Imaging

A 68-year-old man with metastatic periampullary adenocarcinoma presented to his usual clinic for a scheduled biliary stent exchange by endoscopic retrograde cholangiopancreatography (ERCP). The stent had been placed 5 months before, and no complications had been reported during that procedure.

During the stent exchange procedure, the endoscopist advanced the scope to the second part of the duodenum, where a large, ulcerated, friable mass was visualized surrounding the ampulla, consistent with patient’s known periampullary cancer. The biliary stent was removed without much difficulty. However, several attempts to cannulate the common bile duct with a preloaded guidewire failed because of extensive edema and tissue friability, and to avoid further discomfort to the patient, the procedure was aborted. No perforation was visualized during or at the end of the procedure.

During the first hour after the procedure was stopped, the patient suddenly developed abdominal pain and distention and crepitus of the right chest wall. Supine abdominal radiography showed extensive pneumoperitoneum and subcutaneous emphysema in the chest. A nasogastric tube was placed for decompression, and the patient was transferred to the surgical intensive care unit at our hospital.

EVIDENCE OF PERFORATION NOTED

On arrival, the patient’s oxygen saturation was 99% while receiving oxygen at 2 L/minute by nasal cannula. The physical examination revealed neck swelling, abdominal distention, and crepitus in the neck, abdomen, scrotum, and right lower extremity.

Computed tomography (CT) of the abdomen and pelvis with oral and intravenous contrast revealed widespread pneumoretroperitoneum, pneumoperitoneum, and air along the intermuscular planes in the right lower extremity, with no evidence of extravasation of oral contrast (Figure 1). Also noted were bilateral pneumothorax, pneumomediastinum, pneumopericardium, and extensive subcutaneous emphysema (Figure 2).

Despite these impressive findings, the patient remained hemodynamically stable and was managed conservatively with broad-spectrum antibiotics, gastric decompression, and bowel rest. But repeat chest radiography 5 hours after admission to the hospital revealed an enlarging right pneumothorax, which was treated with placement of a pigtail catheter. The patient continued to improve with conservative management and was discharged on the 6th day of hospitalization.

PERFORATION DURING ERCP: INCIDENCE AND COMPLICATIONS

Although perforation is an uncommon complication of ERCP, with an incidence of 1%, mortality rates as high as 18% have been reported.¹ Older age, longer procedural time, anatomic variations, and diseases of the duodenum and common bile duct can increase the risk of perforation.²

Types of perforation

Stapfer et al¹ classified perforation during ERCP into four types, based on etiology and  site of perforation. Type 1 is perforation of the lateral or medial duodenal wall caused by excessive pressure from the endoscope or its acute angulation. Type 2 is periampullary injury, often associated with sphincterotomy or difficulty accessing the biliary tree. Type 3 is injury to the common bile duct or pancreatic duct caused by instrumentation. Type 4 is the presence of retroperitoneal free air with no evidence of actual perforation; this is usually an incidental finding and is of little or no clinical consequence.¹

In 2015, a review of 18 studies described the distribution of ERCP perforation according to the Stapfer classification: 25% were type 1, 46% were type 2, and 22% were type 3.³

Effects of air insufflation

ERCP requires air insufflation for optimal visualization. During difficult or prolonged procedures, a larger amount of air may be insufflated to maintain bowel lumen visibility. Depending on the site and size of the defect, a variable amount of air can leak under pressure once the perforation occurs. A rapid retroperitoneal air leak can spread to multiple body compartments, including the mediastinum, pleura, neck, subcutaneous tissues, scrotum, and musculature by tracking through various fascial planes. Rarely, rapid ingress of air in these areas can lead to compartment syndrome.⁴

Small perforations tend to close spontaneously and may remain clinically silent, but large or persistent perforations are known to cause subcutaneous emphysema, sepsis, and respiratory failure.⁵

Our patient’s type 2 perforation

We presumed that our patient had a type 2 perforation, given the finding of retroperitoneal air. Difficulty cannulating the biliary tree via the friable malignant tissue at the site of the major papilla likely caused punctate perforations, resulting in air leakage into the retroperitoneum. Punctate perforations typically do not allow contrast extravasation, explaining the absence of oral contrast leakage on CT.

TREATMENT OF ENDOSCOPY-RELATED PERFORATION

Conventional supine and upright abdominal radiography is an appropriate initial imaging modality to confirm the diagnosis. However, CT is more sensitive and accurate, especially when air leakage is confined to the retroperitoneum. Intravenous or oral contrast is not necessary but may help localize the perforation and better delineate fluid collections and abscesses.²

Once perforation is suspected, treatment with a broad-spectrum antibiotic, bowel rest, and stomach decompression is imperative.⁶ Further management depends on the type of perforation and the overall clinical picture. Type 1 perforations usually require immediate surgical intervention. Type 2 perforations often seal spontaneously within 2 to 3 days and thus are managed conservatively (ie, a broad-spectrum antibiotic, gastric decompression, and bowel rest), unless there is a persistent leak or a large fluid collection. Type 3 perforations rarely require surgery since most are very small and close spontaneously, and so they are managed conservatively. Type 4 perforations are the least serious. They result in retroperitoneal free air that is thought be related to the use of compressed air for lumen patency. They require only conservative measures.¹ 

A 68-year-old man with metastatic periampullary adenocarcinoma presented to his usual clinic for a scheduled biliary stent exchange by endoscopic retrograde cholangiopancreatography (ERCP). The stent had been placed 5 months before, and no complications had been reported during that procedure.

During the stent exchange procedure, the endoscopist advanced the scope to the second part of the duodenum, where a large, ulcerated, friable mass was visualized surrounding the ampulla, consistent with patient’s known periampullary cancer. The biliary stent was removed without much difficulty. However, several attempts to cannulate the common bile duct with a preloaded guidewire failed because of extensive edema and tissue friability, and to avoid further discomfort to the patient, the procedure was aborted. No perforation was visualized during or at the end of the procedure.

During the first hour after the procedure was stopped, the patient suddenly developed abdominal pain and distention and crepitus of the right chest wall. Supine abdominal radiography showed extensive pneumoperitoneum and subcutaneous emphysema in the chest. A nasogastric tube was placed for decompression, and the patient was transferred to the surgical intensive care unit at our hospital.

EVIDENCE OF PERFORATION NOTED

On arrival, the patient’s oxygen saturation was 99% while receiving oxygen at 2 L/minute by nasal cannula. The physical examination revealed neck swelling, abdominal distention, and crepitus in the neck, abdomen, scrotum, and right lower extremity.

Computed tomography (CT) of the abdomen and pelvis with oral and intravenous contrast revealed widespread pneumoretroperitoneum, pneumoperitoneum, and air along the intermuscular planes in the right lower extremity, with no evidence of extravasation of oral contrast (Figure 1). Also noted were bilateral pneumothorax, pneumomediastinum, pneumopericardium, and extensive subcutaneous emphysema (Figure 2).

Despite these impressive findings, the patient remained hemodynamically stable and was managed conservatively with broad-spectrum antibiotics, gastric decompression, and bowel rest. But repeat chest radiography 5 hours after admission to the hospital revealed an enlarging right pneumothorax, which was treated with placement of a pigtail catheter. The patient continued to improve with conservative management and was discharged on the 6th day of hospitalization.

PERFORATION DURING ERCP: INCIDENCE AND COMPLICATIONS

Although perforation is an uncommon complication of ERCP, with an incidence of 1%, mortality rates as high as 18% have been reported.¹ Older age, longer procedural time, anatomic variations, and diseases of the duodenum and common bile duct can increase the risk of perforation.²

Types of perforation

Stapfer et al¹ classified perforation during ERCP into four types, based on etiology and  site of perforation. Type 1 is perforation of the lateral or medial duodenal wall caused by excessive pressure from the endoscope or its acute angulation. Type 2 is periampullary injury, often associated with sphincterotomy or difficulty accessing the biliary tree. Type 3 is injury to the common bile duct or pancreatic duct caused by instrumentation. Type 4 is the presence of retroperitoneal free air with no evidence of actual perforation; this is usually an incidental finding and is of little or no clinical consequence.¹

In 2015, a review of 18 studies described the distribution of ERCP perforation according to the Stapfer classification: 25% were type 1, 46% were type 2, and 22% were type 3.³

Effects of air insufflation

ERCP requires air insufflation for optimal visualization. During difficult or prolonged procedures, a larger amount of air may be insufflated to maintain bowel lumen visibility. Depending on the site and size of the defect, a variable amount of air can leak under pressure once the perforation occurs. A rapid retroperitoneal air leak can spread to multiple body compartments, including the mediastinum, pleura, neck, subcutaneous tissues, scrotum, and musculature by tracking through various fascial planes. Rarely, rapid ingress of air in these areas can lead to compartment syndrome.⁴

Small perforations tend to close spontaneously and may remain clinically silent, but large or persistent perforations are known to cause subcutaneous emphysema, sepsis, and respiratory failure.⁵

Our patient’s type 2 perforation

We presumed that our patient had a type 2 perforation, given the finding of retroperitoneal air. Difficulty cannulating the biliary tree via the friable malignant tissue at the site of the major papilla likely caused punctate perforations, resulting in air leakage into the retroperitoneum. Punctate perforations typically do not allow contrast extravasation, explaining the absence of oral contrast leakage on CT.

TREATMENT OF ENDOSCOPY-RELATED PERFORATION

Conventional supine and upright abdominal radiography is an appropriate initial imaging modality to confirm the diagnosis. However, CT is more sensitive and accurate, especially when air leakage is confined to the retroperitoneum. Intravenous or oral contrast is not necessary but may help localize the perforation and better delineate fluid collections and abscesses.²

Once perforation is suspected, treatment with a broad-spectrum antibiotic, bowel rest, and stomach decompression is imperative.⁶ Further management depends on the type of perforation and the overall clinical picture. Type 1 perforations usually require immediate surgical intervention. Type 2 perforations often seal spontaneously within 2 to 3 days and thus are managed conservatively (ie, a broad-spectrum antibiotic, gastric decompression, and bowel rest), unless there is a persistent leak or a large fluid collection. Type 3 perforations rarely require surgery since most are very small and close spontaneously, and so they are managed conservatively. Type 4 perforations are the least serious. They result in retroperitoneal free air that is thought be related to the use of compressed air for lumen patency. They require only conservative measures.¹ 

A 68-year-old man with metastatic periampullary adenocarcinoma presented to his usual clinic for a scheduled biliary stent exchange by endoscopic retrograde cholangiopancreatography (ERCP). The stent had been placed 5 months before, and no complications had been reported during that procedure.

During the stent exchange procedure, the endoscopist advanced the scope to the second part of the duodenum, where a large, ulcerated, friable mass was visualized surrounding the ampulla, consistent with patient’s known periampullary cancer. The biliary stent was removed without much difficulty. However, several attempts to cannulate the common bile duct with a preloaded guidewire failed because of extensive edema and tissue friability, and to avoid further discomfort to the patient, the procedure was aborted. No perforation was visualized during or at the end of the procedure.

During the first hour after the procedure was stopped, the patient suddenly developed abdominal pain and distention and crepitus of the right chest wall. Supine abdominal radiography showed extensive pneumoperitoneum and subcutaneous emphysema in the chest. A nasogastric tube was placed for decompression, and the patient was transferred to the surgical intensive care unit at our hospital.

EVIDENCE OF PERFORATION NOTED

On arrival, the patient’s oxygen saturation was 99% while receiving oxygen at 2 L/minute by nasal cannula. The physical examination revealed neck swelling, abdominal distention, and crepitus in the neck, abdomen, scrotum, and right lower extremity.

Computed tomography (CT) of the abdomen and pelvis with oral and intravenous contrast revealed widespread pneumoretroperitoneum, pneumoperitoneum, and air along the intermuscular planes in the right lower extremity, with no evidence of extravasation of oral contrast (Figure 1). Also noted were bilateral pneumothorax, pneumomediastinum, pneumopericardium, and extensive subcutaneous emphysema (Figure 2).

Despite these impressive findings, the patient remained hemodynamically stable and was managed conservatively with broad-spectrum antibiotics, gastric decompression, and bowel rest. But repeat chest radiography 5 hours after admission to the hospital revealed an enlarging right pneumothorax, which was treated with placement of a pigtail catheter. The patient continued to improve with conservative management and was discharged on the 6th day of hospitalization.

PERFORATION DURING ERCP: INCIDENCE AND COMPLICATIONS

Although perforation is an uncommon complication of ERCP, with an incidence of 1%, mortality rates as high as 18% have been reported.¹ Older age, longer procedural time, anatomic variations, and diseases of the duodenum and common bile duct can increase the risk of perforation.²

Types of perforation

Stapfer et al¹ classified perforation during ERCP into four types, based on etiology and  site of perforation. Type 1 is perforation of the lateral or medial duodenal wall caused by excessive pressure from the endoscope or its acute angulation. Type 2 is periampullary injury, often associated with sphincterotomy or difficulty accessing the biliary tree. Type 3 is injury to the common bile duct or pancreatic duct caused by instrumentation. Type 4 is the presence of retroperitoneal free air with no evidence of actual perforation; this is usually an incidental finding and is of little or no clinical consequence.¹

In 2015, a review of 18 studies described the distribution of ERCP perforation according to the Stapfer classification: 25% were type 1, 46% were type 2, and 22% were type 3.³

Effects of air insufflation

ERCP requires air insufflation for optimal visualization. During difficult or prolonged procedures, a larger amount of air may be insufflated to maintain bowel lumen visibility. Depending on the site and size of the defect, a variable amount of air can leak under pressure once the perforation occurs. A rapid retroperitoneal air leak can spread to multiple body compartments, including the mediastinum, pleura, neck, subcutaneous tissues, scrotum, and musculature by tracking through various fascial planes. Rarely, rapid ingress of air in these areas can lead to compartment syndrome.⁴

Small perforations tend to close spontaneously and may remain clinically silent, but large or persistent perforations are known to cause subcutaneous emphysema, sepsis, and respiratory failure.⁵

Our patient’s type 2 perforation

We presumed that our patient had a type 2 perforation, given the finding of retroperitoneal air. Difficulty cannulating the biliary tree via the friable malignant tissue at the site of the major papilla likely caused punctate perforations, resulting in air leakage into the retroperitoneum. Punctate perforations typically do not allow contrast extravasation, explaining the absence of oral contrast leakage on CT.

TREATMENT OF ENDOSCOPY-RELATED PERFORATION

Conventional supine and upright abdominal radiography is an appropriate initial imaging modality to confirm the diagnosis. However, CT is more sensitive and accurate, especially when air leakage is confined to the retroperitoneum. Intravenous or oral contrast is not necessary but may help localize the perforation and better delineate fluid collections and abscesses.²

Once perforation is suspected, treatment with a broad-spectrum antibiotic, bowel rest, and stomach decompression is imperative.⁶ Further management depends on the type of perforation and the overall clinical picture. Type 1 perforations usually require immediate surgical intervention. Type 2 perforations often seal spontaneously within 2 to 3 days and thus are managed conservatively (ie, a broad-spectrum antibiotic, gastric decompression, and bowel rest), unless there is a persistent leak or a large fluid collection. Type 3 perforations rarely require surgery since most are very small and close spontaneously, and so they are managed conservatively. Type 4 perforations are the least serious. They result in retroperitoneal free air that is thought be related to the use of compressed air for lumen patency. They require only conservative measures.¹ 

Timely diagnosis of limb ischemia is critical to limb health and limb salvage. The cause in most cases is related to atherosclerosis, and patients with limb ischemia are usually older and have risk factors for atherosclerosis, such as smoking, diabetes, hypertension, hyperlipidemia, and coronary artery disease. When younger patients develop limb ischemia, the diagnosis is often delayed since the index of suspicion is quite low in the absence of the usual risk factors.

Here, we discuss several nonatherosclerotic causes of limb ischemia: popliteal artery entrapment syndrome, popliteal artery aneurysm, cystic adventitial disease, persistent sciatic artery, phlegmasia cerulea dolens, Buerger disease, Takayasu arteritis, arterial thoracic outlet syndrome, and external iliac endofibrosis (Table 1). Our goal is to help clinicians make a timely diagnosis and ultimately save  the patient’s limb.

POPLITEAL ARTERY ENTRAPMENT SYNDROME

Popliteal artery entrapment syndrome occurs when the popliteal artery becomes compressed in the popliteal fossa, particularly during exercise.^1,2 The underlying problem may be that the popliteal artery has an aberrant course lateral to the medial head of the gastrocnemius muscle, or the medial head of the gastrocnemius may have an abnormal insertion, or there may be fibrous bands in the popliteal fossa, or a combination of these (Figure 1).^1–3 Functional popliteal artery entrapment syndrome occurs when there is compression of the artery without an anatomic cause.^1–3

The classic clinical presentation is a young athletic patient with calf or foot claudication (crampy pain with exercise, relieved with rest), but other symptoms can include coldness, paresthesias, and numbness. Pain at rest and tissue loss are rare on presentation but may develop if the diagnosis and treatment are delayed.³

Continued compression and microtrauma to the artery may lead to an intramural hematoma, thrombus formation, aneurysmal degeneration, dissection, or even acute thrombosis.² If the diagnosis is delayed, the patient’s condition may progress from intermittent arterial compression with plantar flexion to complete arterial thrombosis and critical limb ischemia, putting the patient at risk of limb loss.

Diagnosing popliteal artery entrapment syndrome

The diagnostic workup includes a detailed history with a focus on the cause of pain (usually exercise), a comprehensive physical examination that includes looking for wounds, and a thorough pulse examination.

The workup should start with noninvasive imaging such as duplex arterial ultrasonography with and without provocative measures (plantar flexion), the ankle-brachial index with and without provocative measures, and exercise treadmill testing with ankle-brachial index measurement.^1,2 Plantar flexion may be necessary to elicit arterial compression that is usually absent at rest.

Magnetic resonance imaging (MRI) and computed tomography (CT) of the lower extremity are useful to identify an arterial abnormality and aberrant muscle anatomy^1,3; MRI is currently the gold standard for delineating the muscles of the popliteal fossa.⁴ If these studies do not shed light on the diagnosis, arterial angiography with and without provocative maneuvers is useful in identifying compression of the popliteal artery.^1–3

Treating popliteal artery entrapment syndrome

Treatment depends on the level of arterial injury.

For patients with symptoms but no evidence of arterial injury, the most common procedure offered is popliteal fossa decompression.^1–3 This involves surgical release of the medial head of the gastrocnemius muscle and other muscles compressing the popliteal artery.

For patients with evidence of arterial injury such as stenosis, dissection, or aneurysm,  bypass grafting may be required.

For patients who present with acute limb ischemia, both surgical thrombectomy with possible bypass and intraarterial lysis have been described.^1,2,5

POPLITEAL ARTERY ANEURYSM

Popliteal artery aneurysm (Figure 2) is the most common type of aneurysm of the peripheral arteries of the lower extremity and is present in about 1% of men over age 65. Fifty percent are bilateral, and 50% are associated with an abdominal aortic aneurysm.^6,7 While up to 80% patients with this type of aneurysm have no symptoms at the time of diagnosis, symptoms develop at a rate of 14% per year, with acute limb ischemia occurring in up to one-third of cases.^6,7

When popliteal artery aneurysm progresses to acute limb ischemia, the consequences are often deleterious, as the tibial arteries distal to the popliteal artery are often occluded, limiting treatment options.

Popliteal artery aneurysm is defined as a local dilation of the artery of 2 cm or greater or an increase in the diameter to 1.5 times normal.⁶

Acute thrombosis of the aneurysm with limb ischemia is the most common presenting symptom and occurs in 50% of symptomatic cases of popliteal artery aneurysm.⁷ Almost 25% of patients present with intermittent claudication secondary to thrombosis, partial thrombosis with distal embolization, or combined aneurysmal and atherosclerotic disease. Compression of the popliteal vein by the popliteal artery aneurysm can cause leg swelling with or without deep vein thrombosis in up to 5% of patients.⁶ Rupture is very rare, with a rate of 2% to 4%.^6,7

Diagnosing popliteal artery aneurysm

The diagnosis can be made with arterial duplex ultrasonography, which is also useful for follow-up surveillance.^6–8 In the acute setting, computed tomographic angiography (CTA) or magnetic resonance angiography (MRA) is useful not only to identify the popliteal aneurysm, but also to define the distal tibial outflow vessels.^6,7

Treating popliteal artery aneurysm

Management of an acutely thrombosed popliteal artery aneurysm starts with systemic anticoagulation with intravenous heparin, followed initially by arterial angiography and lysis.^8–11 This approach has been shown to be safe and effective even in the absence of arterial runoff distal to the thrombosed popliteal aneurysm. Conversion to open thrombectomy and bypass can be done if initial lytic therapy fails, if the patient develops complications of lytic therapy, or if the patient needs emergency revascularization because of motor and neurologic deficits in the affected extremity.^8,10,11

How to manage the asymptomatic patient depends on the size of the aneurysm. Most studies recommend 2 cm or larger as the criterion for repair,^6–8,12 while others suggest treating even smaller aneurysms if thrombus is detected.⁹ Preoperative imaging before elective treatment of an asymptomatic popliteal artery aneurysm includes either CTA or MRA,^8,10 which allows the surgeon to visualize the full extent of the aneurysm to best plan the surgical approach. Diagnostic angiography can help determine the most suitable bypass target and can better characterize tibial outflow.

Asymptomatic popliteal artery aneurysm has traditionally been treated with surgical bypass with exclusion of the aneurysm,^6–8,12 but more recently, endovascular approaches using self-expanding stent grafts have been described. Further study is needed to determine the long-term efficacy of the endovascular approach.^8,10

CYSTIC ADVENTITIAL DISEASE

Cystic adventitial disease is a rare condition in which a blood vessel is narrowed due to mucin-containing cysts in the adventitia. More than 80% of cases occur in the popliteal artery, but it has been described in other peripheral arteries and veins.^13,14 It is more common in men than in women and typically occurs in the 4th or 5th decade of life. Most patients present with the sudden onset of calf claudication without the usual risk factors for peripheral vascular disease.¹³

Diagnosing cystic adventitial disease

Noninvasive arterial or venous duplex ultrasonography can be a good screening tool, as the cysts appear hypoechoic, but results are operator-dependent. CTA and MRA are the imaging tests of choice, as they can detect the cystic lesions and define vessel anatomy for intervention. Diagnostic angiography does not show the cysts themselves but instead reveals a classic “hourglass” and “scimitar” pattern of arterial narrowing that suggests the underlying pathology.^13,14

Treating cystic adventitial disease

Usual treatment is complete cyst resection and vessel reconstruction by surgical bypass. Other therapies include open surgical cyst evacuation and removal of the cyst wall, open surgical cyst aspiration, aspiration guided by ultrasonography or CT, and percutaneous angioplasty. However, these nonsurgical treatments have not been shown to be as effective and long-lasting as cyst excision and bypass.^13,14

PERSISTENT SCIATIC ARTERY

Persistent sciatic artery is a rare developmental abnormality.^15–17 Normally, as the femoral artery develops in the embryo, the sciatic artery involutes to form the inferior gluteal artery. But if the femoral system fails to mature, the sciatic artery, which is adjacent to the sciatic nerve posteriorly as it goes through the sciatic foramen, persists and functions as the major artery supplying the lower extremity, continuing to the posterior thigh and joining the popliteal artery (Figure 3).^15,17

Persistent sciatic artery has an incidence of 2.5 to 4 per 10,000 per year¹⁵ and is bilateral in almost half of cases.¹⁶ Up to 40% of patients have no symptoms, but symptoms may develop by age 40 to 50. Because of repeated trauma to the vessel as it passes through the sciatic foramen,¹⁸ the persistent sciatic artery typically sustains accelerated atherosclerotic changes that make it susceptible to aneurysm formation,¹⁵ and up to 46% of patients present with aneurysmal degeneration.¹⁷

Classically, patients present with lower extremity ischemia from atherosclerotic changes in the persistent sciatic artery or aneurysmal degeneration and thromboembolism.¹⁵ Rarely, these aneurysms rupture.^15,17 Other signs and symptoms include a pulsatile mass in the buttock, lower extremity numbness, motor weakness, and radicular pain along the sciatic nerve distribution from nerve compression.^15–17

Physical findings vary but are distinguished by the lack of femoral pulses in the presence of pedal pulses. A pulsatile buttock mass with evidence of lower extremity nerve compression or limb ischemia or both is pathognomonic of a persistent sciatic artery aneurysm.^16,18

Diagnosing persistent sciatic artery

Diagnostic angiography is the gold standard imaging test,^15,19 although CTA is starting to replace it.^16,18

Treating persistent sciatic artery

Persistent sciatic artery that is asymptomatic and is found incidentally does not require repair; however, it should be followed with duplex ultrasonography to look for evidence of aneurysm degeneration. Degeneration requires repair in most cases.^15,16,18,19 When the persistent sciatic artery is the only blood supply to the distal extremity, open aneurysm excision and bypass is the treatment of choice.^15,16,19 If collateral flow is adequate, endovascular coil embolization is an option.¹⁵ Endovascular stent graft placement has also been described.^16,19

PHLEGMASIA CERULEA DOLENS

Phlegmasia cerulea dolens is a rare syndrome caused by extensive acute thrombosis of the ileofemoral vein.^20–23 It is defined as total or near-total occlusion of the venous outflow of an extremity, causing massive swelling and congestion that impedes arterial inflow.^20,22

Phlegmasia cerulea dolens is associated with four cardinal signs: edema, violaceous discoloration, pain, and severe venous outflow obstruction (Figure 4).²² Patients present with sudden onset of lower extremity pain, swelling, cyanosis, and arterial ischemia with or without loss of distal pulses.^20,22

This syndrome can progress to gangrene and massive fluid sequestration leading to shock and death.^21–23 From 25% to 40% of patients die, and of those who survive, 20% to 50% require amputation of the limb.^20,23

Risk factors include malignancy, immobility, heart failure, heparin-induced thrombocytopenia, antiphospholipid syndrome, pregnancy, venous catheterization (eg, to insert an inferior vena cava filter), and surgery.^20–22

Diagnosing phlegmasia cerulea dolens

The diagnosis is made on clinical suspicion with evidence of iliofemoral deep vein thrombosis. Most experts suggest venous duplex ultrasonography to identify the deep vein thrombosis,²³ although CT or MR venography can be used to better delineate the proximal extent of the thrombus.^20,23

Treating phlegmasia cerulea dolens

Initial management is aggressive fluid resuscitation, elevation of the affected limb, strict bed rest, and anticoagulation with intravenous heparin.^20,23 Interventions are aimed at urgently restoring venous outflow to prevent progression to venous gangrene and limb loss.

