Acute Exercise-Induced Compartment Syndrome of the Lower Leg

INTRODUCTION Acute compartment syndrome can put an athlete at risk for muscle and limb loss. The classic presentation is a posttraumatic painful limb with a tense compartment and pain with passive range of motion. However, there are times when the problem does not present with the classic history and physical findings. Physicians and others caring for athletes should have a high index of suspicion for acute compartment syndrome to avoid an adverse outcome for the athlete. CASE PRESENTATION A 33-yr-old distance runner presented to the office complaining of leg pain approximately 28 h after completing a 100-mile ultra-marathon on a 73°F (mean), 70% humidity (average) August day in northeastern Ohio. He finished the race in 26 h and 57 min without difficulty and went home to take a nap. He had attempted this same 100-mile race the previous year on a much more hot and humid day, but stopped running at mile 80 due to dizziness. He awoke from sleep 4 h later with extreme right lower leg pain associated with swelling and redness. He had not taken any medications during or after the race and was not on any daily medications. With progressively worsening pain, he went to the local emergency department (ED), where a plain film of the tibia and fibulae was ordered. The radiographic films were negative and the discharge diagnosis was "shin splints." The athlete was sent home with instructions to use antiinflammatories, ice, and elevation. He continued to have difficulty sleeping that night secondary to worsening pain in his lower leg, with increasing difficulty walking secondary to pain. He presented to our office approximately 24 h after his initial pain for further evaluation where he described the pain as deep and achy. The pain peaked at a 9/10, worsening with any motion of his lower leg. The athlete denied any numbness or tingling, foot drop, fevers, chills, unexplained weight loss, or previous injury. There was no change in his urine color. There were no complaints of headaches or history of bug bites, rashes, or recent travel history. His past medical, family, surgical, and social history were noncontributory. On physical exam, the patient was afebrile with blood pressure of 110/64, pulse of 60, and respirations of 10. He had swelling of his anterior and lateral lower leg compartments with mild erythema and warmth. The anterior and lateral compartments were moderately tense compared with the corresponding compartments on the contralateral lower leg. He had a normal gross sensory exam and normal dorsalis pedis and posterior tibial pulses bilaterally. The capillary refill was normal. There was decreased motion with plantarflexion, dorsiflexion, inversion, and eversion on the right side compared with the left, and these motions elicited the pain. There was significant pain with passive dorsiflexion and eversion of the foot. He was able to flex his toes freely and without pain. There was normal flexion and extension of the lumbar spine and knees bilaterally, and the patellar and Achilles reflexes were normal bilaterally. There was a negative Tinel's at the fibular head bilaterally and no palpable popliteal cords that might indicate deep venous thrombosis. Strength testing was severely limited by the pain and could not be assessed. Compartment pressures were measured in the office using a handheld intra-compartmental pressure-monitoring system (Stryker Surgical, Kalamazoo, MI). The resting pressure was 35 mm Hg in the anterior compartment and 39 mm Hg in the lateral compartment. The high resting pressures confirmed the diagnosis of acute compartment syndrome. Bloodwork included normal chemistries with a serum creatinine of 0.9 mg·dL−1; however, the creatine kinase (CK) level was 6920 (24-195 Units·L−1). He was taken to the operating room where all four of his right lower leg compartment pressures were measured. Preoperative compartment pressures in the posterior compartments were 20 mm Hg in the deep posterior and 20 mm Hg in the superficial posterior compartment. Compartment pressure in the anterior compartment was 38 Hg and 41 mm Hg in the lateral compartment. Fasciotomy was performed in the anterior and anterior lateral compartments, and the surgeon reported that the muscle tissue appeared viable. The skin was closed primarily after the fasciotomy without the need for skin grafting. In the recovery room, the patient felt relief of the leg pain. He was placed in a posterior splint, instructed in non-weightbearing crutch use, and discharged home with an activity restriction and instructions to elevate the extremity. On post-operative day 8, the splint and sutures were removed. He was instructed in gentle passive range of motion movements to be performed on his own, and he was permitted to progress to active range of motion and full weightbearing as tolerated. On post-operative day 15, the patient was feeling very good and had no pain with walking, except on one occasion when he caught his toe, causing a rapid plantar flexion with brief 2/10 pain. He was started in formalized physical therapy after this office visit. The athlete returned to the office on post-operative day 25 feeling "almost 100%" with no pain or aching in his