogate for an overdose event. During the study period, naloxone take-home kits were not available in the Veterans Affairs (VA) setting.

A 2010 ED study described demographic information and comorbidities in opioid overdose, but the study did not include veterans.¹⁶ The clinical characteristics of veterans treated for opioid overdose have not been published. Because identifying characteristics of veterans who overdose may help tailor overdose-prevention efforts, the objective of this study is to describe clinical characteristics of veterans treated for opioid overdose.

Methods

A retrospective chart review and archived data study was approved by the University of Utah and VA Institutional Review Boards, and conducted at the George E. Wahlen Veterans Affairs Medical Center (VAMC) in Salt Lake City, Utah. This chart review included veterans who were admitted to the ED and treated with naloxone between January 1, 2009 and January 1, 2013. 

The authors used the Pharmacy Benefits Management Data Manager to extract data from the VA Data Warehouse and verified the data by open chart review (Table). The following data were collected: ED visit date (overdose date); demographic information, including age, gender, and race; evidence of next of kin or other contact at the same address as the veteran; diagnoses based on International Classification of Diseases, 9th Revision (ICD-9) codes, including sleep apnea, obesity, cardiac disease, pulmonary disease, mental health diagnoses (ICD-9 codes 290-302 [wild card characters (*) included many subdiagnoses]), cancer, and substance use disorders and/or dependencies (SUDD); tobacco use; VA-issued prescription opioid and BZD availability, including dose, fill dates, quantities dispensed, and day supplies; specialty of opioid prescriber; urine-drug screening (UDS) results; and outcome of the overdose. 

No standardized research criteria identify overdose in medical chart review.¹⁷ For each identified patient, the authors reviewed provider and nursing notes charted during an ED visit that included naloxone administration. The event was included as an opioid overdose when notes indicated that the veteran was unresponsive and given naloxone, which resulted in increased respirations or increased responsiveness. Cases were excluded if the reason for naloxone administration was anything other than opioid overdose.

Medical, mental health, and SUDD diagnoses were included only if the veteran had more than three patient-care encounters (PCE) with ICD-9 codes for a specific diagnosis entered by providers. A PCE used in the electronic medical record (EMR) helps collect, manage, and display outpatient encounter data, including providers, procedure codes, and diagnostic codes. Tobacco use was extracted from health factors documented during primary care visit screenings. (Health factors help capture data entered in note templates in the EMR and can be used to query trends.) A diagnosis of obesity was based on a calculated body mass index of at or greater than 30 kg/m² on the day of the ED visit date or the most recently charted height and weight. The type of SUDD was stratified into opioids (ICD-9 codes 304.0*), sedatives (ICD-9 codes 304.1*), alcohol (ICD-9 codes 303.*), and other (ICD-9 codes 304.2-305.9).

The dosage of opioids and BZDs available to a veteran was determined by using methods similar to those described by Gomes et al¹⁸: the dose of opioids and BZDs available based on prescriptions dispensed during the 120 days prior to the ED visit date and the dose available on the day of the ED visit date if prescription instructions were being followed. Prescription opioids and BZDs were converted to daily morphineequivalent dose (MED) and daily lorazepam equivalent dose (LED), using established methods.^19,20

Veterans were stratified into four groups based on prescribed medication availability: opioids only, BZDs only, opioids and BZDs, and neither opioids nor BZDs. The specialty of the opioid prescribers was categorized as primary care, pain specialist, surgeon, emergency specialist, or hospitalist (discharge prescription). Veteran EMRs contain a list of medications obtained outside the VA facility, referred to as non-VA prescriptions. These medications were not included in the analysis because accuracy could not be verified.

A study author reviewed the results of any UDS performed up to 120 days before the ED visit date to determine whether the result reflected the currently prescribed prescription medications. If the UDS was positive for the prescribed opioids and/or BZDs and for any nonprescribed drug, including alcohol, the UDS was classified as not reflective. If the prescribed BZD was alprazolam, clonazepam, or lorazepam, a BZD-positive UDS was not required for the UDS to be considered reflective because of the sensitivity of the UDS BZD immunoassay used at the George E. Wahlen VAMC clinical laboratory.²¹

Outcomes of the overdose were categorized as discharged, hospitalized, or deceased. Descriptive statistical analyses were performed using Microsoft Excel. Group comparisons were performed using Pearson chi-square or Student t test.

Results

The ED at the George E. Wahlen VAMC averages 64 visits per day, almost 94,000 visits within the study period. One hundred seventy ED visits between January 1, 2009 and January 1, 2013, involved naloxone administration. Ninety-two visits met the inclusion criteria of opioid overdose, representing about 0.002% of all ED visits at this facility (Figure 1). Six veterans had multiple ED visits within the study period, including four veterans who were in the opioid-only group.

The majority of veterans in this study were non-Hispanic white (n = 83, 90%), male (n = 88, 96%), with a mean age of 63 years. Less than 40% listed a next of kin or contact person living at their address.

Based on prescriptions available within 120 days before the overdose, 67 veterans (73%) possessed opioid and/or BZD prescriptions. In this group, the MED available on the day of the ED visit ranged from 7.5 mg to 830 mg. The MED was less than or equal to 200 mg in 71.6% and less than or equal to 50 mg in 34.3% of these cases. Veterans prescribed both opioids and BZDs had higher MED (average, 259 mg) available within 120 days of the ED visit than did those prescribed opioids only (average, 118 mg) (P = .015; standard deviation [SD], 132.9). The LED ranged from 1 mg to 12 mg for veterans with available BZDs.

Based on prescriptions available on the day of opioid overdose, 53 veterans (58%) had opioid prescriptions. The ranges of MED and LED available on the day of overdose were the same as the 120-day availability period. The average MED was 183 mg in veterans prescribed both opioids and BZDs and 126 mg in those prescribed opioids only (P = .283; SD, 168.65; Figure 2). The time between the last opioid fill date and the overdose visit date averaged 20 days (range, 0 to 28 days) in veterans prescribed opioids.

Discussion

This retrospective review identified 92 veterans who were treated with naloxone in the ED for opioid overdose during a 4-year period at the George E. Wahlen VAMC. Seventy-eight cases were excluded because the reason entered in charts for naloxone administration was itching, constipation, altered mental status, or unclear documentation.

Veterans in this study were, on average, older than the overdose fatalities in the United States. Opioid-overdose deaths in all US states and in Utah alone occur most frequently in non-Hispanic white men aged between 35 and 54 years.^7,22,23 In the 2010 Nationwide Emergency Department Sample of 136,000 opioid overdoses, of which 98% survived, most were aged 18 to 54 years.¹⁶ The older age in this study most likely reflects the age range of veterans served in the Veterans Health Administration (VHA); however, as more young veterans enter the VHA, the age range of overdose victims may more closely resemble the age ranges found in previous studies. Post hoc analysis showed eight veterans (9%) with probable intentional opioid overdose based on chart review, whereas the incidence of intentional prescription drug overdose in the United States is 17.1%.²⁴

In Utah, almost 93% of fatal overdoses occur at a residential location.²² Less than half of the veterans in this study had a contact or next of kin listed as living at the same address. Although veterans may not have identified someone living with them, in many cases, it is likely another person witnessed the overdose. Relying on EMRs to identify who should receive prevention education in addition to the veteran, may result in missed opportunities to include another person likely to witness an overdose.²⁵ Prescribers should make a conscious effort to ask veterans to identify someone who may be able to assist with rescue efforts in the event of an overdose.

Diagnoses associated with increased risk of opioid-overdose death include sleep apnea, morbid obesity, pulmonary disease or CVD, and/or a history of psychiatric disorders and SUDD.^8,9,16 In a large sample of older veterans, only 64% had at least one medical or psychiatric diagnosis.²⁶ Less than half of the 18,000 VA primary care patients in five VA centers had any psychiatric condition, and less than 65% had CVD, pulmonary disease, or cancer.²⁷ All veterans in this study had medical and psychiatric comorbidity.

In contrast, a large ED sample described by Yokell et al¹⁶ found chronic mental conditions in 33.9%, circulatory disorders in 29.1%, and respiratory conditions in 25.6% of their sample. Bohnert et al⁹ found a significantly elevated hazard ratio (HR) for any psychiatric disorder in a sample of nearly 4,500 veterans. There was variation in the HR when individual psychiatric diagnoses were broken out, with bipolar disorder having the largest HR and schizophrenia having the lowest but still elevated HR.⁹ In this study, individual diagnoses were not broken out because the smaller sample size could diminish the clinical significance of any apparent differences.

Edlund et al¹⁰ found that less than 8% of veterans treated with opioids for chronic noncancer pain had nonopioid SUDD. Bohnert et al⁹ found an HR of 21.95 for overdose death among those with opioid-use disorders. The sample in this study had a much higher incidence of nonopioid SUDD compared with that of the study by Edlund et al,¹⁰ but none of the veterans in this study had a documented history of opioid-use disorder. The absence of opioid-use disorders in this sample is unexpected and points to a need for providers to screen for opioid-use disorder whenever opioids are prescribed or renewed. If prevention practices were directed only to those with opioid SUDDs, none of the veterans in this study would have been included in those efforts. Non-SUDD providers should address the risks of opioid overdose in veterans with sleep apnea, morbid obesity, pulmonary disease or CVD, and/or a history of psychiatric disorders.

Gomes et al¹⁸ found that greater than 100 mg MED available on the day of overdose doubled the risk of opioid-related mortality. The VA/Department of Defense Clinical Practice Guideline for Management of Opioid Therapy for Chronic Pain identifies 200 mg MED as a threshold to define high-dose opioid therapy.²⁸ Fulton-Kehoe et al²⁹ found that 28% of overdose victims were prescribed less than 50 mg MED. In this study, the average dose available to veterans was greater than 100 mg MED; however, one-third of all study veterans had less than 50 mg MED available. Using a threshold dose of 50 mg MED to target prevention efforts would capture only two-thirds of those who experienced overdose; a 200-mg MED threshold would exclude the majority, based on the average MED in each group in this study. Overdose education should be provided to veterans with access to opioids, regardless of dose.

Use of BZDs with opioids may result in greater central nervous system (CNS) depression, pharmacokinetic interactions, or pharmacodynamic interactions at the µ- opioid receptor.^30-32 About one-third of veterans in this study were prescribed opioids and BZDs concurrently, a combination noted in about 33% of opioid overdose deaths reported by the Centers for Disease Control and Prevention.²⁴ Individuals taking methadone combined with BZDs have been found to have severe medical outcomes.³³ If preventive efforts are targeted to those receiving opioids and other CNS depressants, such as BZDs, about half (42%) of the veterans in this study would not receive a potentially life-saving message about preventing overdoses. All veterans with opioids should be educated about the additional risk of overdose posed by drug interactions with other CNS depressants.

The time since the last fill of an opioid prescription ranged from 0 to 28 days. This time frame indicates that some overdoses may have occurred on the day an opioid was filled but most occurred near the end of the expected days’ supply. Because information about adherence or use of the opioid was not studied, it cannot be assumed that medication misuse is the primary reason for the overdose. Providing prevention efforts only at the time of medication dispensing would be insufficient. Clinicians should review local and remote prescription data, including via their states’ prescription drug monitoring program, when discussing the risk of overdose with veterans.

Most veterans had at least one UDS result in the chart. Although half the UDSs obtained reflected prescribed medications, the possibility of aberrant behaviors, which increases the risk of overdose, cannot be ruled out with the methods used in this study.³⁴ Medication management agreements that require UDSs for veterans with chronic pain were not mandatory at the George E. Wahlen VAMC during the study period, and those used did not mandate discontinuation of opioid therapy if suspected aberrant behaviors were present.

