An 18-yr-old female lacrosse player at a local college presented complaining of bilateral anterior and posterior lower leg pain that had started 3 yr before presentation. Initially, the pain appeared during exercise, 5-10 min into running, and lasted for a few hours after the run. She felt pressure and tightness in both of her lower legs. Her pain improved with rest. It eventually progressed to chronic pain that worsened with activity. She also had paresthesias on the dorsal surfaces of both feet while running. She reported having a foot slap bilaterally that occurred during stacked exercise sessions and resolved after exercise. She was able to run through the pain. She had mild low back pain but denied hip and knee pain.
She had a past medical history of asthma and a benign heart murmur. She had no family history of heart disease, vascular disease, aneurysm, bleeding, or clotting disorders. She denied using alcohol, illicit drugs, and tobacco. She was taking meloxicam, iron, magnesium, albuterol, fluticasone, salmeterol, and montelukast.
Her exam showed that she was 5'9" tall and weighed 150 lb. Her vital signs were normal, including blood pressure in both upper extremities. Her general appearance was healthy. Her musculoskeletal exam was symmetric bilaterally. Her lower leg strength was normal. Her lower leg sensation to light touch was normal. She had index pain with sustained passive dorsiflexion created by standing and leaning against a wall as well as pain with prolonged active plantar flexion with a standing heel raise. A one-legged hop test was positive for reproducing her index pain. She had palpable dorsalis pedis and posterior tibial pulses bilaterally. She had more tenderness with palpation of the gastrocnemius than of the tibia.
- Radiographs. Two-view bilateral tibia and fibula were normal.
- Ankle Brachial Index (ABI) Before and After Treadmill Exercise. At rest, ABI was slightly low, with right 0.94 and left 0.92. After treadmill exercise at 2 mph 12% grade for 5 min, the patient had mild to moderate symptoms. Her post-exercise ABI values were right 0.83 and left 0.75. After 5 min of rest, right ABI was 0.80 and left was 0.78. A normal ABI value is 0.95 or higher.
- Doppler Ultrasound of Popliteal Artery, with Stress Maneuvers. There was no evidence of popliteal artery aneurysm or intramural cystic lesions. At rest, the Doppler wave forms in the dorsalis pedis arteries were normal and triphasic; with forced passive dorsiflexion and active plantar flexion against resistance, the dorsalis pedis pulse became monophasic bilaterally.
- Compartment Testing. Bilateral anterior, lateral, and posterior compartment pressures were evaluated before and after treadmill exercise. Her pre-exercise anterior compartment pressure was 23 and increased to 38 mm Hg post-exercise. Her pre-exercise lateral compartment pressure was 20 and increased to 23 mm Hg post-exercise. Her pre-exercise deep posterior compartment pressure was 14 mm Hg and increased to 18 mm Hg post-exercise. Compartment testing is considered abnormal if the resting pressure is higher than 15 mm Hg or if post-exercise pressure is higher than 30 mm Hg.
- Arteriogram of Popliteal Artery with Stress Maneuvers. Patient was tested with active plantar flexion, passive plantar flexion, active dorsiflexion, and passive dorsiflexion with legs straight as well as with legs bent to 30°. Evaluation was performed in the anterior posterior and oblique lateral projections bilaterally. She had normal arterial flow in all positions without evidence of anatomic or functional obstruction.
The patient was found to have features of both anterior compartment syndrome and popliteal artery entrapment. Because the arteriogram with stress maneuvers did not show occlusion of popliteal artery, she was referred for bilateral anterior fasciotomies. After the bilateral anterior fasciotomies, she had improved anterior shin pain but continued to have severe posterior lower leg pain with activities of daily living. A repeat arteriogram was personally performed by the attending vascular surgeon (SWM) at a different facility. This showed complete occlusion of both popliteal arteries with active plantar flexion against resistance. See Figures 1 and 2. He also visualized dynamic lateral motion of the artery during plantar flexion. She was diagnosed with Type VI functional popliteal artery entrapment.
