Acute limb ischemia (ALI) is an emergent medical condition that is characterized by a precipitous decrease in limb perfusion that threatens the viability of the affected limb, and symptoms that have been present for 14 days or less.^1-5 The incidence of lower extremity ALI in the US is nine to 16 cases per 100,000 persons per year, and one to three cases per 100,000 persons per year for upper extremity ALI.³ Symptoms suggestive of this condition classically include pain in the effected limb at rest, loss of sensation, impaired motor function, and cyanosis/pallor. Irreparable damage can occur in as quickly as 4 to 6 hours with complete arterial occlusion. A majority of ALI is caused by thrombosis, with the remainder of cases caused by embolism, 85% and 15% respectively.^1-6 If not addressed promptly, this condition carries a high degree of morbidity (ie, limb loss) and mortality. Immediate initiation of anticoagulation therapy and vascular surgery consultation are mainstays of ED management. Time-to-treatment is a predictor of success and is an area where the emergency physician (EP) can make a significant difference in patient outcomes.⁷ Although vascular interruption via traumatic mechanism is not addressed in this review, it should remain a consideration in relation to the historical features of each case.

Presentation

Traditionally, symptoms of ALI can be remembered as the “six Ps”: pain, pallor, paresthesia, paralysis, pulselessness, and poikilothermia. Note that ALI represents a spectrum of disease, and the presenting features depend heavily on the level and degree of obstruction. Pain, however, is most frequently the first presenting symptom of patients with ALI.^1-6 Pain will occur in muscle groups distal to the occlusion. Obstruction of the aortoiliac region might produce pain in the buttocks, thigh, and hip, whereas occlusion of the femoral artery may produce pain in the calf. Single-level disease will often produce claudication, but multilevel disease may present as a nonhealing ulcer or with focal gangrene. The differential diagnosis of ALI includes direct arterial injury, vasospasm, compartment syndrome, chronic peripheral artery disease, stroke, spinal cord injury, vasculitis, muscular trauma, and radiculopathy.^3,5

Etiology

As stated previously, ALI is a result of either thrombotic or embolic phenomena that either partially or completely occludes a vessel such that adequate perfusion is no longer achieved. Consequently, there is a decrease in the metabolism of the tissue supplied in those territories, which can rapidly progress to necrosis. Thrombosis is the most common cause of ALI, accounting for approximately 85%.^2,3Typically, thrombosis presents in the setting of pre-existing peripheral artery disease (PAD).⁸ As PAD worsens, damage to the arterial endothelium triggers platelet activation, and accumulation in a manner conceptually similar to thrombosis in myocardial infarction.⁹ Hypercoagulable states increase the risk of thrombi development.¹⁰ Symptoms of thrombosis are often more insidious in onset when compared to embolism, and signs/symptoms of prior claudication are almost always present. Consequently, there is a greater chance that collateral circulation has developed over time.^2,6,11,12

By contrast, ALI caused by embolism is more acute in onset, and is often more emergent due to complete occlusion without chance of collateral vessel development.^1,3,6,12 See Table 1 for differences in risk factors and presentation between thrombotic and embolic occlusion.

Historical Features

Information should be obtained systematically in all presentations and should include time of symptom onset, duration, severity, and location; however, special attention should be paid to the evolution of symptoms over time. One historical pearl that should raise suspicion of embolism vs thrombus is a patient history with a specific time of symptom onset. Specific questioning about history of claudication, including description of typical symptoms, is critical. A full list of other medical comorbidities should be obtained. This may reveal risk factors for thrombotic and embolic disease.^1,3-5 This also may alter available treatment options.^7,8,12,13 At presentation, the EP should obtain a list of the patient’s current medications, and special attention should be given to prothrombotic medications and medications that may interact with anticoagulants.

Physical Examination

On physical examination, the EP should pay particular attention to both the external appearance and temperature of the skin of the patient’s affected extremity. The presence or absence of peripheral pulses is an important feature when assessing for ALI; however, the presence of peripheral pulses does not exclude ALI from the differential.

Precise evaluation of sensation is important to attempt to quantify the extent of injury, localize a possible obstruction, and differentiate ALI from other possible causes of sensation deficits. Though not referenced in the six Ps, the patient’s limb may also appear mottled or marbled. Embolic phenomena occur at sites of vascular bifurcation. In a patient with aortic embolism, femoral pulses will be absent with bilateral mottling and paralysis of the lower extremities. Iliac artery embolism will produce the same symptoms, except unilateral. Femoral artery embolism will yield coolness and mottling distal to the inguinal ligament. Similarly, popliteal artery embolism will produce those same findings, except distal to the knee with preserved femoral pulses.

Diagnosis and Evaluation

After the history and physical examination are completed, further diagnostic methodologies should be considered, including laboratory evaluation and additional imaging studies.

Imaging Studies

Doppler ultrasound examination to assess for pulses on the affected limb should be performed immediately. Bedside continuous-wave Doppler may be used to differentiate arterial vs venous signal.^6,14-16 An ankle brachial index may be calculated through either direct auscultation of pulses or Doppler signal. A ratio of less than 0.9 is suggestive of ischemia, while a ratio of less than 0.5 is considered critical ischemia.²

Laboratory Evaluation

Laboratory evaluation of hematocrit, coagulation studies, renal function, electrolyte levels, lactate, and creatinine kinase should be completed.^1,5 An electrocardiogram and bedside/formal echocardiogram may be considered if embolism is suspected.^1,6,17

Imaging

Angiography is currently the gold standard imaging modality to diagnose ALI.¹⁶ However, other imaging modalities exist that expose the patient to less radiation and are generally preferred by patients.¹⁸ Duplex ultrasonography is the least invasive imaging modality, with a reported sensitivity of 88% and specificity of 96% for the detection of greater than 50% stenosis.^6,19 Contrast-enhanced magnetic resonance angiography (MRA) of the lower extremity is also relatively noninvasive, but is more limited in its application. It carries a reported sensitivity of 95% and a specificity of 97% for detection of stenosis of greater than 50%.^6,19 An MRA without contrast may be considered for patients with an estimated glomerular filtration rate of less than 30 mL/min/1.73 m² and who are not on dialysis, but the diagnostic efficacy is reduced.¹⁶ Finally, the sensitivity and specificity of computed tomography angiography (CTA) to detect aortoiliac stenosis of greater than 50% is 96% and 98% respectively.^6,18,19 Other studies demonstrated similar results for other arterial locations in the lower extremities.^18,19 A principal advantage of CTA is that direct visualization of calcifications, clips, stents, and prior bypasses is possible without the limitations of MRA.¹⁶ The American College of Radiology (ACR) lists ultrasound duplex Doppler and noncontrast MRA of the lower extremity as “may be appropriate.”¹⁶ In contrast, the ACR classifies MRA with contrast, CTA with contrast, and angiography of the lower extremity as “usually appropriate.”¹⁶ Selecting the optimal imaging study for a patient may require involvement of a facility’s radiology department and/or a vascular surgeon.^14,15

Management in the ED

Even before the definitive diagnosis of ALI is made, steps can be taken to minimize and/or slow progression of injury. Placing the affected limb in a dependent position and providing intravenous (IV) fluid hydration will maximize perfusion.^1,3,5 Even with consideration of the diagnostic modalities previously described, ALI is often considered a clinical diagnosis. Since time is critical, early consultation with vascular surgery services is imperative if ALI is suspected.

Intravenous Fluid Therapy

Suspected ALI should be treated in the ED with an IV heparin bolus, followed by constant IV infusion. Heparin prevents proximal and distal propagation of the thrombus.^{1,3,5,6,15,17,20} Additionally, it helps maintain the microcirculation surrounding the affected area.⁶ A heparin bolus dose of 100 U/kg followed by a continuous infusion of heparin 1,000 U/h is the recommended standard.^1,3,5,6,15 A goal partial thromboplastin time of 60 to 100 seconds, or an international normalized ratio of 2 to 3 is desirable.^8,21

Staging: The Rutherford Classification System

Once immediate therapies are started, the stage of PAD should be determined using the Rutherford classification system in collaboration with vascular surgery services; this will further guide treatment and disposition.

Category I. In category I ALI, the affected limb is considered viable and not immediately threatened.

Category IIa. The limb is considered to be marginally threatened and salvageable.

Category IIb. An ALI classified as a category IIb is the most urgent type in which the limb is immediately threatened.

Category III. The limb is classified as having irreversible damage.^2,3,17,22

(See Table 2 for a more detailed summary of the Rutherford classification system.)

Treatment

Definitive treatment decisions should be made in consultation with vascular surgery services. The results of three clinical trials developed the foundation for management of ALI: the Thrombolysis or Peripheral Arterial Surgery (TOPAS) trial, Surgery Versus Thrombolysis for Ischemia of the Lower Extremity (STILE) trial, and Rutherford trial.^22-24 Table 3 provides a summary of the treatment techniques utilized, which include mechanical recanalization with percutaneous aspiration thrombectomy, percutaneous mechanical thrombectomy,^6,12,25-28 pharmacological recanalization via catheter-directed thrombolysis,^{6,8,12,20,23-28} and/or surgical management via thrombectomy or embolectomy.^{6,11,23,24,27}

Complications

The complications of treating ALI can be stratified into three subsets: pharmacologic, mechanical, and reperfusion injury-related. Medical treatment with heparin is not without risk. Intracranial hemorrhage, major bleeding at other sites, and compartment syndrome secondary to bleeding can all occur. Treatment may also cause distal embolization and lead to mechanical occlusion of another site. Finally, reperfusion injury predisposes the patient to a host of new problems. Reperfusion injury occurs when fresh blood enters a previously ischemic zone. When this occurs, oxygen free radicals, inflammatory mediators, and catabolism byproducts mix with the blood. This process can damage surrounding epithelial cells and lead to increased interstitial permeability. As a result, compartment syndrome may also develop via this mechanism.^1,3,5,6 The anterior compartment of the lower extremity is most at risk. As such, assessment of peroneal nerve activity via dorsiflexion of the foot and sensation testing is important after the initiation of treatment.⁶ Systemic distribution of these harmful byproducts can also cause arrhythmias, renal failure, and systemic acadisos.^1,3,5,6 It is important for physicians and staff to monitor the patient closely for the development of these complications and be prepared to intervene.