A Utah study based on interviews of overdose victims’ next of kin found that 76% were concerned about victims’ aberrant behaviors, such as medication misuse, prior to the death.²² In contrast, a study of commercial and Medicaid recipients estimated medication misuse rates in at or less than 30% of the sample.³⁵ Urine-drug screening results not reflective of the prescribed regimens have been found in up to 50% of patients receiving chronic opioid therapy.

The UDS findings in this study were determined by the authors and did not capture clinical decisions or interpretations made after results were available or whether these decisions resulted in overdose-prevention strategies, such as targeted education or changes in prescription availability. Targeting preventive efforts toward veterans only with UDS results suggesting medication misuse would have missed more than half the veterans in this study. Urine-drug screening should be used as a clinical monitoring tool whenever opioids, BZDs, or other substances are used or prescribed.

The VA now has a nationwide program, Opioid Overdose Education and Naloxone Distribution (OEND), promoting overdose education and take-home naloxone distribution for providers and patients to prevent opioid-related overdose deaths. A national SharePoint site has been created within the VA that lists resources to support this effort.

Almost all veterans in this review survived the overdose and were hospitalized following the ED visit. Other investigators also have found that the majority (51% to 98%) of overdose victims reaching the ED survived, but fewer patients (3% to 51%) in those studies were hospitalized.^16,36 It is unknown whether there are differences in risk factors associated with survived or fatal overdoses.

Limitations

Although Utah ranked third for drug-overdose death rates in 2008 and had the highest death rate among veterans from 2001 to 2009, this review captured only overdoses among veterans treated during the study period at the George E. Wahlen VAMC ED.^5,6 The number and characteristics of veterans during this same period who were treated for overdose in other community EDs or urgent care centers throughout Utah is unknown.

The definition of opioid and BZD dose available in this study may not represent actual use of opioids or BZDs because it was based on chart review of prescription dispensing information and UDS procedures at the George E. Wahlen VAMC, and medication misuse cannot be ruled out. This study did not evaluate specific aberrant behaviors.

Conclusion

Current overdose-prevention screening efforts primarily identify patients on high-dose opioids and those with SUDD. Many veterans in this study were older than the average US victims’ age, did not have SUDD, were prescribed opioid doses not considered high risk by current guidelines, were nearer the end of their medication supply, and had UDS reflective of prescribed medications. This study suggests that any veteran with access to opioids, whether prescribed or not, is at risk for an opioid overdose. Established risk factors may aid in developing overdose-prevention programs, but prevention should not be limited to veterans with prescribed opioids and known risk factors. Clinicians should screen patients for opioid-use disorder whenever opioids are prescribed and continue to screen them throughout therapy. Broader screening for overdose risk is needed to avoid missing important opportunities for overdose prevention.

Acknowledgments

Gale Anderson, VISN 19 PBM Data Manager, performed initial data query for the study.

Editor’s Note: This article has been adapted from an article originally published in Federal Practitioner (Clement C, Stock C. Who overdoses at a VA emergency department? Fed Prac. 2016;33[11]:14-19. http://www.fedprac.com).

Overdose deaths remain epidemic throughout the United States. The rates of unintentional overdose deaths, increasing by 137% between 2000 and 2014, have been driven by a 4-fold increase in prescription opioid overdoses during that period.^1-3

Veterans died of accidental overdose at a rate of 19.85 deaths/100,000 people compared with a rate of 10.49 deaths in the general population, based on 2005 data.⁴ There is wide state-by-state variation, with the lowest age-adjusted opioid overdose death rate of 1.9 deaths/100,000 person-years among veterans in Mississippi and the highest rate in Utah of 33.9 deaths/100,000 person-years, using 2001 to 2009 data.⁵ These data can be compared with a crude general population overdose death rate of 10.6 deaths per 100,000 person-years in Mississippi and 18.4 deaths per 100,000 person-years in the general Utah population during that same period.⁶

Overdose deaths in the United States occur most often in persons aged 25 to 54 years.⁷ Older age has been associated with iatrogenic opioid overdose in hospitalized patients.⁸ Pulmonary disease, cardiovascular disease (CVD), and psychiatric disorders, including past or present substance use, have been associated with an increased risk of opioid overdose.⁹ However, veterans with substance use disorders are less likely to be prescribed opioids than are nonveterans with substance use disorders.¹⁰ Also, concomitant use of sedating medications, such as benzodiazepines (BZDs), can increase mortality from opioid overdose.¹¹ Patients prescribed opioids for chronic pain conditions often take BZDs for various reasons.¹² Veterans seem more likely to receive opioids to treat chronic pain but at lower average daily doses than doses prescribed to nonveterans.¹⁰

Emergency management of life-threatening opioid overdose includes prompt administration of naloxone.¹³ Naloxone is approved by the US Food and Drug Administration for complete or partial reversal of opioid-induced clinical effects, most critically respiratory depression.^14,15 Naloxone administration in the ED may serve as a surrogate for an overdose event. During the study period, naloxone take-home kits were not available in the Veterans Affairs (VA) setting.

A 2010 ED study described demographic information and comorbidities in opioid overdose, but the study did not include veterans.¹⁶ The clinical characteristics of veterans treated for opioid overdose have not been published. Because identifying characteristics of veterans who overdose may help tailor overdose-prevention efforts, the objective of this study is to describe clinical characteristics of veterans treated for opioid overdose.

Methods

A retrospective chart review and archived data study was approved by the University of Utah and VA Institutional Review Boards, and conducted at the George E. Wahlen Veterans Affairs Medical Center (VAMC) in Salt Lake City, Utah. This chart review included veterans who were admitted to the ED and treated with naloxone between January 1, 2009 and January 1, 2013. 

The authors used the Pharmacy Benefits Management Data Manager to extract data from the VA Data Warehouse and verified the data by open chart review (Table). The following data were collected: ED visit date (overdose date); demographic information, including age, gender, and race; evidence of next of kin or other contact at the same address as the veteran; diagnoses based on International Classification of Diseases, 9th Revision (ICD-9) codes, including sleep apnea, obesity, cardiac disease, pulmonary disease, mental health diagnoses (ICD-9 codes 290-302 [wild card characters (*) included many subdiagnoses]), cancer, and substance use disorders and/or dependencies (SUDD); tobacco use; VA-issued prescription opioid and BZD availability, including dose, fill dates, quantities dispensed, and day supplies; specialty of opioid prescriber; urine-drug screening (UDS) results; and outcome of the overdose. 

No standardized research criteria identify overdose in medical chart review.¹⁷ For each identified patient, the authors reviewed provider and nursing notes charted during an ED visit that included naloxone administration. The event was included as an opioid overdose when notes indicated that the veteran was unresponsive and given naloxone, which resulted in increased respirations or increased responsiveness. Cases were excluded if the reason for naloxone administration was anything other than opioid overdose.

Medical, mental health, and SUDD diagnoses were included only if the veteran had more than three patient-care encounters (PCE) with ICD-9 codes for a specific diagnosis entered by providers. A PCE used in the electronic medical record (EMR) helps collect, manage, and display outpatient encounter data, including providers, procedure codes, and diagnostic codes. Tobacco use was extracted from health factors documented during primary care visit screenings. (Health factors help capture data entered in note templates in the EMR and can be used to query trends.) A diagnosis of obesity was based on a calculated body mass index of at or greater than 30 kg/m² on the day of the ED visit date or the most recently charted height and weight. The type of SUDD was stratified into opioids (ICD-9 codes 304.0*), sedatives (ICD-9 codes 304.1*), alcohol (ICD-9 codes 303.*), and other (ICD-9 codes 304.2-305.9).

The dosage of opioids and BZDs available to a veteran was determined by using methods similar to those described by Gomes et al¹⁸: the dose of opioids and BZDs available based on prescriptions dispensed during the 120 days prior to the ED visit date and the dose available on the day of the ED visit date if prescription instructions were being followed. Prescription opioids and BZDs were converted to daily morphineequivalent dose (MED) and daily lorazepam equivalent dose (LED), using established methods.^19,20

Veterans were stratified into four groups based on prescribed medication availability: opioids only, BZDs only, opioids and BZDs, and neither opioids nor BZDs. The specialty of the opioid prescribers was categorized as primary care, pain specialist, surgeon, emergency specialist, or hospitalist (discharge prescription). Veteran EMRs contain a list of medications obtained outside the VA facility, referred to as non-VA prescriptions. These medications were not included in the analysis because accuracy could not be verified.

A study author reviewed the results of any UDS performed up to 120 days before the ED visit date to determine whether the result reflected the currently prescribed prescription medications. If the UDS was positive for the prescribed opioids and/or BZDs and for any nonprescribed drug, including alcohol, the UDS was classified as not reflective. If the prescribed BZD was alprazolam, clonazepam, or lorazepam, a BZD-positive UDS was not required for the UDS to be considered reflective because of the sensitivity of the UDS BZD immunoassay used at the George E. Wahlen VAMC clinical laboratory.²¹

Outcomes of the overdose were categorized as discharged, hospitalized, or deceased. Descriptive statistical analyses were performed using Microsoft Excel. Group comparisons were performed using Pearson chi-square or Student t test.

Results

The ED at the George E. Wahlen VAMC averages 64 visits per day, almost 94,000 visits within the study period. One hundred seventy ED visits between January 1, 2009 and January 1, 2013, involved naloxone administration. Ninety-two visits met the inclusion criteria of opioid overdose, representing about 0.002% of all ED visits at this facility (Figure 1). Six veterans had multiple ED visits within the study period, including four veterans who were in the opioid-only group.

The majority of veterans in this study were non-Hispanic white (n = 83, 90%), male (n = 88, 96%), with a mean age of 63 years. Less than 40% listed a next of kin or contact person living at their address.

Based on prescriptions available within 120 days before the overdose, 67 veterans (73%) possessed opioid and/or BZD prescriptions. In this group, the MED available on the day of the ED visit ranged from 7.5 mg to 830 mg. The MED was less than or equal to 200 mg in 71.6% and less than or equal to 50 mg in 34.3% of these cases. Veterans prescribed both opioids and BZDs had higher MED (average, 259 mg) available within 120 days of the ED visit than did those prescribed opioids only (average, 118 mg) (P = .015; standard deviation [SD], 132.9). The LED ranged from 1 mg to 12 mg for veterans with available BZDs.

Based on prescriptions available on the day of opioid overdose, 53 veterans (58%) had opioid prescriptions. The ranges of MED and LED available on the day of overdose were the same as the 120-day availability period. The average MED was 183 mg in veterans prescribed both opioids and BZDs and 126 mg in those prescribed opioids only (P = .283; SD, 168.65; Figure 2). The time between the last opioid fill date and the overdose visit date averaged 20 days (range, 0 to 28 days) in veterans prescribed opioids.

Discussion

This retrospective review identified 92 veterans who were treated with naloxone in the ED for opioid overdose during a 4-year period at the George E. Wahlen VAMC. Seventy-eight cases were excluded because the reason entered in charts for naloxone administration was itching, constipation, altered mental status, or unclear documentation.