Although conservative therapy can succeed by itself,²³ if the condition does not improve or has already progressed to an advanced stage, the two mainstays of treatment are open venous thrombectomy and endovascular treatment.^21–23 Endovascular treatment includes catheter-directed thrombolytic therapy (with or without percutaneous mechanical or pharmacomechanical thrombectomy) and stenting.^20,23 The success rate for endovascular therapy can be as high as 90% with near-complete resolution of thrombosis.²⁰ A disadvantage is that, compared with open surgical thrombectomy, more time is needed to achieve venous outflow.^20,22

If endovascular therapy is ineffective, if lytic therapy is contraindicated, or if the disease has progressed to gangrene, open surgical thrombectomy with possible fasciotomy is the preferred option.^20,21,23 Open surgery has the advantage of restoring venous outflow faster, but disadvantages include the inability to open the smaller veins of the extremity, blood loss, and risks associated with general anesthesia.^20–22

BUERGER DISEASE

Buerger disease (thromboangiitis obliterans) is a nonatherosclerotic segmental inflammatory disease involving the small and medium-sized vessels of the arms and legs.^24–27 It is differentiated from other vasculitides by its marked male predominance, its close association with smoking, the rarity of systemic signs and symptoms, and the absence of elevated inflammatory markers.²⁶

The rate of major amputation is reported to be 11% at 5 years and 23% at 20 years.²⁴

The classic patient is a young male smoker with symptoms of arterial disease before age 45.^24,26 Patients can present with migratory thrombophlebitis or signs of arterial insufficiency in the upper or lower extremities. Two or more limbs are commonly involved. Arterial insufficiency can range from claudication and exertional discomfort of the extremity to ischemic pain at rest leading to ulceration of the distal fingers and toes. Physical findings are similar to those seen in peripheral vascular disease and arterial insufficiency, with decreased arterial brachial index, cool extremities, and wounds.

Diagnosing Buerger disease

• The Shionoya diagnostic criteria for Buerger disease are the following five clinical features^24,27:
• History of smoking
• Onset before age 50
• Infrapopliteal arterial occlusive disease
• Upper-limb involvement or phlebitis migrans
• Absence of atherosclerotic risk factors other than heavy smoking.

Various other major and minor criteria have been described to make the diagnosis as well.²⁴

There is no specific laboratory test to confirm the diagnosis of Buerger disease. A full panel of laboratory tests should be sent to rule out other causes of arterial insufficiency and vasculitides; these tests should include C-reactive protein, rheumatoid factor, erythrocyte sedimentation rate, antinuclear antibodies, antiphospholipid antibodies, anti-Scl-70 antibodies, anticentromere antibodies, complement level measurement, and hypercoagulability workup.

Imaging studies include arterial duplex ultrasonography with ankle-brachial indices and segmental pressures and CTA or MRA.²⁶ Angiography can show a “corkscrew” pattern of occlusive disease and collateral formation, which is highly associated with Buerger disease.²⁴

Treating Buerger disease

The only treatment shown to reduce the risk of amputation is complete abstention from tobacco and nicotine (smoking, secondhand smoke, and nicotine patches and gum).^24,26

Symptoms of claudication can be managed with aspirin, clopidogrel, vasodilators, pentoxifylline, and cilostazol.²⁶

Surgical bypass is rarely an option, as Buerger disease typically affects the distal blood vessels, thus precluding bypass, and the 5-year patency rate is only 49%.²⁶ Other treatments including arterial thrombolysis, sympathectomy, stem cell injection, spinal cord stimulators, omental grafting, and immunomodulation have been described, but there are only limited data to offer guidance in choosing the appropriate one.²⁴

TAKAYASU ARTERITIS

Takayasu arteritis is a form of vasculitis involving the aorta and its main branches (Figure 5).²⁸ Although seen around the world, it has a higher incidence in young Asian women. Patients can present with systemic symptoms such as fever, fatigue, vague pain, and cardinal signs of limb ischemia associated with Takayasu arteritis, such as weak or absent pulses, differences between the arms in pulses and blood pressures, unobtainable blood pressure measurement in one or both arms, limb fatigability, and pain.²⁸

Diagnosing Takayasu arteritis

Multiple diagnostic criteria have been proposed to define Takayasu arteritis.²⁸ CTA, MRA, and positron emission tomography have replaced invasive angiography as the diagnostic imaging tests of choice.²⁹

Treating Takayasu arteritis

Takayasu arteritis has an acute and chronic course. Interventions are typically reserved for severe cases, with indications that include uncontrollable hypertension from renal artery stenosis, severe coronary or cerebrovascular disease, severe aortic regurgitation or coarctation, stenotic or occlusive lesions resulting in critical limb ischemia, and aneurysm at risk of rupture.^28–30

THORACIC OUTLET SYNDROME

Thoracic outlet syndrome is compression of the brachial plexus, subclavian vein, or subclavian artery as it exits the thoracic outlet through an area known as the scalene triangle, which is bordered by the anterior scalene, first rib, and clavicle.³¹ Presenting symptoms depend on the structure compressed.

By far the most common presentation³² is neurogenic thoracic outlet syndrome, accounting for more than 90% of cases, followed by venous thoracic outlet syndrome. Arterial thoracic outlet syndrome is the least frequent at less than 1%, but carries the greatest morbidity with potential for limb loss.^31–33

The subclavian artery exits the thoracic outlet between the anterior and middle scalene muscles, and then travels over the first rib and underneath the clavicle.³¹ Repeated trauma from compression of the artery results in intimal injury leading to compression, stenosis, occlusion, or aneurysm formation.^31,32

Symptoms of arterial thoracic outlet syndrome can start out as effort fatigue of the upper extremity secondary to compression. These symptoms are usually vague and difficult to define,³¹ as these patients typically are young and do not have atherosclerotic risk factors that would prompt suspicion of a vascular cause.

The most common presentation of arterial thoracic outlet syndrome is upper extremity embolization from a partially thrombosed aneurysm or area of stenosis with ischemia.³² Symptoms can range from ischemia of the fingers due to  microembolization to acute limb ischemia due to complete thrombosis of the subclavian artery.^31,32 Arterial thoracic outlet syndrome is most commonly associated with a bony abnormality (ie, cervical rib or anomalous first rib),^31–33 and on physical examination the bony abnormality may be palpated in the supraclavicular fossa.³¹

Other physical findings include a bruit over the subclavian artery, a blood pressure difference of 20 mm Hg or more between the affected and unaffected arms, loss of brachial, radial, or ulnar pulses with arm abduction, and loss of the radial pulse with the head rotated to the affected side as the patient takes a deep breath (the Adson maneuver).³¹ While postural changes in the pulse examination hint at arterial thoracic outlet syndrome, extremity pulses may be reduced or even absent in up to 60% of normal patients.³²

Diagnosing thoracic outlet syndrome

The workup should start with noninvasive imaging with pulse volume recording and wrist and finger systolic pressures, followed by arterial duplex ultrasonography.

Chest radiography may be able to identify bony abnormalities, and MRA or CTA with the patient in two positions—ie, arms down at  the sides, and arms held above the head—can help identify arterial compression from bony or muscular structures in the thoracic outlet. Upper extremity angiography provides high-resolution imaging of the digital arteries and can help identify a subclavian artery aneurysm, which may be a subtle finding.³¹

It is important to have objective evidence of arterial or venous mechanical obstruction before deciding to remove the first rib.

Treating thoracic outlet syndrome

Treatment is determined by the severity and acuity of symptoms. If the patient presents with acute limb ischemia, prompt treatment with either open surgery or endovascular treatment is required.^31,32,34 Once the acute phase has resolved or if the patient presents with chronic disease, open surgical repair is needed to remove the compression of the artery. If an arterial abnormality is identified (aneurysm or significant stenosis), an arterial reconstruction with bypass may be required.³¹

The standard treatment for thoracic outlet syndrome is resection of the first rib (and removal of the cervical rib if present).^31,34 This can be by a transaxillary approach unless arterial reconstruction is needed, in which case a supraclavicular approach is used.^31,34 When a patient without symptoms is found to have evidence of arterial compression, most experts would recommend resection of the first rib if there is evidence of an arterial abnormality, or follow-up with duplex imaging for patients with only subtle findings.³¹

EXTERNAL ILIAC ENDOFIBROSIS

External iliac endofibrosis is a rare cause of intermittent claudication, typically in high-performance athletes, resulting from thickening of the intima in the external iliac artery causing luminal narrowing and resultant ischemia.^35–37 The estimated incidence is as high as 20% in elite competitive cyclists, and the condition has been described in other sports as well.³⁷

External iliac endofibrosis typically presents as unilateral leg pain or cramping at near-maximal exercise with an associated feeling of swelling and numbness on the affected side.^35,37 It is bilateral in up to 15% of cases.³⁵ While claudication of the thigh is the predominant presenting symptom, dissection and thrombosis of the external iliac artery have been described, presenting with acute limb ischemia in up to 4% of patients.^35,36

The condition has been attributed to factors such as physical position, psoas hypertrophy, tethering of the external iliac artery to the psoas muscle, kinking and tortuosity of the vessel, and high-flow states secondary to increased cardiac output and adaptive systolic hypertension.^36,37

Diagnosing external iliac endofibrosis

The diagnosis is difficult, as symptoms typically manifest only during maximal exercise. Delays of 12 to 41 months between the onset of symptoms and diagnosis have been reported.³⁷ Physical findings are nonspecific, and pulses and ankle-brachial indices are typically normal at rest. A careful history with a focus on location and duration of symptoms and a high index of suspicion have been shown to increase the sensitivity of diagnosis.³⁶

Noninvasive vascular imaging with arterial duplex ultrasonography with physiologic studies (the ankle-brachial index) at rest and at maximal exertion should be obtained first.^35,37 If findings on ultrasonography are positive, CTA or MRA can be used to identify a suspected stenosis.

Diagnostic angiography is still the gold standard for imaging, as real-time images of the artery with different leg positions can be obtained and pressure gradients can be measured with or without the use of a vasodilator to determine the hemodynamic significance of a lesion.^35–37

Treating external iliac endofibrosis

Treatment should initially be conservative. Recreational athletes should consider changing to a sport that does not require hip flexion, and cyclists should be advised to reduce the amount of time spent cycling and to raise the handlebars or bring the saddle position forward to minimize hip flexion.³⁷

Definitive treatment is open surgical repair. Surgical options include arterial release of the tethered artery, endofibrosectomy and vessel shortening, endofibrosectomy and patch angioplasty, and interposition bypass grafting.^35–37

Timely diagnosis of limb ischemia is critical to limb health and limb salvage. The cause in most cases is related to atherosclerosis, and patients with limb ischemia are usually older and have risk factors for atherosclerosis, such as smoking, diabetes, hypertension, hyperlipidemia, and coronary artery disease. When younger patients develop limb ischemia, the diagnosis is often delayed since the index of suspicion is quite low in the absence of the usual risk factors.

Here, we discuss several nonatherosclerotic causes of limb ischemia: popliteal artery entrapment syndrome, popliteal artery aneurysm, cystic adventitial disease, persistent sciatic artery, phlegmasia cerulea dolens, Buerger disease, Takayasu arteritis, arterial thoracic outlet syndrome, and external iliac endofibrosis (Table 1). Our goal is to help clinicians make a timely diagnosis and ultimately save  the patient’s limb.

POPLITEAL ARTERY ENTRAPMENT SYNDROME

Popliteal artery entrapment syndrome occurs when the popliteal artery becomes compressed in the popliteal fossa, particularly during exercise.^1,2 The underlying problem may be that the popliteal artery has an aberrant course lateral to the medial head of the gastrocnemius muscle, or the medial head of the gastrocnemius may have an abnormal insertion, or there may be fibrous bands in the popliteal fossa, or a combination of these (Figure 1).^1–3 Functional popliteal artery entrapment syndrome occurs when there is compression of the artery without an anatomic cause.^1–3

The classic clinical presentation is a young athletic patient with calf or foot claudication (crampy pain with exercise, relieved with rest), but other symptoms can include coldness, paresthesias, and numbness. Pain at rest and tissue loss are rare on presentation but may develop if the diagnosis and treatment are delayed.³

Continued compression and microtrauma to the artery may lead to an intramural hematoma, thrombus formation, aneurysmal degeneration, dissection, or even acute thrombosis.² If the diagnosis is delayed, the patient’s condition may progress from intermittent arterial compression with plantar flexion to complete arterial thrombosis and critical limb ischemia, putting the patient at risk of limb loss.

Diagnosing popliteal artery entrapment syndrome

The diagnostic workup includes a detailed history with a focus on the cause of pain (usually exercise), a comprehensive physical examination that includes looking for wounds, and a thorough pulse examination.

The workup should start with noninvasive imaging such as duplex arterial ultrasonography with and without provocative measures (plantar flexion), the ankle-brachial index with and without provocative measures, and exercise treadmill testing with ankle-brachial index measurement.^1,2 Plantar flexion may be necessary to elicit arterial compression that is usually absent at rest.

Magnetic resonance imaging (MRI) and computed tomography (CT) of the lower extremity are useful to identify an arterial abnormality and aberrant muscle anatomy^1,3; MRI is currently the gold standard for delineating the muscles of the popliteal fossa.⁴ If these studies do not shed light on the diagnosis, arterial angiography with and without provocative maneuvers is useful in identifying compression of the popliteal artery.^1–3

Treating popliteal artery entrapment syndrome

Treatment depends on the level of arterial injury.

For patients with symptoms but no evidence of arterial injury, the most common procedure offered is popliteal fossa decompression.^1–3 This involves surgical release of the medial head of the gastrocnemius muscle and other muscles compressing the popliteal artery.

For patients with evidence of arterial injury such as stenosis, dissection, or aneurysm,  bypass grafting may be required.

For patients who present with acute limb ischemia, both surgical thrombectomy with possible bypass and intraarterial lysis have been described.^1,2,5

POPLITEAL ARTERY ANEURYSM

Popliteal artery aneurysm (Figure 2) is the most common type of aneurysm of the peripheral arteries of the lower extremity and is present in about 1% of men over age 65. Fifty percent are bilateral, and 50% are associated with an abdominal aortic aneurysm.^6,7 While up to 80% patients with this type of aneurysm have no symptoms at the time of diagnosis, symptoms develop at a rate of 14% per year, with acute limb ischemia occurring in up to one-third of cases.^6,7

When popliteal artery aneurysm progresses to acute limb ischemia, the consequences are often deleterious, as the tibial arteries distal to the popliteal artery are often occluded, limiting treatment options.

Popliteal artery aneurysm is defined as a local dilation of the artery of 2 cm or greater or an increase in the diameter to 1.5 times normal.⁶

Acute thrombosis of the aneurysm with limb ischemia is the most common presenting symptom and occurs in 50% of symptomatic cases of popliteal artery aneurysm.⁷ Almost 25% of patients present with intermittent claudication secondary to thrombosis, partial thrombosis with distal embolization, or combined aneurysmal and atherosclerotic disease. Compression of the popliteal vein by the popliteal artery aneurysm can cause leg swelling with or without deep vein thrombosis in up to 5% of patients.⁶ Rupture is very rare, with a rate of 2% to 4%.^6,7

Diagnosing popliteal artery aneurysm

The diagnosis can be made with arterial duplex ultrasonography, which is also useful for follow-up surveillance.^6–8 In the acute setting, computed tomographic angiography (CTA) or magnetic resonance angiography (MRA) is useful not only to identify the popliteal aneurysm, but also to define the distal tibial outflow vessels.^6,7

Treating popliteal artery aneurysm

Management of an acutely thrombosed popliteal artery aneurysm starts with systemic anticoagulation with intravenous heparin, followed initially by arterial angiography and lysis.^8–11 This approach has been shown to be safe and effective even in the absence of arterial runoff distal to the thrombosed popliteal aneurysm. Conversion to open thrombectomy and bypass can be done if initial lytic therapy fails, if the patient develops complications of lytic therapy, or if the patient needs emergency revascularization because of motor and neurologic deficits in the affected extremity.^8,10,11

How to manage the asymptomatic patient depends on the size of the aneurysm. Most studies recommend 2 cm or larger as the criterion for repair,^6–8,12 while others suggest treating even smaller aneurysms if thrombus is detected.⁹ Preoperative imaging before elective treatment of an asymptomatic popliteal artery aneurysm includes either CTA or MRA,^8,10 which allows the surgeon to visualize the full extent of the aneurysm to best plan the surgical approach. Diagnostic angiography can help determine the most suitable bypass target and can better characterize tibial outflow.

Asymptomatic popliteal artery aneurysm has traditionally been treated with surgical bypass with exclusion of the aneurysm,^6–8,12 but more recently, endovascular approaches using self-expanding stent grafts have been described. Further study is needed to determine the long-term efficacy of the endovascular approach.^8,10

CYSTIC ADVENTITIAL DISEASE

Cystic adventitial disease is a rare condition in which a blood vessel is narrowed due to mucin-containing cysts in the adventitia. More than 80% of cases occur in the popliteal artery, but it has been described in other peripheral arteries and veins.^13,14 It is more common in men than in women and typically occurs in the 4th or 5th decade of life. Most patients present with the sudden onset of calf claudication without the usual risk factors for peripheral vascular disease.¹³

Diagnosing cystic adventitial disease

Noninvasive arterial or venous duplex ultrasonography can be a good screening tool, as the cysts appear hypoechoic, but results are operator-dependent. CTA and MRA are the imaging tests of choice, as they can detect the cystic lesions and define vessel anatomy for intervention. Diagnostic angiography does not show the cysts themselves but instead reveals a classic “hourglass” and “scimitar” pattern of arterial narrowing that suggests the underlying pathology.^13,14

Treating cystic adventitial disease

Usual treatment is complete cyst resection and vessel reconstruction by surgical bypass. Other therapies include open surgical cyst evacuation and removal of the cyst wall, open surgical cyst aspiration, aspiration guided by ultrasonography or CT, and percutaneous angioplasty. However, these nonsurgical treatments have not been shown to be as effective and long-lasting as cyst excision and bypass.^13,14

PERSISTENT SCIATIC ARTERY

Persistent sciatic artery is a rare developmental abnormality.^15–17 Normally, as the femoral artery develops in the embryo, the sciatic artery involutes to form the inferior gluteal artery. But if the femoral system fails to mature, the sciatic artery, which is adjacent to the sciatic nerve posteriorly as it goes through the sciatic foramen, persists and functions as the major artery supplying the lower extremity, continuing to the posterior thigh and joining the popliteal artery (Figure 3).^15,17

Persistent sciatic artery has an incidence of 2.5 to 4 per 10,000 per year¹⁵ and is bilateral in almost half of cases.¹⁶ Up to 40% of patients have no symptoms, but symptoms may develop by age 40 to 50. Because of repeated trauma to the vessel as it passes through the sciatic foramen,¹⁸ the persistent sciatic artery typically sustains accelerated atherosclerotic changes that make it susceptible to aneurysm formation,¹⁵ and up to 46% of patients present with aneurysmal degeneration.¹⁷

Classically, patients present with lower extremity ischemia from atherosclerotic changes in the persistent sciatic artery or aneurysmal degeneration and thromboembolism.¹⁵ Rarely, these aneurysms rupture.^15,17 Other signs and symptoms include a pulsatile mass in the buttock, lower extremity numbness, motor weakness, and radicular pain along the sciatic nerve distribution from nerve compression.^15–17

Physical findings vary but are distinguished by the lack of femoral pulses in the presence of pedal pulses. A pulsatile buttock mass with evidence of lower extremity nerve compression or limb ischemia or both is pathognomonic of a persistent sciatic artery aneurysm.^16,18

Diagnosing persistent sciatic artery

Diagnostic angiography is the gold standard imaging test,^15,19 although CTA is starting to replace it.^16,18

Treating persistent sciatic artery

Persistent sciatic artery that is asymptomatic and is found incidentally does not require repair; however, it should be followed with duplex ultrasonography to look for evidence of aneurysm degeneration. Degeneration requires repair in most cases.^15,16,18,19 When the persistent sciatic artery is the only blood supply to the distal extremity, open aneurysm excision and bypass is the treatment of choice.^15,16,19 If collateral flow is adequate, endovascular coil embolization is an option.¹⁵ Endovascular stent graft placement has also been described.^16,19

PHLEGMASIA CERULEA DOLENS

Phlegmasia cerulea dolens is a rare syndrome caused by extensive acute thrombosis of the ileofemoral vein.^20–23 It is defined as total or near-total occlusion of the venous outflow of an extremity, causing massive swelling and congestion that impedes arterial inflow.^20,22

Phlegmasia cerulea dolens is associated with four cardinal signs: edema, violaceous discoloration, pain, and severe venous outflow obstruction (Figure 4).²² Patients present with sudden onset of lower extremity pain, swelling, cyanosis, and arterial ischemia with or without loss of distal pulses.^20,22

This syndrome can progress to gangrene and massive fluid sequestration leading to shock and death.^21–23 From 25% to 40% of patients die, and of those who survive, 20% to 50% require amputation of the limb.^20,23

Risk factors include malignancy, immobility, heart failure, heparin-induced thrombocytopenia, antiphospholipid syndrome, pregnancy, venous catheterization (eg, to insert an inferior vena cava filter), and surgery.^20–22

Diagnosing phlegmasia cerulea dolens

The diagnosis is made on clinical suspicion with evidence of iliofemoral deep vein thrombosis. Most experts suggest venous duplex ultrasonography to identify the deep vein thrombosis,²³ although CT or MR venography can be used to better delineate the proximal extent of the thrombus.^20,23

Treating phlegmasia cerulea dolens

Initial management is aggressive fluid resuscitation, elevation of the affected limb, strict bed rest, and anticoagulation with intravenous heparin.^20,23 Interventions are aimed at urgently restoring venous outflow to prevent progression to venous gangrene and limb loss.