Opportunities for Improvement

In a condition where minutes matter, expedient action is critical. Time-to-recognition, imaging, consultation, and intervention all are potential sources of delay. Two recent studies have investigated the treatment timeline of ALI. The first study showed that the greatest source of delay is time from symptom onset to presentation in the ED; an average of 11.35 hours. The second largest source of delay was time from recognition of ALI to imaging, with an average delay of 4.75 hours. The average ED evaluation time was 40 minutes, and the average total time to intervention was 10.2 hours. While time-to-symptom presentation may represent a failure of public health, time-to-imaging was identified as an area of unacceptable delay by the authors.²⁹ A second study examined the effect of pre-hospital care on the time-to-treatment. Persons who were transported via emergency medical services (EMS) arrived to the hospital at a median time of 5 hours after symptom onset, were seen by a physician at a median time of 51 minutes, and had revascularization at a median time of 23 hours. Those not transported by EMS arrived to the hospital at a median time of 48 hours after symptom onset, were seen by a physician at a median time of 80 minutes, and had revascularization at a median time of 93 hours. As a secondary goal, the study examined the effect of heparinization in the ED and showed that treatment with heparin was associated with a favorable outcome.³⁰ While the total treatment times in each study vary widely, they share several important commonalities and reinforce expedient management as an important goal.

Outcomes

Advances in the treatment of this condition began in the 1970s, with an explosion of new techniques and data in the past several years. Still, ALI is a high morbidity and high mortality condition. Rates of limb loss are approximately 30% for all cases, and it is a fatal condition for as many as one-in-five. As discussed earlier, the patients who are most likely to experience ALI typically have several medical comorbidities. Perhaps unsurprisingly, ALI portends a poor prognosis even if the limb is salvaged. Approximately 15% to 20% of patients with ALI will die within 1 year of diagnosis.^3,4,6,12

Conclusion

Acute limb ischemia is a rare condition, but a true medical emergency. Prompt recognition of the signs and symptoms of ALI are critical for optimizing patient outcomes. A high index of clinical suspicion in patients with risk factors may lead to early diagnosis. Early vascular surgery consultation and early IV heparin treatment are important aspects of care. Prompt imaging and staging guide further management. Special care should be paid to possible post-treatment complications and to the investigation of contributing factors. The EP has a great opportunity to positively impact care with expeditious management. Early diagnosis, targeted history and physical examination, prompt treatment, collaboration with specialists, and prevention and treatment of life-threatening complications are all hallmarks of emergency medicine.

Acute limb ischemia (ALI) is an emergent medical condition that is characterized by a precipitous decrease in limb perfusion that threatens the viability of the affected limb, and symptoms that have been present for 14 days or less.^1-5 The incidence of lower extremity ALI in the US is nine to 16 cases per 100,000 persons per year, and one to three cases per 100,000 persons per year for upper extremity ALI.³ Symptoms suggestive of this condition classically include pain in the effected limb at rest, loss of sensation, impaired motor function, and cyanosis/pallor. Irreparable damage can occur in as quickly as 4 to 6 hours with complete arterial occlusion. A majority of ALI is caused by thrombosis, with the remainder of cases caused by embolism, 85% and 15% respectively.^1-6 If not addressed promptly, this condition carries a high degree of morbidity (ie, limb loss) and mortality. Immediate initiation of anticoagulation therapy and vascular surgery consultation are mainstays of ED management. Time-to-treatment is a predictor of success and is an area where the emergency physician (EP) can make a significant difference in patient outcomes.⁷ Although vascular interruption via traumatic mechanism is not addressed in this review, it should remain a consideration in relation to the historical features of each case.

Presentation

Traditionally, symptoms of ALI can be remembered as the “six Ps”: pain, pallor, paresthesia, paralysis, pulselessness, and poikilothermia. Note that ALI represents a spectrum of disease, and the presenting features depend heavily on the level and degree of obstruction. Pain, however, is most frequently the first presenting symptom of patients with ALI.^1-6 Pain will occur in muscle groups distal to the occlusion. Obstruction of the aortoiliac region might produce pain in the buttocks, thigh, and hip, whereas occlusion of the femoral artery may produce pain in the calf. Single-level disease will often produce claudication, but multilevel disease may present as a nonhealing ulcer or with focal gangrene. The differential diagnosis of ALI includes direct arterial injury, vasospasm, compartment syndrome, chronic peripheral artery disease, stroke, spinal cord injury, vasculitis, muscular trauma, and radiculopathy.^3,5

Etiology

As stated previously, ALI is a result of either thrombotic or embolic phenomena that either partially or completely occludes a vessel such that adequate perfusion is no longer achieved. Consequently, there is a decrease in the metabolism of the tissue supplied in those territories, which can rapidly progress to necrosis. Thrombosis is the most common cause of ALI, accounting for approximately 85%.^2,3Typically, thrombosis presents in the setting of pre-existing peripheral artery disease (PAD).⁸ As PAD worsens, damage to the arterial endothelium triggers platelet activation, and accumulation in a manner conceptually similar to thrombosis in myocardial infarction.⁹ Hypercoagulable states increase the risk of thrombi development.¹⁰ Symptoms of thrombosis are often more insidious in onset when compared to embolism, and signs/symptoms of prior claudication are almost always present. Consequently, there is a greater chance that collateral circulation has developed over time.^2,6,11,12

By contrast, ALI caused by embolism is more acute in onset, and is often more emergent due to complete occlusion without chance of collateral vessel development.^1,3,6,12 See Table 1 for differences in risk factors and presentation between thrombotic and embolic occlusion.

Historical Features

Information should be obtained systematically in all presentations and should include time of symptom onset, duration, severity, and location; however, special attention should be paid to the evolution of symptoms over time. One historical pearl that should raise suspicion of embolism vs thrombus is a patient history with a specific time of symptom onset. Specific questioning about history of claudication, including description of typical symptoms, is critical. A full list of other medical comorbidities should be obtained. This may reveal risk factors for thrombotic and embolic disease.^1,3-5 This also may alter available treatment options.^7,8,12,13 At presentation, the EP should obtain a list of the patient’s current medications, and special attention should be given to prothrombotic medications and medications that may interact with anticoagulants.

Physical Examination

On physical examination, the EP should pay particular attention to both the external appearance and temperature of the skin of the patient’s affected extremity. The presence or absence of peripheral pulses is an important feature when assessing for ALI; however, the presence of peripheral pulses does not exclude ALI from the differential.

Precise evaluation of sensation is important to attempt to quantify the extent of injury, localize a possible obstruction, and differentiate ALI from other possible causes of sensation deficits. Though not referenced in the six Ps, the patient’s limb may also appear mottled or marbled. Embolic phenomena occur at sites of vascular bifurcation. In a patient with aortic embolism, femoral pulses will be absent with bilateral mottling and paralysis of the lower extremities. Iliac artery embolism will produce the same symptoms, except unilateral. Femoral artery embolism will yield coolness and mottling distal to the inguinal ligament. Similarly, popliteal artery embolism will produce those same findings, except distal to the knee with preserved femoral pulses.

Diagnosis and Evaluation

After the history and physical examination are completed, further diagnostic methodologies should be considered, including laboratory evaluation and additional imaging studies.

Imaging Studies

Doppler ultrasound examination to assess for pulses on the affected limb should be performed immediately. Bedside continuous-wave Doppler may be used to differentiate arterial vs venous signal.^6,14-16 An ankle brachial index may be calculated through either direct auscultation of pulses or Doppler signal. A ratio of less than 0.9 is suggestive of ischemia, while a ratio of less than 0.5 is considered critical ischemia.²

Laboratory Evaluation

Laboratory evaluation of hematocrit, coagulation studies, renal function, electrolyte levels, lactate, and creatinine kinase should be completed.^1,5 An electrocardiogram and bedside/formal echocardiogram may be considered if embolism is suspected.^1,6,17

Imaging

Angiography is currently the gold standard imaging modality to diagnose ALI.¹⁶ However, other imaging modalities exist that expose the patient to less radiation and are generally preferred by patients.¹⁸ Duplex ultrasonography is the least invasive imaging modality, with a reported sensitivity of 88% and specificity of 96% for the detection of greater than 50% stenosis.^6,19 Contrast-enhanced magnetic resonance angiography (MRA) of the lower extremity is also relatively noninvasive, but is more limited in its application. It carries a reported sensitivity of 95% and a specificity of 97% for detection of stenosis of greater than 50%.^6,19 An MRA without contrast may be considered for patients with an estimated glomerular filtration rate of less than 30 mL/min/1.73 m² and who are not on dialysis, but the diagnostic efficacy is reduced.¹⁶ Finally, the sensitivity and specificity of computed tomography angiography (CTA) to detect aortoiliac stenosis of greater than 50% is 96% and 98% respectively.^6,18,19 Other studies demonstrated similar results for other arterial locations in the lower extremities.^18,19 A principal advantage of CTA is that direct visualization of calcifications, clips, stents, and prior bypasses is possible without the limitations of MRA.¹⁶ The American College of Radiology (ACR) lists ultrasound duplex Doppler and noncontrast MRA of the lower extremity as “may be appropriate.”¹⁶ In contrast, the ACR classifies MRA with contrast, CTA with contrast, and angiography of the lower extremity as “usually appropriate.”¹⁶ Selecting the optimal imaging study for a patient may require involvement of a facility’s radiology department and/or a vascular surgeon.^14,15

Management in the ED

Even before the definitive diagnosis of ALI is made, steps can be taken to minimize and/or slow progression of injury. Placing the affected limb in a dependent position and providing intravenous (IV) fluid hydration will maximize perfusion.^1,3,5 Even with consideration of the diagnostic modalities previously described, ALI is often considered a clinical diagnosis. Since time is critical, early consultation with vascular surgery services is imperative if ALI is suspected.

Intravenous Fluid Therapy

Suspected ALI should be treated in the ED with an IV heparin bolus, followed by constant IV infusion. Heparin prevents proximal and distal propagation of the thrombus.^{1,3,5,6,15,17,20} Additionally, it helps maintain the microcirculation surrounding the affected area.⁶ A heparin bolus dose of 100 U/kg followed by a continuous infusion of heparin 1,000 U/h is the recommended standard.^1,3,5,6,15 A goal partial thromboplastin time of 60 to 100 seconds, or an international normalized ratio of 2 to 3 is desirable.^8,21

Staging: The Rutherford Classification System

Once immediate therapies are started, the stage of PAD should be determined using the Rutherford classification system in collaboration with vascular surgery services; this will further guide treatment and disposition.

Category I. In category I ALI, the affected limb is considered viable and not immediately threatened.

Category IIa. The limb is considered to be marginally threatened and salvageable.

Category IIb. An ALI classified as a category IIb is the most urgent type in which the limb is immediately threatened.