Veterans in this study were, on average, older than the overdose fatalities in the United States. Opioid-overdose deaths in all US states and in Utah alone occur most frequently in non-Hispanic white men aged between 35 and 54 years.^7,22,23 In the 2010 Nationwide Emergency Department Sample of 136,000 opioid overdoses, of which 98% survived, most were aged 18 to 54 years.¹⁶ The older age in this study most likely reflects the age range of veterans served in the Veterans Health Administration (VHA); however, as more young veterans enter the VHA, the age range of overdose victims may more closely resemble the age ranges found in previous studies. Post hoc analysis showed eight veterans (9%) with probable intentional opioid overdose based on chart review, whereas the incidence of intentional prescription drug overdose in the United States is 17.1%.²⁴

In Utah, almost 93% of fatal overdoses occur at a residential location.²² Less than half of the veterans in this study had a contact or next of kin listed as living at the same address. Although veterans may not have identified someone living with them, in many cases, it is likely another person witnessed the overdose. Relying on EMRs to identify who should receive prevention education in addition to the veteran, may result in missed opportunities to include another person likely to witness an overdose.²⁵ Prescribers should make a conscious effort to ask veterans to identify someone who may be able to assist with rescue efforts in the event of an overdose.

Diagnoses associated with increased risk of opioid-overdose death include sleep apnea, morbid obesity, pulmonary disease or CVD, and/or a history of psychiatric disorders and SUDD.^8,9,16 In a large sample of older veterans, only 64% had at least one medical or psychiatric diagnosis.²⁶ Less than half of the 18,000 VA primary care patients in five VA centers had any psychiatric condition, and less than 65% had CVD, pulmonary disease, or cancer.²⁷ All veterans in this study had medical and psychiatric comorbidity.

In contrast, a large ED sample described by Yokell et al¹⁶ found chronic mental conditions in 33.9%, circulatory disorders in 29.1%, and respiratory conditions in 25.6% of their sample. Bohnert et al⁹ found a significantly elevated hazard ratio (HR) for any psychiatric disorder in a sample of nearly 4,500 veterans. There was variation in the HR when individual psychiatric diagnoses were broken out, with bipolar disorder having the largest HR and schizophrenia having the lowest but still elevated HR.⁹ In this study, individual diagnoses were not broken out because the smaller sample size could diminish the clinical significance of any apparent differences.

Edlund et al¹⁰ found that less than 8% of veterans treated with opioids for chronic noncancer pain had nonopioid SUDD. Bohnert et al⁹ found an HR of 21.95 for overdose death among those with opioid-use disorders. The sample in this study had a much higher incidence of nonopioid SUDD compared with that of the study by Edlund et al,¹⁰ but none of the veterans in this study had a documented history of opioid-use disorder. The absence of opioid-use disorders in this sample is unexpected and points to a need for providers to screen for opioid-use disorder whenever opioids are prescribed or renewed. If prevention practices were directed only to those with opioid SUDDs, none of the veterans in this study would have been included in those efforts. Non-SUDD providers should address the risks of opioid overdose in veterans with sleep apnea, morbid obesity, pulmonary disease or CVD, and/or a history of psychiatric disorders.

Gomes et al¹⁸ found that greater than 100 mg MED available on the day of overdose doubled the risk of opioid-related mortality. The VA/Department of Defense Clinical Practice Guideline for Management of Opioid Therapy for Chronic Pain identifies 200 mg MED as a threshold to define high-dose opioid therapy.²⁸ Fulton-Kehoe et al²⁹ found that 28% of overdose victims were prescribed less than 50 mg MED. In this study, the average dose available to veterans was greater than 100 mg MED; however, one-third of all study veterans had less than 50 mg MED available. Using a threshold dose of 50 mg MED to target prevention efforts would capture only two-thirds of those who experienced overdose; a 200-mg MED threshold would exclude the majority, based on the average MED in each group in this study. Overdose education should be provided to veterans with access to opioids, regardless of dose.

Use of BZDs with opioids may result in greater central nervous system (CNS) depression, pharmacokinetic interactions, or pharmacodynamic interactions at the µ- opioid receptor.^30-32 About one-third of veterans in this study were prescribed opioids and BZDs concurrently, a combination noted in about 33% of opioid overdose deaths reported by the Centers for Disease Control and Prevention.²⁴ Individuals taking methadone combined with BZDs have been found to have severe medical outcomes.³³ If preventive efforts are targeted to those receiving opioids and other CNS depressants, such as BZDs, about half (42%) of the veterans in this study would not receive a potentially life-saving message about preventing overdoses. All veterans with opioids should be educated about the additional risk of overdose posed by drug interactions with other CNS depressants.

The time since the last fill of an opioid prescription ranged from 0 to 28 days. This time frame indicates that some overdoses may have occurred on the day an opioid was filled but most occurred near the end of the expected days’ supply. Because information about adherence or use of the opioid was not studied, it cannot be assumed that medication misuse is the primary reason for the overdose. Providing prevention efforts only at the time of medication dispensing would be insufficient. Clinicians should review local and remote prescription data, including via their states’ prescription drug monitoring program, when discussing the risk of overdose with veterans.

Most veterans had at least one UDS result in the chart. Although half the UDSs obtained reflected prescribed medications, the possibility of aberrant behaviors, which increases the risk of overdose, cannot be ruled out with the methods used in this study.³⁴ Medication management agreements that require UDSs for veterans with chronic pain were not mandatory at the George E. Wahlen VAMC during the study period, and those used did not mandate discontinuation of opioid therapy if suspected aberrant behaviors were present.

A Utah study based on interviews of overdose victims’ next of kin found that 76% were concerned about victims’ aberrant behaviors, such as medication misuse, prior to the death.²² In contrast, a study of commercial and Medicaid recipients estimated medication misuse rates in at or less than 30% of the sample.³⁵ Urine-drug screening results not reflective of the prescribed regimens have been found in up to 50% of patients receiving chronic opioid therapy.

The UDS findings in this study were determined by the authors and did not capture clinical decisions or interpretations made after results were available or whether these decisions resulted in overdose-prevention strategies, such as targeted education or changes in prescription availability. Targeting preventive efforts toward veterans only with UDS results suggesting medication misuse would have missed more than half the veterans in this study. Urine-drug screening should be used as a clinical monitoring tool whenever opioids, BZDs, or other substances are used or prescribed.

The VA now has a nationwide program, Opioid Overdose Education and Naloxone Distribution (OEND), promoting overdose education and take-home naloxone distribution for providers and patients to prevent opioid-related overdose deaths. A national SharePoint site has been created within the VA that lists resources to support this effort.

Almost all veterans in this review survived the overdose and were hospitalized following the ED visit. Other investigators also have found that the majority (51% to 98%) of overdose victims reaching the ED survived, but fewer patients (3% to 51%) in those studies were hospitalized.^16,36 It is unknown whether there are differences in risk factors associated with survived or fatal overdoses.

Limitations

Although Utah ranked third for drug-overdose death rates in 2008 and had the highest death rate among veterans from 2001 to 2009, this review captured only overdoses among veterans treated during the study period at the George E. Wahlen VAMC ED.^5,6 The number and characteristics of veterans during this same period who were treated for overdose in other community EDs or urgent care centers throughout Utah is unknown.

The definition of opioid and BZD dose available in this study may not represent actual use of opioids or BZDs because it was based on chart review of prescription dispensing information and UDS procedures at the George E. Wahlen VAMC, and medication misuse cannot be ruled out. This study did not evaluate specific aberrant behaviors.

Conclusion

Current overdose-prevention screening efforts primarily identify patients on high-dose opioids and those with SUDD. Many veterans in this study were older than the average US victims’ age, did not have SUDD, were prescribed opioid doses not considered high risk by current guidelines, were nearer the end of their medication supply, and had UDS reflective of prescribed medications. This study suggests that any veteran with access to opioids, whether prescribed or not, is at risk for an opioid overdose. Established risk factors may aid in developing overdose-prevention programs, but prevention should not be limited to veterans with prescribed opioids and known risk factors. Clinicians should screen patients for opioid-use disorder whenever opioids are prescribed and continue to screen them throughout therapy. Broader screening for overdose risk is needed to avoid missing important opportunities for overdose prevention.

Acknowledgments

Gale Anderson, VISN 19 PBM Data Manager, performed initial data query for the study.

Case

A 2-year-old boy and his mother were referred to the ED by the child’s pediatrician after a routine venous blood lead level (BLL) taken at the boy’s recent well visit revealed an elevated lead level of 52 mcg/dL (normal range, <5 mcg/dL). The child’s mother reported that although her son had always been a picky eater, he had recently been complaining of abdominal pain.

The patient’s well-child visits had been normal until his recent 2-year checkup, at which time his pediatrician noticed some speech delay. On further history taking, the emergency physician (EP) learned the patient and his mother resided in an older home (built in the 1950s) that was in disrepair. The mother asked the EP if the elevation in the child’s BLL could be due to the drinking water in their town.

What are the most likely sources of environmental lead exposure?

In 2016, the topic of lead poisoning grabbed national attention when a pediatrician in Flint, Michigan detected an abrupt doubling of the number of children with elevated lead levels in her practice.¹ Upon further investigation, it was discovered that these kids had one thing in common: the source of their drinking water. The City of Flint had recently switched the source of its potable water from Lake Huron to the Flint River. The lower quality water, which was not properly treated with an anticorrosive agent such as orthophosphate, led to widespread pipe corrosion and lead contamination. This finding resulted in a cascade of water testing by other municipalities and school systems, many of which identified lead concentrations above the currently accepted drinking water standard of 15 parts per billion (ppb).

Thousands of children each year are identified to have elevated BLLs, based on the Centers for Disease Control and Prevention definition of a “level of concern” as more than 5 mcg/dL.² The majority of these exposures stem from environmental exposure to lead paint dust in the home, but drinking water normally contributes as a low-level, constant, “basal” exposure. While lead-contaminated drinking water is not acceptable, it is unlikely to generate many ED visits. However, there are a variety of other lead sources that may prompt children to present to the ED with acute or subacute lead poisoning.

Lead is a heavy metal whose physical properties indicate its common uses. It provides durability and opacity to pigments, which is why it is found in oil paint, house paint used before 1976, and on paint for large outdoor structures, where it is still used. Lead is also found in the pigments used in cosmetics, stained glass, and painted pottery, and as an adulterant in highly colored foodstuffs such as imported turmeric.³

The physicochemical characteristics of lead make it an ideal component of solder. Many plumbing pipes in use today are not lead, but join one another using lead solder at the joints, sites that are vulnerable to corrosion. The heavy molecular weight of lead makes it a useful component of bullets and munitions.

Tetraethyl lead was used as an “anti-knock” agent to smooth out the combustion of heterogenous compounds in automotive fuel before it was removed in the mid-1970s.⁴ Prior to its removal, leaded gasoline was the largest source of air, soil, and groundwater contamination leading to environmental exposures.⁴ At present, the most common source of environmental lead exposure among young children is through peeling paint in deteriorating residential buildings. Hazardous occupational lead exposures arise from work involving munitions, reclamation and salvage, painting, welding, and numerous other settings—particularly sites where industrial hygiene is suboptimal. Lead from these sites can be inadvertently transported home on clothing or shoes, raising the exposure risk for children in the household.⁴

What are the health effects of lead exposure?

Like most heavy metals, lead is toxic to many organ systems in the body. The signs and symptoms of lead poisoning vary depending on the patient’s BLL and age (Table 1).⁵ The most common clinical effect of lead in the adult population is hypertension.⁶ Additional renal effects include a Fanconi-type syndrome with glycosuria and proteinuria. Lead can cause a peripheral neuropathy that is predominantly motor, classically causing foot or wrist drop. Abdominal pain from lead exposure is sometimes termed “lead colic” due to its intermittent and often severe nature. Abnormalities in urate metabolism cause a gouty arthritis referred to as “saturnine gout.” ⁶

The young pediatric central nervous system (CNS) is much more vulnerable to the effects of lead than the adult CNS. Even low-level lead exposure to the developing brain causes deficits in intelligence quotient, attention, impulse control, and other neurocognitive functions that are largely irreversible.⁷

Children with an elevated BLL may also develop constipation, anorexia, pallor, and pica.⁸ The development of geophagia (subtype of pica in which one craves and ingests nonfood clay or soil-like materials), represents a “chicken-or-egg” phenomena as it both causes and results from lead poisoning.