lower leg or surgical site. He had progressed to running 2.5 miles pain free and was ready to return to his job as a firefighter. He was given permission at that point to increase his activity as tolerated. A phone interview 7 months after his surgery revealed he was having no problems and was running 60 miles·wk−1. DISCUSSION Richard von Volkmann published his observation over 100 yr ago describing contractures and paralysis of muscle that result from the lack of arterial blood supply due to excessive tissue pressure from trauma (31). This observation laid the groundwork for understanding acute compartment syndrome. Dr. Paul Jepson, a fellow in orthopedic surgery at the Mayo Clinic, was the first to show that this paralysis and contracture could be prevented by prompt decompression of the affected compartments (13). Most cases of acute compartment syndrome in sports activity are secondary to trauma. More rare causes of acute compartment syndrome in the extremities have been described, including post-ischemic, arterial thrombosis, prolonged decubitus position, thrombolytic therapy/anticoagulation, infection, pneumatic antishock trousers, and exercise-induced etiologies for pressure increases (2-18,21-28,30,33). This case represents one of a handful of cases in the literature of acute exercise-induced compartment syndrome (3-5,8,10-12,14,16-18,21,23,24,33). Most of these reports are related to novel exercise in athletes and nonathletes. Some of the events described include running, spinning on a stationary bike, toe kicking a football, walking, soccer, basketball, volleyball, high jump, and repetitive squatting. The pathophysiology of this type of compartment syndrome has not been described fully. Intense or novel exercise bouts can lead to increased compartment pressure by fluid accumulation and acute muscular swelling. These increases in intra-compartmental pressure may be a result of increased arterial blood flow and/or fluid shifts based on increased muscle oncotic pressure from metabolites and muscle breakdown or from electrolyte shifts. Increasing pressure within a closed compartment eventually exceeds venous pressure impairing blood flow. As compartment pressures overcome perfusion pressure, the result is muscle and nerve ischemia. Muscle ischemia increases compartmental pressure and sets up a vicious cycle of increasing compartment pressure, ischemia, and pain. Early recognition of acute compartment syndrome is important to minimize morbidity and improve the chances for a good outcome. Considering the diagnosis in the differential of acute lower leg pain combined with a good history and physical exam are paramount to early recognition of this problem. Important physical examination points include tense compartments, pain with passive motion, and pain out of proportion for the clinical presentation. Compartment pressure testing should be performed in cases where the diagnosis is not clinically evident or the patient has an impaired level of consciousness. The consequences of a delayed or missed compartment syndrome diagnosis can be grave. If not treated, the muscles and nerves undergo necrosis, and limb contracture can result. Subsequent to the necrosis risk of infection and rarely limb loss is possible. In one study, patients with a fasciotomy performed 12 h or more after the onset of pain had a return of full function only 8% of the time (29). The differential diagnosis should include infection, deep venous thrombosis, stress fracture, fracture, nerve entrapment, compression neuropathy, and chronic exertional compartment syndrome. Threshold intra-compartment pressure values that confirm the diagnosis have ranged from 30 to 50 mm Hg in the literature (1,19,20). Whitesides (32) proposed comparing the diastolic blood pressure with the intra-compartmental pressures (Δp). A Δp value (diastolic blood pressure minus the intra-compartmental pressure) less than or equal to 30 mm Hg would constitute a positive test. In cases such as these, the Δp value should be tempered with clinical suspicion to arrive at the diagnosis. Our patient had an excellent outcome. He was able to return to full activity 4 wk postoperatively. This was a very fortunate outcome despite his late presentation for surgical treatment. Complications can result from delayed treatment, including necrosis, contracture, and infection. Return to activity after fasciotomy should be accelerated as soon as the incisions heal. This is an atypical case of acute compartment syndrome, and many times, other injuries preclude rapid advancement of activity. Gentle active range of motion may be started prior to suture removal based on pain level and should definitely be started after suture removal. The patient should be progressed to weightbearing as tolerated when the wounds are healed. In cases of fasciotomy after chronic exertional compartment syndrome, ambulation is encouraged the day of surgery. Formal physical therapy can start as early as 7 d post-surgery and should be instituted by 2 wk postoperatively. Once the athlete is at full weightbearing without pain, the progression to a jogging program can begin. This generally occurs at approximately 4 wk post-surgery. Return to full activity may take anywhere from 6 to 12 wk.