Category III. The limb is classified as having irreversible damage.^2,3,17,22

(See Table 2 for a more detailed summary of the Rutherford classification system.)

Treatment

Definitive treatment decisions should be made in consultation with vascular surgery services. The results of three clinical trials developed the foundation for management of ALI: the Thrombolysis or Peripheral Arterial Surgery (TOPAS) trial, Surgery Versus Thrombolysis for Ischemia of the Lower Extremity (STILE) trial, and Rutherford trial.^22-24 Table 3 provides a summary of the treatment techniques utilized, which include mechanical recanalization with percutaneous aspiration thrombectomy, percutaneous mechanical thrombectomy,^6,12,25-28 pharmacological recanalization via catheter-directed thrombolysis,^{6,8,12,20,23-28} and/or surgical management via thrombectomy or embolectomy.^{6,11,23,24,27}

Complications

The complications of treating ALI can be stratified into three subsets: pharmacologic, mechanical, and reperfusion injury-related. Medical treatment with heparin is not without risk. Intracranial hemorrhage, major bleeding at other sites, and compartment syndrome secondary to bleeding can all occur. Treatment may also cause distal embolization and lead to mechanical occlusion of another site. Finally, reperfusion injury predisposes the patient to a host of new problems. Reperfusion injury occurs when fresh blood enters a previously ischemic zone. When this occurs, oxygen free radicals, inflammatory mediators, and catabolism byproducts mix with the blood. This process can damage surrounding epithelial cells and lead to increased interstitial permeability. As a result, compartment syndrome may also develop via this mechanism.^1,3,5,6 The anterior compartment of the lower extremity is most at risk. As such, assessment of peroneal nerve activity via dorsiflexion of the foot and sensation testing is important after the initiation of treatment.⁶ Systemic distribution of these harmful byproducts can also cause arrhythmias, renal failure, and systemic acadisos.^1,3,5,6 It is important for physicians and staff to monitor the patient closely for the development of these complications and be prepared to intervene.

Opportunities for Improvement

In a condition where minutes matter, expedient action is critical. Time-to-recognition, imaging, consultation, and intervention all are potential sources of delay. Two recent studies have investigated the treatment timeline of ALI. The first study showed that the greatest source of delay is time from symptom onset to presentation in the ED; an average of 11.35 hours. The second largest source of delay was time from recognition of ALI to imaging, with an average delay of 4.75 hours. The average ED evaluation time was 40 minutes, and the average total time to intervention was 10.2 hours. While time-to-symptom presentation may represent a failure of public health, time-to-imaging was identified as an area of unacceptable delay by the authors.²⁹ A second study examined the effect of pre-hospital care on the time-to-treatment. Persons who were transported via emergency medical services (EMS) arrived to the hospital at a median time of 5 hours after symptom onset, were seen by a physician at a median time of 51 minutes, and had revascularization at a median time of 23 hours. Those not transported by EMS arrived to the hospital at a median time of 48 hours after symptom onset, were seen by a physician at a median time of 80 minutes, and had revascularization at a median time of 93 hours. As a secondary goal, the study examined the effect of heparinization in the ED and showed that treatment with heparin was associated with a favorable outcome.³⁰ While the total treatment times in each study vary widely, they share several important commonalities and reinforce expedient management as an important goal.

Outcomes

Advances in the treatment of this condition began in the 1970s, with an explosion of new techniques and data in the past several years. Still, ALI is a high morbidity and high mortality condition. Rates of limb loss are approximately 30% for all cases, and it is a fatal condition for as many as one-in-five. As discussed earlier, the patients who are most likely to experience ALI typically have several medical comorbidities. Perhaps unsurprisingly, ALI portends a poor prognosis even if the limb is salvaged. Approximately 15% to 20% of patients with ALI will die within 1 year of diagnosis.^3,4,6,12

Conclusion

Acute limb ischemia is a rare condition, but a true medical emergency. Prompt recognition of the signs and symptoms of ALI are critical for optimizing patient outcomes. A high index of clinical suspicion in patients with risk factors may lead to early diagnosis. Early vascular surgery consultation and early IV heparin treatment are important aspects of care. Prompt imaging and staging guide further management. Special care should be paid to possible post-treatment complications and to the investigation of contributing factors. The EP has a great opportunity to positively impact care with expeditious management. Early diagnosis, targeted history and physical examination, prompt treatment, collaboration with specialists, and prevention and treatment of life-threatening complications are all hallmarks of emergency medicine.

Acute limb ischemia (ALI) is an emergent medical condition that is characterized by a precipitous decrease in limb perfusion that threatens the viability of the affected limb, and symptoms that have been present for 14 days or less.^1-5 The incidence of lower extremity ALI in the US is nine to 16 cases per 100,000 persons per year, and one to three cases per 100,000 persons per year for upper extremity ALI.³ Symptoms suggestive of this condition classically include pain in the effected limb at rest, loss of sensation, impaired motor function, and cyanosis/pallor. Irreparable damage can occur in as quickly as 4 to 6 hours with complete arterial occlusion. A majority of ALI is caused by thrombosis, with the remainder of cases caused by embolism, 85% and 15% respectively.^1-6 If not addressed promptly, this condition carries a high degree of morbidity (ie, limb loss) and mortality. Immediate initiation of anticoagulation therapy and vascular surgery consultation are mainstays of ED management. Time-to-treatment is a predictor of success and is an area where the emergency physician (EP) can make a significant difference in patient outcomes.⁷ Although vascular interruption via traumatic mechanism is not addressed in this review, it should remain a consideration in relation to the historical features of each case.

Presentation

Traditionally, symptoms of ALI can be remembered as the “six Ps”: pain, pallor, paresthesia, paralysis, pulselessness, and poikilothermia. Note that ALI represents a spectrum of disease, and the presenting features depend heavily on the level and degree of obstruction. Pain, however, is most frequently the first presenting symptom of patients with ALI.^1-6 Pain will occur in muscle groups distal to the occlusion. Obstruction of the aortoiliac region might produce pain in the buttocks, thigh, and hip, whereas occlusion of the femoral artery may produce pain in the calf. Single-level disease will often produce claudication, but multilevel disease may present as a nonhealing ulcer or with focal gangrene. The differential diagnosis of ALI includes direct arterial injury, vasospasm, compartment syndrome, chronic peripheral artery disease, stroke, spinal cord injury, vasculitis, muscular trauma, and radiculopathy.^3,5

Etiology

As stated previously, ALI is a result of either thrombotic or embolic phenomena that either partially or completely occludes a vessel such that adequate perfusion is no longer achieved. Consequently, there is a decrease in the metabolism of the tissue supplied in those territories, which can rapidly progress to necrosis. Thrombosis is the most common cause of ALI, accounting for approximately 85%.^2,3Typically, thrombosis presents in the setting of pre-existing peripheral artery disease (PAD).⁸ As PAD worsens, damage to the arterial endothelium triggers platelet activation, and accumulation in a manner conceptually similar to thrombosis in myocardial infarction.⁹ Hypercoagulable states increase the risk of thrombi development.¹⁰ Symptoms of thrombosis are often more insidious in onset when compared to embolism, and signs/symptoms of prior claudication are almost always present. Consequently, there is a greater chance that collateral circulation has developed over time.^2,6,11,12

By contrast, ALI caused by embolism is more acute in onset, and is often more emergent due to complete occlusion without chance of collateral vessel development.^1,3,6,12 See Table 1 for differences in risk factors and presentation between thrombotic and embolic occlusion.

Historical Features

Information should be obtained systematically in all presentations and should include time of symptom onset, duration, severity, and location; however, special attention should be paid to the evolution of symptoms over time. One historical pearl that should raise suspicion of embolism vs thrombus is a patient history with a specific time of symptom onset. Specific questioning about history of claudication, including description of typical symptoms, is critical. A full list of other medical comorbidities should be obtained. This may reveal risk factors for thrombotic and embolic disease.^1,3-5 This also may alter available treatment options.^7,8,12,13 At presentation, the EP should obtain a list of the patient’s current medications, and special attention should be given to prothrombotic medications and medications that may interact with anticoagulants.

Physical Examination

On physical examination, the EP should pay particular attention to both the external appearance and temperature of the skin of the patient’s affected extremity. The presence or absence of peripheral pulses is an important feature when assessing for ALI; however, the presence of peripheral pulses does not exclude ALI from the differential.

Precise evaluation of sensation is important to attempt to quantify the extent of injury, localize a possible obstruction, and differentiate ALI from other possible causes of sensation deficits. Though not referenced in the six Ps, the patient’s limb may also appear mottled or marbled. Embolic phenomena occur at sites of vascular bifurcation. In a patient with aortic embolism, femoral pulses will be absent with bilateral mottling and paralysis of the lower extremities. Iliac artery embolism will produce the same symptoms, except unilateral. Femoral artery embolism will yield coolness and mottling distal to the inguinal ligament. Similarly, popliteal artery embolism will produce those same findings, except distal to the knee with preserved femoral pulses.

Diagnosis and Evaluation

After the history and physical examination are completed, further diagnostic methodologies should be considered, including laboratory evaluation and additional imaging studies.

Imaging Studies

Doppler ultrasound examination to assess for pulses on the affected limb should be performed immediately. Bedside continuous-wave Doppler may be used to differentiate arterial vs venous signal.^6,14-16 An ankle brachial index may be calculated through either direct auscultation of pulses or Doppler signal. A ratio of less than 0.9 is suggestive of ischemia, while a ratio of less than 0.5 is considered critical ischemia.²

Laboratory Evaluation

Laboratory evaluation of hematocrit, coagulation studies, renal function, electrolyte levels, lactate, and creatinine kinase should be completed.^1,5 An electrocardiogram and bedside/formal echocardiogram may be considered if embolism is suspected.^1,6,17

Imaging

Angiography is currently the gold standard imaging modality to diagnose ALI.¹⁶ However, other imaging modalities exist that expose the patient to less radiation and are generally preferred by patients.¹⁸ Duplex ultrasonography is the least invasive imaging modality, with a reported sensitivity of 88% and specificity of 96% for the detection of greater than 50% stenosis.^6,19 Contrast-enhanced magnetic resonance angiography (MRA) of the lower extremity is also relatively noninvasive, but is more limited in its application. It carries a reported sensitivity of 95% and a specificity of 97% for detection of stenosis of greater than 50%.^6,19 An MRA without contrast may be considered for patients with an estimated glomerular filtration rate of less than 30 mL/min/1.73 m² and who are not on dialysis, but the diagnostic efficacy is reduced.¹⁶ Finally, the sensitivity and specificity of computed tomography angiography (CTA) to detect aortoiliac stenosis of greater than 50% is 96% and 98% respectively.^6,18,19 Other studies demonstrated similar results for other arterial locations in the lower extremities.^18,19 A principal advantage of CTA is that direct visualization of calcifications, clips, stents, and prior bypasses is possible without the limitations of MRA.¹⁶ The American College of Radiology (ACR) lists ultrasound duplex Doppler and noncontrast MRA of the lower extremity as “may be appropriate.”¹⁶ In contrast, the ACR classifies MRA with contrast, CTA with contrast, and angiography of the lower extremity as “usually appropriate.”¹⁶ Selecting the optimal imaging study for a patient may require involvement of a facility’s radiology department and/or a vascular surgeon.^14,15

Management in the ED

Even before the definitive diagnosis of ALI is made, steps can be taken to minimize and/or slow progression of injury. Placing the affected limb in a dependent position and providing intravenous (IV) fluid hydration will maximize perfusion.^1,3,5 Even with consideration of the diagnostic modalities previously described, ALI is often considered a clinical diagnosis. Since time is critical, early consultation with vascular surgery services is imperative if ALI is suspected.