Although conservative therapy can succeed by itself,²³ if the condition does not improve or has already progressed to an advanced stage, the two mainstays of treatment are open venous thrombectomy and endovascular treatment.^21–23 Endovascular treatment includes catheter-directed thrombolytic therapy (with or without percutaneous mechanical or pharmacomechanical thrombectomy) and stenting.^20,23 The success rate for endovascular therapy can be as high as 90% with near-complete resolution of thrombosis.²⁰ A disadvantage is that, compared with open surgical thrombectomy, more time is needed to achieve venous outflow.^20,22

If endovascular therapy is ineffective, if lytic therapy is contraindicated, or if the disease has progressed to gangrene, open surgical thrombectomy with possible fasciotomy is the preferred option.^20,21,23 Open surgery has the advantage of restoring venous outflow faster, but disadvantages include the inability to open the smaller veins of the extremity, blood loss, and risks associated with general anesthesia.^20–22

BUERGER DISEASE

Buerger disease (thromboangiitis obliterans) is a nonatherosclerotic segmental inflammatory disease involving the small and medium-sized vessels of the arms and legs.^24–27 It is differentiated from other vasculitides by its marked male predominance, its close association with smoking, the rarity of systemic signs and symptoms, and the absence of elevated inflammatory markers.²⁶

The rate of major amputation is reported to be 11% at 5 years and 23% at 20 years.²⁴

The classic patient is a young male smoker with symptoms of arterial disease before age 45.^24,26 Patients can present with migratory thrombophlebitis or signs of arterial insufficiency in the upper or lower extremities. Two or more limbs are commonly involved. Arterial insufficiency can range from claudication and exertional discomfort of the extremity to ischemic pain at rest leading to ulceration of the distal fingers and toes. Physical findings are similar to those seen in peripheral vascular disease and arterial insufficiency, with decreased arterial brachial index, cool extremities, and wounds.

Diagnosing Buerger disease

• The Shionoya diagnostic criteria for Buerger disease are the following five clinical features^24,27:
• History of smoking
• Onset before age 50
• Infrapopliteal arterial occlusive disease
• Upper-limb involvement or phlebitis migrans
• Absence of atherosclerotic risk factors other than heavy smoking.

Various other major and minor criteria have been described to make the diagnosis as well.²⁴

There is no specific laboratory test to confirm the diagnosis of Buerger disease. A full panel of laboratory tests should be sent to rule out other causes of arterial insufficiency and vasculitides; these tests should include C-reactive protein, rheumatoid factor, erythrocyte sedimentation rate, antinuclear antibodies, antiphospholipid antibodies, anti-Scl-70 antibodies, anticentromere antibodies, complement level measurement, and hypercoagulability workup.

Imaging studies include arterial duplex ultrasonography with ankle-brachial indices and segmental pressures and CTA or MRA.²⁶ Angiography can show a “corkscrew” pattern of occlusive disease and collateral formation, which is highly associated with Buerger disease.²⁴

Treating Buerger disease

The only treatment shown to reduce the risk of amputation is complete abstention from tobacco and nicotine (smoking, secondhand smoke, and nicotine patches and gum).^24,26

Symptoms of claudication can be managed with aspirin, clopidogrel, vasodilators, pentoxifylline, and cilostazol.²⁶

Surgical bypass is rarely an option, as Buerger disease typically affects the distal blood vessels, thus precluding bypass, and the 5-year patency rate is only 49%.²⁶ Other treatments including arterial thrombolysis, sympathectomy, stem cell injection, spinal cord stimulators, omental grafting, and immunomodulation have been described, but there are only limited data to offer guidance in choosing the appropriate one.²⁴

TAKAYASU ARTERITIS

Takayasu arteritis is a form of vasculitis involving the aorta and its main branches (Figure 5).²⁸ Although seen around the world, it has a higher incidence in young Asian women. Patients can present with systemic symptoms such as fever, fatigue, vague pain, and cardinal signs of limb ischemia associated with Takayasu arteritis, such as weak or absent pulses, differences between the arms in pulses and blood pressures, unobtainable blood pressure measurement in one or both arms, limb fatigability, and pain.²⁸

Diagnosing Takayasu arteritis

Multiple diagnostic criteria have been proposed to define Takayasu arteritis.²⁸ CTA, MRA, and positron emission tomography have replaced invasive angiography as the diagnostic imaging tests of choice.²⁹

Treating Takayasu arteritis

Takayasu arteritis has an acute and chronic course. Interventions are typically reserved for severe cases, with indications that include uncontrollable hypertension from renal artery stenosis, severe coronary or cerebrovascular disease, severe aortic regurgitation or coarctation, stenotic or occlusive lesions resulting in critical limb ischemia, and aneurysm at risk of rupture.^28–30

THORACIC OUTLET SYNDROME

Thoracic outlet syndrome is compression of the brachial plexus, subclavian vein, or subclavian artery as it exits the thoracic outlet through an area known as the scalene triangle, which is bordered by the anterior scalene, first rib, and clavicle.³¹ Presenting symptoms depend on the structure compressed.

By far the most common presentation³² is neurogenic thoracic outlet syndrome, accounting for more than 90% of cases, followed by venous thoracic outlet syndrome. Arterial thoracic outlet syndrome is the least frequent at less than 1%, but carries the greatest morbidity with potential for limb loss.^31–33

The subclavian artery exits the thoracic outlet between the anterior and middle scalene muscles, and then travels over the first rib and underneath the clavicle.³¹ Repeated trauma from compression of the artery results in intimal injury leading to compression, stenosis, occlusion, or aneurysm formation.^31,32

Symptoms of arterial thoracic outlet syndrome can start out as effort fatigue of the upper extremity secondary to compression. These symptoms are usually vague and difficult to define,³¹ as these patients typically are young and do not have atherosclerotic risk factors that would prompt suspicion of a vascular cause.

The most common presentation of arterial thoracic outlet syndrome is upper extremity embolization from a partially thrombosed aneurysm or area of stenosis with ischemia.³² Symptoms can range from ischemia of the fingers due to  microembolization to acute limb ischemia due to complete thrombosis of the subclavian artery.^31,32 Arterial thoracic outlet syndrome is most commonly associated with a bony abnormality (ie, cervical rib or anomalous first rib),^31–33 and on physical examination the bony abnormality may be palpated in the supraclavicular fossa.³¹

Other physical findings include a bruit over the subclavian artery, a blood pressure difference of 20 mm Hg or more between the affected and unaffected arms, loss of brachial, radial, or ulnar pulses with arm abduction, and loss of the radial pulse with the head rotated to the affected side as the patient takes a deep breath (the Adson maneuver).³¹ While postural changes in the pulse examination hint at arterial thoracic outlet syndrome, extremity pulses may be reduced or even absent in up to 60% of normal patients.³²

Diagnosing thoracic outlet syndrome

The workup should start with noninvasive imaging with pulse volume recording and wrist and finger systolic pressures, followed by arterial duplex ultrasonography.

Chest radiography may be able to identify bony abnormalities, and MRA or CTA with the patient in two positions—ie, arms down at  the sides, and arms held above the head—can help identify arterial compression from bony or muscular structures in the thoracic outlet. Upper extremity angiography provides high-resolution imaging of the digital arteries and can help identify a subclavian artery aneurysm, which may be a subtle finding.³¹

It is important to have objective evidence of arterial or venous mechanical obstruction before deciding to remove the first rib.

Treating thoracic outlet syndrome

Treatment is determined by the severity and acuity of symptoms. If the patient presents with acute limb ischemia, prompt treatment with either open surgery or endovascular treatment is required.^31,32,34 Once the acute phase has resolved or if the patient presents with chronic disease, open surgical repair is needed to remove the compression of the artery. If an arterial abnormality is identified (aneurysm or significant stenosis), an arterial reconstruction with bypass may be required.³¹

The standard treatment for thoracic outlet syndrome is resection of the first rib (and removal of the cervical rib if present).^31,34 This can be by a transaxillary approach unless arterial reconstruction is needed, in which case a supraclavicular approach is used.^31,34 When a patient without symptoms is found to have evidence of arterial compression, most experts would recommend resection of the first rib if there is evidence of an arterial abnormality, or follow-up with duplex imaging for patients with only subtle findings.³¹

EXTERNAL ILIAC ENDOFIBROSIS

External iliac endofibrosis is a rare cause of intermittent claudication, typically in high-performance athletes, resulting from thickening of the intima in the external iliac artery causing luminal narrowing and resultant ischemia.^35–37 The estimated incidence is as high as 20% in elite competitive cyclists, and the condition has been described in other sports as well.³⁷

External iliac endofibrosis typically presents as unilateral leg pain or cramping at near-maximal exercise with an associated feeling of swelling and numbness on the affected side.^35,37 It is bilateral in up to 15% of cases.³⁵ While claudication of the thigh is the predominant presenting symptom, dissection and thrombosis of the external iliac artery have been described, presenting with acute limb ischemia in up to 4% of patients.^35,36

The condition has been attributed to factors such as physical position, psoas hypertrophy, tethering of the external iliac artery to the psoas muscle, kinking and tortuosity of the vessel, and high-flow states secondary to increased cardiac output and adaptive systolic hypertension.^36,37

Diagnosing external iliac endofibrosis

The diagnosis is difficult, as symptoms typically manifest only during maximal exercise. Delays of 12 to 41 months between the onset of symptoms and diagnosis have been reported.³⁷ Physical findings are nonspecific, and pulses and ankle-brachial indices are typically normal at rest. A careful history with a focus on location and duration of symptoms and a high index of suspicion have been shown to increase the sensitivity of diagnosis.³⁶

Noninvasive vascular imaging with arterial duplex ultrasonography with physiologic studies (the ankle-brachial index) at rest and at maximal exertion should be obtained first.^35,37 If findings on ultrasonography are positive, CTA or MRA can be used to identify a suspected stenosis.

Diagnostic angiography is still the gold standard for imaging, as real-time images of the artery with different leg positions can be obtained and pressure gradients can be measured with or without the use of a vasodilator to determine the hemodynamic significance of a lesion.^35–37

Treating external iliac endofibrosis

Treatment should initially be conservative. Recreational athletes should consider changing to a sport that does not require hip flexion, and cyclists should be advised to reduce the amount of time spent cycling and to raise the handlebars or bring the saddle position forward to minimize hip flexion.³⁷

Definitive treatment is open surgical repair. Surgical options include arterial release of the tethered artery, endofibrosectomy and vessel shortening, endofibrosectomy and patch angioplasty, and interposition bypass grafting.^35–37

Timely diagnosis of limb ischemia is critical to limb health and limb salvage. The cause in most cases is related to atherosclerosis, and patients with limb ischemia are usually older and have risk factors for atherosclerosis, such as smoking, diabetes, hypertension, hyperlipidemia, and coronary artery disease. When younger patients develop limb ischemia, the diagnosis is often delayed since the index of suspicion is quite low in the absence of the usual risk factors.

Here, we discuss several nonatherosclerotic causes of limb ischemia: popliteal artery entrapment syndrome, popliteal artery aneurysm, cystic adventitial disease, persistent sciatic artery, phlegmasia cerulea dolens, Buerger disease, Takayasu arteritis, arterial thoracic outlet syndrome, and external iliac endofibrosis (Table 1). Our goal is to help clinicians make a timely diagnosis and ultimately save  the patient’s limb.

POPLITEAL ARTERY ENTRAPMENT SYNDROME

Popliteal artery entrapment syndrome occurs when the popliteal artery becomes compressed in the popliteal fossa, particularly during exercise.^1,2 The underlying problem may be that the popliteal artery has an aberrant course lateral to the medial head of the gastrocnemius muscle, or the medial head of the gastrocnemius may have an abnormal insertion, or there may be fibrous bands in the popliteal fossa, or a combination of these (Figure 1).^1–3 Functional popliteal artery entrapment syndrome occurs when there is compression of the artery without an anatomic cause.^1–3

The classic clinical presentation is a young athletic patient with calf or foot claudication (crampy pain with exercise, relieved with rest), but other symptoms can include coldness, paresthesias, and numbness. Pain at rest and tissue loss are rare on presentation but may develop if the diagnosis and treatment are delayed.³

Continued compression and microtrauma to the artery may lead to an intramural hematoma, thrombus formation, aneurysmal degeneration, dissection, or even acute thrombosis.² If the diagnosis is delayed, the patient’s condition may progress from intermittent arterial compression with plantar flexion to complete arterial thrombosis and critical limb ischemia, putting the patient at risk of limb loss.

Diagnosing popliteal artery entrapment syndrome

The diagnostic workup includes a detailed history with a focus on the cause of pain (usually exercise), a comprehensive physical examination that includes looking for wounds, and a thorough pulse examination.

The workup should start with noninvasive imaging such as duplex arterial ultrasonography with and without provocative measures (plantar flexion), the ankle-brachial index with and without provocative measures, and exercise treadmill testing with ankle-brachial index measurement.^1,2 Plantar flexion may be necessary to elicit arterial compression that is usually absent at rest.

Magnetic resonance imaging (MRI) and computed tomography (CT) of the lower extremity are useful to identify an arterial abnormality and aberrant muscle anatomy^1,3; MRI is currently the gold standard for delineating the muscles of the popliteal fossa.⁴ If these studies do not shed light on the diagnosis, arterial angiography with and without provocative maneuvers is useful in identifying compression of the popliteal artery.^1–3

Treating popliteal artery entrapment syndrome

Treatment depends on the level of arterial injury.

For patients with symptoms but no evidence of arterial injury, the most common procedure offered is popliteal fossa decompression.^1–3 This involves surgical release of the medial head of the gastrocnemius muscle and other muscles compressing the popliteal artery.

For patients with evidence of arterial injury such as stenosis, dissection, or aneurysm,  bypass grafting may be required.

For patients who present with acute limb ischemia, both surgical thrombectomy with possible bypass and intraarterial lysis have been described.^1,2,5

POPLITEAL ARTERY ANEURYSM

Popliteal artery aneurysm (Figure 2) is the most common type of aneurysm of the peripheral arteries of the lower extremity and is present in about 1% of men over age 65. Fifty percent are bilateral, and 50% are associated with an abdominal aortic aneurysm.^6,7 While up to 80% patients with this type of aneurysm have no symptoms at the time of diagnosis, symptoms develop at a rate of 14% per year, with acute limb ischemia occurring in up to one-third of cases.^6,7

When popliteal artery aneurysm progresses to acute limb ischemia, the consequences are often deleterious, as the tibial arteries distal to the popliteal artery are often occluded, limiting treatment options.

Popliteal artery aneurysm is defined as a local dilation of the artery of 2 cm or greater or an increase in the diameter to 1.5 times normal.⁶

Acute thrombosis of the aneurysm with limb ischemia is the most common presenting symptom and occurs in 50% of symptomatic cases of popliteal artery aneurysm.⁷ Almost 25% of patients present with intermittent claudication secondary to thrombosis, partial thrombosis with distal embolization, or combined aneurysmal and atherosclerotic disease. Compression of the popliteal vein by the popliteal artery aneurysm can cause leg swelling with or without deep vein thrombosis in up to 5% of patients.⁶ Rupture is very rare, with a rate of 2% to 4%.^6,7

Diagnosing popliteal artery aneurysm

The diagnosis can be made with arterial duplex ultrasonography, which is also useful for follow-up surveillance.^6–8 In the acute setting, computed tomographic angiography (CTA) or magnetic resonance angiography (MRA) is useful not only to identify the popliteal aneurysm, but also to define the distal tibial outflow vessels.^6,7

Treating popliteal artery aneurysm

Management of an acutely thrombosed popliteal artery aneurysm starts with systemic anticoagulation with intravenous heparin, followed initially by arterial angiography and lysis.^8–11 This approach has been shown to be safe and effective even in the absence of arterial runoff distal to the thrombosed popliteal aneurysm. Conversion to open thrombectomy and bypass can be done if initial lytic therapy fails, if the patient develops complications of lytic therapy, or if the patient needs emergency revascularization because of motor and neurologic deficits in the affected extremity.^8,10,11

How to manage the asymptomatic patient depends on the size of the aneurysm. Most studies recommend 2 cm or larger as the criterion for repair,^6–8,12 while others suggest treating even smaller aneurysms if thrombus is detected.⁹ Preoperative imaging before elective treatment of an asymptomatic popliteal artery aneurysm includes either CTA or MRA,^8,10 which allows the surgeon to visualize the full extent of the aneurysm to best plan the surgical approach. Diagnostic angiography can help determine the most suitable bypass target and can better characterize tibial outflow.

Asymptomatic popliteal artery aneurysm has traditionally been treated with surgical bypass with exclusion of the aneurysm,^6–8,12 but more recently, endovascular approaches using self-expanding stent grafts have been described. Further study is needed to determine the long-term efficacy of the endovascular approach.^8,10

CYSTIC ADVENTITIAL DISEASE

Cystic adventitial disease is a rare condition in which a blood vessel is narrowed due to mucin-containing cysts in the adventitia. More than 80% of cases occur in the popliteal artery, but it has been described in other peripheral arteries and veins.^13,14 It is more common in men than in women and typically occurs in the 4th or 5th decade of life. Most patients present with the sudden onset of calf claudication without the usual risk factors for peripheral vascular disease.¹³

Diagnosing cystic adventitial disease

Noninvasive arterial or venous duplex ultrasonography can be a good screening tool, as the cysts appear hypoechoic, but results are operator-dependent. CTA and MRA are the imaging tests of choice, as they can detect the cystic lesions and define vessel anatomy for intervention. Diagnostic angiography does not show the cysts themselves but instead reveals a classic “hourglass” and “scimitar” pattern of arterial narrowing that suggests the underlying pathology.^13,14

Treating cystic adventitial disease

Usual treatment is complete cyst resection and vessel reconstruction by surgical bypass. Other therapies include open surgical cyst evacuation and removal of the cyst wall, open surgical cyst aspiration, aspiration guided by ultrasonography or CT, and percutaneous angioplasty. However, these nonsurgical treatments have not been shown to be as effective and long-lasting as cyst excision and bypass.^13,14

PERSISTENT SCIATIC ARTERY

Persistent sciatic artery is a rare developmental abnormality.^15–17 Normally, as the femoral artery develops in the embryo, the sciatic artery involutes to form the inferior gluteal artery. But if the femoral system fails to mature, the sciatic artery, which is adjacent to the sciatic nerve posteriorly as it goes through the sciatic foramen, persists and functions as the major artery supplying the lower extremity, continuing to the posterior thigh and joining the popliteal artery (Figure 3).^15,17

Persistent sciatic artery has an incidence of 2.5 to 4 per 10,000 per year¹⁵ and is bilateral in almost half of cases.¹⁶ Up to 40% of patients have no symptoms, but symptoms may develop by age 40 to 50. Because of repeated trauma to the vessel as it passes through the sciatic foramen,¹⁸ the persistent sciatic artery typically sustains accelerated atherosclerotic changes that make it susceptible to aneurysm formation,¹⁵ and up to 46% of patients present with aneurysmal degeneration.¹⁷

Classically, patients present with lower extremity ischemia from atherosclerotic changes in the persistent sciatic artery or aneurysmal degeneration and thromboembolism.¹⁵ Rarely, these aneurysms rupture.^15,17 Other signs and symptoms include a pulsatile mass in the buttock, lower extremity numbness, motor weakness, and radicular pain along the sciatic nerve distribution from nerve compression.^15–17

Physical findings vary but are distinguished by the lack of femoral pulses in the presence of pedal pulses. A pulsatile buttock mass with evidence of lower extremity nerve compression or limb ischemia or both is pathognomonic of a persistent sciatic artery aneurysm.^16,18

Diagnosing persistent sciatic artery

Diagnostic angiography is the gold standard imaging test,^15,19 although CTA is starting to replace it.^16,18

Treating persistent sciatic artery

Persistent sciatic artery that is asymptomatic and is found incidentally does not require repair; however, it should be followed with duplex ultrasonography to look for evidence of aneurysm degeneration. Degeneration requires repair in most cases.^15,16,18,19 When the persistent sciatic artery is the only blood supply to the distal extremity, open aneurysm excision and bypass is the treatment of choice.^15,16,19 If collateral flow is adequate, endovascular coil embolization is an option.¹⁵ Endovascular stent graft placement has also been described.^16,19

PHLEGMASIA CERULEA DOLENS

Phlegmasia cerulea dolens is a rare syndrome caused by extensive acute thrombosis of the ileofemoral vein.^20–23 It is defined as total or near-total occlusion of the venous outflow of an extremity, causing massive swelling and congestion that impedes arterial inflow.^20,22

Phlegmasia cerulea dolens is associated with four cardinal signs: edema, violaceous discoloration, pain, and severe venous outflow obstruction (Figure 4).²² Patients present with sudden onset of lower extremity pain, swelling, cyanosis, and arterial ischemia with or without loss of distal pulses.^20,22

This syndrome can progress to gangrene and massive fluid sequestration leading to shock and death.^21–23 From 25% to 40% of patients die, and of those who survive, 20% to 50% require amputation of the limb.^20,23

Risk factors include malignancy, immobility, heart failure, heparin-induced thrombocytopenia, antiphospholipid syndrome, pregnancy, venous catheterization (eg, to insert an inferior vena cava filter), and surgery.^20–22

Diagnosing phlegmasia cerulea dolens

The diagnosis is made on clinical suspicion with evidence of iliofemoral deep vein thrombosis. Most experts suggest venous duplex ultrasonography to identify the deep vein thrombosis,²³ although CT or MR venography can be used to better delineate the proximal extent of the thrombus.^20,23

Treating phlegmasia cerulea dolens

Initial management is aggressive fluid resuscitation, elevation of the affected limb, strict bed rest, and anticoagulation with intravenous heparin.^20,23 Interventions are aimed at urgently restoring venous outflow to prevent progression to venous gangrene and limb loss.

Although conservative therapy can succeed by itself,²³ if the condition does not improve or has already progressed to an advanced stage, the two mainstays of treatment are open venous thrombectomy and endovascular treatment.^21–23 Endovascular treatment includes catheter-directed thrombolytic therapy (with or without percutaneous mechanical or pharmacomechanical thrombectomy) and stenting.^20,23 The success rate for endovascular therapy can be as high as 90% with near-complete resolution of thrombosis.²⁰ A disadvantage is that, compared with open surgical thrombectomy, more time is needed to achieve venous outflow.^20,22

If endovascular therapy is ineffective, if lytic therapy is contraindicated, or if the disease has progressed to gangrene, open surgical thrombectomy with possible fasciotomy is the preferred option.^20,21,23 Open surgery has the advantage of restoring venous outflow faster, but disadvantages include the inability to open the smaller veins of the extremity, blood loss, and risks associated with general anesthesia.^20–22

BUERGER DISEASE

Buerger disease (thromboangiitis obliterans) is a nonatherosclerotic segmental inflammatory disease involving the small and medium-sized vessels of the arms and legs.^24–27 It is differentiated from other vasculitides by its marked male predominance, its close association with smoking, the rarity of systemic signs and symptoms, and the absence of elevated inflammatory markers.²⁶

The rate of major amputation is reported to be 11% at 5 years and 23% at 20 years.²⁴

The classic patient is a young male smoker with symptoms of arterial disease before age 45.^24,26 Patients can present with migratory thrombophlebitis or signs of arterial insufficiency in the upper or lower extremities. Two or more limbs are commonly involved. Arterial insufficiency can range from claudication and exertional discomfort of the extremity to ischemic pain at rest leading to ulceration of the distal fingers and toes. Physical findings are similar to those seen in peripheral vascular disease and arterial insufficiency, with decreased arterial brachial index, cool extremities, and wounds.

Diagnosing Buerger disease

• The Shionoya diagnostic criteria for Buerger disease are the following five clinical features^24,27:
• History of smoking
• Onset before age 50
• Infrapopliteal arterial occlusive disease
• Upper-limb involvement or phlebitis migrans
• Absence of atherosclerotic risk factors other than heavy smoking.

Various other major and minor criteria have been described to make the diagnosis as well.²⁴

There is no specific laboratory test to confirm the diagnosis of Buerger disease. A full panel of laboratory tests should be sent to rule out other causes of arterial insufficiency and vasculitides; these tests should include C-reactive protein, rheumatoid factor, erythrocyte sedimentation rate, antinuclear antibodies, antiphospholipid antibodies, anti-Scl-70 antibodies, anticentromere antibodies, complement level measurement, and hypercoagulability workup.