Lead impairs multiple steps of the heme synthesis pathway, causing microcytic anemia with basophilic stippling. Lead-induced anemia exacerbates pica as anemic patients are more likely to eat leaded paint chips and other lead-containing materials such as pottery.⁸ Of note, leaded white paint is reported to have a pleasant taste due to the sweet-tasting lead acetate used as a pigment.

The most dramatic and consequential manifestation of lead poisoning is lead encephalopathy. This can occur at any age, but manifests in children at much lower BLLs than in adults. Patients can be altered or obtunded, have convulsive activity, and may develop cerebral edema. Encephalopathy is a life-threatening emergency and must be recognized and treated immediately. Lead encephalopathy should be suspected in any young child with hand-to-mouth behavior who has any of the above environmental risk factors.⁴ The findings of anemia or the other diagnostic signs described below are too unreliable and take too long to be truly helpful in making the diagnosis.

How is the diagnosis of lead poisoning made?

The gold standard for the diagnosis of lead poisoning is the measurement of BLL. However, the turnaround time for this test is usually at least 24 hours, but may take up to several days. As such, adjunctive testing can accelerate obtaining a diagnosis. A complete blood count (CBC) to evaluate for microcytic anemia may demonstrate a characteristic pattern of basophilic stippling.⁹ A protoporphyrin level—either a free erythrocyte protoporphyrin (FEP) or a zinc protoporphyrin level—will be elevated, a result of heme synthesis disruption.⁹ Urinalysis may demonstrate glycosuria or proteinuria.⁶ Hypertension is often present, even in pediatric patients.

An abdominal radiograph is essential in children to determine whether a lead foreign body, such as a paint chip, is present in the intestinal lumen. Long bone films may demonstrate “lead lines” at the metaphysis, which in fact do not reflect lead itself but abnormal calcium deposition in growing bone due to lead’s interference with bone remodeling. A computed tomography (CT) scan of the brain in patients with encephalopathy will often demonstrate cerebral edema.⁶

Of note, capillary BLLs taken via finger-stick can be falsely elevated due contamination during collection (eg, the presence of lead dust on the skin). However, this screening method is often used by clinicians in the pediatric primary care setting because of its feasibility. Elevated BLLs from capillary testing should always be followed by a BLL obtained by venipuncture.²

Case Continuation

The patient’s mother was counseled on sources of lead contamination. She was informed that although drinking water may contribute some amount to an elevated BLL, the most likely source of contamination is still lead paint found in older homes such as the one in which she and her son resided.

Diagnostic studies to support the diagnosis of lead poisoning were performed. A CBC revealed a hemoglobin of 9.8 g/dL with a mean corpuscular volume of 68 fL. A microscopic smear of blood demonstrated basophilic stippling of red blood cells. An FEP level was 386 mcg/dL. An abdominal radiograph demonstrated small radiopacities throughout the large intestine, without obstruction, which was suggestive of ingested lead paint chips.

What is the best management approach to patients with suspected lead poisoning?

The first-line treatment for patients with lead poisoning is removal from the exposure source, which first and foremost requires identification of the hazard through careful history taking and scene investigation by the local health department. This will avoid recurrent visits following successful chelation for repeat exposure to an unidentified source. Relocation to another dwelling will often be required for patients with presumed exposure until the hazard can be identified and abated.

Patients who have ingested or have embedded leaded foreign bodies will require removal via whole bowel irrigation or surgical means.

Following decontamination, chelation is required for children with a BLL more than 45 mcg/dL, and adults with CNS symptomatology and a BLL more than 70 mcg/dL. Table 2 provides guidelines for chelation therapy based on BLL.⁵

Work-up and Management in the ED

The patient with lead poisoning, while an unusual presentation in the ED, requires specialized management to minimize sequelae of exposure. Careful attention to history is vital. When in doubt, the EP should consult with her or his regional poison control center (800-222-1222) or with a medical toxicologist or other expert.

There are several scenarios in which a patient may present to the ED with lead toxicity. The following scenarios, along with their respective clinical approach strategies, represent three of the most common presentations.

Scenario 1: The Pediatric Patient With Elevated Venous Blood Lead Levels

The EP should employ the following clinical approach when evaluating and managing the pediatric patient with normal mental status whose routine screening reveals a BLL sufficiently elevated to warrant evaluation or admission—perhaps to discontinue exposure or initiate chelation therapy.

• Obtain a history, including possible lead sources; perform a complete physical examination; and obtain a repeat BLL, CBC with microscopic examination, and renal function test.
• Obtain an abdominal film to look for radiopacities, including paint chips or larger ingested foreign bodies.
• If radiopaque foreign bodies are present on abdominal radiograph, whole bowel irrigation with polyethylene glycol solution given via a nasogastric tube at 250 to 500 cc/h for a pediatric patient (1 to 2 L/h for adult patients) should be given until no residual foreign bodies remain.
• Obtain a radiograph of the long bone, which may demonstrate metaphyseal enhancement in the pediatric patient, suggesting long-term exposure.
• Ensure local or state health departments are contacted to arrange for environmental inspection of the home. This is essential prior to discharge to the home environment.
• Begin chelation therapy according to the BLL (Table 2).

Scenario 2: Adult Patients Presenting With Signs and Symptoms of Lead Toxicity

The adult patient who presents to the ED with complaints suggestive of lead poisoning and whose history is indicative of lead exposure should be evaluated and managed as follows:

• Obtain a thorough history, including the occupation and hobbies of the patient and all family members.
• Obtain vital signs to evaluate for hypertension; repeat BLL, CBC with smear, and serum creatinine test. Perform a physical examination to evaluate for lead lines.
• Obtain radiographic images, which may demonstrate a leaded foreign body, such as in the patient with prior history of gunshot wounds.
• If the BLL is sufficiently elevated or clinical findings are sufficiently severe, admit for chelation.

Scenario 3: The Pediatric or Adult Patient Presenting With Altered Mental Status

The patient presenting with altered mental status of unclear etiology—regardless of age—and in whom lead encephalopathy is a possible cause, should be worked-up and managed as follows:

• Obtain BLL, CBC, FEP levels. Consider radiographic imaging to assess for ingested or embedded foreign bodies.
• If abnormalities in the above laboratory studies are consistent with lead poisoning, initiate chelation immediately—prior to receiving repeat BLL result.
• Obtain a CT scan of the head to assess for cerebral edema.
• Provide supportive care for encephalopathy, including airway control and management of increased intracranial pressure.

Case Conclusion

The patient was admitted to the hospital for whole bowel irrigation and chelation therapy with succimer. The local health department conducted an investigation of the home and found multiple areas of peeling lead paint and lead dust, and ordered remediation of the property before it could be re-occupied by the family. A test of the home’s drinking water found no elevation above the 15 ppb standard.

The patient was discharged from the hospital in the care of his mother. They were relocated to a lead-free home, with follow-up by the pediatrician for ongoing monitoring of the BLL and developmental milestones.

Case

A 2-year-old boy and his mother were referred to the ED by the child’s pediatrician after a routine venous blood lead level (BLL) taken at the boy’s recent well visit revealed an elevated lead level of 52 mcg/dL (normal range, <5 mcg/dL). The child’s mother reported that although her son had always been a picky eater, he had recently been complaining of abdominal pain.

The patient’s well-child visits had been normal until his recent 2-year checkup, at which time his pediatrician noticed some speech delay. On further history taking, the emergency physician (EP) learned the patient and his mother resided in an older home (built in the 1950s) that was in disrepair. The mother asked the EP if the elevation in the child’s BLL could be due to the drinking water in their town.

What are the most likely sources of environmental lead exposure?

In 2016, the topic of lead poisoning grabbed national attention when a pediatrician in Flint, Michigan detected an abrupt doubling of the number of children with elevated lead levels in her practice.¹ Upon further investigation, it was discovered that these kids had one thing in common: the source of their drinking water. The City of Flint had recently switched the source of its potable water from Lake Huron to the Flint River. The lower quality water, which was not properly treated with an anticorrosive agent such as orthophosphate, led to widespread pipe corrosion and lead contamination. This finding resulted in a cascade of water testing by other municipalities and school systems, many of which identified lead concentrations above the currently accepted drinking water standard of 15 parts per billion (ppb).

Thousands of children each year are identified to have elevated BLLs, based on the Centers for Disease Control and Prevention definition of a “level of concern” as more than 5 mcg/dL.² The majority of these exposures stem from environmental exposure to lead paint dust in the home, but drinking water normally contributes as a low-level, constant, “basal” exposure. While lead-contaminated drinking water is not acceptable, it is unlikely to generate many ED visits. However, there are a variety of other lead sources that may prompt children to present to the ED with acute or subacute lead poisoning.

Lead is a heavy metal whose physical properties indicate its common uses. It provides durability and opacity to pigments, which is why it is found in oil paint, house paint used before 1976, and on paint for large outdoor structures, where it is still used. Lead is also found in the pigments used in cosmetics, stained glass, and painted pottery, and as an adulterant in highly colored foodstuffs such as imported turmeric.³

The physicochemical characteristics of lead make it an ideal component of solder. Many plumbing pipes in use today are not lead, but join one another using lead solder at the joints, sites that are vulnerable to corrosion. The heavy molecular weight of lead makes it a useful component of bullets and munitions.

Tetraethyl lead was used as an “anti-knock” agent to smooth out the combustion of heterogenous compounds in automotive fuel before it was removed in the mid-1970s.⁴ Prior to its removal, leaded gasoline was the largest source of air, soil, and groundwater contamination leading to environmental exposures.⁴ At present, the most common source of environmental lead exposure among young children is through peeling paint in deteriorating residential buildings. Hazardous occupational lead exposures arise from work involving munitions, reclamation and salvage, painting, welding, and numerous other settings—particularly sites where industrial hygiene is suboptimal. Lead from these sites can be inadvertently transported home on clothing or shoes, raising the exposure risk for children in the household.⁴

What are the health effects of lead exposure?

Like most heavy metals, lead is toxic to many organ systems in the body. The signs and symptoms of lead poisoning vary depending on the patient’s BLL and age (Table 1).⁵ The most common clinical effect of lead in the adult population is hypertension.⁶ Additional renal effects include a Fanconi-type syndrome with glycosuria and proteinuria. Lead can cause a peripheral neuropathy that is predominantly motor, classically causing foot or wrist drop. Abdominal pain from lead exposure is sometimes termed “lead colic” due to its intermittent and often severe nature. Abnormalities in urate metabolism cause a gouty arthritis referred to as “saturnine gout.” ⁶

The young pediatric central nervous system (CNS) is much more vulnerable to the effects of lead than the adult CNS. Even low-level lead exposure to the developing brain causes deficits in intelligence quotient, attention, impulse control, and other neurocognitive functions that are largely irreversible.⁷

Children with an elevated BLL may also develop constipation, anorexia, pallor, and pica.⁸ The development of geophagia (subtype of pica in which one craves and ingests nonfood clay or soil-like materials), represents a “chicken-or-egg” phenomena as it both causes and results from lead poisoning.

Lead impairs multiple steps of the heme synthesis pathway, causing microcytic anemia with basophilic stippling. Lead-induced anemia exacerbates pica as anemic patients are more likely to eat leaded paint chips and other lead-containing materials such as pottery.⁸ Of note, leaded white paint is reported to have a pleasant taste due to the sweet-tasting lead acetate used as a pigment.