Intravenous Fluid Therapy

Suspected ALI should be treated in the ED with an IV heparin bolus, followed by constant IV infusion. Heparin prevents proximal and distal propagation of the thrombus.^{1,3,5,6,15,17,20} Additionally, it helps maintain the microcirculation surrounding the affected area.⁶ A heparin bolus dose of 100 U/kg followed by a continuous infusion of heparin 1,000 U/h is the recommended standard.^1,3,5,6,15 A goal partial thromboplastin time of 60 to 100 seconds, or an international normalized ratio of 2 to 3 is desirable.^8,21

Staging: The Rutherford Classification System

Once immediate therapies are started, the stage of PAD should be determined using the Rutherford classification system in collaboration with vascular surgery services; this will further guide treatment and disposition.

Category I. In category I ALI, the affected limb is considered viable and not immediately threatened.

Category IIa. The limb is considered to be marginally threatened and salvageable.

Category IIb. An ALI classified as a category IIb is the most urgent type in which the limb is immediately threatened.

Category III. The limb is classified as having irreversible damage.^2,3,17,22

(See Table 2 for a more detailed summary of the Rutherford classification system.)

Treatment

Definitive treatment decisions should be made in consultation with vascular surgery services. The results of three clinical trials developed the foundation for management of ALI: the Thrombolysis or Peripheral Arterial Surgery (TOPAS) trial, Surgery Versus Thrombolysis for Ischemia of the Lower Extremity (STILE) trial, and Rutherford trial.^22-24 Table 3 provides a summary of the treatment techniques utilized, which include mechanical recanalization with percutaneous aspiration thrombectomy, percutaneous mechanical thrombectomy,^6,12,25-28 pharmacological recanalization via catheter-directed thrombolysis,^{6,8,12,20,23-28} and/or surgical management via thrombectomy or embolectomy.^{6,11,23,24,27}

Complications

The complications of treating ALI can be stratified into three subsets: pharmacologic, mechanical, and reperfusion injury-related. Medical treatment with heparin is not without risk. Intracranial hemorrhage, major bleeding at other sites, and compartment syndrome secondary to bleeding can all occur. Treatment may also cause distal embolization and lead to mechanical occlusion of another site. Finally, reperfusion injury predisposes the patient to a host of new problems. Reperfusion injury occurs when fresh blood enters a previously ischemic zone. When this occurs, oxygen free radicals, inflammatory mediators, and catabolism byproducts mix with the blood. This process can damage surrounding epithelial cells and lead to increased interstitial permeability. As a result, compartment syndrome may also develop via this mechanism.^1,3,5,6 The anterior compartment of the lower extremity is most at risk. As such, assessment of peroneal nerve activity via dorsiflexion of the foot and sensation testing is important after the initiation of treatment.⁶ Systemic distribution of these harmful byproducts can also cause arrhythmias, renal failure, and systemic acadisos.^1,3,5,6 It is important for physicians and staff to monitor the patient closely for the development of these complications and be prepared to intervene.

Opportunities for Improvement

In a condition where minutes matter, expedient action is critical. Time-to-recognition, imaging, consultation, and intervention all are potential sources of delay. Two recent studies have investigated the treatment timeline of ALI. The first study showed that the greatest source of delay is time from symptom onset to presentation in the ED; an average of 11.35 hours. The second largest source of delay was time from recognition of ALI to imaging, with an average delay of 4.75 hours. The average ED evaluation time was 40 minutes, and the average total time to intervention was 10.2 hours. While time-to-symptom presentation may represent a failure of public health, time-to-imaging was identified as an area of unacceptable delay by the authors.²⁹ A second study examined the effect of pre-hospital care on the time-to-treatment. Persons who were transported via emergency medical services (EMS) arrived to the hospital at a median time of 5 hours after symptom onset, were seen by a physician at a median time of 51 minutes, and had revascularization at a median time of 23 hours. Those not transported by EMS arrived to the hospital at a median time of 48 hours after symptom onset, were seen by a physician at a median time of 80 minutes, and had revascularization at a median time of 93 hours. As a secondary goal, the study examined the effect of heparinization in the ED and showed that treatment with heparin was associated with a favorable outcome.³⁰ While the total treatment times in each study vary widely, they share several important commonalities and reinforce expedient management as an important goal.

Outcomes

Advances in the treatment of this condition began in the 1970s, with an explosion of new techniques and data in the past several years. Still, ALI is a high morbidity and high mortality condition. Rates of limb loss are approximately 30% for all cases, and it is a fatal condition for as many as one-in-five. As discussed earlier, the patients who are most likely to experience ALI typically have several medical comorbidities. Perhaps unsurprisingly, ALI portends a poor prognosis even if the limb is salvaged. Approximately 15% to 20% of patients with ALI will die within 1 year of diagnosis.^3,4,6,12

Conclusion

Acute limb ischemia is a rare condition, but a true medical emergency. Prompt recognition of the signs and symptoms of ALI are critical for optimizing patient outcomes. A high index of clinical suspicion in patients with risk factors may lead to early diagnosis. Early vascular surgery consultation and early IV heparin treatment are important aspects of care. Prompt imaging and staging guide further management. Special care should be paid to possible post-treatment complications and to the investigation of contributing factors. The EP has a great opportunity to positively impact care with expeditious management. Early diagnosis, targeted history and physical examination, prompt treatment, collaboration with specialists, and prevention and treatment of life-threatening complications are all hallmarks of emergency medicine.

Significant changes have occurred in the updated American Heart Association Stroke Council’s recommendations for early management of acute ischemic stroke (AIS). Conceptually, early management can be separated into initial triage and decisions about intervention to restore blood flow with thrombolysis or mechanical thrombectomy. If reperfusion therapy is not appropriate, then the focus is on management to minimize further damage from the stroke, decrease the likelihood of recurrence, and lessen secondary problems related to the stroke.

All patients with AIS should receive noncontrast CT to determine if there is evidence of a hemorrhagic stroke and, if such evidence exists, than the patient is not a candidate for thrombolysis. Intravenous alteplase should be considered for patients who present within 3 hours of stroke onset and for selected patients presenting between 3-4.5 hours after stroke onset (for more details, see Table 6 in the guidelines). Selected patients with AIS who present within 6-24 hours of last time they were known to be normal and who have large vessel occlusion in the anterior circulation, may be candidates for mechanical thrombectomy in specialized centers. Patients who are not candidates for acute interventions should then be managed according to early stroke management guidelines.

Early stroke management for patients with AIS admitted to medical floors involves attention to blood pressure, glucose, and antiplatelet therapy. For patients with blood pressure lower than 220/120 mm Hg who did not receive IV alteplase or thrombectomy, treatment of hypertension in the first 48-72 hours after an AIS does not change the outcome. It is reasonable when patients have BP greater than or equal to 220/120 mm Hg, to lower blood pressure by 15% during the first 24 hours after onset of stroke. Starting or restarting antihypertensive therapy during hospitalization in patients with blood pressure higher than 140/90 mm Hg who are neurologically stable improves long-term blood pressure control and is considered a reasonable strategy.

For patients with noncardioembolic AIS, the use of antiplatelet agents rather than oral anticoagulation is recommended. Patients should be treated with aspirin 160 mg-325 mg within 24-48 hours of presentation. In patients unsafe or unable to swallow, rectal or nasogastric administration is recommended. In patients with minor stroke, 21 days of dual-antiplatelet therapy (aspirin and clopidogrel) started within 24 hours can decrease stroke recurrence for the first 90 days after a stroke. This recommendation is based on a single study, the CHANCE trial, in a homogeneous population in China, and its generalizability is not known. If a patient had an AIS while already on aspirin, there is some evidence supporting a decreased risk of major cardiovascular events and recurrent stroke in patients switching to an alternative antiplatelet agent or combination antiplatelet therapy. Because of methodologic issues in the those studies, the guideline concludes that, for those already on aspirin, it is of unclear benefit to increase the dose of aspirin, switch to a different antiplatelet agent, or add a second antiplatelet agent. Switching to warfarin is not beneficial for secondary stroke prevention. High-dose statin therapy should be initiated. For patients with AIS in the setting of atrial fibrillation, oral anticoagulation can be started within 4-14 days after the stroke. One study showed that anticoagulation should not be started before 4 days after the stroke, with a hazard ratio of 0.53 for starting anticoagulation at 4-14 days, compared with less than 4 days.

Hyperglycemia should be controlled to a range of 140-180 mg/dL, because higher values are associated with worse outcomes. Oxygen should be used if needed to maintain oxygen saturation greater than 94%. High-intensity statin therapy should be used, and smoking cessation is strongly encouraged for those who use tobacco, with avoidance of secondhand smoke whenever possible.

Patients should be screened for dysphagia before taking anything per oral, including medications. A nasogastric tube may be considered within the first 7 days, if patients are dysphagic. Oral hygiene protocols may include antibacterial mouth rinse, systematic oral care, and decontamination gel to decrease the risk of pneumonia .

For deep vein thrombosis prophylaxis, intermittent pneumatic compression, in addition to the aspirin that a patient is on is reasonable, and the benefit of prophylactic-dose subcutaneous heparin (unfractionated heparin or low-molecular-weight heparin) in immobile patients with AIS is not well established.