Imaging studies include arterial duplex ultrasonography with ankle-brachial indices and segmental pressures and CTA or MRA.²⁶ Angiography can show a “corkscrew” pattern of occlusive disease and collateral formation, which is highly associated with Buerger disease.²⁴

Treating Buerger disease

The only treatment shown to reduce the risk of amputation is complete abstention from tobacco and nicotine (smoking, secondhand smoke, and nicotine patches and gum).^24,26

Symptoms of claudication can be managed with aspirin, clopidogrel, vasodilators, pentoxifylline, and cilostazol.²⁶

Surgical bypass is rarely an option, as Buerger disease typically affects the distal blood vessels, thus precluding bypass, and the 5-year patency rate is only 49%.²⁶ Other treatments including arterial thrombolysis, sympathectomy, stem cell injection, spinal cord stimulators, omental grafting, and immunomodulation have been described, but there are only limited data to offer guidance in choosing the appropriate one.²⁴

TAKAYASU ARTERITIS

Takayasu arteritis is a form of vasculitis involving the aorta and its main branches (Figure 5).²⁸ Although seen around the world, it has a higher incidence in young Asian women. Patients can present with systemic symptoms such as fever, fatigue, vague pain, and cardinal signs of limb ischemia associated with Takayasu arteritis, such as weak or absent pulses, differences between the arms in pulses and blood pressures, unobtainable blood pressure measurement in one or both arms, limb fatigability, and pain.²⁸

Diagnosing Takayasu arteritis

Multiple diagnostic criteria have been proposed to define Takayasu arteritis.²⁸ CTA, MRA, and positron emission tomography have replaced invasive angiography as the diagnostic imaging tests of choice.²⁹

Treating Takayasu arteritis

Takayasu arteritis has an acute and chronic course. Interventions are typically reserved for severe cases, with indications that include uncontrollable hypertension from renal artery stenosis, severe coronary or cerebrovascular disease, severe aortic regurgitation or coarctation, stenotic or occlusive lesions resulting in critical limb ischemia, and aneurysm at risk of rupture.^28–30

THORACIC OUTLET SYNDROME

Thoracic outlet syndrome is compression of the brachial plexus, subclavian vein, or subclavian artery as it exits the thoracic outlet through an area known as the scalene triangle, which is bordered by the anterior scalene, first rib, and clavicle.³¹ Presenting symptoms depend on the structure compressed.

By far the most common presentation³² is neurogenic thoracic outlet syndrome, accounting for more than 90% of cases, followed by venous thoracic outlet syndrome. Arterial thoracic outlet syndrome is the least frequent at less than 1%, but carries the greatest morbidity with potential for limb loss.^31–33

The subclavian artery exits the thoracic outlet between the anterior and middle scalene muscles, and then travels over the first rib and underneath the clavicle.³¹ Repeated trauma from compression of the artery results in intimal injury leading to compression, stenosis, occlusion, or aneurysm formation.^31,32

Symptoms of arterial thoracic outlet syndrome can start out as effort fatigue of the upper extremity secondary to compression. These symptoms are usually vague and difficult to define,³¹ as these patients typically are young and do not have atherosclerotic risk factors that would prompt suspicion of a vascular cause.

The most common presentation of arterial thoracic outlet syndrome is upper extremity embolization from a partially thrombosed aneurysm or area of stenosis with ischemia.³² Symptoms can range from ischemia of the fingers due to  microembolization to acute limb ischemia due to complete thrombosis of the subclavian artery.^31,32 Arterial thoracic outlet syndrome is most commonly associated with a bony abnormality (ie, cervical rib or anomalous first rib),^31–33 and on physical examination the bony abnormality may be palpated in the supraclavicular fossa.³¹

Other physical findings include a bruit over the subclavian artery, a blood pressure difference of 20 mm Hg or more between the affected and unaffected arms, loss of brachial, radial, or ulnar pulses with arm abduction, and loss of the radial pulse with the head rotated to the affected side as the patient takes a deep breath (the Adson maneuver).³¹ While postural changes in the pulse examination hint at arterial thoracic outlet syndrome, extremity pulses may be reduced or even absent in up to 60% of normal patients.³²

Diagnosing thoracic outlet syndrome

The workup should start with noninvasive imaging with pulse volume recording and wrist and finger systolic pressures, followed by arterial duplex ultrasonography.

Chest radiography may be able to identify bony abnormalities, and MRA or CTA with the patient in two positions—ie, arms down at  the sides, and arms held above the head—can help identify arterial compression from bony or muscular structures in the thoracic outlet. Upper extremity angiography provides high-resolution imaging of the digital arteries and can help identify a subclavian artery aneurysm, which may be a subtle finding.³¹

It is important to have objective evidence of arterial or venous mechanical obstruction before deciding to remove the first rib.

Treating thoracic outlet syndrome

Treatment is determined by the severity and acuity of symptoms. If the patient presents with acute limb ischemia, prompt treatment with either open surgery or endovascular treatment is required.^31,32,34 Once the acute phase has resolved or if the patient presents with chronic disease, open surgical repair is needed to remove the compression of the artery. If an arterial abnormality is identified (aneurysm or significant stenosis), an arterial reconstruction with bypass may be required.³¹

The standard treatment for thoracic outlet syndrome is resection of the first rib (and removal of the cervical rib if present).^31,34 This can be by a transaxillary approach unless arterial reconstruction is needed, in which case a supraclavicular approach is used.^31,34 When a patient without symptoms is found to have evidence of arterial compression, most experts would recommend resection of the first rib if there is evidence of an arterial abnormality, or follow-up with duplex imaging for patients with only subtle findings.³¹

EXTERNAL ILIAC ENDOFIBROSIS

External iliac endofibrosis is a rare cause of intermittent claudication, typically in high-performance athletes, resulting from thickening of the intima in the external iliac artery causing luminal narrowing and resultant ischemia.^35–37 The estimated incidence is as high as 20% in elite competitive cyclists, and the condition has been described in other sports as well.³⁷

External iliac endofibrosis typically presents as unilateral leg pain or cramping at near-maximal exercise with an associated feeling of swelling and numbness on the affected side.^35,37 It is bilateral in up to 15% of cases.³⁵ While claudication of the thigh is the predominant presenting symptom, dissection and thrombosis of the external iliac artery have been described, presenting with acute limb ischemia in up to 4% of patients.^35,36

The condition has been attributed to factors such as physical position, psoas hypertrophy, tethering of the external iliac artery to the psoas muscle, kinking and tortuosity of the vessel, and high-flow states secondary to increased cardiac output and adaptive systolic hypertension.^36,37

Diagnosing external iliac endofibrosis

The diagnosis is difficult, as symptoms typically manifest only during maximal exercise. Delays of 12 to 41 months between the onset of symptoms and diagnosis have been reported.³⁷ Physical findings are nonspecific, and pulses and ankle-brachial indices are typically normal at rest. A careful history with a focus on location and duration of symptoms and a high index of suspicion have been shown to increase the sensitivity of diagnosis.³⁶

Noninvasive vascular imaging with arterial duplex ultrasonography with physiologic studies (the ankle-brachial index) at rest and at maximal exertion should be obtained first.^35,37 If findings on ultrasonography are positive, CTA or MRA can be used to identify a suspected stenosis.

Diagnostic angiography is still the gold standard for imaging, as real-time images of the artery with different leg positions can be obtained and pressure gradients can be measured with or without the use of a vasodilator to determine the hemodynamic significance of a lesion.^35–37

Treating external iliac endofibrosis

Treatment should initially be conservative. Recreational athletes should consider changing to a sport that does not require hip flexion, and cyclists should be advised to reduce the amount of time spent cycling and to raise the handlebars or bring the saddle position forward to minimize hip flexion.³⁷

Definitive treatment is open surgical repair. Surgical options include arterial release of the tethered artery, endofibrosectomy and vessel shortening, endofibrosectomy and patch angioplasty, and interposition bypass grafting.^35–37

Current smoking, as well as higher levels of cumulative cigarette exposure from past smoking, were both associated with higher left ventricular mass, a higher LV mass-to-volume ratio, and worse diastolic function in an elderly community-based population with no overt indications of coronary artery disease or heart failure, according to a report published online Sept. 13 in Circulation: Cardiovascular Imaging.

“These findings suggest that smoking is associated with subtle alterations in LV structure and function, which might help explain the higher risk of heart failure [HF] reported for smokers, independent of coronary artery disease [CAD],” said Wilson Nadruz Jr., MD, of the cardiovascular division, Brigham and Women’s Hospital, Boston, and his associates.

©Zoonar/A.Mijatovic/Thinkstock.com

They analyzed links between smoking and echocardiographic features using data from the Atherosclerosis Risk in Communities (ARIC) study, an ongoing prospective observational study involving community-dwelling adults who were aged 45-64 years at baseline in 1987-1989. For their study, Dr. Nadruz and his colleagues assessed echocardiographic images taken for 4,580 ARIC participants at follow-up roughly 25 years later. None of these adults had any indication of CAD or HF; 287 (6.3%) were current smokers, 2,316 (50.5%) were former smokers, and 1,977 (43.2%) never smoked.

Compared with never smokers, current smokers showed a greater LV mass index (80.4 vs. 76.7), a greater LV mass-to-volume ratio (1.93 vs. 1.83), and a higher prevalence of LV hypertrophy (15% vs. 9%), as well as a higher prevalence of concentric LV hypertrophy and worse LV diastolic function. The same association was found between never smokers and former smokers who had higher levels of cumulative cigarette exposure, the investigators said (Circ Cardiovasc Imag. 2016 Sep 13. doi: 10.1161/circimaging.116.004950).

This association between smoking and altered LV structure and function remained robust after the data were adjusted to account for numerous cardiac risk factors such as older age, higher BMI, diabetes, hypertension, greater alcohol consumption, and higher heart rate. It also didn’t vary by patient sex, race, or income level. In contrast, there was no association between smoking and right ventricular structure or function.

“These data suggest that smoking can independently lead to thickening of the heart and worsening of heart function, which may lead to a higher risk for heart failure, even in people who don’t have heart attacks,” Dr. Nadruz said in a statement.

Looking at the results in a more positive light, senior author Scott D. Solomon, MD, professor of medicine at Harvard University, Boston, said “The good news is that former smokers had similar heart structure and function, compared with never smokers,” suggesting that “the potential effects of tobacco on the myocardium might be reversible after smoking cessation.”

Current smoking, as well as higher levels of cumulative cigarette exposure from past smoking, were both associated with higher left ventricular mass, a higher LV mass-to-volume ratio, and worse diastolic function in an elderly community-based population with no overt indications of coronary artery disease or heart failure, according to a report published online Sept. 13 in Circulation: Cardiovascular Imaging.

“These findings suggest that smoking is associated with subtle alterations in LV structure and function, which might help explain the higher risk of heart failure [HF] reported for smokers, independent of coronary artery disease [CAD],” said Wilson Nadruz Jr., MD, of the cardiovascular division, Brigham and Women’s Hospital, Boston, and his associates.

©Zoonar/A.Mijatovic/Thinkstock.com

They analyzed links between smoking and echocardiographic features using data from the Atherosclerosis Risk in Communities (ARIC) study, an ongoing prospective observational study involving community-dwelling adults who were aged 45-64 years at baseline in 1987-1989. For their study, Dr. Nadruz and his colleagues assessed echocardiographic images taken for 4,580 ARIC participants at follow-up roughly 25 years later. None of these adults had any indication of CAD or HF; 287 (6.3%) were current smokers, 2,316 (50.5%) were former smokers, and 1,977 (43.2%) never smoked.

Compared with never smokers, current smokers showed a greater LV mass index (80.4 vs. 76.7), a greater LV mass-to-volume ratio (1.93 vs. 1.83), and a higher prevalence of LV hypertrophy (15% vs. 9%), as well as a higher prevalence of concentric LV hypertrophy and worse LV diastolic function. The same association was found between never smokers and former smokers who had higher levels of cumulative cigarette exposure, the investigators said (Circ Cardiovasc Imag. 2016 Sep 13. doi: 10.1161/circimaging.116.004950).

This association between smoking and altered LV structure and function remained robust after the data were adjusted to account for numerous cardiac risk factors such as older age, higher BMI, diabetes, hypertension, greater alcohol consumption, and higher heart rate. It also didn’t vary by patient sex, race, or income level. In contrast, there was no association between smoking and right ventricular structure or function.

“These data suggest that smoking can independently lead to thickening of the heart and worsening of heart function, which may lead to a higher risk for heart failure, even in people who don’t have heart attacks,” Dr. Nadruz said in a statement.

Looking at the results in a more positive light, senior author Scott D. Solomon, MD, professor of medicine at Harvard University, Boston, said “The good news is that former smokers had similar heart structure and function, compared with never smokers,” suggesting that “the potential effects of tobacco on the myocardium might be reversible after smoking cessation.”

Current smoking, as well as higher levels of cumulative cigarette exposure from past smoking, were both associated with higher left ventricular mass, a higher LV mass-to-volume ratio, and worse diastolic function in an elderly community-based population with no overt indications of coronary artery disease or heart failure, according to a report published online Sept. 13 in Circulation: Cardiovascular Imaging.

“These findings suggest that smoking is associated with subtle alterations in LV structure and function, which might help explain the higher risk of heart failure [HF] reported for smokers, independent of coronary artery disease [CAD],” said Wilson Nadruz Jr., MD, of the cardiovascular division, Brigham and Women’s Hospital, Boston, and his associates.

©Zoonar/A.Mijatovic/Thinkstock.com

They analyzed links between smoking and echocardiographic features using data from the Atherosclerosis Risk in Communities (ARIC) study, an ongoing prospective observational study involving community-dwelling adults who were aged 45-64 years at baseline in 1987-1989. For their study, Dr. Nadruz and his colleagues assessed echocardiographic images taken for 4,580 ARIC participants at follow-up roughly 25 years later. None of these adults had any indication of CAD or HF; 287 (6.3%) were current smokers, 2,316 (50.5%) were former smokers, and 1,977 (43.2%) never smoked.

Compared with never smokers, current smokers showed a greater LV mass index (80.4 vs. 76.7), a greater LV mass-to-volume ratio (1.93 vs. 1.83), and a higher prevalence of LV hypertrophy (15% vs. 9%), as well as a higher prevalence of concentric LV hypertrophy and worse LV diastolic function. The same association was found between never smokers and former smokers who had higher levels of cumulative cigarette exposure, the investigators said (Circ Cardiovasc Imag. 2016 Sep 13. doi: 10.1161/circimaging.116.004950).

This association between smoking and altered LV structure and function remained robust after the data were adjusted to account for numerous cardiac risk factors such as older age, higher BMI, diabetes, hypertension, greater alcohol consumption, and higher heart rate. It also didn’t vary by patient sex, race, or income level. In contrast, there was no association between smoking and right ventricular structure or function.

“These data suggest that smoking can independently lead to thickening of the heart and worsening of heart function, which may lead to a higher risk for heart failure, even in people who don’t have heart attacks,” Dr. Nadruz said in a statement.

Looking at the results in a more positive light, senior author Scott D. Solomon, MD, professor of medicine at Harvard University, Boston, said “The good news is that former smokers had similar heart structure and function, compared with never smokers,” suggesting that “the potential effects of tobacco on the myocardium might be reversible after smoking cessation.”

Clinicians familiar with point-of-care (POC) ultrasound know that structures such as the hands and feet require the use of the linear high-frequency transducer to obtain quality images. In reality, however, employing the standard technique (ie, applying gel to the probe surface and scanning the structure) can be challenging due to the uneven surfaces of the fingers and toes; therefore, obtaining good contact with the transducer is harder than it may seem at first glance. Additionally, since these structures are superficial, they are usually seen on the top half of the ultrasound display, while the focal zone of most ultrasound machines is located in the middle of the display and is nonadjustable.

We describe two simple adjuncts to POC ultrasound that can assist in visualizing digital structures with greater ease and improved image resolution: the water bath^1,2 and standoff pad techniques.

Water Bath Technique

In the water bath technique, one fills a small basin with lukewarm water to a depth point where the extremity being studied (ie, hand or foot) is mostly—but not completely—submerged in the water bath.  After the extremity is submerged, the high-frequency probe is then placed into the water bath (Figure 1). When employing this technique, the transducer does not need to make contact with the patient’s skin. Since the water acts as an excellent conduction medium for sound waves, no ultrasound gel is required. For a video demonstrating the use of the water bath technique to evaluate the distal tip of the finger, see below.

Standoff Pad

Another technique that enhances POC imaging of the digits involves a standoff pad. A variety of commercially available standoff pads can be used for this technique. Alternatively, the clinician can easily create a standoff pad using supplies that are readily available in the ED. One such method is to fill a latex glove with water, tie off the filled glove, and place it on top of the extremity to be imaged (Figure 2). The water in the glove will facilitate sound-wave transmission.

Pathology

The water bath and standoff pad techniques can facilitate visualization of several pathologies, including felons (Figure 3), flexor tenosynovitis, phalangeal and metacarpal/metatarsal fractures, and interphalangeal, metacarpophalangeal, and metatarsophalangeal joint effusions (Figure 4). In addition, these techniques also assist in visualizing digit tendons to evaluate for tears in these structures (Figure 5).

Summary

Point-of-care ultrasound imaging to evaluate superficial body parts such as hands or feet can be challenging due to the irregular shape and uneven surface of these structures. The employment of adjuncts such as the water bath or standoff pad techniques can mitigate these challenges, facilitating the acquisition of high-resolution images and providing easier identification of pathology.

Clinicians familiar with point-of-care (POC) ultrasound know that structures such as the hands and feet require the use of the linear high-frequency transducer to obtain quality images. In reality, however, employing the standard technique (ie, applying gel to the probe surface and scanning the structure) can be challenging due to the uneven surfaces of the fingers and toes; therefore, obtaining good contact with the transducer is harder than it may seem at first glance. Additionally, since these structures are superficial, they are usually seen on the top half of the ultrasound display, while the focal zone of most ultrasound machines is located in the middle of the display and is nonadjustable.

We describe two simple adjuncts to POC ultrasound that can assist in visualizing digital structures with greater ease and improved image resolution: the water bath^1,2 and standoff pad techniques.

Water Bath Technique

In the water bath technique, one fills a small basin with lukewarm water to a depth point where the extremity being studied (ie, hand or foot) is mostly—but not completely—submerged in the water bath.  After the extremity is submerged, the high-frequency probe is then placed into the water bath (Figure 1). When employing this technique, the transducer does not need to make contact with the patient’s skin. Since the water acts as an excellent conduction medium for sound waves, no ultrasound gel is required. For a video demonstrating the use of the water bath technique to evaluate the distal tip of the finger, see below.

Standoff Pad

Another technique that enhances POC imaging of the digits involves a standoff pad. A variety of commercially available standoff pads can be used for this technique. Alternatively, the clinician can easily create a standoff pad using supplies that are readily available in the ED. One such method is to fill a latex glove with water, tie off the filled glove, and place it on top of the extremity to be imaged (Figure 2). The water in the glove will facilitate sound-wave transmission.

Pathology

The water bath and standoff pad techniques can facilitate visualization of several pathologies, including felons (Figure 3), flexor tenosynovitis, phalangeal and metacarpal/metatarsal fractures, and interphalangeal, metacarpophalangeal, and metatarsophalangeal joint effusions (Figure 4). In addition, these techniques also assist in visualizing digit tendons to evaluate for tears in these structures (Figure 5).

Summary

Point-of-care ultrasound imaging to evaluate superficial body parts such as hands or feet can be challenging due to the irregular shape and uneven surface of these structures. The employment of adjuncts such as the water bath or standoff pad techniques can mitigate these challenges, facilitating the acquisition of high-resolution images and providing easier identification of pathology.

Clinicians familiar with point-of-care (POC) ultrasound know that structures such as the hands and feet require the use of the linear high-frequency transducer to obtain quality images. In reality, however, employing the standard technique (ie, applying gel to the probe surface and scanning the structure) can be challenging due to the uneven surfaces of the fingers and toes; therefore, obtaining good contact with the transducer is harder than it may seem at first glance. Additionally, since these structures are superficial, they are usually seen on the top half of the ultrasound display, while the focal zone of most ultrasound machines is located in the middle of the display and is nonadjustable.

We describe two simple adjuncts to POC ultrasound that can assist in visualizing digital structures with greater ease and improved image resolution: the water bath^1,2 and standoff pad techniques.

Water Bath Technique

In the water bath technique, one fills a small basin with lukewarm water to a depth point where the extremity being studied (ie, hand or foot) is mostly—but not completely—submerged in the water bath.  After the extremity is submerged, the high-frequency probe is then placed into the water bath (Figure 1). When employing this technique, the transducer does not need to make contact with the patient’s skin. Since the water acts as an excellent conduction medium for sound waves, no ultrasound gel is required. For a video demonstrating the use of the water bath technique to evaluate the distal tip of the finger, see below.

Standoff Pad

Another technique that enhances POC imaging of the digits involves a standoff pad. A variety of commercially available standoff pads can be used for this technique. Alternatively, the clinician can easily create a standoff pad using supplies that are readily available in the ED. One such method is to fill a latex glove with water, tie off the filled glove, and place it on top of the extremity to be imaged (Figure 2). The water in the glove will facilitate sound-wave transmission.

Pathology

The water bath and standoff pad techniques can facilitate visualization of several pathologies, including felons (Figure 3), flexor tenosynovitis, phalangeal and metacarpal/metatarsal fractures, and interphalangeal, metacarpophalangeal, and metatarsophalangeal joint effusions (Figure 4). In addition, these techniques also assist in visualizing digit tendons to evaluate for tears in these structures (Figure 5).

Summary

Point-of-care ultrasound imaging to evaluate superficial body parts such as hands or feet can be challenging due to the irregular shape and uneven surface of these structures. The employment of adjuncts such as the water bath or standoff pad techniques can mitigate these challenges, facilitating the acquisition of high-resolution images and providing easier identification of pathology.

A 39-year-old Filipino man presented with nausea, vomiting, and abdominal pain of 2 weeks’ duration. He did not report trauma, and he had no history of medical illness or surgery.

On arrival, his blood pressure was 123/83 mm Hg, pulse 122 beats per minute, respiratory rate 18 breaths per minute, and temperature 100.7°F (38.1°C). On physical examination, he exhibited marked tenderness of the right upper quadrant on palpation. The abdomen was otherwise soft with no guarding or rebound tenderness.

Results of initial laboratory testing were as follows:

• Leukocyte count 17.0 × 10⁹/L (reference range 4.5–11.0)
• Serum glucose 558 mg/dL without ketoacidosis
• Aspartate aminotransferase 109 U/L (2–40)
• Alanine aminotranferase 28 U/L (2–50)
• Total serum bilirubin 4.0 mg/dL (0.0–1.5).

Plain chest radiography showed dramatic elevation of the right hemidiaphragm with a large subphrenic air-fluid level (Figure 1). Abdominal computed tomography (CT) demonstrated a multiloculated hepatic abscess 18 × 13.5 cm subjacent to the diaphragm (Figure 2). Cultures of blood and the abscess yielded Klebsiella pneumoniae. The patient recovered after percutaneous drainage and a course of ceftriaxone.

PRIMARY KLEBSIELLA LIVER ABSCESS

K pneumoniae, a gram-negative aerobic encapsulated bacillus of the normal human intestinal flora, is closely related to Escherichia coli, historically the most frequent bacterial cause of pyogenic liver abscess.¹ Over the last 30 years, K pneumoniae has eclipsed E coli as the most common causative agent, with the epicenter of this trend being located in Taiwan and South Korea, perhaps because rates of fecal Klebsiella carriage in that region are particularly high.^1,2

Concurrently, there has been increasing recognition—initially across Asia, but lately in Europe and the Western Hemisphere—of the so-called invasive Klebsiella liver abscess (KLA) syndrome, virtually unique to the hypervirulent K1 and K2 capsular serotypes of K pneumoniae prevalent in Asia.^3–6 This community-acquired syndrome is characterized by hematogenous deposition of the organism at distant sites, such as the lung, soft tissues, central nervous system, and eyes. Impairment of phagocytic function, as occurs in diabetes mellitus, and the resistance to phagocytosis conferred by the K1 and K2 serotypes have been identified as predisposing factors for dissemination.^7,8 The mucoid phenotype of K pneumoniae, very common in Asian isolates of the K1 and K2 serotypes, is also associated with hypervirulence and extrahepatic spread, presumably through evasion of phagocytosis and complement-mediated opsonization.^2,9

Our patient’s risk factors for KLA were his Asian origin and uncontrolled diabetes. No evidence of remote infection was detected during his hospitalization.

HEMIDIAPHRAGM ELEVATION

Acquired hemidiaphragm elevation is most commonly unilateral and typically represents an incidental radiologic finding attributable to paralysis of the corresponding diaphragm after phrenic nerve injury caused by trauma, surgery, or infection. Unilateral diaphragmatic paralysis is classically confirmed by performing a fluoroscopic sniff test, which is positive if the affected hemidiaphragm is observed in real time to paradoxically move upward during forced inhalation.¹⁰ This condition is usually asymptomatic at rest but could cause exertional dyspnea and contribute to ventilatory failure when pulmonary disease coexists.¹¹

Occasionally, as in our patient, hemidiaphragm elevation is part of the presentation of active abdominal pathology that displaces the corresponding hemidiaphragm cephalad by mass effect. Examples of such space-occupying abdominal lesions include infections, malignancy, hepatosplenomegaly, and pneumoperitoneum from a ruptured viscus. Pneumoperitoneum is suggested by the presence of an air crescent immediately subjacent to the affected hemidiaphragm on an upright radiograph accompanied by peritoneal signs.

