PFATS Articles

Sudden Onset of Exercise Induced Ischemia

Dan Lorenz, MS, PT, ATC/L, CSCS; David Price, ATC/L

This case study describes the development of sudden onset exercise induced lower extremity ischemia which developed as a result of multiple knee surgeries. The following details the progression of treatment and surgical intervention to alleviate a lower extremity arterial blockage.

History

The 34-year-old offensive athlete’s medical history is significant for multiple knee surgeries, as well as a lumbar spondylolysis. In August of 1999, the athlete sustained a left knee ACL tear, MCL tear, and lateral meniscus tear during a pre-season game. His ACL was subsequently reconstructed with an autologous bone-tendon-bone graft, and the lateral meniscus tear was resected. The surgeon did not repair the MCL leaving it to heal without intervention. Six months post-operatively, the athlete did not gain full range of motion suffering from a three degree loss of extension, as well as, decreased flexion. An MRI showed scarring of the fat pad and the patellar tendon in addition to a small popliteal cyst. Range of motion restrictions due to post-op arthrofibrosis, particularly of the patella, as well as early scar tissue formation led to the need for a second surgery.

Five months after his first surgery, the athlete underwent arthroscopic manipulation including the excision of scar tissue and drainage of a Baker’s cyst in the posterior capsule. He had the cyst drained several times with recurrence, which continued to limit his motion. Three months following his second surgery, he had a third arthroscopic surgery to remove the cyst and debride and manipulate the joint. Because of the cyst removal, the posterior capsule was reinforced with a hamstring graft to ensure that it would maintain structural integrity. He was able to play during the 2000 season with a brace locked at 10°, despite not having a normal knee. Even with aggressive physical therapy and adequate time for healing, he failed to regain the motion desired. His final range of motion could not be manipulated in the clinic, mostly due to significant patella baja that developed over time. In February of 2001, he had a final procedure done arthroscopically to manipulate the knee to correct his loss of flexion and to have scar tissue debrided. Additionally, his final procedure included chondroplasty with microfracture of the trochlear groove, medial and lateral release of the patella, and notchplasty. Most of his rehabilitation was done off-site at the location of the treating surgeon. Following his third knee surgery, he successfully played symptom free with limited range of motion (10°-125°) for four seasons.

Injury and Treatment Timeline
August 24, 2005:

During practice while running a series of plays, the athlete complained of tightness and soreness in his lower leg and pain in the region of his proximal anterior/lateral shin and lateral calf. The pain was accompanied by mild numbness in the fourth and fifth toes, occasionally the numbness spread into the plantar surface of his foot.
Drill work did not reproduce symptoms but repetitive running of plays caused the fatiguing sensation. His symptoms resolved with rest. Initially, the athlete thought that his knee sleeve may have been too tight and that his ankle taping may have also caused his pain. He subsequently removed both the sleeve and ankle taping, however neither approach provided any relief of his symptoms.
The condition was considered a muscle spasm/cramp of the lower leg. He was removed from practice and treated with massage, stretching, and ice.

August 25, 2005:

The athlete had no complaints with activities of daily living (ADL’s) except when walking up inclined surfaces (i.e. the tunnel leading from the players’ parking lot to the stadium).
He was re-evaluated by the head athletic trainer who continued to treat the athlete for muscle cramps/spasms.

August 26, 2005:

Still complaining of the same symptoms, the athlete was evaluated by the team physician. The physician’s examination revealed:
- Standing posture in varus alignment with a lack of approximately 5-10° of extension in his left knee.
- Normal gait with the ability to walk on his tip-toes without exacerbation of symptoms.
- No evidence of effusion or added loss of motion in his knee.
Examination of the lower leg showed:
- Trace pitting edema in the medial aspect of his left lower leg. This pitting edema was present in the opposite lower leg but to a lesser degree.
- Soreness in the calf that was elicited by palpation of the proximal anterior/lateral muscle compartment as well as the lateral head of the gastrocnemius at the musculotendinous junction that coursed to the mid-calf region.
- No symptoms with Tinel’s sign over the proximal peroneal nerve below the fibular head.
- Normal Achilles tendon function and normal strength of the plantar flexors, dorsiflexors, invertors, evertors and toes.
- Radiographs of the tibia and fibula showed no bony abnormality.
Sensation testing revealed:
- No evidence of decreased sensation in the dorsal distribution of the superficial peroneal nerve or in the first webspace .
- Normal light touch in the lateral foot, plantar surface, and lateral hindfoot.
- No evidence of disc pathology. Lower back screening and provocative straight-leg raising did not reproduce any symptoms in the back or leg.
Following examination, the physician concluded that the athlete had a possible exercise induced compartment syndrome or a possible chronic progressive muscle strain with an unusual peroneal nerve irritation secondary to his varus left knee. Lumbar and lumbosacral radiculopathies were ruled out. It was recommended that the athlete have an MRI of the low back and leg with the possibility of further EMG studies to include compartment pressure measurements. Treatment interventions included unloader braces and a heel lift as well as a cleat evaluation.