The bottom line

Early management of stroke involves first determining whether someone is a candidate for reperfusion therapy with alteplase or thrombectomy and then, if not, admitting them to a monitored setting to screen for atrial fibrillation and evaluation for carotid stenosis. Patients should be evaluated for both depression and swallowing function, and there should be initiation of deep vein thrombosis prevention, appropriate management of elevated blood pressures, anti-platelet therapy, and statin therapy as well as plans for rehabilitation services.

Reference

Powers WJ et al. on behalf of the American Heart Association Stroke Council. 2018 Guidelines for the early management of patients with acute ischemic stroke: A guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2018 Mar;49(3):e46-e110.

Dr. Skolnik is a professor of family and community medicine at Jefferson Medical College, Philadelphia, and an associate director of the family medicine residency program at Abington (Pa.) Jefferson Health. Dr. Callahan is an attending physician and preceptor in the family medicine residency program at Abington Jefferson Health.

Significant changes have occurred in the updated American Heart Association Stroke Council’s recommendations for early management of acute ischemic stroke (AIS). Conceptually, early management can be separated into initial triage and decisions about intervention to restore blood flow with thrombolysis or mechanical thrombectomy. If reperfusion therapy is not appropriate, then the focus is on management to minimize further damage from the stroke, decrease the likelihood of recurrence, and lessen secondary problems related to the stroke.

All patients with AIS should receive noncontrast CT to determine if there is evidence of a hemorrhagic stroke and, if such evidence exists, than the patient is not a candidate for thrombolysis. Intravenous alteplase should be considered for patients who present within 3 hours of stroke onset and for selected patients presenting between 3-4.5 hours after stroke onset (for more details, see Table 6 in the guidelines). Selected patients with AIS who present within 6-24 hours of last time they were known to be normal and who have large vessel occlusion in the anterior circulation, may be candidates for mechanical thrombectomy in specialized centers. Patients who are not candidates for acute interventions should then be managed according to early stroke management guidelines.

Early stroke management for patients with AIS admitted to medical floors involves attention to blood pressure, glucose, and antiplatelet therapy. For patients with blood pressure lower than 220/120 mm Hg who did not receive IV alteplase or thrombectomy, treatment of hypertension in the first 48-72 hours after an AIS does not change the outcome. It is reasonable when patients have BP greater than or equal to 220/120 mm Hg, to lower blood pressure by 15% during the first 24 hours after onset of stroke. Starting or restarting antihypertensive therapy during hospitalization in patients with blood pressure higher than 140/90 mm Hg who are neurologically stable improves long-term blood pressure control and is considered a reasonable strategy.

For patients with noncardioembolic AIS, the use of antiplatelet agents rather than oral anticoagulation is recommended. Patients should be treated with aspirin 160 mg-325 mg within 24-48 hours of presentation. In patients unsafe or unable to swallow, rectal or nasogastric administration is recommended. In patients with minor stroke, 21 days of dual-antiplatelet therapy (aspirin and clopidogrel) started within 24 hours can decrease stroke recurrence for the first 90 days after a stroke. This recommendation is based on a single study, the CHANCE trial, in a homogeneous population in China, and its generalizability is not known. If a patient had an AIS while already on aspirin, there is some evidence supporting a decreased risk of major cardiovascular events and recurrent stroke in patients switching to an alternative antiplatelet agent or combination antiplatelet therapy. Because of methodologic issues in the those studies, the guideline concludes that, for those already on aspirin, it is of unclear benefit to increase the dose of aspirin, switch to a different antiplatelet agent, or add a second antiplatelet agent. Switching to warfarin is not beneficial for secondary stroke prevention. High-dose statin therapy should be initiated. For patients with AIS in the setting of atrial fibrillation, oral anticoagulation can be started within 4-14 days after the stroke. One study showed that anticoagulation should not be started before 4 days after the stroke, with a hazard ratio of 0.53 for starting anticoagulation at 4-14 days, compared with less than 4 days.

Hyperglycemia should be controlled to a range of 140-180 mg/dL, because higher values are associated with worse outcomes. Oxygen should be used if needed to maintain oxygen saturation greater than 94%. High-intensity statin therapy should be used, and smoking cessation is strongly encouraged for those who use tobacco, with avoidance of secondhand smoke whenever possible.

Patients should be screened for dysphagia before taking anything per oral, including medications. A nasogastric tube may be considered within the first 7 days, if patients are dysphagic. Oral hygiene protocols may include antibacterial mouth rinse, systematic oral care, and decontamination gel to decrease the risk of pneumonia .

For deep vein thrombosis prophylaxis, intermittent pneumatic compression, in addition to the aspirin that a patient is on is reasonable, and the benefit of prophylactic-dose subcutaneous heparin (unfractionated heparin or low-molecular-weight heparin) in immobile patients with AIS is not well established.

The bottom line

Early management of stroke involves first determining whether someone is a candidate for reperfusion therapy with alteplase or thrombectomy and then, if not, admitting them to a monitored setting to screen for atrial fibrillation and evaluation for carotid stenosis. Patients should be evaluated for both depression and swallowing function, and there should be initiation of deep vein thrombosis prevention, appropriate management of elevated blood pressures, anti-platelet therapy, and statin therapy as well as plans for rehabilitation services.

Reference

Powers WJ et al. on behalf of the American Heart Association Stroke Council. 2018 Guidelines for the early management of patients with acute ischemic stroke: A guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2018 Mar;49(3):e46-e110.

Dr. Skolnik is a professor of family and community medicine at Jefferson Medical College, Philadelphia, and an associate director of the family medicine residency program at Abington (Pa.) Jefferson Health. Dr. Callahan is an attending physician and preceptor in the family medicine residency program at Abington Jefferson Health.

Significant changes have occurred in the updated American Heart Association Stroke Council’s recommendations for early management of acute ischemic stroke (AIS). Conceptually, early management can be separated into initial triage and decisions about intervention to restore blood flow with thrombolysis or mechanical thrombectomy. If reperfusion therapy is not appropriate, then the focus is on management to minimize further damage from the stroke, decrease the likelihood of recurrence, and lessen secondary problems related to the stroke.

All patients with AIS should receive noncontrast CT to determine if there is evidence of a hemorrhagic stroke and, if such evidence exists, than the patient is not a candidate for thrombolysis. Intravenous alteplase should be considered for patients who present within 3 hours of stroke onset and for selected patients presenting between 3-4.5 hours after stroke onset (for more details, see Table 6 in the guidelines). Selected patients with AIS who present within 6-24 hours of last time they were known to be normal and who have large vessel occlusion in the anterior circulation, may be candidates for mechanical thrombectomy in specialized centers. Patients who are not candidates for acute interventions should then be managed according to early stroke management guidelines.

Early stroke management for patients with AIS admitted to medical floors involves attention to blood pressure, glucose, and antiplatelet therapy. For patients with blood pressure lower than 220/120 mm Hg who did not receive IV alteplase or thrombectomy, treatment of hypertension in the first 48-72 hours after an AIS does not change the outcome. It is reasonable when patients have BP greater than or equal to 220/120 mm Hg, to lower blood pressure by 15% during the first 24 hours after onset of stroke. Starting or restarting antihypertensive therapy during hospitalization in patients with blood pressure higher than 140/90 mm Hg who are neurologically stable improves long-term blood pressure control and is considered a reasonable strategy.

For patients with noncardioembolic AIS, the use of antiplatelet agents rather than oral anticoagulation is recommended. Patients should be treated with aspirin 160 mg-325 mg within 24-48 hours of presentation. In patients unsafe or unable to swallow, rectal or nasogastric administration is recommended. In patients with minor stroke, 21 days of dual-antiplatelet therapy (aspirin and clopidogrel) started within 24 hours can decrease stroke recurrence for the first 90 days after a stroke. This recommendation is based on a single study, the CHANCE trial, in a homogeneous population in China, and its generalizability is not known. If a patient had an AIS while already on aspirin, there is some evidence supporting a decreased risk of major cardiovascular events and recurrent stroke in patients switching to an alternative antiplatelet agent or combination antiplatelet therapy. Because of methodologic issues in the those studies, the guideline concludes that, for those already on aspirin, it is of unclear benefit to increase the dose of aspirin, switch to a different antiplatelet agent, or add a second antiplatelet agent. Switching to warfarin is not beneficial for secondary stroke prevention. High-dose statin therapy should be initiated. For patients with AIS in the setting of atrial fibrillation, oral anticoagulation can be started within 4-14 days after the stroke. One study showed that anticoagulation should not be started before 4 days after the stroke, with a hazard ratio of 0.53 for starting anticoagulation at 4-14 days, compared with less than 4 days.

Hyperglycemia should be controlled to a range of 140-180 mg/dL, because higher values are associated with worse outcomes. Oxygen should be used if needed to maintain oxygen saturation greater than 94%. High-intensity statin therapy should be used, and smoking cessation is strongly encouraged for those who use tobacco, with avoidance of secondhand smoke whenever possible.

Patients should be screened for dysphagia before taking anything per oral, including medications. A nasogastric tube may be considered within the first 7 days, if patients are dysphagic. Oral hygiene protocols may include antibacterial mouth rinse, systematic oral care, and decontamination gel to decrease the risk of pneumonia .

For deep vein thrombosis prophylaxis, intermittent pneumatic compression, in addition to the aspirin that a patient is on is reasonable, and the benefit of prophylactic-dose subcutaneous heparin (unfractionated heparin or low-molecular-weight heparin) in immobile patients with AIS is not well established.

The bottom line

Early management of stroke involves first determining whether someone is a candidate for reperfusion therapy with alteplase or thrombectomy and then, if not, admitting them to a monitored setting to screen for atrial fibrillation and evaluation for carotid stenosis. Patients should be evaluated for both depression and swallowing function, and there should be initiation of deep vein thrombosis prevention, appropriate management of elevated blood pressures, anti-platelet therapy, and statin therapy as well as plans for rehabilitation services.

Reference

Powers WJ et al. on behalf of the American Heart Association Stroke Council. 2018 Guidelines for the early management of patients with acute ischemic stroke: A guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2018 Mar;49(3):e46-e110.

Dr. Skolnik is a professor of family and community medicine at Jefferson Medical College, Philadelphia, and an associate director of the family medicine residency program at Abington (Pa.) Jefferson Health. Dr. Callahan is an attending physician and preceptor in the family medicine residency program at Abington Jefferson Health.

CHICAGO – Two women in their 30s resumed menstruation about 7 months after one of their ovaries was injected with human mesenchymal stem cells obtained from their hips.

Neither of the women had menstruated for about 5 years; both were in premature menopause and wanted desperately to start a family. Estrogen levels began increasing soon after treatment, and night sweats and other symptoms of menopause almost disappeared. After a year, the treated ovary was almost the size of a normal premenopausal ovary. There weren’t any complications or side effects, and both women are now pursuing pregnancy.