Although there was subphrenic air on this patient’s initial chest radiograph, it was actually part of an air-fluid level without associated peritoneal signs. An air-fluid level is characterized by a sharp horizontal demarcation between the lighter gas component floating at the top and the heavier fluid component settling on the bottom (Figure 1). The subsequent CT excluded free intra-abdominal air while identifying a large hepatic abscess as the cause of hemidiaphragm elevation. In trauma victims, CT is also helpful in ruling out diaphragmatic rupture, which can have a similar radiographic appearance.¹²

Our patient’s presentation was a reminder that an elevated hemidiaphragm may reflect abdominal pathology and that subphrenic air in this context need not be either “free” or a surgical emergency. Drainage of the abscess restored the normal position of our patient’s right hemidiaphragm (Figure 3).

A 39-year-old Filipino man presented with nausea, vomiting, and abdominal pain of 2 weeks’ duration. He did not report trauma, and he had no history of medical illness or surgery.

On arrival, his blood pressure was 123/83 mm Hg, pulse 122 beats per minute, respiratory rate 18 breaths per minute, and temperature 100.7°F (38.1°C). On physical examination, he exhibited marked tenderness of the right upper quadrant on palpation. The abdomen was otherwise soft with no guarding or rebound tenderness.

Results of initial laboratory testing were as follows:

• Leukocyte count 17.0 × 10⁹/L (reference range 4.5–11.0)
• Serum glucose 558 mg/dL without ketoacidosis
• Aspartate aminotransferase 109 U/L (2–40)
• Alanine aminotranferase 28 U/L (2–50)
• Total serum bilirubin 4.0 mg/dL (0.0–1.5).

Plain chest radiography showed dramatic elevation of the right hemidiaphragm with a large subphrenic air-fluid level (Figure 1). Abdominal computed tomography (CT) demonstrated a multiloculated hepatic abscess 18 × 13.5 cm subjacent to the diaphragm (Figure 2). Cultures of blood and the abscess yielded Klebsiella pneumoniae. The patient recovered after percutaneous drainage and a course of ceftriaxone.

PRIMARY KLEBSIELLA LIVER ABSCESS

K pneumoniae, a gram-negative aerobic encapsulated bacillus of the normal human intestinal flora, is closely related to Escherichia coli, historically the most frequent bacterial cause of pyogenic liver abscess.¹ Over the last 30 years, K pneumoniae has eclipsed E coli as the most common causative agent, with the epicenter of this trend being located in Taiwan and South Korea, perhaps because rates of fecal Klebsiella carriage in that region are particularly high.^1,2

Concurrently, there has been increasing recognition—initially across Asia, but lately in Europe and the Western Hemisphere—of the so-called invasive Klebsiella liver abscess (KLA) syndrome, virtually unique to the hypervirulent K1 and K2 capsular serotypes of K pneumoniae prevalent in Asia.^3–6 This community-acquired syndrome is characterized by hematogenous deposition of the organism at distant sites, such as the lung, soft tissues, central nervous system, and eyes. Impairment of phagocytic function, as occurs in diabetes mellitus, and the resistance to phagocytosis conferred by the K1 and K2 serotypes have been identified as predisposing factors for dissemination.^7,8 The mucoid phenotype of K pneumoniae, very common in Asian isolates of the K1 and K2 serotypes, is also associated with hypervirulence and extrahepatic spread, presumably through evasion of phagocytosis and complement-mediated opsonization.^2,9

Our patient’s risk factors for KLA were his Asian origin and uncontrolled diabetes. No evidence of remote infection was detected during his hospitalization.

HEMIDIAPHRAGM ELEVATION

Acquired hemidiaphragm elevation is most commonly unilateral and typically represents an incidental radiologic finding attributable to paralysis of the corresponding diaphragm after phrenic nerve injury caused by trauma, surgery, or infection. Unilateral diaphragmatic paralysis is classically confirmed by performing a fluoroscopic sniff test, which is positive if the affected hemidiaphragm is observed in real time to paradoxically move upward during forced inhalation.¹⁰ This condition is usually asymptomatic at rest but could cause exertional dyspnea and contribute to ventilatory failure when pulmonary disease coexists.¹¹

Occasionally, as in our patient, hemidiaphragm elevation is part of the presentation of active abdominal pathology that displaces the corresponding hemidiaphragm cephalad by mass effect. Examples of such space-occupying abdominal lesions include infections, malignancy, hepatosplenomegaly, and pneumoperitoneum from a ruptured viscus. Pneumoperitoneum is suggested by the presence of an air crescent immediately subjacent to the affected hemidiaphragm on an upright radiograph accompanied by peritoneal signs.

Although there was subphrenic air on this patient’s initial chest radiograph, it was actually part of an air-fluid level without associated peritoneal signs. An air-fluid level is characterized by a sharp horizontal demarcation between the lighter gas component floating at the top and the heavier fluid component settling on the bottom (Figure 1). The subsequent CT excluded free intra-abdominal air while identifying a large hepatic abscess as the cause of hemidiaphragm elevation. In trauma victims, CT is also helpful in ruling out diaphragmatic rupture, which can have a similar radiographic appearance.¹²

Our patient’s presentation was a reminder that an elevated hemidiaphragm may reflect abdominal pathology and that subphrenic air in this context need not be either “free” or a surgical emergency. Drainage of the abscess restored the normal position of our patient’s right hemidiaphragm (Figure 3).

A 39-year-old Filipino man presented with nausea, vomiting, and abdominal pain of 2 weeks’ duration. He did not report trauma, and he had no history of medical illness or surgery.

On arrival, his blood pressure was 123/83 mm Hg, pulse 122 beats per minute, respiratory rate 18 breaths per minute, and temperature 100.7°F (38.1°C). On physical examination, he exhibited marked tenderness of the right upper quadrant on palpation. The abdomen was otherwise soft with no guarding or rebound tenderness.

Results of initial laboratory testing were as follows:

• Leukocyte count 17.0 × 10⁹/L (reference range 4.5–11.0)
• Serum glucose 558 mg/dL without ketoacidosis
• Aspartate aminotransferase 109 U/L (2–40)
• Alanine aminotranferase 28 U/L (2–50)
• Total serum bilirubin 4.0 mg/dL (0.0–1.5).

Plain chest radiography showed dramatic elevation of the right hemidiaphragm with a large subphrenic air-fluid level (Figure 1). Abdominal computed tomography (CT) demonstrated a multiloculated hepatic abscess 18 × 13.5 cm subjacent to the diaphragm (Figure 2). Cultures of blood and the abscess yielded Klebsiella pneumoniae. The patient recovered after percutaneous drainage and a course of ceftriaxone.

PRIMARY KLEBSIELLA LIVER ABSCESS

K pneumoniae, a gram-negative aerobic encapsulated bacillus of the normal human intestinal flora, is closely related to Escherichia coli, historically the most frequent bacterial cause of pyogenic liver abscess.¹ Over the last 30 years, K pneumoniae has eclipsed E coli as the most common causative agent, with the epicenter of this trend being located in Taiwan and South Korea, perhaps because rates of fecal Klebsiella carriage in that region are particularly high.^1,2

Concurrently, there has been increasing recognition—initially across Asia, but lately in Europe and the Western Hemisphere—of the so-called invasive Klebsiella liver abscess (KLA) syndrome, virtually unique to the hypervirulent K1 and K2 capsular serotypes of K pneumoniae prevalent in Asia.^3–6 This community-acquired syndrome is characterized by hematogenous deposition of the organism at distant sites, such as the lung, soft tissues, central nervous system, and eyes. Impairment of phagocytic function, as occurs in diabetes mellitus, and the resistance to phagocytosis conferred by the K1 and K2 serotypes have been identified as predisposing factors for dissemination.^7,8 The mucoid phenotype of K pneumoniae, very common in Asian isolates of the K1 and K2 serotypes, is also associated with hypervirulence and extrahepatic spread, presumably through evasion of phagocytosis and complement-mediated opsonization.^2,9

Our patient’s risk factors for KLA were his Asian origin and uncontrolled diabetes. No evidence of remote infection was detected during his hospitalization.

HEMIDIAPHRAGM ELEVATION

Acquired hemidiaphragm elevation is most commonly unilateral and typically represents an incidental radiologic finding attributable to paralysis of the corresponding diaphragm after phrenic nerve injury caused by trauma, surgery, or infection. Unilateral diaphragmatic paralysis is classically confirmed by performing a fluoroscopic sniff test, which is positive if the affected hemidiaphragm is observed in real time to paradoxically move upward during forced inhalation.¹⁰ This condition is usually asymptomatic at rest but could cause exertional dyspnea and contribute to ventilatory failure when pulmonary disease coexists.¹¹

Occasionally, as in our patient, hemidiaphragm elevation is part of the presentation of active abdominal pathology that displaces the corresponding hemidiaphragm cephalad by mass effect. Examples of such space-occupying abdominal lesions include infections, malignancy, hepatosplenomegaly, and pneumoperitoneum from a ruptured viscus. Pneumoperitoneum is suggested by the presence of an air crescent immediately subjacent to the affected hemidiaphragm on an upright radiograph accompanied by peritoneal signs.

Although there was subphrenic air on this patient’s initial chest radiograph, it was actually part of an air-fluid level without associated peritoneal signs. An air-fluid level is characterized by a sharp horizontal demarcation between the lighter gas component floating at the top and the heavier fluid component settling on the bottom (Figure 1). The subsequent CT excluded free intra-abdominal air while identifying a large hepatic abscess as the cause of hemidiaphragm elevation. In trauma victims, CT is also helpful in ruling out diaphragmatic rupture, which can have a similar radiographic appearance.¹²

Our patient’s presentation was a reminder that an elevated hemidiaphragm may reflect abdominal pathology and that subphrenic air in this context need not be either “free” or a surgical emergency. Drainage of the abscess restored the normal position of our patient’s right hemidiaphragm (Figure 3).

ROME – Functional, noninvasive cardiac imaging using cardiovascular MR or myocardial perfusion scintigraphy was significantly better than was a current and well regarded guideline-based approach to identifying patients with chest pain and suspected coronary artery disease who could safely avoid angiography, thereby cutting the rate of unnecessary angiography by about 75%.

Following the guideline formula adopted by the British National Institute for Health and Care Excellence (NICE) resulted in a 29% rate of unnecessary angiography compared with rates of 7.5% using cardiovascular MR (CMR) and 7.1% using myocardial perfusion scintigraphy (MPS) in a multicenter randomized trial with 1,202 patients, John P. Greenwood, MBChB, said at the annual congress of the European Society of Cardiology.

Mitchel L. Zoler/Frontline Medical News

This universal use of a functional, noninvasive imaging strategy to guide angiography resulted in no significant penalty of missed coronary disease or subsequent coronary events. The rate of positive angiography findings was 12% among the 240 patients managed according to the NICE guidelines, 10% among 481 patients screened by CMR, and 9% among the 481 patients screened using MPS, reported Dr. Greenwood, professor of cardiology at the University of Leeds (England). The rate of major adverse coronary events after 12 months of follow-up were 3% following the NICE protocol and 4% when screening by CMR or with MPS.

Concurrently with Dr. Greenwood’s report, the findings from the Clinical Evaluation of Magnetic Resonance Imaging in Coronary Heart Disease 2 (CE-MARC2) study appeared in an article online (JAMA. 2016 Aug 29. doi: 10.1001/jama.2016.12680).

“We showed that a functional test with CMR or MPS can reduce the rate of unnecessary coronary angiography. Cutting unnecessary angiography is really important to patients, and it may also cost effective,” he said, but cautioned that a formal cost analysis of the options tested in this study is still being run.

The NICE guidelines manage patients with chest pain that could be angina by their pretest probability of having coronary artery disease (CAD), and at the time the study was designed the NICE guidelines, issued in 2010, provided the most up-to-date expert guidance on how to triage these patients. The study enrolled patients with a pretest probability for CAD of 10%-90%; collectively their average probability was 50%. The patients participated in the study at one of six U.K. centers during November 2012 to March 2015. The average age was 56 years.

MPS is “probably the noninvasive imaging approach most commonly used worldwide to detect coronary ischemia,” Dr. Greenwood said. But he led an earlier study that showed that CMR, using a gadolinium-based tracing agent, works even better than MPS (in this study single photon emission CT) to predict a patient’s risk for major cardiac events. He said this superiority is probably because of the greater spatial resolution with CMR.

“The higher spatial resolution of CMR, about 5- to 10-fold greater that MPS, is less likely to produce false negative results,” he said in an interview. “We showed that CMR has higher diagnostic accuracy, is a better prognosticator, and is more cost effective” than MPS. Dr. Greenwood attributed the similar performance of CMR and MPS in CE-MARC2 to the study’s design, which led to fewer patients undergoing each of the two imaging methods and made CE-MARC2 underpowered to discern a difference in specificity. In his earlier study, which included 752 patients who underwent examination with both CMR and MPS, the negative predictive value of CMR was 91% compared with 79% with MPS.

CMR uses conventional MR machines, is now widely available, and is being widely used today as a first-line test in the United Kingdom and Europe, he added.

Dr. Greenwood believes that in his new study functional imaging outperformed the NICE guidelines because the pretest models used in the guidelines “tend to overestimate risk,” the factor that produces angiography overuse.

His report included two additional analyses that assessed the impact of CMR and MPS in the subgroup of patients with a high pretest probability for CAD, 61%-90%, and in the subgroup with a low pretest probability, 10%-29%. Among the patients with a high likelihood for CAD the two functional imaging methods cut the rate of unnecessary angiography by 95%, a statistically significant difference. Among those with a low likelihood functional imaging cut the rate 56%, a difference that did not reach statistical significance.

[email protected]

On Twitter @mitchelzoler

ROME – Functional, noninvasive cardiac imaging using cardiovascular MR or myocardial perfusion scintigraphy was significantly better than was a current and well regarded guideline-based approach to identifying patients with chest pain and suspected coronary artery disease who could safely avoid angiography, thereby cutting the rate of unnecessary angiography by about 75%.

Following the guideline formula adopted by the British National Institute for Health and Care Excellence (NICE) resulted in a 29% rate of unnecessary angiography compared with rates of 7.5% using cardiovascular MR (CMR) and 7.1% using myocardial perfusion scintigraphy (MPS) in a multicenter randomized trial with 1,202 patients, John P. Greenwood, MBChB, said at the annual congress of the European Society of Cardiology.

Mitchel L. Zoler/Frontline Medical News

This universal use of a functional, noninvasive imaging strategy to guide angiography resulted in no significant penalty of missed coronary disease or subsequent coronary events. The rate of positive angiography findings was 12% among the 240 patients managed according to the NICE guidelines, 10% among 481 patients screened by CMR, and 9% among the 481 patients screened using MPS, reported Dr. Greenwood, professor of cardiology at the University of Leeds (England). The rate of major adverse coronary events after 12 months of follow-up were 3% following the NICE protocol and 4% when screening by CMR or with MPS.

Concurrently with Dr. Greenwood’s report, the findings from the Clinical Evaluation of Magnetic Resonance Imaging in Coronary Heart Disease 2 (CE-MARC2) study appeared in an article online (JAMA. 2016 Aug 29. doi: 10.1001/jama.2016.12680).

“We showed that a functional test with CMR or MPS can reduce the rate of unnecessary coronary angiography. Cutting unnecessary angiography is really important to patients, and it may also cost effective,” he said, but cautioned that a formal cost analysis of the options tested in this study is still being run.

The NICE guidelines manage patients with chest pain that could be angina by their pretest probability of having coronary artery disease (CAD), and at the time the study was designed the NICE guidelines, issued in 2010, provided the most up-to-date expert guidance on how to triage these patients. The study enrolled patients with a pretest probability for CAD of 10%-90%; collectively their average probability was 50%. The patients participated in the study at one of six U.K. centers during November 2012 to March 2015. The average age was 56 years.

MPS is “probably the noninvasive imaging approach most commonly used worldwide to detect coronary ischemia,” Dr. Greenwood said. But he led an earlier study that showed that CMR, using a gadolinium-based tracing agent, works even better than MPS (in this study single photon emission CT) to predict a patient’s risk for major cardiac events. He said this superiority is probably because of the greater spatial resolution with CMR.

“The higher spatial resolution of CMR, about 5- to 10-fold greater that MPS, is less likely to produce false negative results,” he said in an interview. “We showed that CMR has higher diagnostic accuracy, is a better prognosticator, and is more cost effective” than MPS. Dr. Greenwood attributed the similar performance of CMR and MPS in CE-MARC2 to the study’s design, which led to fewer patients undergoing each of the two imaging methods and made CE-MARC2 underpowered to discern a difference in specificity. In his earlier study, which included 752 patients who underwent examination with both CMR and MPS, the negative predictive value of CMR was 91% compared with 79% with MPS.

CMR uses conventional MR machines, is now widely available, and is being widely used today as a first-line test in the United Kingdom and Europe, he added.

Dr. Greenwood believes that in his new study functional imaging outperformed the NICE guidelines because the pretest models used in the guidelines “tend to overestimate risk,” the factor that produces angiography overuse.

His report included two additional analyses that assessed the impact of CMR and MPS in the subgroup of patients with a high pretest probability for CAD, 61%-90%, and in the subgroup with a low pretest probability, 10%-29%. Among the patients with a high likelihood for CAD the two functional imaging methods cut the rate of unnecessary angiography by 95%, a statistically significant difference. Among those with a low likelihood functional imaging cut the rate 56%, a difference that did not reach statistical significance.

[email protected]

On Twitter @mitchelzoler

ROME – Functional, noninvasive cardiac imaging using cardiovascular MR or myocardial perfusion scintigraphy was significantly better than was a current and well regarded guideline-based approach to identifying patients with chest pain and suspected coronary artery disease who could safely avoid angiography, thereby cutting the rate of unnecessary angiography by about 75%.

Following the guideline formula adopted by the British National Institute for Health and Care Excellence (NICE) resulted in a 29% rate of unnecessary angiography compared with rates of 7.5% using cardiovascular MR (CMR) and 7.1% using myocardial perfusion scintigraphy (MPS) in a multicenter randomized trial with 1,202 patients, John P. Greenwood, MBChB, said at the annual congress of the European Society of Cardiology.

Mitchel L. Zoler/Frontline Medical News

This universal use of a functional, noninvasive imaging strategy to guide angiography resulted in no significant penalty of missed coronary disease or subsequent coronary events. The rate of positive angiography findings was 12% among the 240 patients managed according to the NICE guidelines, 10% among 481 patients screened by CMR, and 9% among the 481 patients screened using MPS, reported Dr. Greenwood, professor of cardiology at the University of Leeds (England). The rate of major adverse coronary events after 12 months of follow-up were 3% following the NICE protocol and 4% when screening by CMR or with MPS.

Concurrently with Dr. Greenwood’s report, the findings from the Clinical Evaluation of Magnetic Resonance Imaging in Coronary Heart Disease 2 (CE-MARC2) study appeared in an article online (JAMA. 2016 Aug 29. doi: 10.1001/jama.2016.12680).

“We showed that a functional test with CMR or MPS can reduce the rate of unnecessary coronary angiography. Cutting unnecessary angiography is really important to patients, and it may also cost effective,” he said, but cautioned that a formal cost analysis of the options tested in this study is still being run.

The NICE guidelines manage patients with chest pain that could be angina by their pretest probability of having coronary artery disease (CAD), and at the time the study was designed the NICE guidelines, issued in 2010, provided the most up-to-date expert guidance on how to triage these patients. The study enrolled patients with a pretest probability for CAD of 10%-90%; collectively their average probability was 50%. The patients participated in the study at one of six U.K. centers during November 2012 to March 2015. The average age was 56 years.

MPS is “probably the noninvasive imaging approach most commonly used worldwide to detect coronary ischemia,” Dr. Greenwood said. But he led an earlier study that showed that CMR, using a gadolinium-based tracing agent, works even better than MPS (in this study single photon emission CT) to predict a patient’s risk for major cardiac events. He said this superiority is probably because of the greater spatial resolution with CMR.

“The higher spatial resolution of CMR, about 5- to 10-fold greater that MPS, is less likely to produce false negative results,” he said in an interview. “We showed that CMR has higher diagnostic accuracy, is a better prognosticator, and is more cost effective” than MPS. Dr. Greenwood attributed the similar performance of CMR and MPS in CE-MARC2 to the study’s design, which led to fewer patients undergoing each of the two imaging methods and made CE-MARC2 underpowered to discern a difference in specificity. In his earlier study, which included 752 patients who underwent examination with both CMR and MPS, the negative predictive value of CMR was 91% compared with 79% with MPS.

CMR uses conventional MR machines, is now widely available, and is being widely used today as a first-line test in the United Kingdom and Europe, he added.

Dr. Greenwood believes that in his new study functional imaging outperformed the NICE guidelines because the pretest models used in the guidelines “tend to overestimate risk,” the factor that produces angiography overuse.

His report included two additional analyses that assessed the impact of CMR and MPS in the subgroup of patients with a high pretest probability for CAD, 61%-90%, and in the subgroup with a low pretest probability, 10%-29%. Among the patients with a high likelihood for CAD the two functional imaging methods cut the rate of unnecessary angiography by 95%, a statistically significant difference. Among those with a low likelihood functional imaging cut the rate 56%, a difference that did not reach statistical significance.

[email protected]

On Twitter @mitchelzoler

The long head of the biceps (LHB) tendon is a recognized source of shoulder pain. LHB tendon pathology is commonly associated with other shoulder conditions, such as superior labral tears, rotator cuff tears, or subacromial impingement, whereas isolated pathology, such as traumatic ruptures, tendinosis, or medial subluxation, is rare.¹ Treatment of LHB pathology ranges from conservative measures to surgical measures, including tenotomy or tenodesis.² LHB tenodesis offers the advantage of maintaining the length–tension relationship of the biceps muscle to prevent atrophy and avoid the Popeye deformity incurred from tenotomy alone. Tenodesis also prevents muscle cramping associated with contracted biceps muscle and better maintains elbow flexion and supination strength, which may be decreased with tenotomy.³ In addition, when a subpectoral biceps tenodesis technique is used, pain from LHB tendinopathy in the intertubercular groove may be reduced.⁴

Open subpectoral biceps tenodesis is a reproducible, efficient method for LHB tenodesis.^4,5 A variety of fixation devices has been used: bone tunnels,⁶ keyhole fixation,⁷ suture anchors,^6-9 and interference screws.^6-8,10,11 More recently, a bicortical button has been used for LHB tendon tenodesis.¹² Biomechanical studies have shown that load to failure is comparable for bicortical button fixation and interference screw fixation.^13,14 In other models of tendon repair, the bicortical button has strength and stability comparable to those of interference screw fixation and enables earlier rehabilitation.^15-17 However, there is concern that bicortical button fixation may result in axillary nerve (AN) or posterior circumflex humeral artery (PCHA) compromise because of the proximity of these neurovascular structures to the bicortical button.^13,18-21

We conducted a study to functionally and sonographically assess the outcomes of patients who underwent open subpectoral biceps tenodesis with a bicortical button. Functional outcomes were assessed with patient-reported outcomes and physician-reported outcomes. Sonographic studies were used to evaluate the integrity of the tenodesis and determine the proximity of the button to the AN and the PCHA along the posterior proximal humerus.

Methods

After obtaining Institutional Review Board approval for this study, we retrospectively identified 28 consecutive patients who had proximal biceps tenodesis performed by a single surgeon (Dr. K.E. Swanson) using a mini-open subpectoral biceps tenodesis technique with a bicortical button between March 2011 and January 2013. All 28 patients were asked to participate in the study. Twenty-four (86%) agreed to complete 2 surgical outcome surveys, and 18 (64%) completed a 3-part clinical examination at minimum 12-month follow-up.

One of the surveys was Quick Disabilities of the Arm, Shoulder, and Hand (QuickDASH), a validated comprehensive disability survey that scores upper extremity functionality on a scale ranging from 0 (none) to 100 (extreme difficulty).^22,23 The other survey scored pain on a scale ranging from 0 (none) to 100 (worst pain).

The clinical examination was completed during a single visit by an orthopedic surgeon (Dr. Meadows or Dr. Diesselhorst) different from the primary surgeon (Dr. K.E. Swanson) and by a clinician-sonologist (Dr. Finnoff). The examination’s 3 parts were physical examination of arm, biceps supination strength test, and ultrasonographic evaluation.