August 27, 2005:

Due to numbness in the fourth and fifth toes with persistent soreness in the anterior and lateral muscle compartments, the athlete was removed from a preseason game after participating in only two series.

August 28, 2005:

The lumbar spine MRI showed mild degenerative disc disease (DDD) from L4-S1 with dorsal annular thinning and slight posterior lateral bulging of these discs. No evidence of central or neural foraminal impingement was detected, however there were subtle changes of the pars of L5 bilaterally. The right side showed evidence of sclerosis without evidence of spondylolysis. On the left, spondylolysis of L5 was suggested, despite no evidence of spondylolisthesis. These findings did not differ from previous MRI’s of the lumbar spine in this athlete nor had the findings progressed.
MRI of his left calf showed a small amount of edema extending along the anterior and medial left mid-to-distal tibial periosteum, possibly representing an area of shin splints. In addition, a small amount of fluid tracked along the distal flexor hallucis tendon. His calf muscles and bone were normal.

Based on inconclusive studies, he was referred to a vascular surgeon for a Doppler study, which uses ultrasound to reflect sound waves to evaluate blood flow through a particular vessel. This test determines blocked or reduced blood flow through the narrowing of vessels. Subjectively, the athlete reported numbness along the dorsal and plantar surfaces of his left foot with light workout activities. His pain progressed to his forefoot and he reported toe numbness with activity. He had no pain with level ground walking or at rest but decreasing exercise did not result in improvement. Further examination revealed a negative Homan’s sign. There was no suggestion of an underlying deep vein thrombosis (DVT), but his peripheral pulses, especially on the left, were barely palpable.

Ankle Brachial Index (ABI)

The ABI is used to predict the severity of peripheral vascular disease. A decrease in the ABI with exercise is a sensitive indicator that significant peripheral arterial disease is present. A normal ABI of 1 or 1.1 means that blood pressure at the ankle is the same or greater than the pressure in the subject’s arm and that no significant blockage has occurred. Any ABI reading of less than 1 is abnormal. An ABI of less than 0.95 specifically indicates significant narrowing of one or more blood vessels. An ABI of less than 0.8 may result in pain in the foot, leg, or buttock with exercise. Lab data showed the athlete had an ABI of 0.8 at rest an ABI of 0.3 with exercise with abnormal blood flow at the popliteal artery. The Doppler study showed evidence of lower extremity ischemia which led to the diagnosis -- left lower extremity claudication related to a focal popliteal artery dissection.

August 30, 2005:

The athlete had an 8mm stent placed in the distal superficial femoral/proximal popliteal artery after the Doppler study confirmed blockages of significant physiologic importance. He was put on exercise restrictions of walking only.

September 2, 2005:

On his follow-up evaluation, his symptoms had fully resolved and he denied any calf pain when exercising. He also denied discoloration in the leg and only complained of subtle mild numbness of the forefoot. The athlete was placed on Plavix, an anti-coagulant, and the high risk of bleeding from being on this medication was addressed. He was instructed to avoid stretching and massage of his legs.
No formal rehabilitation occurred per physician recommendations. The physician believed rest would be of greatest benefit. Resistance exercises could potentially damage the repair site from vigorous muscle contractions or from fluctuations in blood pressure.

Return to Play

The athlete started and played in the season opener on September 11, 2005 without incident. To ensure that the stent was secure and vascular blood flow was optimized, the athlete underwent bi-weekly Duplex imaging until the end of the season. A type of Doppler study, duplex imaging uses ultrasound to produce a picture of the blood vessel and surrounding organs. The imaging provides details about the speed and direction of blood flow through the blood vessel. The Duplex study confirmed the success of the stent with no compromise of blood flow.

The athlete completed the 2005-06 season without further complaints or incident. Currently, he is symptom free and is completing all conditioning and mini-camp activities without restrictions. As a precaution against a blood clot, he takes an 81 mg aspirin everyday. He will be re-assessed via Duplex prior to training camp for the 2006-07 season.

Conclusion

The vascular surgeon concluded that the athlete had an arterial flow disruption at the site of the previous knee reconstructions, likely a result of the complications related to the surgeries. The surgeon hypothesized that through repeated surgeries, soft tissues in the region healed as one rather than separate entities. Essentially, a "false lumen", or a blood re-entry point, was created in the intimal layers of the blood vessel through repeated manipulations which changed blood flow in that vessel. Since the blood vessel repeatedly healed from the three manipulative procedures, intimal hyperplasia occurred, resulting in blood flow occlusion. The athlete will require life-long surveillance with periodic Duplex imaging and physiologic testing. If recurrent stenosis is identified, a balloon angioplasty, remote arthrectomy, or surgical reconstruction may be indicated.

This case study affirms the importance of the differential diagnosis and how the long term sequelae of previous operations can cause problems in the future. Typically, injuries seen on a daily basis fit neatly into a category and progress normally. However, there are times when certified athletic trainers must "think outside the box" and consider complications that are beyond musculoskeletal origins. In this case, vascular complications occurred as a result of multiple knee surgeries. Even though this athlete clearly did not fit into the "typical" patient with peripheral arterial disease (i.e. as a result of atherosclerosis), it must be considered nonetheless.