The results are “very exciting, very encouraging,” said senior investigator Ayman Al-Hendy, MD, PhD, a gynecology professor at the University of Illinois at Chicago.

Robert Lodge/MDEdge News

[email protected]

SOURCE: Al-Hendy A et al. ENDO 2018, Abstract OR33-6.

CHICAGO – Two women in their 30s resumed menstruation about 7 months after one of their ovaries was injected with human mesenchymal stem cells obtained from their hips.

Neither of the women had menstruated for about 5 years; both were in premature menopause and wanted desperately to start a family. Estrogen levels began increasing soon after treatment, and night sweats and other symptoms of menopause almost disappeared. After a year, the treated ovary was almost the size of a normal premenopausal ovary. There weren’t any complications or side effects, and both women are now pursuing pregnancy.

The results are “very exciting, very encouraging,” said senior investigator Ayman Al-Hendy, MD, PhD, a gynecology professor at the University of Illinois at Chicago.

Robert Lodge/MDEdge News

[email protected]

SOURCE: Al-Hendy A et al. ENDO 2018, Abstract OR33-6.

CHICAGO – Two women in their 30s resumed menstruation about 7 months after one of their ovaries was injected with human mesenchymal stem cells obtained from their hips.

Neither of the women had menstruated for about 5 years; both were in premature menopause and wanted desperately to start a family. Estrogen levels began increasing soon after treatment, and night sweats and other symptoms of menopause almost disappeared. After a year, the treated ovary was almost the size of a normal premenopausal ovary. There weren’t any complications or side effects, and both women are now pursuing pregnancy.

The results are “very exciting, very encouraging,” said senior investigator Ayman Al-Hendy, MD, PhD, a gynecology professor at the University of Illinois at Chicago.

Robert Lodge/MDEdge News

[email protected]

SOURCE: Al-Hendy A et al. ENDO 2018, Abstract OR33-6.

CHICAGO – Testosterone levels dropped by one third for women with polycystic ovary syndrome (PCOS) and hyperandrogenemia when they received a centrally acting medication currently in development. The proof-of-concept phase 2 trial, which saw no concerning safety signals for the medication, fezolinetant, sets the stage for a larger, and perhaps longer, study to learn more about the neurokinin 3 receptor antagonist’s efficacy against PCOS.

“The primary outcome for this phase 2 trial was to see if we could lower testosterone levels in these PCOS patients,” said Graeme Fraser, PhD, chief scientific officer for Ogeda, discussing the poster he and his colleagues presented at the annual meeting of the Endocrine Society.

“Testosterone levels decreased: Measured at about 3 hours postdose, which is the approximate pharmacokinetic Cmax [maximum serum concentration], there was … a more than 30% decrease in testosterone levels,” said Dr. Fraser. By week 12, he said, “there was a very consistent decrease of 30% of testosterone levels. So that was quite good; we successfully hit the primary outcome.”

At 12 weeks, the higher dose of fezolinetant decreased testosterone by 0.64 nmol/L, compared with the 0.04 nmol/L seen with placebo (P less than .01).

[email protected]

SOURCE: Fraser G et al. ENDO 2018, Abstract SAT-305-LB.

CHICAGO – Testosterone levels dropped by one third for women with polycystic ovary syndrome (PCOS) and hyperandrogenemia when they received a centrally acting medication currently in development. The proof-of-concept phase 2 trial, which saw no concerning safety signals for the medication, fezolinetant, sets the stage for a larger, and perhaps longer, study to learn more about the neurokinin 3 receptor antagonist’s efficacy against PCOS.

“The primary outcome for this phase 2 trial was to see if we could lower testosterone levels in these PCOS patients,” said Graeme Fraser, PhD, chief scientific officer for Ogeda, discussing the poster he and his colleagues presented at the annual meeting of the Endocrine Society.

“Testosterone levels decreased: Measured at about 3 hours postdose, which is the approximate pharmacokinetic Cmax [maximum serum concentration], there was … a more than 30% decrease in testosterone levels,” said Dr. Fraser. By week 12, he said, “there was a very consistent decrease of 30% of testosterone levels. So that was quite good; we successfully hit the primary outcome.”

At 12 weeks, the higher dose of fezolinetant decreased testosterone by 0.64 nmol/L, compared with the 0.04 nmol/L seen with placebo (P less than .01).

[email protected]

SOURCE: Fraser G et al. ENDO 2018, Abstract SAT-305-LB.

CHICAGO – Testosterone levels dropped by one third for women with polycystic ovary syndrome (PCOS) and hyperandrogenemia when they received a centrally acting medication currently in development. The proof-of-concept phase 2 trial, which saw no concerning safety signals for the medication, fezolinetant, sets the stage for a larger, and perhaps longer, study to learn more about the neurokinin 3 receptor antagonist’s efficacy against PCOS.

“The primary outcome for this phase 2 trial was to see if we could lower testosterone levels in these PCOS patients,” said Graeme Fraser, PhD, chief scientific officer for Ogeda, discussing the poster he and his colleagues presented at the annual meeting of the Endocrine Society.

“Testosterone levels decreased: Measured at about 3 hours postdose, which is the approximate pharmacokinetic Cmax [maximum serum concentration], there was … a more than 30% decrease in testosterone levels,” said Dr. Fraser. By week 12, he said, “there was a very consistent decrease of 30% of testosterone levels. So that was quite good; we successfully hit the primary outcome.”

At 12 weeks, the higher dose of fezolinetant decreased testosterone by 0.64 nmol/L, compared with the 0.04 nmol/L seen with placebo (P less than .01).

[email protected]

SOURCE: Fraser G et al. ENDO 2018, Abstract SAT-305-LB.

Obstetrics and gynecology helped to make the 2018 Main Residency Match the largest ever as the specialty increased residency slots by 3.7% and accepted 3.3% more applicants, compared with 2017, according to the National Resident Matching Program (NRMP).

Ob.gyn. brought 1,336 first-year positions to the Match Day party this year and filled 78.7% of them with U.S. graduates. The overall fill rate of 99.6% is actually down from last year, when the specialty managed to fill all 1,288 positions offered. For all specialties, U.S. graduates filled 58.7% of the record-high 30,232 available spots, and the overall fill rate was 96.1%, the NRMP said in its 2018 Main Residency Match report.

[email protected]

Obstetrics and gynecology helped to make the 2018 Main Residency Match the largest ever as the specialty increased residency slots by 3.7% and accepted 3.3% more applicants, compared with 2017, according to the National Resident Matching Program (NRMP).

Ob.gyn. brought 1,336 first-year positions to the Match Day party this year and filled 78.7% of them with U.S. graduates. The overall fill rate of 99.6% is actually down from last year, when the specialty managed to fill all 1,288 positions offered. For all specialties, U.S. graduates filled 58.7% of the record-high 30,232 available spots, and the overall fill rate was 96.1%, the NRMP said in its 2018 Main Residency Match report.

[email protected]

Obstetrics and gynecology helped to make the 2018 Main Residency Match the largest ever as the specialty increased residency slots by 3.7% and accepted 3.3% more applicants, compared with 2017, according to the National Resident Matching Program (NRMP).

Ob.gyn. brought 1,336 first-year positions to the Match Day party this year and filled 78.7% of them with U.S. graduates. The overall fill rate of 99.6% is actually down from last year, when the specialty managed to fill all 1,288 positions offered. For all specialties, U.S. graduates filled 58.7% of the record-high 30,232 available spots, and the overall fill rate was 96.1%, the NRMP said in its 2018 Main Residency Match report.

[email protected]

A 54-year-old woman presents with severe abdominal pain lasting 3 hours. The pain came on suddenly and was 10/10 in severity. It was in her right upper quadrant radiating to her back. She has had a 50-pound weight loss in the past year. Her medications include sertraline, phentermine-topiramate, and simvastatin.

She is evaluated in the emergency department, and labs show the following: aspartate aminotransferase, 450; alanine aminotransferase, 500; alkaline phosphatase, 100; bilirubin, 1.2. She receives morphine for her pain with minimal relief. An ultrasound shows no gallstones and no dilated common bile duct (CBD).

Her pain resolves 3 hours after arriving in the ED. Repeat labs 15 minutes after pain resolution show the following: AST, 900; ALT, 1,000; alk phos, 130; bili, 1.2.

What is the most likely diagnosis?

A. Acetaminophen toxicity.

B. Hepatitis A.

C. Ischemic hepatitis.

D. Simvastatin.

E. Passage of gallstone.

The patient has had weight loss, which increases the risk of gallstone formation, and the pain pattern is consistent with passage of a gallstone through the common bile duct.

I have seen a number of cases where the diagnosis was missed when the lab pattern is similar to the labs in this case. The high transaminases and the absence of significant alkaline phosphatase elevation can be confusing. We are taught in our medical training that alkaline phosphatase is a lab value that goes up with obstruction, and that transaminases are liver injury labs. What are the data on liver labs in the setting of acute obstruction as seen with the passage of a gallstone?

Frederick Kiechle, MD, and colleagues reported that alkaline phosphatase levels, either alone or in conjunction with bilirubin levels, were not useful in determining the presence of common bile duct stones.¹ Ming-Hsun Yang et al. found that normal gamma-glutamyl transferase results had the highest negative predictive value for the presence of a common bile duct stone (97%).² The sensitivity for ultrasound detection of CBD stone in this study was only 35%.

Keun Soo Ahn and colleagues found that, in patients with symptomatic CBD stones, the average AST was 275, and the average ALT was 317 – about six to seven times the upper limit of normal for these lab tests.³ In the same study, the average alkaline phosphatase was 213, which is about twice the upper limit of normal.

Pearl: AST and ALT elevations in patients with acute abdominal pain could be due to choledocholithiasis, even if there are minimal or no abnormalities in alkaline phosphatase. Marked elevations (greater than 1,000) can occur.
 

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

References

1. Am J Emerg Med. 1985 Nov;3(6):556-60.

2. Surg Endosc. 2008 Jul;22(7):1620-4.

3. World J Surg. 2016 Aug;40(8):1925-31.

4. J Clin Gastroenterol. 2017 Sep;51(8):728-33.

5. Am J Gastroenterol. 2005 Feb;100(2):295-8.

6. Clin Gastroenterol Hepatol. 2010 Dec;8(12):1077-82.

A 54-year-old woman presents with severe abdominal pain lasting 3 hours. The pain came on suddenly and was 10/10 in severity. It was in her right upper quadrant radiating to her back. She has had a 50-pound weight loss in the past year. Her medications include sertraline, phentermine-topiramate, and simvastatin.