Physical Examination of Arm. Physical examination included palpation of bicipital groove, range of motion (ROM) of shoulder and elbow, and clinical deformity of biceps. Patients were questioned regarding symptoms of AN damage, including sensory and motor findings. Bicipital groove tenderness was assessed with a visual analog scale rating pain 0 to 10. ROM was measured in degrees and was presented as a percentage of full elbow ROM (150°) and full shoulder ROM (180°).

Biceps Supination Strength Test. Biceps supination strength was tested with a baseline hydraulic wrist dynamometer with door handle attachment. Patients were seated with the elbow bent 90° and the forearm in a neutral position. In a series of 3 trials, the patient maintained grip of the dynamometer doorknob while supinating the forearm. The tenodesed (operated) arm and contralateral unaffected (nonoperated) arm were tested in random order and recorded in pounds.

Ultrasonographic Evaluation. Ultrasonography was used to evaluate the tenodesis site. In each case, the biceps tendon was assessed to determine the location of the bicortical button in relation to the AN/PCHA neurovascular bundle. Whereas nerves are difficult to visualize with ultrasonography, arteries are readily seen. Dr. Finnoff used a CX50 ultrasound machine (Philips Medical Systems) with either a 12-3 MHz linear array or a 5-1 MHz curvilinear array transducer to measure the shortest distance from the PCHA to the button.

Each patient was placed in a lateral decubitus or prone position, and the skin of the upper arm was exposed. Tendon integrity was deemed either intact (continuity between biceps tendon and cortical button) or disrupted (lack of continuity between tendon and cortical button). The transducer was then placed in an anatomical sagittal plane over the posterior aspect of the proximal humerus. Power Doppler and cephalad and caudad transducer glides were used to identify the location of the PCHA. The transducer was then glided laterally and anteriorly around the humerus, following the course of the PCHA, until the cortical button was located. The narrowest interval between the PCHA and the cortical button was measured using the ultrasound machine’s software. A still image of each measurement was saved.

Surgical Technique

Biceps tenodesis indications included high-demand heavy laborers, athletes, and patients who preferred the cosmetic results of tenodesis over tenotomy. Most patients had acute symptomatic tears of the superior labrum with instability of the biceps anchor complex. Others had fraying and tenosynovitis of the LHB tendon. Any associated pathology was addressed during the same surgical period.

The surgical technique used was similar to that described by Snir and colleagues.¹² Each patient was placed in the lateral decubitus position. Once pathology confirmed biceps tenodesis, the biceps tendon was tenotomized at the base of the superior labrum. A 3-cm incision was made along the axillary fold centered over the inferior border of the pectoralis major tendon. Blunt dissection was performed to define the inferior border of the pectoralis major tendon and to palpate the underlying biceps tendon as it exited the intertubercular groove. The LHB tendon was removed and prepared with No. 2 Fiberwire (Arthrex) in Krackow fashion starting 2 cm proximal to the musculotendinous junction. The excess tendon was excised.

A 3.2-mm guide wire was centered along the most distal aspect of the biceps groove and then drilled through the anterior cortex and just through the posterior cortex. A cannulated reamer, selected on the basis of the biceps tendon diameter (typically, 5-7 mm), was then drilled over the guide wire through the anterior cortex only. The Food and Drug Administration–approved cortical button (BicepsButton; Arthrex) was then loaded by passing the tendon suture ends through each side of the button in alternating fashion, thus allowing the button to slide along the sutures.

The button was loaded onto the BicepsButton deployment device and inserted through the drilled tunnel of the anterior cortex and just through the posterior cortex. The deployment device was then removed, and 1 suture end was pulled to allow the button to engage the posterior humeral cortex. Pulling on both sutures allowed the biceps tendon to slide through the anterior cortex hole of the humerus until the tendon reached the posterior humeral cortex. Tension was verified, and the sutures were tied over the tendon. The wound was then irrigated and closed.

Rehabilitation Program

Patients completed a standard rehabilitation protocol for biceps tenodesis²⁴ along with rehabilitation protocols for any additional procedures performed. In phase 1 (weeks 0-2), they focused on gradual restoration of passive ROM and remained in a sling. In phase 2 (weeks 2-6), they focused on gradual restoration of active ROM, and by week 3 were weaned out of the sling. In phase 3 (weeks 6-8), they continued ROM and strengthening exercises to normalize strength, endurance, and neuromuscular control. In phase 4 (weeks 8-12), they focused on advanced strengthening exercises and return to activities.

Statistical Analysis

Descriptive statistics included means, medians, and SDs. Comparisons between operated and nonoperated arms and between dominant and nondominant arms were performed by a statistician using paired t tests with P = .05. Confidence intervals were calculated for operated and nonoperated arms and for dominant and nondominant arms by using the differences between them.

Results

Functional Outcomes

Surgical outcome scores and pain scores were obtained from 24 patients (86%) at minimum 12-month follow-up. Mean (SD) DASH score was 15.15 (17.6; median, 9), and mean (median) pain score was 12.61 (7).

Eighteen patients (64%) completed the clinical examination: 16 men (88.9%) and 2 women (11.1%). Mean age was 48.3 years (age range, 33-59 years). Of these 18 patients, 9 (50%) had surgery on the dominant arm, and the other 9 had surgery on the nondominant arm. All patients were right-hand–dominant. In 3 patients, biceps tenodesis was performed with only minimal arthroscopic débridement (20%); in the other 15, biceps tenodesis was performed concomitantly with 1 or more additional arthroscopic procedures: acromioplasty (73%), rotator cuff repair (47%), distal clavicle resection (33%), subacromial bursectomy (13%), microfracture of glenoid (13%), and posterior labral repair (7%).

The clinical examination was performed a mean of 15.2 months (range, 12-26 months) after surgery. Physical examination findings are listed in Table 1.

Forearm supination strength, averaged from 3 trials on each arm, was significantly (P = .01) greater in the nonoperated arm than in the operated arm (Table 2, Figure 1). A 95% confidence interval for the mean (SD) difference in strength was 9.35 (7.76) pounds, meaning that on average, the nonoperated arm will be 1.59 to 17.11 pounds stronger than the operated arm. In addition, strength of the dominant arm was greater than that of the nondominant arm (P = .05) regardless of which arm underwent surgery (Table 2, Figure 1). However, the mean (SD) difference in strength was 6.94 (8.39) pounds, indicating the observed difference was not statistically significant.

Sonographic Evaluation

According to the sonographic evaluations, the tenodesis was intact in all 18 patients (Figure 2). Estimated mean (SD) distance from button to PCHA was 18.17 (9.0) mm (median, 16.1 mm; range, 9.4-48 mm) (Figure 2, Figure 3). No patient indicated any symptoms of AN damage.

Discussion

There are few studies of functional outcomes of biceps tenodesis. Pain is a common measure of patient satisfaction. Mazzocca and colleagues²⁵ reported a mean follow-up pain score of 1.1 (range, 0.5-1.9) out of 10 for a group of 41 patients who had subpectoral tenodesis with an interference screw. Millett and colleagues²⁶ reported a mean postoperative pain score of 2.5 out of 10 for patients who had subpectoral interference screw fixation. Our patients reported a mean pain score of 12.6 out of 100 after minimum 12-month follow-up. We also assessed for pain in the intertubercular groove during palpation. Although some studies have shown that groove pain was eliminated by subpectoral biceps tenodesis,⁵ 3 patients in our study had pain on groove palpation. The cause of this residual pain is unclear, but some studies have suggested a chronic degenerative pathologic process that occurs while the tendon is within the biceps groove.²⁷ Removing the tendon from the groove may not remove the underlying cause of pain.

Our patients’ mean DASH score was 15.15 (within the excellent range). Normative mean (SD) DASH score for the general population is 10.1 (14.68).²⁸

Functional strength of forearm supination, shoulder ROM, and elbow ROM are objective measures of patient performance after fixation. On Cybex testing, Phillips and colleagues²⁹ found no difference in forearm supination strength or elbow flexion (compared with contralateral arm) after biceps tenodesis or conservative treatment for proximal biceps ruptures. Shank and colleagues³⁰ compared elbow flexion and supination strength of the affected and unaffected arms after suture anchor subpectoral biceps tenodesis. There was no significant difference in Cybex results, but there was a 14% to 15% loss of average strength in the tenodesed versus nonsurgical arm. In the present study, we found a significant difference in forearm supination strength between the operated and nonoperated arms, but with only a 7% loss of average strength in the operated arms. The difference in strength ranged from 1.59 to 17.11 pounds, which may not be clinically significant, as supination strength ranged from 60 to 270 pounds.

Of the 18 patients in this study, 9 had surgery on the dominant arm, and the other 9 had surgery on the nondominant arm. Examining the effect of arm dominance on results revealed that patients with surgery on the nondominant arm tended to have substantially reduced supination strength in that arm vs the dominant arm. There was an 11% loss of average strength for nondominant vs dominant arms that had surgery. Examining nondominant arms only revealed a 13% loss of strength for operated vs nonoperated arms. There was no difference in forearm supination strengths between nonoperated arms (dominant vs nondominant) or between dominant arms (operated vs nonoperated). This suggests that, though hand dominance may not play a significant role in control patients’ forearm supination strength,³⁰ it may have a substantial effect on surgical patients’ ability to regain strength when the nondominant arm is the surgical arm.
One objective of this study was to measure the distance between the biceps cortical button on the posterior humeral cortex and the AN/PCHA neurovascular bundle. The AN bundles with the PCHA posterior to the humeral neck.^31-33 As the AN travels with the PCHA, and the PCHA has been reliably identified with Doppler ultrasonography,^34-36 the PCHA was used as a marker for the AN in this study. Our bicortical button technique places the button on the posterior aspect of the humerus, making AN and PCHA the nearest at-risk neurovascular structures. None of our patients had symptoms of AN damage. However, 2 patients indicated pain in the posterior aspect of the humerus during deltoid activation. Distance from the neurovascular structures to the button was 48 mm in one patient and 13.6 mm in the other. DASH scores were 43 and 27, respectively. Both patients’ 1-year pain score was 30. The first patient underwent arthroscopic acromioplasty, distal clavicle resection, and microfracture of the glenoid surface in addition to the subpectoral biceps tenodesis; the second underwent subacromial decompression and distal clavicle resection in addition to the subpectoral biceps tenodesis. Whether the associated pathology contributed to their persistent pain is unknown. However, given the distance from AN/PCHA to button, it is unlikely that their pain was a result of neurovascular compromise from the procedure.

Advantages of the cortical button include the ability to drill a smaller hole in the humerus for fixation, compared with the hole drilled for an interference screw. Despite the biomechanical strength of the screw, large (8 mm) cortical violations have been associated with increased fracture risk of the proximal humerus.^37,38 The tendon may experience less trauma than that caused by being twisted against an interference screw, the most common location of failure of which is the tendon–screw interface.³⁹ In addition, tendon healing may be improved through circumferential healing in the cortical button tunnel.

A concern of using a bicortical button for fixation is drilling through the posterior cortex, because of the proximity of the posterior neurovascular structures. In a case in which the posterior cord was injured, Rhee and colleagues⁴⁰ used a suture pullout technique whereby a Beath pin was passed out of the posterior humerus and soft tissues to then hold tension on the biceps tendon during the tenodesis. The radial nerve potentially could have been injured by pin overpenetration or by becoming wrapped up in the soft tissues as the pin was spinning through them. In our technique, the posterior humeral cortex is drilled cautiously to avoid overpenetration and possibly getting the posterior soft tissues wrapped up in the guide pin. No AN injuries have been reported with this technique. Mean distance from AN to posterior cortical button in this study was 18.17 mm. In 2 cadaver studies of bicortical drilling for subpectoral biceps tenodesis, the ANs were 25.1 mm and 36.7 mm from the posterior drill hole.^41,21

Limitations of this study included its design (case series) and limited number of follow-up patients. Of the 28 consecutive patients identified for the study, 10 did not undergo the clinical examination, as they either lived more than 3 hours away (8 patients) or could not be contacted (2 patients). Another study limitation was the inability to directly image ANs with ultrasound. Therefore, measurements of the distance from the PCHA to the button were used to estimate the distance from the AN/PCHA neurovascular bundle to the button.

In this study, functional outcomes were excellent, and there were no tenodesis failures or neurovascular complications. These preliminary findings indicate that subpectoral biceps tenodesis with a bicortical button is a viable treatment option for patients with the appropriate indications for this procedure.

The long head of the biceps (LHB) tendon is a recognized source of shoulder pain. LHB tendon pathology is commonly associated with other shoulder conditions, such as superior labral tears, rotator cuff tears, or subacromial impingement, whereas isolated pathology, such as traumatic ruptures, tendinosis, or medial subluxation, is rare.¹ Treatment of LHB pathology ranges from conservative measures to surgical measures, including tenotomy or tenodesis.² LHB tenodesis offers the advantage of maintaining the length–tension relationship of the biceps muscle to prevent atrophy and avoid the Popeye deformity incurred from tenotomy alone. Tenodesis also prevents muscle cramping associated with contracted biceps muscle and better maintains elbow flexion and supination strength, which may be decreased with tenotomy.³ In addition, when a subpectoral biceps tenodesis technique is used, pain from LHB tendinopathy in the intertubercular groove may be reduced.⁴

Open subpectoral biceps tenodesis is a reproducible, efficient method for LHB tenodesis.^4,5 A variety of fixation devices has been used: bone tunnels,⁶ keyhole fixation,⁷ suture anchors,^6-9 and interference screws.^6-8,10,11 More recently, a bicortical button has been used for LHB tendon tenodesis.¹² Biomechanical studies have shown that load to failure is comparable for bicortical button fixation and interference screw fixation.^13,14 In other models of tendon repair, the bicortical button has strength and stability comparable to those of interference screw fixation and enables earlier rehabilitation.^15-17 However, there is concern that bicortical button fixation may result in axillary nerve (AN) or posterior circumflex humeral artery (PCHA) compromise because of the proximity of these neurovascular structures to the bicortical button.^13,18-21

We conducted a study to functionally and sonographically assess the outcomes of patients who underwent open subpectoral biceps tenodesis with a bicortical button. Functional outcomes were assessed with patient-reported outcomes and physician-reported outcomes. Sonographic studies were used to evaluate the integrity of the tenodesis and determine the proximity of the button to the AN and the PCHA along the posterior proximal humerus.

Methods

After obtaining Institutional Review Board approval for this study, we retrospectively identified 28 consecutive patients who had proximal biceps tenodesis performed by a single surgeon (Dr. K.E. Swanson) using a mini-open subpectoral biceps tenodesis technique with a bicortical button between March 2011 and January 2013. All 28 patients were asked to participate in the study. Twenty-four (86%) agreed to complete 2 surgical outcome surveys, and 18 (64%) completed a 3-part clinical examination at minimum 12-month follow-up.

One of the surveys was Quick Disabilities of the Arm, Shoulder, and Hand (QuickDASH), a validated comprehensive disability survey that scores upper extremity functionality on a scale ranging from 0 (none) to 100 (extreme difficulty).^22,23 The other survey scored pain on a scale ranging from 0 (none) to 100 (worst pain).

The clinical examination was completed during a single visit by an orthopedic surgeon (Dr. Meadows or Dr. Diesselhorst) different from the primary surgeon (Dr. K.E. Swanson) and by a clinician-sonologist (Dr. Finnoff). The examination’s 3 parts were physical examination of arm, biceps supination strength test, and ultrasonographic evaluation.

Physical Examination of Arm. Physical examination included palpation of bicipital groove, range of motion (ROM) of shoulder and elbow, and clinical deformity of biceps. Patients were questioned regarding symptoms of AN damage, including sensory and motor findings. Bicipital groove tenderness was assessed with a visual analog scale rating pain 0 to 10. ROM was measured in degrees and was presented as a percentage of full elbow ROM (150°) and full shoulder ROM (180°).

Biceps Supination Strength Test. Biceps supination strength was tested with a baseline hydraulic wrist dynamometer with door handle attachment. Patients were seated with the elbow bent 90° and the forearm in a neutral position. In a series of 3 trials, the patient maintained grip of the dynamometer doorknob while supinating the forearm. The tenodesed (operated) arm and contralateral unaffected (nonoperated) arm were tested in random order and recorded in pounds.

Ultrasonographic Evaluation. Ultrasonography was used to evaluate the tenodesis site. In each case, the biceps tendon was assessed to determine the location of the bicortical button in relation to the AN/PCHA neurovascular bundle. Whereas nerves are difficult to visualize with ultrasonography, arteries are readily seen. Dr. Finnoff used a CX50 ultrasound machine (Philips Medical Systems) with either a 12-3 MHz linear array or a 5-1 MHz curvilinear array transducer to measure the shortest distance from the PCHA to the button.

Each patient was placed in a lateral decubitus or prone position, and the skin of the upper arm was exposed. Tendon integrity was deemed either intact (continuity between biceps tendon and cortical button) or disrupted (lack of continuity between tendon and cortical button). The transducer was then placed in an anatomical sagittal plane over the posterior aspect of the proximal humerus. Power Doppler and cephalad and caudad transducer glides were used to identify the location of the PCHA. The transducer was then glided laterally and anteriorly around the humerus, following the course of the PCHA, until the cortical button was located. The narrowest interval between the PCHA and the cortical button was measured using the ultrasound machine’s software. A still image of each measurement was saved.

Surgical Technique

Biceps tenodesis indications included high-demand heavy laborers, athletes, and patients who preferred the cosmetic results of tenodesis over tenotomy. Most patients had acute symptomatic tears of the superior labrum with instability of the biceps anchor complex. Others had fraying and tenosynovitis of the LHB tendon. Any associated pathology was addressed during the same surgical period.

The surgical technique used was similar to that described by Snir and colleagues.¹² Each patient was placed in the lateral decubitus position. Once pathology confirmed biceps tenodesis, the biceps tendon was tenotomized at the base of the superior labrum. A 3-cm incision was made along the axillary fold centered over the inferior border of the pectoralis major tendon. Blunt dissection was performed to define the inferior border of the pectoralis major tendon and to palpate the underlying biceps tendon as it exited the intertubercular groove. The LHB tendon was removed and prepared with No. 2 Fiberwire (Arthrex) in Krackow fashion starting 2 cm proximal to the musculotendinous junction. The excess tendon was excised.

A 3.2-mm guide wire was centered along the most distal aspect of the biceps groove and then drilled through the anterior cortex and just through the posterior cortex. A cannulated reamer, selected on the basis of the biceps tendon diameter (typically, 5-7 mm), was then drilled over the guide wire through the anterior cortex only. The Food and Drug Administration–approved cortical button (BicepsButton; Arthrex) was then loaded by passing the tendon suture ends through each side of the button in alternating fashion, thus allowing the button to slide along the sutures.

The button was loaded onto the BicepsButton deployment device and inserted through the drilled tunnel of the anterior cortex and just through the posterior cortex. The deployment device was then removed, and 1 suture end was pulled to allow the button to engage the posterior humeral cortex. Pulling on both sutures allowed the biceps tendon to slide through the anterior cortex hole of the humerus until the tendon reached the posterior humeral cortex. Tension was verified, and the sutures were tied over the tendon. The wound was then irrigated and closed.

Rehabilitation Program

Patients completed a standard rehabilitation protocol for biceps tenodesis²⁴ along with rehabilitation protocols for any additional procedures performed. In phase 1 (weeks 0-2), they focused on gradual restoration of passive ROM and remained in a sling. In phase 2 (weeks 2-6), they focused on gradual restoration of active ROM, and by week 3 were weaned out of the sling. In phase 3 (weeks 6-8), they continued ROM and strengthening exercises to normalize strength, endurance, and neuromuscular control. In phase 4 (weeks 8-12), they focused on advanced strengthening exercises and return to activities.

Statistical Analysis

Descriptive statistics included means, medians, and SDs. Comparisons between operated and nonoperated arms and between dominant and nondominant arms were performed by a statistician using paired t tests with P = .05. Confidence intervals were calculated for operated and nonoperated arms and for dominant and nondominant arms by using the differences between them.

Results

Functional Outcomes

Surgical outcome scores and pain scores were obtained from 24 patients (86%) at minimum 12-month follow-up. Mean (SD) DASH score was 15.15 (17.6; median, 9), and mean (median) pain score was 12.61 (7).

Eighteen patients (64%) completed the clinical examination: 16 men (88.9%) and 2 women (11.1%). Mean age was 48.3 years (age range, 33-59 years). Of these 18 patients, 9 (50%) had surgery on the dominant arm, and the other 9 had surgery on the nondominant arm. All patients were right-hand–dominant. In 3 patients, biceps tenodesis was performed with only minimal arthroscopic débridement (20%); in the other 15, biceps tenodesis was performed concomitantly with 1 or more additional arthroscopic procedures: acromioplasty (73%), rotator cuff repair (47%), distal clavicle resection (33%), subacromial bursectomy (13%), microfracture of glenoid (13%), and posterior labral repair (7%).

The clinical examination was performed a mean of 15.2 months (range, 12-26 months) after surgery. Physical examination findings are listed in Table 1.

Forearm supination strength, averaged from 3 trials on each arm, was significantly (P = .01) greater in the nonoperated arm than in the operated arm (Table 2, Figure 1). A 95% confidence interval for the mean (SD) difference in strength was 9.35 (7.76) pounds, meaning that on average, the nonoperated arm will be 1.59 to 17.11 pounds stronger than the operated arm. In addition, strength of the dominant arm was greater than that of the nondominant arm (P = .05) regardless of which arm underwent surgery (Table 2, Figure 1). However, the mean (SD) difference in strength was 6.94 (8.39) pounds, indicating the observed difference was not statistically significant.

Sonographic Evaluation

According to the sonographic evaluations, the tenodesis was intact in all 18 patients (Figure 2). Estimated mean (SD) distance from button to PCHA was 18.17 (9.0) mm (median, 16.1 mm; range, 9.4-48 mm) (Figure 2, Figure 3). No patient indicated any symptoms of AN damage.

Discussion

There are few studies of functional outcomes of biceps tenodesis. Pain is a common measure of patient satisfaction. Mazzocca and colleagues²⁵ reported a mean follow-up pain score of 1.1 (range, 0.5-1.9) out of 10 for a group of 41 patients who had subpectoral tenodesis with an interference screw. Millett and colleagues²⁶ reported a mean postoperative pain score of 2.5 out of 10 for patients who had subpectoral interference screw fixation. Our patients reported a mean pain score of 12.6 out of 100 after minimum 12-month follow-up. We also assessed for pain in the intertubercular groove during palpation. Although some studies have shown that groove pain was eliminated by subpectoral biceps tenodesis,⁵ 3 patients in our study had pain on groove palpation. The cause of this residual pain is unclear, but some studies have suggested a chronic degenerative pathologic process that occurs while the tendon is within the biceps groove.²⁷ Removing the tendon from the groove may not remove the underlying cause of pain.

Our patients’ mean DASH score was 15.15 (within the excellent range). Normative mean (SD) DASH score for the general population is 10.1 (14.68).²⁸

Functional strength of forearm supination, shoulder ROM, and elbow ROM are objective measures of patient performance after fixation. On Cybex testing, Phillips and colleagues²⁹ found no difference in forearm supination strength or elbow flexion (compared with contralateral arm) after biceps tenodesis or conservative treatment for proximal biceps ruptures. Shank and colleagues³⁰ compared elbow flexion and supination strength of the affected and unaffected arms after suture anchor subpectoral biceps tenodesis. There was no significant difference in Cybex results, but there was a 14% to 15% loss of average strength in the tenodesed versus nonsurgical arm. In the present study, we found a significant difference in forearm supination strength between the operated and nonoperated arms, but with only a 7% loss of average strength in the operated arms. The difference in strength ranged from 1.59 to 17.11 pounds, which may not be clinically significant, as supination strength ranged from 60 to 270 pounds.