The most dramatic and consequential manifestation of lead poisoning is lead encephalopathy. This can occur at any age, but manifests in children at much lower BLLs than in adults. Patients can be altered or obtunded, have convulsive activity, and may develop cerebral edema. Encephalopathy is a life-threatening emergency and must be recognized and treated immediately. Lead encephalopathy should be suspected in any young child with hand-to-mouth behavior who has any of the above environmental risk factors.⁴ The findings of anemia or the other diagnostic signs described below are too unreliable and take too long to be truly helpful in making the diagnosis.

How is the diagnosis of lead poisoning made?

The gold standard for the diagnosis of lead poisoning is the measurement of BLL. However, the turnaround time for this test is usually at least 24 hours, but may take up to several days. As such, adjunctive testing can accelerate obtaining a diagnosis. A complete blood count (CBC) to evaluate for microcytic anemia may demonstrate a characteristic pattern of basophilic stippling.⁹ A protoporphyrin level—either a free erythrocyte protoporphyrin (FEP) or a zinc protoporphyrin level—will be elevated, a result of heme synthesis disruption.⁹ Urinalysis may demonstrate glycosuria or proteinuria.⁶ Hypertension is often present, even in pediatric patients.

An abdominal radiograph is essential in children to determine whether a lead foreign body, such as a paint chip, is present in the intestinal lumen. Long bone films may demonstrate “lead lines” at the metaphysis, which in fact do not reflect lead itself but abnormal calcium deposition in growing bone due to lead’s interference with bone remodeling. A computed tomography (CT) scan of the brain in patients with encephalopathy will often demonstrate cerebral edema.⁶

Of note, capillary BLLs taken via finger-stick can be falsely elevated due contamination during collection (eg, the presence of lead dust on the skin). However, this screening method is often used by clinicians in the pediatric primary care setting because of its feasibility. Elevated BLLs from capillary testing should always be followed by a BLL obtained by venipuncture.²

Case Continuation

The patient’s mother was counseled on sources of lead contamination. She was informed that although drinking water may contribute some amount to an elevated BLL, the most likely source of contamination is still lead paint found in older homes such as the one in which she and her son resided.

Diagnostic studies to support the diagnosis of lead poisoning were performed. A CBC revealed a hemoglobin of 9.8 g/dL with a mean corpuscular volume of 68 fL. A microscopic smear of blood demonstrated basophilic stippling of red blood cells. An FEP level was 386 mcg/dL. An abdominal radiograph demonstrated small radiopacities throughout the large intestine, without obstruction, which was suggestive of ingested lead paint chips.

What is the best management approach to patients with suspected lead poisoning?

The first-line treatment for patients with lead poisoning is removal from the exposure source, which first and foremost requires identification of the hazard through careful history taking and scene investigation by the local health department. This will avoid recurrent visits following successful chelation for repeat exposure to an unidentified source. Relocation to another dwelling will often be required for patients with presumed exposure until the hazard can be identified and abated.

Patients who have ingested or have embedded leaded foreign bodies will require removal via whole bowel irrigation or surgical means.

Following decontamination, chelation is required for children with a BLL more than 45 mcg/dL, and adults with CNS symptomatology and a BLL more than 70 mcg/dL. Table 2 provides guidelines for chelation therapy based on BLL.⁵

Work-up and Management in the ED

The patient with lead poisoning, while an unusual presentation in the ED, requires specialized management to minimize sequelae of exposure. Careful attention to history is vital. When in doubt, the EP should consult with her or his regional poison control center (800-222-1222) or with a medical toxicologist or other expert.

There are several scenarios in which a patient may present to the ED with lead toxicity. The following scenarios, along with their respective clinical approach strategies, represent three of the most common presentations.

Scenario 1: The Pediatric Patient With Elevated Venous Blood Lead Levels

The EP should employ the following clinical approach when evaluating and managing the pediatric patient with normal mental status whose routine screening reveals a BLL sufficiently elevated to warrant evaluation or admission—perhaps to discontinue exposure or initiate chelation therapy.

• Obtain a history, including possible lead sources; perform a complete physical examination; and obtain a repeat BLL, CBC with microscopic examination, and renal function test.
• Obtain an abdominal film to look for radiopacities, including paint chips or larger ingested foreign bodies.
• If radiopaque foreign bodies are present on abdominal radiograph, whole bowel irrigation with polyethylene glycol solution given via a nasogastric tube at 250 to 500 cc/h for a pediatric patient (1 to 2 L/h for adult patients) should be given until no residual foreign bodies remain.
• Obtain a radiograph of the long bone, which may demonstrate metaphyseal enhancement in the pediatric patient, suggesting long-term exposure.
• Ensure local or state health departments are contacted to arrange for environmental inspection of the home. This is essential prior to discharge to the home environment.
• Begin chelation therapy according to the BLL (Table 2).

Scenario 2: Adult Patients Presenting With Signs and Symptoms of Lead Toxicity

The adult patient who presents to the ED with complaints suggestive of lead poisoning and whose history is indicative of lead exposure should be evaluated and managed as follows:

• Obtain a thorough history, including the occupation and hobbies of the patient and all family members.
• Obtain vital signs to evaluate for hypertension; repeat BLL, CBC with smear, and serum creatinine test. Perform a physical examination to evaluate for lead lines.
• Obtain radiographic images, which may demonstrate a leaded foreign body, such as in the patient with prior history of gunshot wounds.
• If the BLL is sufficiently elevated or clinical findings are sufficiently severe, admit for chelation.

Scenario 3: The Pediatric or Adult Patient Presenting With Altered Mental Status

The patient presenting with altered mental status of unclear etiology—regardless of age—and in whom lead encephalopathy is a possible cause, should be worked-up and managed as follows:

• Obtain BLL, CBC, FEP levels. Consider radiographic imaging to assess for ingested or embedded foreign bodies.
• If abnormalities in the above laboratory studies are consistent with lead poisoning, initiate chelation immediately—prior to receiving repeat BLL result.
• Obtain a CT scan of the head to assess for cerebral edema.
• Provide supportive care for encephalopathy, including airway control and management of increased intracranial pressure.

Case Conclusion

The patient was admitted to the hospital for whole bowel irrigation and chelation therapy with succimer. The local health department conducted an investigation of the home and found multiple areas of peeling lead paint and lead dust, and ordered remediation of the property before it could be re-occupied by the family. A test of the home’s drinking water found no elevation above the 15 ppb standard.

The patient was discharged from the hospital in the care of his mother. They were relocated to a lead-free home, with follow-up by the pediatrician for ongoing monitoring of the BLL and developmental milestones.

Case

A 2-year-old boy and his mother were referred to the ED by the child’s pediatrician after a routine venous blood lead level (BLL) taken at the boy’s recent well visit revealed an elevated lead level of 52 mcg/dL (normal range, <5 mcg/dL). The child’s mother reported that although her son had always been a picky eater, he had recently been complaining of abdominal pain.

The patient’s well-child visits had been normal until his recent 2-year checkup, at which time his pediatrician noticed some speech delay. On further history taking, the emergency physician (EP) learned the patient and his mother resided in an older home (built in the 1950s) that was in disrepair. The mother asked the EP if the elevation in the child’s BLL could be due to the drinking water in their town.

What are the most likely sources of environmental lead exposure?

In 2016, the topic of lead poisoning grabbed national attention when a pediatrician in Flint, Michigan detected an abrupt doubling of the number of children with elevated lead levels in her practice.¹ Upon further investigation, it was discovered that these kids had one thing in common: the source of their drinking water. The City of Flint had recently switched the source of its potable water from Lake Huron to the Flint River. The lower quality water, which was not properly treated with an anticorrosive agent such as orthophosphate, led to widespread pipe corrosion and lead contamination. This finding resulted in a cascade of water testing by other municipalities and school systems, many of which identified lead concentrations above the currently accepted drinking water standard of 15 parts per billion (ppb).

Thousands of children each year are identified to have elevated BLLs, based on the Centers for Disease Control and Prevention definition of a “level of concern” as more than 5 mcg/dL.² The majority of these exposures stem from environmental exposure to lead paint dust in the home, but drinking water normally contributes as a low-level, constant, “basal” exposure. While lead-contaminated drinking water is not acceptable, it is unlikely to generate many ED visits. However, there are a variety of other lead sources that may prompt children to present to the ED with acute or subacute lead poisoning.

Lead is a heavy metal whose physical properties indicate its common uses. It provides durability and opacity to pigments, which is why it is found in oil paint, house paint used before 1976, and on paint for large outdoor structures, where it is still used. Lead is also found in the pigments used in cosmetics, stained glass, and painted pottery, and as an adulterant in highly colored foodstuffs such as imported turmeric.³

The physicochemical characteristics of lead make it an ideal component of solder. Many plumbing pipes in use today are not lead, but join one another using lead solder at the joints, sites that are vulnerable to corrosion. The heavy molecular weight of lead makes it a useful component of bullets and munitions.

Tetraethyl lead was used as an “anti-knock” agent to smooth out the combustion of heterogenous compounds in automotive fuel before it was removed in the mid-1970s.⁴ Prior to its removal, leaded gasoline was the largest source of air, soil, and groundwater contamination leading to environmental exposures.⁴ At present, the most common source of environmental lead exposure among young children is through peeling paint in deteriorating residential buildings. Hazardous occupational lead exposures arise from work involving munitions, reclamation and salvage, painting, welding, and numerous other settings—particularly sites where industrial hygiene is suboptimal. Lead from these sites can be inadvertently transported home on clothing or shoes, raising the exposure risk for children in the household.⁴

What are the health effects of lead exposure?

Like most heavy metals, lead is toxic to many organ systems in the body. The signs and symptoms of lead poisoning vary depending on the patient’s BLL and age (Table 1).⁵ The most common clinical effect of lead in the adult population is hypertension.⁶ Additional renal effects include a Fanconi-type syndrome with glycosuria and proteinuria. Lead can cause a peripheral neuropathy that is predominantly motor, classically causing foot or wrist drop. Abdominal pain from lead exposure is sometimes termed “lead colic” due to its intermittent and often severe nature. Abnormalities in urate metabolism cause a gouty arthritis referred to as “saturnine gout.” ⁶

The young pediatric central nervous system (CNS) is much more vulnerable to the effects of lead than the adult CNS. Even low-level lead exposure to the developing brain causes deficits in intelligence quotient, attention, impulse control, and other neurocognitive functions that are largely irreversible.⁷

Children with an elevated BLL may also develop constipation, anorexia, pallor, and pica.⁸ The development of geophagia (subtype of pica in which one craves and ingests nonfood clay or soil-like materials), represents a “chicken-or-egg” phenomena as it both causes and results from lead poisoning.

Lead impairs multiple steps of the heme synthesis pathway, causing microcytic anemia with basophilic stippling. Lead-induced anemia exacerbates pica as anemic patients are more likely to eat leaded paint chips and other lead-containing materials such as pottery.⁸ Of note, leaded white paint is reported to have a pleasant taste due to the sweet-tasting lead acetate used as a pigment.

The most dramatic and consequential manifestation of lead poisoning is lead encephalopathy. This can occur at any age, but manifests in children at much lower BLLs than in adults. Patients can be altered or obtunded, have convulsive activity, and may develop cerebral edema. Encephalopathy is a life-threatening emergency and must be recognized and treated immediately. Lead encephalopathy should be suspected in any young child with hand-to-mouth behavior who has any of the above environmental risk factors.⁴ The findings of anemia or the other diagnostic signs described below are too unreliable and take too long to be truly helpful in making the diagnosis.

How is the diagnosis of lead poisoning made?