She is evaluated in the emergency department, and labs show the following: aspartate aminotransferase, 450; alanine aminotransferase, 500; alkaline phosphatase, 100; bilirubin, 1.2. She receives morphine for her pain with minimal relief. An ultrasound shows no gallstones and no dilated common bile duct (CBD).

Her pain resolves 3 hours after arriving in the ED. Repeat labs 15 minutes after pain resolution show the following: AST, 900; ALT, 1,000; alk phos, 130; bili, 1.2.

What is the most likely diagnosis?

A. Acetaminophen toxicity.

B. Hepatitis A.

C. Ischemic hepatitis.

D. Simvastatin.

E. Passage of gallstone.

The patient has had weight loss, which increases the risk of gallstone formation, and the pain pattern is consistent with passage of a gallstone through the common bile duct.

I have seen a number of cases where the diagnosis was missed when the lab pattern is similar to the labs in this case. The high transaminases and the absence of significant alkaline phosphatase elevation can be confusing. We are taught in our medical training that alkaline phosphatase is a lab value that goes up with obstruction, and that transaminases are liver injury labs. What are the data on liver labs in the setting of acute obstruction as seen with the passage of a gallstone?

Frederick Kiechle, MD, and colleagues reported that alkaline phosphatase levels, either alone or in conjunction with bilirubin levels, were not useful in determining the presence of common bile duct stones.¹ Ming-Hsun Yang et al. found that normal gamma-glutamyl transferase results had the highest negative predictive value for the presence of a common bile duct stone (97%).² The sensitivity for ultrasound detection of CBD stone in this study was only 35%.

Keun Soo Ahn and colleagues found that, in patients with symptomatic CBD stones, the average AST was 275, and the average ALT was 317 – about six to seven times the upper limit of normal for these lab tests.³ In the same study, the average alkaline phosphatase was 213, which is about twice the upper limit of normal.

Pearl: AST and ALT elevations in patients with acute abdominal pain could be due to choledocholithiasis, even if there are minimal or no abnormalities in alkaline phosphatase. Marked elevations (greater than 1,000) can occur.
 

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

References

1. Am J Emerg Med. 1985 Nov;3(6):556-60.

2. Surg Endosc. 2008 Jul;22(7):1620-4.

3. World J Surg. 2016 Aug;40(8):1925-31.

4. J Clin Gastroenterol. 2017 Sep;51(8):728-33.

5. Am J Gastroenterol. 2005 Feb;100(2):295-8.

6. Clin Gastroenterol Hepatol. 2010 Dec;8(12):1077-82.

A 54-year-old woman presents with severe abdominal pain lasting 3 hours. The pain came on suddenly and was 10/10 in severity. It was in her right upper quadrant radiating to her back. She has had a 50-pound weight loss in the past year. Her medications include sertraline, phentermine-topiramate, and simvastatin.

She is evaluated in the emergency department, and labs show the following: aspartate aminotransferase, 450; alanine aminotransferase, 500; alkaline phosphatase, 100; bilirubin, 1.2. She receives morphine for her pain with minimal relief. An ultrasound shows no gallstones and no dilated common bile duct (CBD).

Her pain resolves 3 hours after arriving in the ED. Repeat labs 15 minutes after pain resolution show the following: AST, 900; ALT, 1,000; alk phos, 130; bili, 1.2.

What is the most likely diagnosis?

A. Acetaminophen toxicity.

B. Hepatitis A.

C. Ischemic hepatitis.

D. Simvastatin.

E. Passage of gallstone.

The patient has had weight loss, which increases the risk of gallstone formation, and the pain pattern is consistent with passage of a gallstone through the common bile duct.

I have seen a number of cases where the diagnosis was missed when the lab pattern is similar to the labs in this case. The high transaminases and the absence of significant alkaline phosphatase elevation can be confusing. We are taught in our medical training that alkaline phosphatase is a lab value that goes up with obstruction, and that transaminases are liver injury labs. What are the data on liver labs in the setting of acute obstruction as seen with the passage of a gallstone?

Frederick Kiechle, MD, and colleagues reported that alkaline phosphatase levels, either alone or in conjunction with bilirubin levels, were not useful in determining the presence of common bile duct stones.¹ Ming-Hsun Yang et al. found that normal gamma-glutamyl transferase results had the highest negative predictive value for the presence of a common bile duct stone (97%).² The sensitivity for ultrasound detection of CBD stone in this study was only 35%.

Keun Soo Ahn and colleagues found that, in patients with symptomatic CBD stones, the average AST was 275, and the average ALT was 317 – about six to seven times the upper limit of normal for these lab tests.³ In the same study, the average alkaline phosphatase was 213, which is about twice the upper limit of normal.

Pearl: AST and ALT elevations in patients with acute abdominal pain could be due to choledocholithiasis, even if there are minimal or no abnormalities in alkaline phosphatase. Marked elevations (greater than 1,000) can occur.
 

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

References

1. Am J Emerg Med. 1985 Nov;3(6):556-60.

2. Surg Endosc. 2008 Jul;22(7):1620-4.

3. World J Surg. 2016 Aug;40(8):1925-31.

4. J Clin Gastroenterol. 2017 Sep;51(8):728-33.

5. Am J Gastroenterol. 2005 Feb;100(2):295-8.

6. Clin Gastroenterol Hepatol. 2010 Dec;8(12):1077-82.

Transitions of care can be rife with communications issues – and subsequent adverse events. They are also a place where hospitalists can take the lead in making improvements.

“They are the team leaders, typically,” said Ana Pujols McKee, MD, the executive vice president and chief medical officer for The Joint Commission. “The hospitalist really owns this process of the transfer of this accurate information.”

To help, The Joint Commission has issued a new Sentinel Event Alert, which provides seven recommendations to improve the communication failures that can occur when patients are transitioned from one caregiver to another, as well as a Targeted Solutions Tool to put the recommendations into action.

“Every organization is challenged in communicating accurate and timely information regarding patients,” Dr. McKee said. “One of the riskiest transitions that patients go through is when they change levels of care from ICU to med-surg, or from the ER to ICU, OR to ICU, med-surg to home, and home to home care. All of those transitions inherently carry a certain amount of risk and are deeply reliant on the transfer of the right information at the right time to the right person.”

Transitions of care can be rife with communications issues – and subsequent adverse events. They are also a place where hospitalists can take the lead in making improvements.

“They are the team leaders, typically,” said Ana Pujols McKee, MD, the executive vice president and chief medical officer for The Joint Commission. “The hospitalist really owns this process of the transfer of this accurate information.”

To help, The Joint Commission has issued a new Sentinel Event Alert, which provides seven recommendations to improve the communication failures that can occur when patients are transitioned from one caregiver to another, as well as a Targeted Solutions Tool to put the recommendations into action.

“Every organization is challenged in communicating accurate and timely information regarding patients,” Dr. McKee said. “One of the riskiest transitions that patients go through is when they change levels of care from ICU to med-surg, or from the ER to ICU, OR to ICU, med-surg to home, and home to home care. All of those transitions inherently carry a certain amount of risk and are deeply reliant on the transfer of the right information at the right time to the right person.”

Transitions of care can be rife with communications issues – and subsequent adverse events. They are also a place where hospitalists can take the lead in making improvements.

“They are the team leaders, typically,” said Ana Pujols McKee, MD, the executive vice president and chief medical officer for The Joint Commission. “The hospitalist really owns this process of the transfer of this accurate information.”

To help, The Joint Commission has issued a new Sentinel Event Alert, which provides seven recommendations to improve the communication failures that can occur when patients are transitioned from one caregiver to another, as well as a Targeted Solutions Tool to put the recommendations into action.

“Every organization is challenged in communicating accurate and timely information regarding patients,” Dr. McKee said. “One of the riskiest transitions that patients go through is when they change levels of care from ICU to med-surg, or from the ER to ICU, OR to ICU, med-surg to home, and home to home care. All of those transitions inherently carry a certain amount of risk and are deeply reliant on the transfer of the right information at the right time to the right person.”

Estrogen tablets and a popular vaginal gel failed to top placebo for relieving vulvovaginal symptoms in postmenopausal women, based on data from a randomized trial of more than 300 patients suffering from genitourinary syndrome of menopause (GSM), a constellation of symptoms including pain on vaginal penetration and vaginal dryness.

“Surveys of postmenopausal women demonstrate a preference for effective, nonhormonal therapies, often due to safety concerns,” wrote Caroline M. Mitchell, MD, of Massachusetts General Hospital, Boston, and her colleagues. The report was published in JAMA Internal Medicine. The researchers randomized 302 postmenopausal women with GSM 1:1:1 to a Vagifem 10-microgram estradiol tablet and placebo gel, a placebo tablet and Replens gel, or a placebo tablet and a placebo gel.

The average age of the women was 61 years, 88% were white, and 81% were sexually active.

The primary outcome was a decrease in the most bothersome symptoms reported by the women after 12 weeks of treatment. The most common of these were pain on penetration (60%) and vulvovaginal dryness (21%).

[email protected]

SOURCE: Mitchell C et al. JAMA Intern Med. 2018 Mar. doi: 10.1001/jamainternmed.2018.0116.

Estrogen tablets and a popular vaginal gel failed to top placebo for relieving vulvovaginal symptoms in postmenopausal women, based on data from a randomized trial of more than 300 patients suffering from genitourinary syndrome of menopause (GSM), a constellation of symptoms including pain on vaginal penetration and vaginal dryness.

“Surveys of postmenopausal women demonstrate a preference for effective, nonhormonal therapies, often due to safety concerns,” wrote Caroline M. Mitchell, MD, of Massachusetts General Hospital, Boston, and her colleagues. The report was published in JAMA Internal Medicine. The researchers randomized 302 postmenopausal women with GSM 1:1:1 to a Vagifem 10-microgram estradiol tablet and placebo gel, a placebo tablet and Replens gel, or a placebo tablet and a placebo gel.

The average age of the women was 61 years, 88% were white, and 81% were sexually active.

The primary outcome was a decrease in the most bothersome symptoms reported by the women after 12 weeks of treatment. The most common of these were pain on penetration (60%) and vulvovaginal dryness (21%).

[email protected]

SOURCE: Mitchell C et al. JAMA Intern Med. 2018 Mar. doi: 10.1001/jamainternmed.2018.0116.