Of the 18 patients in this study, 9 had surgery on the dominant arm, and the other 9 had surgery on the nondominant arm. Examining the effect of arm dominance on results revealed that patients with surgery on the nondominant arm tended to have substantially reduced supination strength in that arm vs the dominant arm. There was an 11% loss of average strength for nondominant vs dominant arms that had surgery. Examining nondominant arms only revealed a 13% loss of strength for operated vs nonoperated arms. There was no difference in forearm supination strengths between nonoperated arms (dominant vs nondominant) or between dominant arms (operated vs nonoperated). This suggests that, though hand dominance may not play a significant role in control patients’ forearm supination strength,³⁰ it may have a substantial effect on surgical patients’ ability to regain strength when the nondominant arm is the surgical arm.
One objective of this study was to measure the distance between the biceps cortical button on the posterior humeral cortex and the AN/PCHA neurovascular bundle. The AN bundles with the PCHA posterior to the humeral neck.^31-33 As the AN travels with the PCHA, and the PCHA has been reliably identified with Doppler ultrasonography,^34-36 the PCHA was used as a marker for the AN in this study. Our bicortical button technique places the button on the posterior aspect of the humerus, making AN and PCHA the nearest at-risk neurovascular structures. None of our patients had symptoms of AN damage. However, 2 patients indicated pain in the posterior aspect of the humerus during deltoid activation. Distance from the neurovascular structures to the button was 48 mm in one patient and 13.6 mm in the other. DASH scores were 43 and 27, respectively. Both patients’ 1-year pain score was 30. The first patient underwent arthroscopic acromioplasty, distal clavicle resection, and microfracture of the glenoid surface in addition to the subpectoral biceps tenodesis; the second underwent subacromial decompression and distal clavicle resection in addition to the subpectoral biceps tenodesis. Whether the associated pathology contributed to their persistent pain is unknown. However, given the distance from AN/PCHA to button, it is unlikely that their pain was a result of neurovascular compromise from the procedure.

Advantages of the cortical button include the ability to drill a smaller hole in the humerus for fixation, compared with the hole drilled for an interference screw. Despite the biomechanical strength of the screw, large (8 mm) cortical violations have been associated with increased fracture risk of the proximal humerus.^37,38 The tendon may experience less trauma than that caused by being twisted against an interference screw, the most common location of failure of which is the tendon–screw interface.³⁹ In addition, tendon healing may be improved through circumferential healing in the cortical button tunnel.

A concern of using a bicortical button for fixation is drilling through the posterior cortex, because of the proximity of the posterior neurovascular structures. In a case in which the posterior cord was injured, Rhee and colleagues⁴⁰ used a suture pullout technique whereby a Beath pin was passed out of the posterior humerus and soft tissues to then hold tension on the biceps tendon during the tenodesis. The radial nerve potentially could have been injured by pin overpenetration or by becoming wrapped up in the soft tissues as the pin was spinning through them. In our technique, the posterior humeral cortex is drilled cautiously to avoid overpenetration and possibly getting the posterior soft tissues wrapped up in the guide pin. No AN injuries have been reported with this technique. Mean distance from AN to posterior cortical button in this study was 18.17 mm. In 2 cadaver studies of bicortical drilling for subpectoral biceps tenodesis, the ANs were 25.1 mm and 36.7 mm from the posterior drill hole.^41,21

Limitations of this study included its design (case series) and limited number of follow-up patients. Of the 28 consecutive patients identified for the study, 10 did not undergo the clinical examination, as they either lived more than 3 hours away (8 patients) or could not be contacted (2 patients). Another study limitation was the inability to directly image ANs with ultrasound. Therefore, measurements of the distance from the PCHA to the button were used to estimate the distance from the AN/PCHA neurovascular bundle to the button.

In this study, functional outcomes were excellent, and there were no tenodesis failures or neurovascular complications. These preliminary findings indicate that subpectoral biceps tenodesis with a bicortical button is a viable treatment option for patients with the appropriate indications for this procedure.

The long head of the biceps (LHB) tendon is a recognized source of shoulder pain. LHB tendon pathology is commonly associated with other shoulder conditions, such as superior labral tears, rotator cuff tears, or subacromial impingement, whereas isolated pathology, such as traumatic ruptures, tendinosis, or medial subluxation, is rare.¹ Treatment of LHB pathology ranges from conservative measures to surgical measures, including tenotomy or tenodesis.² LHB tenodesis offers the advantage of maintaining the length–tension relationship of the biceps muscle to prevent atrophy and avoid the Popeye deformity incurred from tenotomy alone. Tenodesis also prevents muscle cramping associated with contracted biceps muscle and better maintains elbow flexion and supination strength, which may be decreased with tenotomy.³ In addition, when a subpectoral biceps tenodesis technique is used, pain from LHB tendinopathy in the intertubercular groove may be reduced.⁴

Open subpectoral biceps tenodesis is a reproducible, efficient method for LHB tenodesis.^4,5 A variety of fixation devices has been used: bone tunnels,⁶ keyhole fixation,⁷ suture anchors,^6-9 and interference screws.^6-8,10,11 More recently, a bicortical button has been used for LHB tendon tenodesis.¹² Biomechanical studies have shown that load to failure is comparable for bicortical button fixation and interference screw fixation.^13,14 In other models of tendon repair, the bicortical button has strength and stability comparable to those of interference screw fixation and enables earlier rehabilitation.^15-17 However, there is concern that bicortical button fixation may result in axillary nerve (AN) or posterior circumflex humeral artery (PCHA) compromise because of the proximity of these neurovascular structures to the bicortical button.^13,18-21

We conducted a study to functionally and sonographically assess the outcomes of patients who underwent open subpectoral biceps tenodesis with a bicortical button. Functional outcomes were assessed with patient-reported outcomes and physician-reported outcomes. Sonographic studies were used to evaluate the integrity of the tenodesis and determine the proximity of the button to the AN and the PCHA along the posterior proximal humerus.

Methods

After obtaining Institutional Review Board approval for this study, we retrospectively identified 28 consecutive patients who had proximal biceps tenodesis performed by a single surgeon (Dr. K.E. Swanson) using a mini-open subpectoral biceps tenodesis technique with a bicortical button between March 2011 and January 2013. All 28 patients were asked to participate in the study. Twenty-four (86%) agreed to complete 2 surgical outcome surveys, and 18 (64%) completed a 3-part clinical examination at minimum 12-month follow-up.

One of the surveys was Quick Disabilities of the Arm, Shoulder, and Hand (QuickDASH), a validated comprehensive disability survey that scores upper extremity functionality on a scale ranging from 0 (none) to 100 (extreme difficulty).^22,23 The other survey scored pain on a scale ranging from 0 (none) to 100 (worst pain).

The clinical examination was completed during a single visit by an orthopedic surgeon (Dr. Meadows or Dr. Diesselhorst) different from the primary surgeon (Dr. K.E. Swanson) and by a clinician-sonologist (Dr. Finnoff). The examination’s 3 parts were physical examination of arm, biceps supination strength test, and ultrasonographic evaluation.

Physical Examination of Arm. Physical examination included palpation of bicipital groove, range of motion (ROM) of shoulder and elbow, and clinical deformity of biceps. Patients were questioned regarding symptoms of AN damage, including sensory and motor findings. Bicipital groove tenderness was assessed with a visual analog scale rating pain 0 to 10. ROM was measured in degrees and was presented as a percentage of full elbow ROM (150°) and full shoulder ROM (180°).

Biceps Supination Strength Test. Biceps supination strength was tested with a baseline hydraulic wrist dynamometer with door handle attachment. Patients were seated with the elbow bent 90° and the forearm in a neutral position. In a series of 3 trials, the patient maintained grip of the dynamometer doorknob while supinating the forearm. The tenodesed (operated) arm and contralateral unaffected (nonoperated) arm were tested in random order and recorded in pounds.

Ultrasonographic Evaluation. Ultrasonography was used to evaluate the tenodesis site. In each case, the biceps tendon was assessed to determine the location of the bicortical button in relation to the AN/PCHA neurovascular bundle. Whereas nerves are difficult to visualize with ultrasonography, arteries are readily seen. Dr. Finnoff used a CX50 ultrasound machine (Philips Medical Systems) with either a 12-3 MHz linear array or a 5-1 MHz curvilinear array transducer to measure the shortest distance from the PCHA to the button.

Each patient was placed in a lateral decubitus or prone position, and the skin of the upper arm was exposed. Tendon integrity was deemed either intact (continuity between biceps tendon and cortical button) or disrupted (lack of continuity between tendon and cortical button). The transducer was then placed in an anatomical sagittal plane over the posterior aspect of the proximal humerus. Power Doppler and cephalad and caudad transducer glides were used to identify the location of the PCHA. The transducer was then glided laterally and anteriorly around the humerus, following the course of the PCHA, until the cortical button was located. The narrowest interval between the PCHA and the cortical button was measured using the ultrasound machine’s software. A still image of each measurement was saved.

Surgical Technique

Biceps tenodesis indications included high-demand heavy laborers, athletes, and patients who preferred the cosmetic results of tenodesis over tenotomy. Most patients had acute symptomatic tears of the superior labrum with instability of the biceps anchor complex. Others had fraying and tenosynovitis of the LHB tendon. Any associated pathology was addressed during the same surgical period.

The surgical technique used was similar to that described by Snir and colleagues.¹² Each patient was placed in the lateral decubitus position. Once pathology confirmed biceps tenodesis, the biceps tendon was tenotomized at the base of the superior labrum. A 3-cm incision was made along the axillary fold centered over the inferior border of the pectoralis major tendon. Blunt dissection was performed to define the inferior border of the pectoralis major tendon and to palpate the underlying biceps tendon as it exited the intertubercular groove. The LHB tendon was removed and prepared with No. 2 Fiberwire (Arthrex) in Krackow fashion starting 2 cm proximal to the musculotendinous junction. The excess tendon was excised.

A 3.2-mm guide wire was centered along the most distal aspect of the biceps groove and then drilled through the anterior cortex and just through the posterior cortex. A cannulated reamer, selected on the basis of the biceps tendon diameter (typically, 5-7 mm), was then drilled over the guide wire through the anterior cortex only. The Food and Drug Administration–approved cortical button (BicepsButton; Arthrex) was then loaded by passing the tendon suture ends through each side of the button in alternating fashion, thus allowing the button to slide along the sutures.

The button was loaded onto the BicepsButton deployment device and inserted through the drilled tunnel of the anterior cortex and just through the posterior cortex. The deployment device was then removed, and 1 suture end was pulled to allow the button to engage the posterior humeral cortex. Pulling on both sutures allowed the biceps tendon to slide through the anterior cortex hole of the humerus until the tendon reached the posterior humeral cortex. Tension was verified, and the sutures were tied over the tendon. The wound was then irrigated and closed.

Rehabilitation Program

Patients completed a standard rehabilitation protocol for biceps tenodesis²⁴ along with rehabilitation protocols for any additional procedures performed. In phase 1 (weeks 0-2), they focused on gradual restoration of passive ROM and remained in a sling. In phase 2 (weeks 2-6), they focused on gradual restoration of active ROM, and by week 3 were weaned out of the sling. In phase 3 (weeks 6-8), they continued ROM and strengthening exercises to normalize strength, endurance, and neuromuscular control. In phase 4 (weeks 8-12), they focused on advanced strengthening exercises and return to activities.

Statistical Analysis

Descriptive statistics included means, medians, and SDs. Comparisons between operated and nonoperated arms and between dominant and nondominant arms were performed by a statistician using paired t tests with P = .05. Confidence intervals were calculated for operated and nonoperated arms and for dominant and nondominant arms by using the differences between them.

Results

Functional Outcomes

Surgical outcome scores and pain scores were obtained from 24 patients (86%) at minimum 12-month follow-up. Mean (SD) DASH score was 15.15 (17.6; median, 9), and mean (median) pain score was 12.61 (7).

Eighteen patients (64%) completed the clinical examination: 16 men (88.9%) and 2 women (11.1%). Mean age was 48.3 years (age range, 33-59 years). Of these 18 patients, 9 (50%) had surgery on the dominant arm, and the other 9 had surgery on the nondominant arm. All patients were right-hand–dominant. In 3 patients, biceps tenodesis was performed with only minimal arthroscopic débridement (20%); in the other 15, biceps tenodesis was performed concomitantly with 1 or more additional arthroscopic procedures: acromioplasty (73%), rotator cuff repair (47%), distal clavicle resection (33%), subacromial bursectomy (13%), microfracture of glenoid (13%), and posterior labral repair (7%).

The clinical examination was performed a mean of 15.2 months (range, 12-26 months) after surgery. Physical examination findings are listed in Table 1.

Forearm supination strength, averaged from 3 trials on each arm, was significantly (P = .01) greater in the nonoperated arm than in the operated arm (Table 2, Figure 1). A 95% confidence interval for the mean (SD) difference in strength was 9.35 (7.76) pounds, meaning that on average, the nonoperated arm will be 1.59 to 17.11 pounds stronger than the operated arm. In addition, strength of the dominant arm was greater than that of the nondominant arm (P = .05) regardless of which arm underwent surgery (Table 2, Figure 1). However, the mean (SD) difference in strength was 6.94 (8.39) pounds, indicating the observed difference was not statistically significant.

Sonographic Evaluation

According to the sonographic evaluations, the tenodesis was intact in all 18 patients (Figure 2). Estimated mean (SD) distance from button to PCHA was 18.17 (9.0) mm (median, 16.1 mm; range, 9.4-48 mm) (Figure 2, Figure 3). No patient indicated any symptoms of AN damage.

Discussion

There are few studies of functional outcomes of biceps tenodesis. Pain is a common measure of patient satisfaction. Mazzocca and colleagues²⁵ reported a mean follow-up pain score of 1.1 (range, 0.5-1.9) out of 10 for a group of 41 patients who had subpectoral tenodesis with an interference screw. Millett and colleagues²⁶ reported a mean postoperative pain score of 2.5 out of 10 for patients who had subpectoral interference screw fixation. Our patients reported a mean pain score of 12.6 out of 100 after minimum 12-month follow-up. We also assessed for pain in the intertubercular groove during palpation. Although some studies have shown that groove pain was eliminated by subpectoral biceps tenodesis,⁵ 3 patients in our study had pain on groove palpation. The cause of this residual pain is unclear, but some studies have suggested a chronic degenerative pathologic process that occurs while the tendon is within the biceps groove.²⁷ Removing the tendon from the groove may not remove the underlying cause of pain.

Our patients’ mean DASH score was 15.15 (within the excellent range). Normative mean (SD) DASH score for the general population is 10.1 (14.68).²⁸

Functional strength of forearm supination, shoulder ROM, and elbow ROM are objective measures of patient performance after fixation. On Cybex testing, Phillips and colleagues²⁹ found no difference in forearm supination strength or elbow flexion (compared with contralateral arm) after biceps tenodesis or conservative treatment for proximal biceps ruptures. Shank and colleagues³⁰ compared elbow flexion and supination strength of the affected and unaffected arms after suture anchor subpectoral biceps tenodesis. There was no significant difference in Cybex results, but there was a 14% to 15% loss of average strength in the tenodesed versus nonsurgical arm. In the present study, we found a significant difference in forearm supination strength between the operated and nonoperated arms, but with only a 7% loss of average strength in the operated arms. The difference in strength ranged from 1.59 to 17.11 pounds, which may not be clinically significant, as supination strength ranged from 60 to 270 pounds.

Of the 18 patients in this study, 9 had surgery on the dominant arm, and the other 9 had surgery on the nondominant arm. Examining the effect of arm dominance on results revealed that patients with surgery on the nondominant arm tended to have substantially reduced supination strength in that arm vs the dominant arm. There was an 11% loss of average strength for nondominant vs dominant arms that had surgery. Examining nondominant arms only revealed a 13% loss of strength for operated vs nonoperated arms. There was no difference in forearm supination strengths between nonoperated arms (dominant vs nondominant) or between dominant arms (operated vs nonoperated). This suggests that, though hand dominance may not play a significant role in control patients’ forearm supination strength,³⁰ it may have a substantial effect on surgical patients’ ability to regain strength when the nondominant arm is the surgical arm.
One objective of this study was to measure the distance between the biceps cortical button on the posterior humeral cortex and the AN/PCHA neurovascular bundle. The AN bundles with the PCHA posterior to the humeral neck.^31-33 As the AN travels with the PCHA, and the PCHA has been reliably identified with Doppler ultrasonography,^34-36 the PCHA was used as a marker for the AN in this study. Our bicortical button technique places the button on the posterior aspect of the humerus, making AN and PCHA the nearest at-risk neurovascular structures. None of our patients had symptoms of AN damage. However, 2 patients indicated pain in the posterior aspect of the humerus during deltoid activation. Distance from the neurovascular structures to the button was 48 mm in one patient and 13.6 mm in the other. DASH scores were 43 and 27, respectively. Both patients’ 1-year pain score was 30. The first patient underwent arthroscopic acromioplasty, distal clavicle resection, and microfracture of the glenoid surface in addition to the subpectoral biceps tenodesis; the second underwent subacromial decompression and distal clavicle resection in addition to the subpectoral biceps tenodesis. Whether the associated pathology contributed to their persistent pain is unknown. However, given the distance from AN/PCHA to button, it is unlikely that their pain was a result of neurovascular compromise from the procedure.

Advantages of the cortical button include the ability to drill a smaller hole in the humerus for fixation, compared with the hole drilled for an interference screw. Despite the biomechanical strength of the screw, large (8 mm) cortical violations have been associated with increased fracture risk of the proximal humerus.^37,38 The tendon may experience less trauma than that caused by being twisted against an interference screw, the most common location of failure of which is the tendon–screw interface.³⁹ In addition, tendon healing may be improved through circumferential healing in the cortical button tunnel.

A concern of using a bicortical button for fixation is drilling through the posterior cortex, because of the proximity of the posterior neurovascular structures. In a case in which the posterior cord was injured, Rhee and colleagues⁴⁰ used a suture pullout technique whereby a Beath pin was passed out of the posterior humerus and soft tissues to then hold tension on the biceps tendon during the tenodesis. The radial nerve potentially could have been injured by pin overpenetration or by becoming wrapped up in the soft tissues as the pin was spinning through them. In our technique, the posterior humeral cortex is drilled cautiously to avoid overpenetration and possibly getting the posterior soft tissues wrapped up in the guide pin. No AN injuries have been reported with this technique. Mean distance from AN to posterior cortical button in this study was 18.17 mm. In 2 cadaver studies of bicortical drilling for subpectoral biceps tenodesis, the ANs were 25.1 mm and 36.7 mm from the posterior drill hole.^41,21

Limitations of this study included its design (case series) and limited number of follow-up patients. Of the 28 consecutive patients identified for the study, 10 did not undergo the clinical examination, as they either lived more than 3 hours away (8 patients) or could not be contacted (2 patients). Another study limitation was the inability to directly image ANs with ultrasound. Therefore, measurements of the distance from the PCHA to the button were used to estimate the distance from the AN/PCHA neurovascular bundle to the button.

In this study, functional outcomes were excellent, and there were no tenodesis failures or neurovascular complications. These preliminary findings indicate that subpectoral biceps tenodesis with a bicortical button is a viable treatment option for patients with the appropriate indications for this procedure.

A 79-year-old woman presented to the ED with acute shortness of breath. Of note, she had been recently discharged from our hospital after an open reduction and internal fixation of an intertrochanteric fracture of the right hip. The patient’s postoperative course was uncomplicated, and she was discharged home after a brief inpatient stay.

On physical examination, the patient was diaphoretic and tachypneic; oxygen saturation was 68% on room air, but increased to 100% saturation with supplemental oxygen through a nonrebreather mask. Radiographs from the patient’s inpatient hospital stay (Figure 1a) as well as ED visit (Figure 1b) were reviewed; representative images are shown above.
 

What is the diagnosis? What additional imaging tests may be useful to confirm the diagnosis?

Answer

The radiographs taken at the time of the patient’s discharge were normal. The radiograph of the chest obtained in the ED, however, demonstrated a distinct cut-off of the right mainstem bronchus, referred to as a bronchial cut-off sign (white arrow, Figure 2), with a rounded density projecting over the right mainstem bronchus (white asterisk, Figure 2). These radiographic appearances suggested the presence of an aspirated foreign body.

A computed tomography (CT) scan of the chest with contrast was performed to further evaluate the radiographic opacity and to exclude pulmonary embolism (PE), as this patient was at risk for such. The CT scan revealed no evidence of PE but confirmed the diagnosis of an aspirated foreign body. A high-density tablet (black asterisk, Figure 3) was noted to be completely occluding the right mainstem bronchus (white arrow, Figure 3) with resultant mild hyperinflation of the right lung. Upon further questioning, the patient stated that she had choked on a calcium tablet earlier in the day, but thought that the pill had finally “gone down.”

Since aspiration of foreign bodies is far more common in children,^1,2 the diagnosis often is not considered in adults who present with acute onset of shortness of breath. In adults, the most significant predisposing factor to aspiration is alcoholism. However, foreign body aspiration may arise in various clinical scenarios, including in patients with structural abnormalities, in those with neuromuscular disease, and in the postoperative setting. The most common aspirated foreign bodies are food and broken tooth fragments/periodontal devices (eg, periodontal splint).²

Presentation is varied and depends upon the nature and volume of the aspirated foreign body, which may contribute to the airway obstruction or an inflammatory bronchopneumonia. The posterior segment of the upper lobes and the superior segments of the lower lobes are the most commonly involved sites, with the right lung preferentially involved over the left lung.³

The diagnosis of foreign body aspiration begins with an appropriate clinical history. Given our patient’s recent orthopedic surgery, PE was an understandable diagnostic consideration. As with any patient acutely short of breath, radiographs are the initial diagnostic imaging study of choice. An abrupt truncation of a bronchus on radiography suggests obstruction related to a mucous plugging, cancer, or foreign body aspiration. Other findings of foreign body aspiration include segmental/lobar hyperinflation and/or atelectasis.³ In many scenarios, the aspirated foreign body may not be radiodense, which limits the utility and diagnostic accuracy of radiography. Computed tomography improves diagnostic precision and time to diagnosis by directly visualizing the airway lumen and improving visualization of radiolucent objects.⁴

Treatment for obstructive aspiration depends upon the location and nature of the aspirated object. However, bedside bronchoscopy and extraction of the foreign object is the mainstay of treatment, and is how this patient was treated. Rapid diagnosis and treatment is key to alleviating obstruction and preventing potential complications of hemoptysis and infection. 

A 79-year-old woman presented to the ED with acute shortness of breath. Of note, she had been recently discharged from our hospital after an open reduction and internal fixation of an intertrochanteric fracture of the right hip. The patient’s postoperative course was uncomplicated, and she was discharged home after a brief inpatient stay.

On physical examination, the patient was diaphoretic and tachypneic; oxygen saturation was 68% on room air, but increased to 100% saturation with supplemental oxygen through a nonrebreather mask. Radiographs from the patient’s inpatient hospital stay (Figure 1a) as well as ED visit (Figure 1b) were reviewed; representative images are shown above.
 

What is the diagnosis? What additional imaging tests may be useful to confirm the diagnosis?

Answer

The radiographs taken at the time of the patient’s discharge were normal. The radiograph of the chest obtained in the ED, however, demonstrated a distinct cut-off of the right mainstem bronchus, referred to as a bronchial cut-off sign (white arrow, Figure 2), with a rounded density projecting over the right mainstem bronchus (white asterisk, Figure 2). These radiographic appearances suggested the presence of an aspirated foreign body.

A computed tomography (CT) scan of the chest with contrast was performed to further evaluate the radiographic opacity and to exclude pulmonary embolism (PE), as this patient was at risk for such. The CT scan revealed no evidence of PE but confirmed the diagnosis of an aspirated foreign body. A high-density tablet (black asterisk, Figure 3) was noted to be completely occluding the right mainstem bronchus (white arrow, Figure 3) with resultant mild hyperinflation of the right lung. Upon further questioning, the patient stated that she had choked on a calcium tablet earlier in the day, but thought that the pill had finally “gone down.”

Since aspiration of foreign bodies is far more common in children,^1,2 the diagnosis often is not considered in adults who present with acute onset of shortness of breath. In adults, the most significant predisposing factor to aspiration is alcoholism. However, foreign body aspiration may arise in various clinical scenarios, including in patients with structural abnormalities, in those with neuromuscular disease, and in the postoperative setting. The most common aspirated foreign bodies are food and broken tooth fragments/periodontal devices (eg, periodontal splint).²

Presentation is varied and depends upon the nature and volume of the aspirated foreign body, which may contribute to the airway obstruction or an inflammatory bronchopneumonia. The posterior segment of the upper lobes and the superior segments of the lower lobes are the most commonly involved sites, with the right lung preferentially involved over the left lung.³

The diagnosis of foreign body aspiration begins with an appropriate clinical history. Given our patient’s recent orthopedic surgery, PE was an understandable diagnostic consideration. As with any patient acutely short of breath, radiographs are the initial diagnostic imaging study of choice. An abrupt truncation of a bronchus on radiography suggests obstruction related to a mucous plugging, cancer, or foreign body aspiration. Other findings of foreign body aspiration include segmental/lobar hyperinflation and/or atelectasis.³ In many scenarios, the aspirated foreign body may not be radiodense, which limits the utility and diagnostic accuracy of radiography. Computed tomography improves diagnostic precision and time to diagnosis by directly visualizing the airway lumen and improving visualization of radiolucent objects.⁴

Treatment for obstructive aspiration depends upon the location and nature of the aspirated object. However, bedside bronchoscopy and extraction of the foreign object is the mainstay of treatment, and is how this patient was treated. Rapid diagnosis and treatment is key to alleviating obstruction and preventing potential complications of hemoptysis and infection. 