The gold standard for the diagnosis of lead poisoning is the measurement of BLL. However, the turnaround time for this test is usually at least 24 hours, but may take up to several days. As such, adjunctive testing can accelerate obtaining a diagnosis. A complete blood count (CBC) to evaluate for microcytic anemia may demonstrate a characteristic pattern of basophilic stippling.⁹ A protoporphyrin level—either a free erythrocyte protoporphyrin (FEP) or a zinc protoporphyrin level—will be elevated, a result of heme synthesis disruption.⁹ Urinalysis may demonstrate glycosuria or proteinuria.⁶ Hypertension is often present, even in pediatric patients.

An abdominal radiograph is essential in children to determine whether a lead foreign body, such as a paint chip, is present in the intestinal lumen. Long bone films may demonstrate “lead lines” at the metaphysis, which in fact do not reflect lead itself but abnormal calcium deposition in growing bone due to lead’s interference with bone remodeling. A computed tomography (CT) scan of the brain in patients with encephalopathy will often demonstrate cerebral edema.⁶

Of note, capillary BLLs taken via finger-stick can be falsely elevated due contamination during collection (eg, the presence of lead dust on the skin). However, this screening method is often used by clinicians in the pediatric primary care setting because of its feasibility. Elevated BLLs from capillary testing should always be followed by a BLL obtained by venipuncture.²

Case Continuation

The patient’s mother was counseled on sources of lead contamination. She was informed that although drinking water may contribute some amount to an elevated BLL, the most likely source of contamination is still lead paint found in older homes such as the one in which she and her son resided.

Diagnostic studies to support the diagnosis of lead poisoning were performed. A CBC revealed a hemoglobin of 9.8 g/dL with a mean corpuscular volume of 68 fL. A microscopic smear of blood demonstrated basophilic stippling of red blood cells. An FEP level was 386 mcg/dL. An abdominal radiograph demonstrated small radiopacities throughout the large intestine, without obstruction, which was suggestive of ingested lead paint chips.

What is the best management approach to patients with suspected lead poisoning?

The first-line treatment for patients with lead poisoning is removal from the exposure source, which first and foremost requires identification of the hazard through careful history taking and scene investigation by the local health department. This will avoid recurrent visits following successful chelation for repeat exposure to an unidentified source. Relocation to another dwelling will often be required for patients with presumed exposure until the hazard can be identified and abated.

Patients who have ingested or have embedded leaded foreign bodies will require removal via whole bowel irrigation or surgical means.

Following decontamination, chelation is required for children with a BLL more than 45 mcg/dL, and adults with CNS symptomatology and a BLL more than 70 mcg/dL. Table 2 provides guidelines for chelation therapy based on BLL.⁵

Work-up and Management in the ED

The patient with lead poisoning, while an unusual presentation in the ED, requires specialized management to minimize sequelae of exposure. Careful attention to history is vital. When in doubt, the EP should consult with her or his regional poison control center (800-222-1222) or with a medical toxicologist or other expert.

There are several scenarios in which a patient may present to the ED with lead toxicity. The following scenarios, along with their respective clinical approach strategies, represent three of the most common presentations.

Scenario 1: The Pediatric Patient With Elevated Venous Blood Lead Levels

The EP should employ the following clinical approach when evaluating and managing the pediatric patient with normal mental status whose routine screening reveals a BLL sufficiently elevated to warrant evaluation or admission—perhaps to discontinue exposure or initiate chelation therapy.

• Obtain a history, including possible lead sources; perform a complete physical examination; and obtain a repeat BLL, CBC with microscopic examination, and renal function test.
• Obtain an abdominal film to look for radiopacities, including paint chips or larger ingested foreign bodies.
• If radiopaque foreign bodies are present on abdominal radiograph, whole bowel irrigation with polyethylene glycol solution given via a nasogastric tube at 250 to 500 cc/h for a pediatric patient (1 to 2 L/h for adult patients) should be given until no residual foreign bodies remain.
• Obtain a radiograph of the long bone, which may demonstrate metaphyseal enhancement in the pediatric patient, suggesting long-term exposure.
• Ensure local or state health departments are contacted to arrange for environmental inspection of the home. This is essential prior to discharge to the home environment.
• Begin chelation therapy according to the BLL (Table 2).

Scenario 2: Adult Patients Presenting With Signs and Symptoms of Lead Toxicity

The adult patient who presents to the ED with complaints suggestive of lead poisoning and whose history is indicative of lead exposure should be evaluated and managed as follows:

• Obtain a thorough history, including the occupation and hobbies of the patient and all family members.
• Obtain vital signs to evaluate for hypertension; repeat BLL, CBC with smear, and serum creatinine test. Perform a physical examination to evaluate for lead lines.
• Obtain radiographic images, which may demonstrate a leaded foreign body, such as in the patient with prior history of gunshot wounds.
• If the BLL is sufficiently elevated or clinical findings are sufficiently severe, admit for chelation.

Scenario 3: The Pediatric or Adult Patient Presenting With Altered Mental Status

The patient presenting with altered mental status of unclear etiology—regardless of age—and in whom lead encephalopathy is a possible cause, should be worked-up and managed as follows:

• Obtain BLL, CBC, FEP levels. Consider radiographic imaging to assess for ingested or embedded foreign bodies.
• If abnormalities in the above laboratory studies are consistent with lead poisoning, initiate chelation immediately—prior to receiving repeat BLL result.
• Obtain a CT scan of the head to assess for cerebral edema.
• Provide supportive care for encephalopathy, including airway control and management of increased intracranial pressure.

Case Conclusion

The patient was admitted to the hospital for whole bowel irrigation and chelation therapy with succimer. The local health department conducted an investigation of the home and found multiple areas of peeling lead paint and lead dust, and ordered remediation of the property before it could be re-occupied by the family. A test of the home’s drinking water found no elevation above the 15 ppb standard.

The patient was discharged from the hospital in the care of his mother. They were relocated to a lead-free home, with follow-up by the pediatrician for ongoing monitoring of the BLL and developmental milestones.

Case

A 21-year-old woman presented to the ED with pain and swelling on the right side of her neck. She stated the pain started earlier that morning and worsened when she ate or swallowed. The patient denied a recent or remote history of drooling, voice changes, or neck swelling. She reported no fevers, chills, or any other complaints, and had no pertinent medical history—specifically, no history of recent dental work. Her surgical history included tonsillectomy and cholecystectomy. There was no family history of diabetes, thyroid disease, autoimmune disease, or any other diseases. The patient stated that she was not on any prescription or over-the-counter medications. Regarding her social history, she denied past or cu

Vital signs at presentation were: blood pressure, 124/63 mm Hg (sitting); heart rate, 73 beats/min; respiratory rate, 15 breaths/min; and temperature, 98°F. Oxygen saturation was 99% on room air. On clinical examination, pain was noted in the patient’s right submandibular area and was tender to palpation. The swelling extended to the angle of the mandible posteriorly (Figure 1a and 1b). There was no erythema or increased surface temperature to suggest overlying cellulitis. The oral examination showed no evidence of dental infection, angioedema, or Ludwig angina. The pharynx was normal in appearance. The otological examination was unremarkable, and there was no evidence of mastoiditis.

Laboratory evaluation included a complete blood count (CBC), basic metabolic profile (BMP), and rapid streptococcal test (RST). The results of the patient’s CBC revealed a white blood cell count (WBC) of 11.1 x 10⁹/L; the BMP was unremarkable; and the RST was negative.

A soft tissue neck computed tomography (CT) scan with contrast was obtained, which revealed mild right submandibular gland enlargement with abnormal enhancement (Figure 2). Stranding was also noted in the right submandibular space along with thickening of the right platysma muscle, and few surrounding lymph nodes were prominent (Figure 3). The findings were consistent with acute submandibular sialadenitis.

Discussion

Comparatively little has been published on acute submandibular sialadenitis over the past three decades, and much of that which is cited in the literature comes from a rather small pool of case reports.¹ In a literature review, Raad et al¹ noted, “Pertinent literature on [this] subject includes case reports but no studies describing the microbial and clinical characteristics of this disease.” Further, many of the published case reports describe neonatal presentations of submandibular sialadenitis, the incidence of which is rare in this patient population.^2-4

Submandibular and Parotid Glands

The submandibular gland is the second largest salivary gland, the parotid gland being the largest. The duct of the salivary gland, the Wharton’s duct, opens under the tongue in the area of the lingual frenulum. Ductal obstruction is more frequently seen with the submandibular gland than with the parotid gland.¹ The reason for this is unclear, but may be related to several factors. One factor may be that, unlike the Stenson’s duct of the parotid gland, the Wharton’s duct does not pass through a muscle; thus, there is no muscular massage supporting the movement of secretion, as there is with buccinator muscle massage of Stenson’s duct. In addition, submandibular saliva is more viscous than parotid saliva due to its higher protein content and higher concentration of calcium phosphate.¹

Etiology

Submandibular gland obstruction can occur in the absence of infection. Noninfectious cases typically present with pain upon eating and swallowing. A bacterial infectious etiology is associated with odynophagia, but also includes persistent pain and tenderness. This presents as pain associated with eating. Bacterial infection of the submandibular gland adds the element of persistent pain, associated with such features as tenderness. In addition, purulent discharge from the Wharton’s duct may be present in infectious cases, and accompanied by fever, chills, and an elevated WBC.¹

Several bacteria have been isolated in infectious submandibular sialadenitis, the most common pathogens being Staphylococcus aureus. However, streptococci, Pseudomonas aeruginosa, Moraxella catarrhalis, and Escherichia coli bacteria have also been identified in cases of infectious submandibular sialadenitis.⁵

Viral etiologies of sialadenitis, such as mumps, are generally bilateral and nonsuppurative. The human immunodeficiency virus can also cause bilateral nonsuppurative salivary gland infections.⁶

Imaging Studies

As illustrated in our case, CT imaging can assist in confirming the diagnosis of acute submandibular sialadenitis by defining the anatomic involvement and identifying the presence of an abscess. Ultrasound can also be used and has been described as a first-line imaging procedure.^7,8

Treatment

Surgical Intervention. Abscesses may require surgical intervention. However, most cases without abscess formation respond to outpatient treatment with antibiotics.⁵ If ductal obstruction is identified, removal of the calculus may be needed. This may involve ductal dilation, sialolithectomy, or even ductoplasty if a stricture is identified.¹

Antibiotic Therapy. With respect to antibiotic selection, Chandak et al⁵ recommend oral amoxicillin-clavulanic acid. Other antistaphylococcal coverage recommendations have been made in the literature. Gland massage may be helpful after the tenderness has resolved,⁵ and sialogogues (eg, lemon drops, vitamin C lozenges) can also provide some relief.⁶ In addition, to avoid disease recurrence and prevent dental complications, Chandak et al⁵ emphasize the crucial role of hydration and excellent oral hygiene.

Conclusion

We suspected acute submandibular sialadenitis in our patient based on clinical findings, which were confirmed on CT imaging. Patients with acute submandibular sialadenitis may present with submandibular gland obstruction in the absence of bacterial infection. Noninfectious obstruction typically presents as pain associated with eating and swallowing, whereas infectious cases include constant pain and tenderness in the affected area. In addition, patients with infectious etiology may also have purulent discharge from Wharton’s duct, fever, chills, and an elevated WBC. Several bacteria have been isolated, the most common being S aureus. However, streptococci, P aeruginosa, M catarrhalis and E coli have also been identified. Computed tomography studies are helpful in confirming the diagnosis, defining anatomical involvement, and in identifying abscess formation.