TREATMENT AND OUTCOMES
The patient had surgical treatment to minimize pressure on her popliteal artery. The surgery consisted of neurolysis of the tibial nerve, subtotal resection of medial head of the gastrocnemius muscle, wedge resection of the upper soleus muscle, and complete resection of the plantaris muscle. She had 100% relief of her pain in one leg and was able to return to her sport. Her other leg was decompressed after recovery of the first and she had 90% improvement in her pain 3 months after surgery. There are no defined return to play guidelines after this surgery. The recovery will depend on the surgery needed to prevent popliteal artery entrapment. In general, recommendations include using crutches after surgery but transitioning to weight bearing as tolerated over the first week. During the second week we recommend the patient work on obtaining a normal gait with full leg extension. The patient can progress to a slow jog once they can walk with normal mechanics. At week three they can start a progressive return to usual activity, including intense training, as long as the incision is healing appropriately. Return to sport will vary anywhere from four to eight weeks.
Popliteal artery entrapment arises when there is anatomic (Types I-V) or functional (Type VI) compression of the neurovascular bundle in the popliteal fossa. Anatomic causes include an abnormal pathway of the artery around or through the medial head of the gastrocnemius, or compression by the plantaris, popliteus or aberrant fibrous bands. These can lead to poststenotic aneurismal dilatation requiring grafting. Type VI arises on the basis of "big muscle in a small/fixed space" which compresses the artery with gastrocnemius activation. PAES will produce typical claudication-like symptoms with exercise, which usually resolve fairly quickly with exercise cessation. The artery, vein, and nerve descend together and can all be compressed by the same mechanism. This can produce compartment hypertension due to occlusion of venous outflow and give a false impression of isolated chronic exertional compartment syndrome. Compartment release, however, will not relieve all of the patient's symptoms as there is also concomitant arterial compression and insufficiency.
This case highlights several points. First, making the correct diagnosis of functional popliteal artery entrapment is difficult and highly dependent on the proper performance of stress maneuvers during the examination and investigations. Second, there can be overlap of popliteal artery entrapment with chronic exertional compartment syndrome and tibial nerve compression. Third, the treatment should be tailored to address the specific abnormalities for each patient.
Initially a careful history and physical exam can help direct further work-up. Examination and imaging will be normal in the neutral position. Office work up includes stress testing the patient with provocative maneuvers. Bruits over the popliteal fossa are reported, but are rare. Initially have the patient maintain passive plantar flexion, which has no significant muscle activity and should not provoke compartment syndrome. Next the patient is asked to perform and maintain a, static toe raise in maximal active plantar flexion. Provocation should reproduce the patient's index symptoms within a maximum of 60-90 seconds. Typical vascular laboratory work-up can include bilateral ABI performed before and after treadmill exercise sufficient to reproduce symptoms, and a Doppler ultrasound of the popliteal arteries in both the neutral position and with provocative maneuvers of active plantar flexion and forced passive dorsiflexion. These can show diminution of flow, increased flow velocity and change of the normal waveforms from triphasic to monophasic. It is critical to perform all of the provocative maneuvers with the knee maintained in full extension, as any knee flexion will relieve the arterial compression. The gold standard for popliteal artery entrapment is an arteriogram of the popliteal arteries at rest and during active plantar flexion against resistance. It is critical to evaluate all of the patient's symptoms and lab studies together, as false positive provocative lab tests can occur in normal individuals.
In this case, the reason for the discrepancy in the tests was unclear. It is possible that the patient was unable to generate enough force in plantar flexion to reproduce the occlusion. There should be slight shortening of the gastrocnemius with minimal motion artifact to optimize the view of the popliteal artery. Because the initial arteriogram was normal, the vascular surgeon felt she would benefit from anterior fasciotomies for chronic exertional compartment syndrome. This did resolve her anterior leg pain but not the more significant and disabling posterior leg pain. She had almost complete resolution in her pain after the surgery for functional popliteal artery entrapment.Copyright © 2009 by the American College of Sports Medicine.