A 79-year-old woman presented to the ED with acute shortness of breath. Of note, she had been recently discharged from our hospital after an open reduction and internal fixation of an intertrochanteric fracture of the right hip. The patient’s postoperative course was uncomplicated, and she was discharged home after a brief inpatient stay.

On physical examination, the patient was diaphoretic and tachypneic; oxygen saturation was 68% on room air, but increased to 100% saturation with supplemental oxygen through a nonrebreather mask. Radiographs from the patient’s inpatient hospital stay (Figure 1a) as well as ED visit (Figure 1b) were reviewed; representative images are shown above.
 

What is the diagnosis? What additional imaging tests may be useful to confirm the diagnosis?

Answer

The radiographs taken at the time of the patient’s discharge were normal. The radiograph of the chest obtained in the ED, however, demonstrated a distinct cut-off of the right mainstem bronchus, referred to as a bronchial cut-off sign (white arrow, Figure 2), with a rounded density projecting over the right mainstem bronchus (white asterisk, Figure 2). These radiographic appearances suggested the presence of an aspirated foreign body.

A computed tomography (CT) scan of the chest with contrast was performed to further evaluate the radiographic opacity and to exclude pulmonary embolism (PE), as this patient was at risk for such. The CT scan revealed no evidence of PE but confirmed the diagnosis of an aspirated foreign body. A high-density tablet (black asterisk, Figure 3) was noted to be completely occluding the right mainstem bronchus (white arrow, Figure 3) with resultant mild hyperinflation of the right lung. Upon further questioning, the patient stated that she had choked on a calcium tablet earlier in the day, but thought that the pill had finally “gone down.”

Since aspiration of foreign bodies is far more common in children,^1,2 the diagnosis often is not considered in adults who present with acute onset of shortness of breath. In adults, the most significant predisposing factor to aspiration is alcoholism. However, foreign body aspiration may arise in various clinical scenarios, including in patients with structural abnormalities, in those with neuromuscular disease, and in the postoperative setting. The most common aspirated foreign bodies are food and broken tooth fragments/periodontal devices (eg, periodontal splint).²

Presentation is varied and depends upon the nature and volume of the aspirated foreign body, which may contribute to the airway obstruction or an inflammatory bronchopneumonia. The posterior segment of the upper lobes and the superior segments of the lower lobes are the most commonly involved sites, with the right lung preferentially involved over the left lung.³

The diagnosis of foreign body aspiration begins with an appropriate clinical history. Given our patient’s recent orthopedic surgery, PE was an understandable diagnostic consideration. As with any patient acutely short of breath, radiographs are the initial diagnostic imaging study of choice. An abrupt truncation of a bronchus on radiography suggests obstruction related to a mucous plugging, cancer, or foreign body aspiration. Other findings of foreign body aspiration include segmental/lobar hyperinflation and/or atelectasis.³ In many scenarios, the aspirated foreign body may not be radiodense, which limits the utility and diagnostic accuracy of radiography. Computed tomography improves diagnostic precision and time to diagnosis by directly visualizing the airway lumen and improving visualization of radiolucent objects.⁴

Treatment for obstructive aspiration depends upon the location and nature of the aspirated object. However, bedside bronchoscopy and extraction of the foreign object is the mainstay of treatment, and is how this patient was treated. Rapid diagnosis and treatment is key to alleviating obstruction and preventing potential complications of hemoptysis and infection. 

MIAMI – Patients with psoriatic arthritis had a higher prevalence and greater extent of coronary artery plaque in a pilot study comparison with healthy control patients that may point to increased risk independent of traditional cardiovascular risk factors.

In the study, coronary artery plaque as assessed by cardiac computed tomography angiography (CCTA) occurred in 39 (78%) of 50 patients with psoriatic arthritis, a significantly higher rate than that observed for healthy controls (11 of 25, 44%).

©vizualis/thinkstockphotos.com

Investigators not only measured plaque volume, but also assessed the type of plaque: calcified, noncalcified, or mixed. Mixed plaque predominated. This could be important because “noncalcified and mixed carry higher risk for rupture and later cardiovascular events,” Agnes Szentpetery, MD, a research fellow at St. Vincent’s University Hospital in Dublin, said at the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis.

She and her colleagues also found more clinically significant stenosis among the 50 participants with psoriatic arthritis, compared with 25 healthy controls matched for age, sex, smoking status, and presence of metabolic syndrome. “This pilot study is the first to assess coronary plaques in asymptomatic patients with psoriatic arthritis with CCTA,” Dr. Szentpetery said.

Total plaque volume was higher in the psoriatic arthritis group versus controls, and higher in the left main artery for psoriatic arthritis patients, both with and without metabolic syndrome.

The study points to increased risk independent of traditional cardiovascular risk factors. For example, CCTA revealed no difference in plaque volume between patients with and without metabolic disease. In addition, a previous study suggests “the burden of carotid artery plaques is higher in patients with psoriatic arthritis compared to those with psoriasis alone,” Dr. Szentpetery said, citing a cross-sectional study comparing 125 people with psoriasis to 114 others with psoriatic arthritis (Ann Rheum Dis. 2013 May;72[5]:715-20).

Perhaps not surprisingly, inflammation could be driving the association between psoriatic and cardiovascular disease risk. Other investigators suggest chronic, low-grade inflammation leads to atherosclerosis through a maladaptive immune response and altered lipid metabolism, for example (Nat Med. 2011 Nov;17[11]:1410-22).

In the current study, the patients with psoriatic arthritis had well-established disease, occurring for a mean duration of 19 years. Mean age was 58 years, and 54% were men. Approximately 60% were taking disease-modifying antirheumatic drugs, two-thirds were taking biologics, and about one-third were on combination treatment. Controls were similar demographically with a mean age of 57 years, and 52% were men.

Interestingly, Psoriasis Area and Severity Index (PASI) scores did not correlate with increased risk. During discussion after the presentation of the study, a researcher unaffiliated with the study offered an answer. “It could be their skin disease was controlled by the biologics. You had 67% on biologics,” said Nehal Mehta, MD, Clinical Research Scholar in the section of inflammation and cardiometabolic disease at the National Heart, Lung, and Blood Institute. “We at the NIH see a strong correlation between PASI and coronary artery disease risk.”

“We know methotrexate and anti-TNF agents can have a protective effect on atherosclerosis, but we did not look at this specifically,” Dr. Szentpetery said. Overall, PASI scores were relatively low in the study population, she added, which “may explain why we did not see the correlation with PASI scores.”

Dr. Szentpetery and Dr. Mehta had no relevant financial disclosures.

MIAMI – Patients with psoriatic arthritis had a higher prevalence and greater extent of coronary artery plaque in a pilot study comparison with healthy control patients that may point to increased risk independent of traditional cardiovascular risk factors.

In the study, coronary artery plaque as assessed by cardiac computed tomography angiography (CCTA) occurred in 39 (78%) of 50 patients with psoriatic arthritis, a significantly higher rate than that observed for healthy controls (11 of 25, 44%).

©vizualis/thinkstockphotos.com

Investigators not only measured plaque volume, but also assessed the type of plaque: calcified, noncalcified, or mixed. Mixed plaque predominated. This could be important because “noncalcified and mixed carry higher risk for rupture and later cardiovascular events,” Agnes Szentpetery, MD, a research fellow at St. Vincent’s University Hospital in Dublin, said at the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis.

She and her colleagues also found more clinically significant stenosis among the 50 participants with psoriatic arthritis, compared with 25 healthy controls matched for age, sex, smoking status, and presence of metabolic syndrome. “This pilot study is the first to assess coronary plaques in asymptomatic patients with psoriatic arthritis with CCTA,” Dr. Szentpetery said.

Total plaque volume was higher in the psoriatic arthritis group versus controls, and higher in the left main artery for psoriatic arthritis patients, both with and without metabolic syndrome.

The study points to increased risk independent of traditional cardiovascular risk factors. For example, CCTA revealed no difference in plaque volume between patients with and without metabolic disease. In addition, a previous study suggests “the burden of carotid artery plaques is higher in patients with psoriatic arthritis compared to those with psoriasis alone,” Dr. Szentpetery said, citing a cross-sectional study comparing 125 people with psoriasis to 114 others with psoriatic arthritis (Ann Rheum Dis. 2013 May;72[5]:715-20).

Perhaps not surprisingly, inflammation could be driving the association between psoriatic and cardiovascular disease risk. Other investigators suggest chronic, low-grade inflammation leads to atherosclerosis through a maladaptive immune response and altered lipid metabolism, for example (Nat Med. 2011 Nov;17[11]:1410-22).

In the current study, the patients with psoriatic arthritis had well-established disease, occurring for a mean duration of 19 years. Mean age was 58 years, and 54% were men. Approximately 60% were taking disease-modifying antirheumatic drugs, two-thirds were taking biologics, and about one-third were on combination treatment. Controls were similar demographically with a mean age of 57 years, and 52% were men.

Interestingly, Psoriasis Area and Severity Index (PASI) scores did not correlate with increased risk. During discussion after the presentation of the study, a researcher unaffiliated with the study offered an answer. “It could be their skin disease was controlled by the biologics. You had 67% on biologics,” said Nehal Mehta, MD, Clinical Research Scholar in the section of inflammation and cardiometabolic disease at the National Heart, Lung, and Blood Institute. “We at the NIH see a strong correlation between PASI and coronary artery disease risk.”

“We know methotrexate and anti-TNF agents can have a protective effect on atherosclerosis, but we did not look at this specifically,” Dr. Szentpetery said. Overall, PASI scores were relatively low in the study population, she added, which “may explain why we did not see the correlation with PASI scores.”

Dr. Szentpetery and Dr. Mehta had no relevant financial disclosures.

MIAMI – Patients with psoriatic arthritis had a higher prevalence and greater extent of coronary artery plaque in a pilot study comparison with healthy control patients that may point to increased risk independent of traditional cardiovascular risk factors.

In the study, coronary artery plaque as assessed by cardiac computed tomography angiography (CCTA) occurred in 39 (78%) of 50 patients with psoriatic arthritis, a significantly higher rate than that observed for healthy controls (11 of 25, 44%).

©vizualis/thinkstockphotos.com

Investigators not only measured plaque volume, but also assessed the type of plaque: calcified, noncalcified, or mixed. Mixed plaque predominated. This could be important because “noncalcified and mixed carry higher risk for rupture and later cardiovascular events,” Agnes Szentpetery, MD, a research fellow at St. Vincent’s University Hospital in Dublin, said at the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis.

She and her colleagues also found more clinically significant stenosis among the 50 participants with psoriatic arthritis, compared with 25 healthy controls matched for age, sex, smoking status, and presence of metabolic syndrome. “This pilot study is the first to assess coronary plaques in asymptomatic patients with psoriatic arthritis with CCTA,” Dr. Szentpetery said.

Total plaque volume was higher in the psoriatic arthritis group versus controls, and higher in the left main artery for psoriatic arthritis patients, both with and without metabolic syndrome.

The study points to increased risk independent of traditional cardiovascular risk factors. For example, CCTA revealed no difference in plaque volume between patients with and without metabolic disease. In addition, a previous study suggests “the burden of carotid artery plaques is higher in patients with psoriatic arthritis compared to those with psoriasis alone,” Dr. Szentpetery said, citing a cross-sectional study comparing 125 people with psoriasis to 114 others with psoriatic arthritis (Ann Rheum Dis. 2013 May;72[5]:715-20).

Perhaps not surprisingly, inflammation could be driving the association between psoriatic and cardiovascular disease risk. Other investigators suggest chronic, low-grade inflammation leads to atherosclerosis through a maladaptive immune response and altered lipid metabolism, for example (Nat Med. 2011 Nov;17[11]:1410-22).

In the current study, the patients with psoriatic arthritis had well-established disease, occurring for a mean duration of 19 years. Mean age was 58 years, and 54% were men. Approximately 60% were taking disease-modifying antirheumatic drugs, two-thirds were taking biologics, and about one-third were on combination treatment. Controls were similar demographically with a mean age of 57 years, and 52% were men.

Interestingly, Psoriasis Area and Severity Index (PASI) scores did not correlate with increased risk. During discussion after the presentation of the study, a researcher unaffiliated with the study offered an answer. “It could be their skin disease was controlled by the biologics. You had 67% on biologics,” said Nehal Mehta, MD, Clinical Research Scholar in the section of inflammation and cardiometabolic disease at the National Heart, Lung, and Blood Institute. “We at the NIH see a strong correlation between PASI and coronary artery disease risk.”

“We know methotrexate and anti-TNF agents can have a protective effect on atherosclerosis, but we did not look at this specifically,” Dr. Szentpetery said. Overall, PASI scores were relatively low in the study population, she added, which “may explain why we did not see the correlation with PASI scores.”

Dr. Szentpetery and Dr. Mehta had no relevant financial disclosures.

Failure to achieve a rounded and unobstructed ostia in children who have surgery to repair anomalous coronary arteries can put these children at continued risk for sudden death, but cardiac MRI with virtual angioscopy (VA) before and after the operation can give cardiologists a clear picture of a patient’s risk for sudden death and help direct ongoing management, according to a study in the July issue of the Journal of Thoracic and Cardiovascular Surgery (2016;152:205-10).

“Cardiac MRI with virtual angioscopy is an important tool for evaluating anomalous coronary anatomy, myocardial function, and ischemia and should be considered for initial and postoperative assessment of children with anomalous coronary arteries,” lead author Julie A. Brothers, MD, and her coauthors said in reporting their findings.

Anomalous coronary artery is a rare congenital condition in which the left coronary artery (LCA) originates from the right sinus or the right coronary artery (RCA) originates from the left coronary sinus. Dr. Brothers, a pediatric cardiologist, and her colleagues from the Children’s Hospital of Philadelphia and the University of Pennsylvania, also in Philadelphia, studied nine male patients who had operations for anomalous coronary arteries during Feb. 2009-May 2015 in what they said is the first study to document anomalous coronary artery anatomy both before and after surgery. The patients’ average age was 14.1 years; seven had right anomalous coronary arteries and two had left anomalous arteries. After the operations, MRI-VA revealed that two patients still had narrowing in the neo-orifices.

Previous reports recommend surgical repair for all patients with anomalous LCA and for symptomatic patients with anomalous RCA anatomy (Ann Thorac Surg. 2011;92:691-7; Ann Thorac Surg. 2014;98:941-5). MRI-VA allows the surgical team to survey the ostial stenosis before the operation “as if standing within the vessel itself,” Dr. Brothers and her coauthors wrote. Afterward, MRI-VA lets the surgeon and team see if the operation succeeded in repairing the orifices.

In the study population, VA before surgery confirmed elliptical, slit-like orifices in all patients. The operations involved unroofing procedures; two patients also had detachment and resuspension procedures during surgery. After surgery, VA showed that seven patients had round, patent, unobstructed repaired orifices; but two had orifices that were still narrow and somewhat stenotic, Dr. Brothers and her coauthors said. The study group had postoperative MRI-VA an average of 8.6 months after surgery.

“The significance of these findings is unknown; however, if the proposed mechanism of ischemia is due to a slit-like orifice, a continued stenotic orifice may place subjects at risk for sudden death,” the researchers said. The two study patients with the narrowed, stenotic orifices have remained symptom free, with no evidence of ischemia on exercise stress test or cardiac MRI. “These subjects will need to be followed up in the future to monitor for progression or resolution,” the study authors wrote.

Sudden cardiac death (SCD) is more common in anomalous aortic origin of the LCA than the RCA, Dr. Brothers and her colleagues said. Thus, an elliptical, slit-like neo-orifice is a concern because it can become blocked during exercise, possibly leading to lethal ventricular arrhythmia, they said. Ischemia in patients with anomalous coronary artery seems to result from a cumulative effect of exercise.

Patients who undergo the modified unroofing procedure typically have electrocardiography and echocardiography afterward and then get cleared to return to competitive sports in about 3 months if their stress test indicates it. Dr. Brothers and her colleagues said this activity recommendation may need alteration for those patients who have had a heart attack or sudden cardiac arrest, because they may remain at increased risk of SCD after surgery. “At the very least, additional imaging, such as with MRI-VA, should be used in this population,” the study authors said.

While Dr. Brothers and her colleagues acknowledged the small sample size is a limitation of the study, they also pointed out that anomalous coronary artery is a rare disease. They also noted that high-quality VA images can be difficult to obtain in noncompliant patients or those have arrhythmia or irregular breathing. “The images obtained in this study were acquired at an institution very familiar with pediatric cardiac coronary MRI and would be appropriate for assessing the coronary ostia with VA,” they said.

Dr. Brothers and her coauthors had no financial disclosures.

Failure to achieve a rounded and unobstructed ostia in children who have surgery to repair anomalous coronary arteries can put these children at continued risk for sudden death, but cardiac MRI with virtual angioscopy (VA) before and after the operation can give cardiologists a clear picture of a patient’s risk for sudden death and help direct ongoing management, according to a study in the July issue of the Journal of Thoracic and Cardiovascular Surgery (2016;152:205-10).

“Cardiac MRI with virtual angioscopy is an important tool for evaluating anomalous coronary anatomy, myocardial function, and ischemia and should be considered for initial and postoperative assessment of children with anomalous coronary arteries,” lead author Julie A. Brothers, MD, and her coauthors said in reporting their findings.

Anomalous coronary artery is a rare congenital condition in which the left coronary artery (LCA) originates from the right sinus or the right coronary artery (RCA) originates from the left coronary sinus. Dr. Brothers, a pediatric cardiologist, and her colleagues from the Children’s Hospital of Philadelphia and the University of Pennsylvania, also in Philadelphia, studied nine male patients who had operations for anomalous coronary arteries during Feb. 2009-May 2015 in what they said is the first study to document anomalous coronary artery anatomy both before and after surgery. The patients’ average age was 14.1 years; seven had right anomalous coronary arteries and two had left anomalous arteries. After the operations, MRI-VA revealed that two patients still had narrowing in the neo-orifices.

Previous reports recommend surgical repair for all patients with anomalous LCA and for symptomatic patients with anomalous RCA anatomy (Ann Thorac Surg. 2011;92:691-7; Ann Thorac Surg. 2014;98:941-5). MRI-VA allows the surgical team to survey the ostial stenosis before the operation “as if standing within the vessel itself,” Dr. Brothers and her coauthors wrote. Afterward, MRI-VA lets the surgeon and team see if the operation succeeded in repairing the orifices.

In the study population, VA before surgery confirmed elliptical, slit-like orifices in all patients. The operations involved unroofing procedures; two patients also had detachment and resuspension procedures during surgery. After surgery, VA showed that seven patients had round, patent, unobstructed repaired orifices; but two had orifices that were still narrow and somewhat stenotic, Dr. Brothers and her coauthors said. The study group had postoperative MRI-VA an average of 8.6 months after surgery.

“The significance of these findings is unknown; however, if the proposed mechanism of ischemia is due to a slit-like orifice, a continued stenotic orifice may place subjects at risk for sudden death,” the researchers said. The two study patients with the narrowed, stenotic orifices have remained symptom free, with no evidence of ischemia on exercise stress test or cardiac MRI. “These subjects will need to be followed up in the future to monitor for progression or resolution,” the study authors wrote.

Sudden cardiac death (SCD) is more common in anomalous aortic origin of the LCA than the RCA, Dr. Brothers and her colleagues said. Thus, an elliptical, slit-like neo-orifice is a concern because it can become blocked during exercise, possibly leading to lethal ventricular arrhythmia, they said. Ischemia in patients with anomalous coronary artery seems to result from a cumulative effect of exercise.

Patients who undergo the modified unroofing procedure typically have electrocardiography and echocardiography afterward and then get cleared to return to competitive sports in about 3 months if their stress test indicates it. Dr. Brothers and her colleagues said this activity recommendation may need alteration for those patients who have had a heart attack or sudden cardiac arrest, because they may remain at increased risk of SCD after surgery. “At the very least, additional imaging, such as with MRI-VA, should be used in this population,” the study authors said.

While Dr. Brothers and her colleagues acknowledged the small sample size is a limitation of the study, they also pointed out that anomalous coronary artery is a rare disease. They also noted that high-quality VA images can be difficult to obtain in noncompliant patients or those have arrhythmia or irregular breathing. “The images obtained in this study were acquired at an institution very familiar with pediatric cardiac coronary MRI and would be appropriate for assessing the coronary ostia with VA,” they said.

Dr. Brothers and her coauthors had no financial disclosures.

Failure to achieve a rounded and unobstructed ostia in children who have surgery to repair anomalous coronary arteries can put these children at continued risk for sudden death, but cardiac MRI with virtual angioscopy (VA) before and after the operation can give cardiologists a clear picture of a patient’s risk for sudden death and help direct ongoing management, according to a study in the July issue of the Journal of Thoracic and Cardiovascular Surgery (2016;152:205-10).

“Cardiac MRI with virtual angioscopy is an important tool for evaluating anomalous coronary anatomy, myocardial function, and ischemia and should be considered for initial and postoperative assessment of children with anomalous coronary arteries,” lead author Julie A. Brothers, MD, and her coauthors said in reporting their findings.

Anomalous coronary artery is a rare congenital condition in which the left coronary artery (LCA) originates from the right sinus or the right coronary artery (RCA) originates from the left coronary sinus. Dr. Brothers, a pediatric cardiologist, and her colleagues from the Children’s Hospital of Philadelphia and the University of Pennsylvania, also in Philadelphia, studied nine male patients who had operations for anomalous coronary arteries during Feb. 2009-May 2015 in what they said is the first study to document anomalous coronary artery anatomy both before and after surgery. The patients’ average age was 14.1 years; seven had right anomalous coronary arteries and two had left anomalous arteries. After the operations, MRI-VA revealed that two patients still had narrowing in the neo-orifices.

Previous reports recommend surgical repair for all patients with anomalous LCA and for symptomatic patients with anomalous RCA anatomy (Ann Thorac Surg. 2011;92:691-7; Ann Thorac Surg. 2014;98:941-5). MRI-VA allows the surgical team to survey the ostial stenosis before the operation “as if standing within the vessel itself,” Dr. Brothers and her coauthors wrote. Afterward, MRI-VA lets the surgeon and team see if the operation succeeded in repairing the orifices.

In the study population, VA before surgery confirmed elliptical, slit-like orifices in all patients. The operations involved unroofing procedures; two patients also had detachment and resuspension procedures during surgery. After surgery, VA showed that seven patients had round, patent, unobstructed repaired orifices; but two had orifices that were still narrow and somewhat stenotic, Dr. Brothers and her coauthors said. The study group had postoperative MRI-VA an average of 8.6 months after surgery.

“The significance of these findings is unknown; however, if the proposed mechanism of ischemia is due to a slit-like orifice, a continued stenotic orifice may place subjects at risk for sudden death,” the researchers said. The two study patients with the narrowed, stenotic orifices have remained symptom free, with no evidence of ischemia on exercise stress test or cardiac MRI. “These subjects will need to be followed up in the future to monitor for progression or resolution,” the study authors wrote.

Sudden cardiac death (SCD) is more common in anomalous aortic origin of the LCA than the RCA, Dr. Brothers and her colleagues said. Thus, an elliptical, slit-like neo-orifice is a concern because it can become blocked during exercise, possibly leading to lethal ventricular arrhythmia, they said. Ischemia in patients with anomalous coronary artery seems to result from a cumulative effect of exercise.

Patients who undergo the modified unroofing procedure typically have electrocardiography and echocardiography afterward and then get cleared to return to competitive sports in about 3 months if their stress test indicates it. Dr. Brothers and her colleagues said this activity recommendation may need alteration for those patients who have had a heart attack or sudden cardiac arrest, because they may remain at increased risk of SCD after surgery. “At the very least, additional imaging, such as with MRI-VA, should be used in this population,” the study authors said.

While Dr. Brothers and her colleagues acknowledged the small sample size is a limitation of the study, they also pointed out that anomalous coronary artery is a rare disease. They also noted that high-quality VA images can be difficult to obtain in noncompliant patients or those have arrhythmia or irregular breathing. “The images obtained in this study were acquired at an institution very familiar with pediatric cardiac coronary MRI and would be appropriate for assessing the coronary ostia with VA,” they said.

Dr. Brothers and her coauthors had no financial disclosures.