Abscesses may require surgical intervention. However, most cases without abscess formation respond to outpatient treatment with antibiotics. Antibiotic selection involves antistaphylococcal coverage, such as amoxicillin-clavulanic acid. Glandular massage may be helpful after the tenderness has resolved. In addition, the literature emphasizes the crucial role of hydration and excellent oral hygiene in disease recurrence and to prevent dental complications.

Case

A 21-year-old woman presented to the ED with pain and swelling on the right side of her neck. She stated the pain started earlier that morning and worsened when she ate or swallowed. The patient denied a recent or remote history of drooling, voice changes, or neck swelling. She reported no fevers, chills, or any other complaints, and had no pertinent medical history—specifically, no history of recent dental work. Her surgical history included tonsillectomy and cholecystectomy. There was no family history of diabetes, thyroid disease, autoimmune disease, or any other diseases. The patient stated that she was not on any prescription or over-the-counter medications. Regarding her social history, she denied past or cu

Vital signs at presentation were: blood pressure, 124/63 mm Hg (sitting); heart rate, 73 beats/min; respiratory rate, 15 breaths/min; and temperature, 98°F. Oxygen saturation was 99% on room air. On clinical examination, pain was noted in the patient’s right submandibular area and was tender to palpation. The swelling extended to the angle of the mandible posteriorly (Figure 1a and 1b). There was no erythema or increased surface temperature to suggest overlying cellulitis. The oral examination showed no evidence of dental infection, angioedema, or Ludwig angina. The pharynx was normal in appearance. The otological examination was unremarkable, and there was no evidence of mastoiditis.

Laboratory evaluation included a complete blood count (CBC), basic metabolic profile (BMP), and rapid streptococcal test (RST). The results of the patient’s CBC revealed a white blood cell count (WBC) of 11.1 x 10⁹/L; the BMP was unremarkable; and the RST was negative.

A soft tissue neck computed tomography (CT) scan with contrast was obtained, which revealed mild right submandibular gland enlargement with abnormal enhancement (Figure 2). Stranding was also noted in the right submandibular space along with thickening of the right platysma muscle, and few surrounding lymph nodes were prominent (Figure 3). The findings were consistent with acute submandibular sialadenitis.

Discussion

Comparatively little has been published on acute submandibular sialadenitis over the past three decades, and much of that which is cited in the literature comes from a rather small pool of case reports.¹ In a literature review, Raad et al¹ noted, “Pertinent literature on [this] subject includes case reports but no studies describing the microbial and clinical characteristics of this disease.” Further, many of the published case reports describe neonatal presentations of submandibular sialadenitis, the incidence of which is rare in this patient population.^2-4

Submandibular and Parotid Glands

The submandibular gland is the second largest salivary gland, the parotid gland being the largest. The duct of the salivary gland, the Wharton’s duct, opens under the tongue in the area of the lingual frenulum. Ductal obstruction is more frequently seen with the submandibular gland than with the parotid gland.¹ The reason for this is unclear, but may be related to several factors. One factor may be that, unlike the Stenson’s duct of the parotid gland, the Wharton’s duct does not pass through a muscle; thus, there is no muscular massage supporting the movement of secretion, as there is with buccinator muscle massage of Stenson’s duct. In addition, submandibular saliva is more viscous than parotid saliva due to its higher protein content and higher concentration of calcium phosphate.¹

Etiology

Submandibular gland obstruction can occur in the absence of infection. Noninfectious cases typically present with pain upon eating and swallowing. A bacterial infectious etiology is associated with odynophagia, but also includes persistent pain and tenderness. This presents as pain associated with eating. Bacterial infection of the submandibular gland adds the element of persistent pain, associated with such features as tenderness. In addition, purulent discharge from the Wharton’s duct may be present in infectious cases, and accompanied by fever, chills, and an elevated WBC.¹

Several bacteria have been isolated in infectious submandibular sialadenitis, the most common pathogens being Staphylococcus aureus. However, streptococci, Pseudomonas aeruginosa, Moraxella catarrhalis, and Escherichia coli bacteria have also been identified in cases of infectious submandibular sialadenitis.⁵

Viral etiologies of sialadenitis, such as mumps, are generally bilateral and nonsuppurative. The human immunodeficiency virus can also cause bilateral nonsuppurative salivary gland infections.⁶

Imaging Studies

As illustrated in our case, CT imaging can assist in confirming the diagnosis of acute submandibular sialadenitis by defining the anatomic involvement and identifying the presence of an abscess. Ultrasound can also be used and has been described as a first-line imaging procedure.^7,8

Treatment

Surgical Intervention. Abscesses may require surgical intervention. However, most cases without abscess formation respond to outpatient treatment with antibiotics.⁵ If ductal obstruction is identified, removal of the calculus may be needed. This may involve ductal dilation, sialolithectomy, or even ductoplasty if a stricture is identified.¹

Antibiotic Therapy. With respect to antibiotic selection, Chandak et al⁵ recommend oral amoxicillin-clavulanic acid. Other antistaphylococcal coverage recommendations have been made in the literature. Gland massage may be helpful after the tenderness has resolved,⁵ and sialogogues (eg, lemon drops, vitamin C lozenges) can also provide some relief.⁶ In addition, to avoid disease recurrence and prevent dental complications, Chandak et al⁵ emphasize the crucial role of hydration and excellent oral hygiene.

Conclusion

We suspected acute submandibular sialadenitis in our patient based on clinical findings, which were confirmed on CT imaging. Patients with acute submandibular sialadenitis may present with submandibular gland obstruction in the absence of bacterial infection. Noninfectious obstruction typically presents as pain associated with eating and swallowing, whereas infectious cases include constant pain and tenderness in the affected area. In addition, patients with infectious etiology may also have purulent discharge from Wharton’s duct, fever, chills, and an elevated WBC. Several bacteria have been isolated, the most common being S aureus. However, streptococci, P aeruginosa, M catarrhalis and E coli have also been identified. Computed tomography studies are helpful in confirming the diagnosis, defining anatomical involvement, and in identifying abscess formation.

Abscesses may require surgical intervention. However, most cases without abscess formation respond to outpatient treatment with antibiotics. Antibiotic selection involves antistaphylococcal coverage, such as amoxicillin-clavulanic acid. Glandular massage may be helpful after the tenderness has resolved. In addition, the literature emphasizes the crucial role of hydration and excellent oral hygiene in disease recurrence and to prevent dental complications.

Case

A 21-year-old woman presented to the ED with pain and swelling on the right side of her neck. She stated the pain started earlier that morning and worsened when she ate or swallowed. The patient denied a recent or remote history of drooling, voice changes, or neck swelling. She reported no fevers, chills, or any other complaints, and had no pertinent medical history—specifically, no history of recent dental work. Her surgical history included tonsillectomy and cholecystectomy. There was no family history of diabetes, thyroid disease, autoimmune disease, or any other diseases. The patient stated that she was not on any prescription or over-the-counter medications. Regarding her social history, she denied past or cu

Vital signs at presentation were: blood pressure, 124/63 mm Hg (sitting); heart rate, 73 beats/min; respiratory rate, 15 breaths/min; and temperature, 98°F. Oxygen saturation was 99% on room air. On clinical examination, pain was noted in the patient’s right submandibular area and was tender to palpation. The swelling extended to the angle of the mandible posteriorly (Figure 1a and 1b). There was no erythema or increased surface temperature to suggest overlying cellulitis. The oral examination showed no evidence of dental infection, angioedema, or Ludwig angina. The pharynx was normal in appearance. The otological examination was unremarkable, and there was no evidence of mastoiditis.

Laboratory evaluation included a complete blood count (CBC), basic metabolic profile (BMP), and rapid streptococcal test (RST). The results of the patient’s CBC revealed a white blood cell count (WBC) of 11.1 x 10⁹/L; the BMP was unremarkable; and the RST was negative.

A soft tissue neck computed tomography (CT) scan with contrast was obtained, which revealed mild right submandibular gland enlargement with abnormal enhancement (Figure 2). Stranding was also noted in the right submandibular space along with thickening of the right platysma muscle, and few surrounding lymph nodes were prominent (Figure 3). The findings were consistent with acute submandibular sialadenitis.

Discussion

Comparatively little has been published on acute submandibular sialadenitis over the past three decades, and much of that which is cited in the literature comes from a rather small pool of case reports.¹ In a literature review, Raad et al¹ noted, “Pertinent literature on [this] subject includes case reports but no studies describing the microbial and clinical characteristics of this disease.” Further, many of the published case reports describe neonatal presentations of submandibular sialadenitis, the incidence of which is rare in this patient population.^2-4

Submandibular and Parotid Glands

The submandibular gland is the second largest salivary gland, the parotid gland being the largest. The duct of the salivary gland, the Wharton’s duct, opens under the tongue in the area of the lingual frenulum. Ductal obstruction is more frequently seen with the submandibular gland than with the parotid gland.¹ The reason for this is unclear, but may be related to several factors. One factor may be that, unlike the Stenson’s duct of the parotid gland, the Wharton’s duct does not pass through a muscle; thus, there is no muscular massage supporting the movement of secretion, as there is with buccinator muscle massage of Stenson’s duct. In addition, submandibular saliva is more viscous than parotid saliva due to its higher protein content and higher concentration of calcium phosphate.¹

Etiology

Submandibular gland obstruction can occur in the absence of infection. Noninfectious cases typically present with pain upon eating and swallowing. A bacterial infectious etiology is associated with odynophagia, but also includes persistent pain and tenderness. This presents as pain associated with eating. Bacterial infection of the submandibular gland adds the element of persistent pain, associated with such features as tenderness. In addition, purulent discharge from the Wharton’s duct may be present in infectious cases, and accompanied by fever, chills, and an elevated WBC.¹

Several bacteria have been isolated in infectious submandibular sialadenitis, the most common pathogens being Staphylococcus aureus. However, streptococci, Pseudomonas aeruginosa, Moraxella catarrhalis, and Escherichia coli bacteria have also been identified in cases of infectious submandibular sialadenitis.⁵

Viral etiologies of sialadenitis, such as mumps, are generally bilateral and nonsuppurative. The human immunodeficiency virus can also cause bilateral nonsuppurative salivary gland infections.⁶

Imaging Studies

As illustrated in our case, CT imaging can assist in confirming the diagnosis of acute submandibular sialadenitis by defining the anatomic involvement and identifying the presence of an abscess. Ultrasound can also be used and has been described as a first-line imaging procedure.^7,8

Treatment

Surgical Intervention. Abscesses may require surgical intervention. However, most cases without abscess formation respond to outpatient treatment with antibiotics.⁵ If ductal obstruction is identified, removal of the calculus may be needed. This may involve ductal dilation, sialolithectomy, or even ductoplasty if a stricture is identified.¹

Antibiotic Therapy. With respect to antibiotic selection, Chandak et al⁵ recommend oral amoxicillin-clavulanic acid. Other antistaphylococcal coverage recommendations have been made in the literature. Gland massage may be helpful after the tenderness has resolved,⁵ and sialogogues (eg, lemon drops, vitamin C lozenges) can also provide some relief.⁶ In addition, to avoid disease recurrence and prevent dental complications, Chandak et al⁵ emphasize the crucial role of hydration and excellent oral hygiene.

Conclusion

We suspected acute submandibular sialadenitis in our patient based on clinical findings, which were confirmed on CT imaging. Patients with acute submandibular sialadenitis may present with submandibular gland obstruction in the absence of bacterial infection. Noninfectious obstruction typically presents as pain associated with eating and swallowing, whereas infectious cases include constant pain and tenderness in the affected area. In addition, patients with infectious etiology may also have purulent discharge from Wharton’s duct, fever, chills, and an elevated WBC. Several bacteria have been isolated, the most common being S aureus. However, streptococci, P aeruginosa, M catarrhalis and E coli have also been identified. Computed tomography studies are helpful in confirming the diagnosis, defining anatomical involvement, and in identifying abscess formation.