Estrogen tablets and a popular vaginal gel failed to top placebo for relieving vulvovaginal symptoms in postmenopausal women, based on data from a randomized trial of more than 300 patients suffering from genitourinary syndrome of menopause (GSM), a constellation of symptoms including pain on vaginal penetration and vaginal dryness.

“Surveys of postmenopausal women demonstrate a preference for effective, nonhormonal therapies, often due to safety concerns,” wrote Caroline M. Mitchell, MD, of Massachusetts General Hospital, Boston, and her colleagues. The report was published in JAMA Internal Medicine. The researchers randomized 302 postmenopausal women with GSM 1:1:1 to a Vagifem 10-microgram estradiol tablet and placebo gel, a placebo tablet and Replens gel, or a placebo tablet and a placebo gel.

The average age of the women was 61 years, 88% were white, and 81% were sexually active.

The primary outcome was a decrease in the most bothersome symptoms reported by the women after 12 weeks of treatment. The most common of these were pain on penetration (60%) and vulvovaginal dryness (21%).

[email protected]

SOURCE: Mitchell C et al. JAMA Intern Med. 2018 Mar. doi: 10.1001/jamainternmed.2018.0116.

Question: After many years of diabetes, a 60-year-old office worker develops nephropathy followed by end-stage renal disease, and now requires dialysis. He has opted for peritoneal dialysis rather than hemodialysis, so that he does not have to be away from the workplace for treatment. His diabetes is insulin requiring, and he has occasional hypoglycemic reactions. Although he qualifies for Social Security disability benefits, he prefers to continue working full time. The employer is considering terminating him.

Which of the following is best?

A. The Americans with Disabilities Act prohibits job discrimination against patients with disabilities, so long as they are otherwise qualified for every aspect of the job.

B. Renal insufficiency and diabetes are considered disabilities under the ADA.

C. The employer is obligated to provide full accommodation to enable this employee to continue working.

D. If the accommodations needed for a disabled person are unreasonable, or prove too disruptive or expensive, then the employer is not obligated to provide them.

E. This patient should simply retire and enjoy his SS disability benefits.

In addition, the law prohibits discrimination against people with disabilities from accessing public accommodations (Title III), which include doctors’ offices and health care facilities, as well as restaurants, retail stores, etc. Other areas under the purview of the omnibus ADA include transportation, communications, and access to state and local government programs and services.

The Equal Employment Opportunity Commission (EEOC) enforces Title I of the ADA, the section that deals with job discrimination. Its compliance manual sets out guidelines for determining whether an individual in fact has a disability.

The word “disability” has three components, and the term is not synonymous with “impairment.” However, a disability begins with having an impairment, defined as a physiological disorder affecting one or more of a number of body systems or a mental or psychological disorder.

An example given by the EEOC: If a person cannot find a job because that person has the equivalent of a second-grade education and therefore cannot read, that person does not have an impairment for purposes of the ADA. If, however, that person cannot read because of severe dyslexia, that person has an impairment. Likewise, being overweight is not considered an impairment (unless due to an underlying physical condition, e.g., hypothyroidism), although extreme obesity in excess of 100% ideal body weight is.

Having determined that an impairment exists, the next step in the analysis is to ascertain if the impairment limits one or more “major life activities.” These have classically included activities such as caring for oneself, performing manual tasks, walking, seeing, hearing, speaking, and breathing.

Dr. Tan is emeritus professor of medicine and a former adjunct professor of law at the University of Hawaii, Honolulu. This article is meant to be educational and does not constitute medical, ethical or legal advice. For additional information, readers may contact the author at [email protected].

References

1. Americans with Disabilities Act of 1990 (ADA), 104 Stat. 327, 42 U. S. C. § 12101 et seq.

2. Bragdon v. Abbott et al. 524 U.S. 624 (1998).

3. Cathy A. Fiscus v. Wal-Mart Stores Inc., 385 F.3d 378 (3d Cir. 2004).

4. 42 U. S. C. § 12182(b)(3).

5. Available at www.kidney.org/atoz/content/employersguide.

Question: After many years of diabetes, a 60-year-old office worker develops nephropathy followed by end-stage renal disease, and now requires dialysis. He has opted for peritoneal dialysis rather than hemodialysis, so that he does not have to be away from the workplace for treatment. His diabetes is insulin requiring, and he has occasional hypoglycemic reactions. Although he qualifies for Social Security disability benefits, he prefers to continue working full time. The employer is considering terminating him.

Which of the following is best?

A. The Americans with Disabilities Act prohibits job discrimination against patients with disabilities, so long as they are otherwise qualified for every aspect of the job.

B. Renal insufficiency and diabetes are considered disabilities under the ADA.

C. The employer is obligated to provide full accommodation to enable this employee to continue working.

D. If the accommodations needed for a disabled person are unreasonable, or prove too disruptive or expensive, then the employer is not obligated to provide them.

E. This patient should simply retire and enjoy his SS disability benefits.

In addition, the law prohibits discrimination against people with disabilities from accessing public accommodations (Title III), which include doctors’ offices and health care facilities, as well as restaurants, retail stores, etc. Other areas under the purview of the omnibus ADA include transportation, communications, and access to state and local government programs and services.

The Equal Employment Opportunity Commission (EEOC) enforces Title I of the ADA, the section that deals with job discrimination. Its compliance manual sets out guidelines for determining whether an individual in fact has a disability.

The word “disability” has three components, and the term is not synonymous with “impairment.” However, a disability begins with having an impairment, defined as a physiological disorder affecting one or more of a number of body systems or a mental or psychological disorder.

An example given by the EEOC: If a person cannot find a job because that person has the equivalent of a second-grade education and therefore cannot read, that person does not have an impairment for purposes of the ADA. If, however, that person cannot read because of severe dyslexia, that person has an impairment. Likewise, being overweight is not considered an impairment (unless due to an underlying physical condition, e.g., hypothyroidism), although extreme obesity in excess of 100% ideal body weight is.

Having determined that an impairment exists, the next step in the analysis is to ascertain if the impairment limits one or more “major life activities.” These have classically included activities such as caring for oneself, performing manual tasks, walking, seeing, hearing, speaking, and breathing.

Dr. Tan is emeritus professor of medicine and a former adjunct professor of law at the University of Hawaii, Honolulu. This article is meant to be educational and does not constitute medical, ethical or legal advice. For additional information, readers may contact the author at [email protected].

References

1. Americans with Disabilities Act of 1990 (ADA), 104 Stat. 327, 42 U. S. C. § 12101 et seq.

2. Bragdon v. Abbott et al. 524 U.S. 624 (1998).

3. Cathy A. Fiscus v. Wal-Mart Stores Inc., 385 F.3d 378 (3d Cir. 2004).

4. 42 U. S. C. § 12182(b)(3).

5. Available at www.kidney.org/atoz/content/employersguide.

Question: After many years of diabetes, a 60-year-old office worker develops nephropathy followed by end-stage renal disease, and now requires dialysis. He has opted for peritoneal dialysis rather than hemodialysis, so that he does not have to be away from the workplace for treatment. His diabetes is insulin requiring, and he has occasional hypoglycemic reactions. Although he qualifies for Social Security disability benefits, he prefers to continue working full time. The employer is considering terminating him.

Which of the following is best?

A. The Americans with Disabilities Act prohibits job discrimination against patients with disabilities, so long as they are otherwise qualified for every aspect of the job.

B. Renal insufficiency and diabetes are considered disabilities under the ADA.

C. The employer is obligated to provide full accommodation to enable this employee to continue working.

D. If the accommodations needed for a disabled person are unreasonable, or prove too disruptive or expensive, then the employer is not obligated to provide them.

E. This patient should simply retire and enjoy his SS disability benefits.

In addition, the law prohibits discrimination against people with disabilities from accessing public accommodations (Title III), which include doctors’ offices and health care facilities, as well as restaurants, retail stores, etc. Other areas under the purview of the omnibus ADA include transportation, communications, and access to state and local government programs and services.

The Equal Employment Opportunity Commission (EEOC) enforces Title I of the ADA, the section that deals with job discrimination. Its compliance manual sets out guidelines for determining whether an individual in fact has a disability.

The word “disability” has three components, and the term is not synonymous with “impairment.” However, a disability begins with having an impairment, defined as a physiological disorder affecting one or more of a number of body systems or a mental or psychological disorder.

An example given by the EEOC: If a person cannot find a job because that person has the equivalent of a second-grade education and therefore cannot read, that person does not have an impairment for purposes of the ADA. If, however, that person cannot read because of severe dyslexia, that person has an impairment. Likewise, being overweight is not considered an impairment (unless due to an underlying physical condition, e.g., hypothyroidism), although extreme obesity in excess of 100% ideal body weight is.

Having determined that an impairment exists, the next step in the analysis is to ascertain if the impairment limits one or more “major life activities.” These have classically included activities such as caring for oneself, performing manual tasks, walking, seeing, hearing, speaking, and breathing.

Dr. Tan is emeritus professor of medicine and a former adjunct professor of law at the University of Hawaii, Honolulu. This article is meant to be educational and does not constitute medical, ethical or legal advice. For additional information, readers may contact the author at [email protected].

References

1. Americans with Disabilities Act of 1990 (ADA), 104 Stat. 327, 42 U. S. C. § 12101 et seq.

2. Bragdon v. Abbott et al. 524 U.S. 624 (1998).

3. Cathy A. Fiscus v. Wal-Mart Stores Inc., 385 F.3d 378 (3d Cir. 2004).

4. 42 U. S. C. § 12182(b)(3).

5. Available at www.kidney.org/atoz/content/employersguide.

Registration and housing for the 2018 Vascular Annual Meeting are now open. Register today for VAM, June 20 to 23 in Boston, including looking over housing options. Following a full day of postgraduate courses, VESS abstracts, workshops and international programming on Wednesday, June 20, abstract-based scientific sessions will open June 21 and continue to June 23. The Exhibit Hall will be open June 21 to 22.

Registration and housing for the 2018 Vascular Annual Meeting are now open. Register today for VAM, June 20 to 23 in Boston, including looking over housing options. Following a full day of postgraduate courses, VESS abstracts, workshops and international programming on Wednesday, June 20, abstract-based scientific sessions will open June 21 and continue to June 23. The Exhibit Hall will be open June 21 to 22.

Registration and housing for the 2018 Vascular Annual Meeting are now open. Register today for VAM, June 20 to 23 in Boston, including looking over housing options. Following a full day of postgraduate courses, VESS abstracts, workshops and international programming on Wednesday, June 20, abstract-based scientific sessions will open June 21 and continue to June 23. The Exhibit Hall will be open June 21 to 22.