Abscesses may require surgical intervention. However, most cases without abscess formation respond to outpatient treatment with antibiotics. Antibiotic selection involves antistaphylococcal coverage, such as amoxicillin-clavulanic acid. Glandular massage may be helpful after the tenderness has resolved. In addition, the literature emphasizes the crucial role of hydration and excellent oral hygiene in disease recurrence and to prevent dental complications.

The diagnosis of aortic dissection is often challenging due to its various presentations and the frequent absence of classic findings. This high-morbidity and high-mortality condition may present with nonspecific chest, back, or abdominal pain, and is often associated with hypotension.¹ Point-of-care (POC) ultrasound in the ED allows for rapid diagnosis of this time-sensitive disease.

Case

A 70-year-old woman presented to the ED for evaluation of acute sharp chest pain, which she stated began while she was exercising earlier that day. The pain was substernal and radiated to her upper back. The patient also described associated lightheadedness and dyspnea, but denied any focal weakness or paresthesias. Her vital signs were remarkable for a blood pressure of 90/31 mm Hg and a heart rate of 42 beats/min. A bedside ultrasound of the patient’s aortic root and abdominal aorta was performed to assess for evidence of aortic dissection.

Imaging Technique

To evaluate for aortic dissection using POC ultrasound, views of the aortic root and the abdominal aorta should be obtained with the patient in the supine position. The phased array (cardiac) probe is used to obtain the parasternal long axis (PSLA) view of the heart to visualize the aortic root. The PSLA view is obtained by placing the probe in the third or fourth intercostal space, adjacent to the left sternal border, with the probe parallel to the long axis of the left ventricle (Figure 1). The American Society of Echocardiography recommends measuring the aortic diameter at the sinus of Valsalva, but measurement of the largest visible portion of the aortic root may be more practical.^2,3 Measurement of the aortic root diameter should occur at end diastole.^2,3 Tricks for better visualization of the aortic root include tilting the probe tail 10° toward the patient’s right elbow (ie, aiming the probe footprint toward the patient’s left shoulder), or placing the patient in the left lateral decubitus position. Values greater than 4 cm indicate aortic root dilatation.⁴ Figure 2 demonstrates the PSLA view in our patient, showing the dilated aortic root, which measured roughly 5 cm. 

The abdominal aorta is best visualized using a low-frequency curvilinear (abdominal) probe. The aorta should be visualized in the transverse plane from the diaphragm to its bifurcation by placing the probe in the epigastrium and slowly moving it inferiorly to the level of the umbilicus (Figure 3). The aorta can then be visualized in the longitudinal plane by rotating the probe clockwise until it is parallel with the long axis of the aorta (Figure 4). Visualization of an intimal flap is the most common sonographic finding associated with an abdominal aortic dissection. In our patient, an intimal flap was visualized in both the transverse and longitudinal views (Figures 5 and 6).

Discussion

Aortic dissection is a medical emergency—one that has a reported in-hospital mortality of 27.4%.¹ Therefore, prompt diagnosis of an aortic dissection in the ED is crucial to improving patient outcomes. Traditionally, emergency physicians (EPs) have relied on aortography and contrast-enhanced computed tomography (CT) to diagnose aortic dissection. However, both of these modalities require a considerable length of time, injection of contrast material, and often transportation of the patient from the ED.

Point-of-care ultrasound provides a fast and noninvasive tool for the diagnosis of aortic dissection. Several recent case reports and case series have highlighted the utility of POC ultrasound to diagnose aortic dissection in the ED.^5-7

Case Conclusion

After the results of the POC transthoracic and transabdominal ultrasound were reviewed, we promptly consulted the vascular surgery team. They performed a CT scan verifying a DeBakey type I aortic dissection involving both the ascending aorta and the descending aorta. The patient was subsequently taken to the operating room for definitive repair with a graft. She was discharged home on hospital day 9 in good condition.

Summary

Point-of-care ultrasound is a useful bedside tool for the rapid diagnosis of aortic dissection in the ED. The aortic root dilatation seen on the PSLA view and the presence of an intimal flap seen on either transthoracic or transabdominal views of the aorta are both highly sensitive for aortic dissection.

The diagnosis of aortic dissection is often challenging due to its various presentations and the frequent absence of classic findings. This high-morbidity and high-mortality condition may present with nonspecific chest, back, or abdominal pain, and is often associated with hypotension.¹ Point-of-care (POC) ultrasound in the ED allows for rapid diagnosis of this time-sensitive disease.

Case

A 70-year-old woman presented to the ED for evaluation of acute sharp chest pain, which she stated began while she was exercising earlier that day. The pain was substernal and radiated to her upper back. The patient also described associated lightheadedness and dyspnea, but denied any focal weakness or paresthesias. Her vital signs were remarkable for a blood pressure of 90/31 mm Hg and a heart rate of 42 beats/min. A bedside ultrasound of the patient’s aortic root and abdominal aorta was performed to assess for evidence of aortic dissection.

Imaging Technique

To evaluate for aortic dissection using POC ultrasound, views of the aortic root and the abdominal aorta should be obtained with the patient in the supine position. The phased array (cardiac) probe is used to obtain the parasternal long axis (PSLA) view of the heart to visualize the aortic root. The PSLA view is obtained by placing the probe in the third or fourth intercostal space, adjacent to the left sternal border, with the probe parallel to the long axis of the left ventricle (Figure 1). The American Society of Echocardiography recommends measuring the aortic diameter at the sinus of Valsalva, but measurement of the largest visible portion of the aortic root may be more practical.^2,3 Measurement of the aortic root diameter should occur at end diastole.^2,3 Tricks for better visualization of the aortic root include tilting the probe tail 10° toward the patient’s right elbow (ie, aiming the probe footprint toward the patient’s left shoulder), or placing the patient in the left lateral decubitus position. Values greater than 4 cm indicate aortic root dilatation.⁴ Figure 2 demonstrates the PSLA view in our patient, showing the dilated aortic root, which measured roughly 5 cm. 

The abdominal aorta is best visualized using a low-frequency curvilinear (abdominal) probe. The aorta should be visualized in the transverse plane from the diaphragm to its bifurcation by placing the probe in the epigastrium and slowly moving it inferiorly to the level of the umbilicus (Figure 3). The aorta can then be visualized in the longitudinal plane by rotating the probe clockwise until it is parallel with the long axis of the aorta (Figure 4). Visualization of an intimal flap is the most common sonographic finding associated with an abdominal aortic dissection. In our patient, an intimal flap was visualized in both the transverse and longitudinal views (Figures 5 and 6).

Discussion

Aortic dissection is a medical emergency—one that has a reported in-hospital mortality of 27.4%.¹ Therefore, prompt diagnosis of an aortic dissection in the ED is crucial to improving patient outcomes. Traditionally, emergency physicians (EPs) have relied on aortography and contrast-enhanced computed tomography (CT) to diagnose aortic dissection. However, both of these modalities require a considerable length of time, injection of contrast material, and often transportation of the patient from the ED.

Point-of-care ultrasound provides a fast and noninvasive tool for the diagnosis of aortic dissection. Several recent case reports and case series have highlighted the utility of POC ultrasound to diagnose aortic dissection in the ED.^5-7

Case Conclusion

After the results of the POC transthoracic and transabdominal ultrasound were reviewed, we promptly consulted the vascular surgery team. They performed a CT scan verifying a DeBakey type I aortic dissection involving both the ascending aorta and the descending aorta. The patient was subsequently taken to the operating room for definitive repair with a graft. She was discharged home on hospital day 9 in good condition.

Summary

Point-of-care ultrasound is a useful bedside tool for the rapid diagnosis of aortic dissection in the ED. The aortic root dilatation seen on the PSLA view and the presence of an intimal flap seen on either transthoracic or transabdominal views of the aorta are both highly sensitive for aortic dissection.

The diagnosis of aortic dissection is often challenging due to its various presentations and the frequent absence of classic findings. This high-morbidity and high-mortality condition may present with nonspecific chest, back, or abdominal pain, and is often associated with hypotension.¹ Point-of-care (POC) ultrasound in the ED allows for rapid diagnosis of this time-sensitive disease.

Case

A 70-year-old woman presented to the ED for evaluation of acute sharp chest pain, which she stated began while she was exercising earlier that day. The pain was substernal and radiated to her upper back. The patient also described associated lightheadedness and dyspnea, but denied any focal weakness or paresthesias. Her vital signs were remarkable for a blood pressure of 90/31 mm Hg and a heart rate of 42 beats/min. A bedside ultrasound of the patient’s aortic root and abdominal aorta was performed to assess for evidence of aortic dissection.

Imaging Technique

To evaluate for aortic dissection using POC ultrasound, views of the aortic root and the abdominal aorta should be obtained with the patient in the supine position. The phased array (cardiac) probe is used to obtain the parasternal long axis (PSLA) view of the heart to visualize the aortic root. The PSLA view is obtained by placing the probe in the third or fourth intercostal space, adjacent to the left sternal border, with the probe parallel to the long axis of the left ventricle (Figure 1). The American Society of Echocardiography recommends measuring the aortic diameter at the sinus of Valsalva, but measurement of the largest visible portion of the aortic root may be more practical.^2,3 Measurement of the aortic root diameter should occur at end diastole.^2,3 Tricks for better visualization of the aortic root include tilting the probe tail 10° toward the patient’s right elbow (ie, aiming the probe footprint toward the patient’s left shoulder), or placing the patient in the left lateral decubitus position. Values greater than 4 cm indicate aortic root dilatation.⁴ Figure 2 demonstrates the PSLA view in our patient, showing the dilated aortic root, which measured roughly 5 cm. 

The abdominal aorta is best visualized using a low-frequency curvilinear (abdominal) probe. The aorta should be visualized in the transverse plane from the diaphragm to its bifurcation by placing the probe in the epigastrium and slowly moving it inferiorly to the level of the umbilicus (Figure 3). The aorta can then be visualized in the longitudinal plane by rotating the probe clockwise until it is parallel with the long axis of the aorta (Figure 4). Visualization of an intimal flap is the most common sonographic finding associated with an abdominal aortic dissection. In our patient, an intimal flap was visualized in both the transverse and longitudinal views (Figures 5 and 6).

Discussion

Aortic dissection is a medical emergency—one that has a reported in-hospital mortality of 27.4%.¹ Therefore, prompt diagnosis of an aortic dissection in the ED is crucial to improving patient outcomes. Traditionally, emergency physicians (EPs) have relied on aortography and contrast-enhanced computed tomography (CT) to diagnose aortic dissection. However, both of these modalities require a considerable length of time, injection of contrast material, and often transportation of the patient from the ED.

Point-of-care ultrasound provides a fast and noninvasive tool for the diagnosis of aortic dissection. Several recent case reports and case series have highlighted the utility of POC ultrasound to diagnose aortic dissection in the ED.^5-7

Case Conclusion

After the results of the POC transthoracic and transabdominal ultrasound were reviewed, we promptly consulted the vascular surgery team. They performed a CT scan verifying a DeBakey type I aortic dissection involving both the ascending aorta and the descending aorta. The patient was subsequently taken to the operating room for definitive repair with a graft. She was discharged home on hospital day 9 in good condition.

Summary

Point-of-care ultrasound is a useful bedside tool for the rapid diagnosis of aortic dissection in the ED. The aortic root dilatation seen on the PSLA view and the presence of an intimal flap seen on either transthoracic or transabdominal views of the aorta are both highly sensitive for aortic dissection.