Bilateral Lower Extremity Compartment Syndrome and Anterior Tibial Stress Fractures Following an Army Physical Fitness Test

Introduction

A 30-year-old active-duty soldier presented to the Walter Reed Army Medical Center emergency department for evaluation of sudden-onset bilateral leg and thigh pain immediately following completion of his 2.5-mile army physical fitness test walk. On evaluation he was found to have grade 4 anterior tibial stress fractures and bilateral lower extremity compartment syndrome.

Case Report

A 30-year-old active-duty soldier with bilateral patellofemoral syndrome came to the Walter Reed Army Medical Center emergency department for evaluation of sudden-onset bilateral leg and thigh pain immediately following completion of his 2.5-mile army physical fitness test (APFT) walk. He stated that during the preceding 3 weeks he had been training for the APFT by walking 2 to 3 miles three times per week. Plain films of the lower extremities demonstrated bilateral anterior tibia stress fractures (Figures 1 and 2). Laboratory results were significant for a creatine kinase level of 718 and normal liver associated enzymes. The patient was given narcotics for pain control and an outpatient appointment for a bone scan. Six days later he returned for his bone scan (Figures 3 and 4), immediately after which he presented to the internal medicine clinic complaining of intractable pain and lower extremity swelling. Repeat laboratory results demonstrated a creatine kinase level of 10,609. The orthopaedic surgery department was consulted. Over the ensuing 8 hours sensory loss in the distribution of his deep fibular nerve developed. Right and left leg compartment pressures were measured as 85 and 30, respectively. The patient was taken to surgery where bilateral 4 compartment fasciotomies were performed along with debridement of the left anterior compartment and right deep posterior compartment.

Figure 1.

X-ray showing anterior cortical stress fracture of the left tibia.

Figure 2.

X-ray showing anterior cortical stress fracture of the right tibia.

Figure 3.

Delayed anterior and posterior images from technetium 99 bone scan showing mild diffuse soft tissue increased activity in the calf regions.

Figure 4.

Blood flow and blood pool images from technetium 99 bone scan showing multiple focal and diffuse areas of increased abnormal radiotracer accumulation noted throughout the bilateral tibiae and fibulas. Some of the more intense areas appear to involve the full cortical thickness, suggestive of grade 4 (or severe) stress fractures.

Discussion

Both acute exertional compartment syndrome and anterior tibial stress fractures are rare causes of leg pain in young athletes.[1,2] As demonstrated by this case, their combined presentation can pose a diagnostic dilemma. However, because of the associated morbidity, it is imperative that both be excluded in patients with exercise-related leg pain.

Stress fractures occur as a result of frequent stressing of a bone with compression or stretch. Abrupt increases in the duration, frequency, or intensity of physical activity without sufficient rest is thought to lead to an imbalance between bone resorption and formation.[3] This results in microfractures that can coalesce into stress fractures. The incidence of stress fractures varies widely based on the population being assessed. In an athletic population, the incidence is approximately 0.12%, but this rises to as much as 20% in runners.[4,5]

Risk factors for stress fractures can be divided into 3 subclasses: activity related, biomechanical, and metabolic. Activity-related risk factors include poor footwear, excessive training, and irregular terrain.[6] Inflexible or weak calf muscles, unequal leg length, flat or high-arched feet, forefoot varus, subtalar varus, and tibia vara comprise the biomechanical risk factors.[4] In addition, any disease state that leads to demineralization of the bone is a risk factor for stress fractures.

Patients with stress fractures typically have a gradual increase in pain with activity, which may progress to rest pain. Occasionally, the patient may experience an abrupt increase in pain when an area under stress finally fractures. An acute onset of severe pain as described in the case example is an unusual presentation for stress fractures. A diagnosis is made based on history and physical examination with confirmatory radiography or bone scan. X-rays have a low sensitivity in the first 2 to 3 weeks of injury, but can be very specific. Bone scans are able to detect evidence of stress fractures within 2 to 3 days of injury with a high sensitivity (74%). However, the specificity is low, with as many as 50% of positive findings being falsely positive.[7] Magnetic resonance imaging is a viable alternative to bone scan because it has equal sensitivity (88%) but improved specificity (100%).[8]

Treatment of stress fractures in the primary care setting is based on whether the fracture is in a high- or low-risk site. Low-risk sites include the second through fourth metacarpal shafts, posterior/medial tibial shaft, humerus, ribs, sacrum, and pubic rami. In these low-risk sites stress fractures can be treated with a brief period of rest followed by gradual return to normal function. High-risk sites include the superior side of the femoral neck, patella, anterior cortex of the tibia, medial malleolus, talus, tarsal navicular, proximal fifth metatarsal shaft, great toe sesamoids, and base of the second metatarsal bone. These patients should be referred to the orthopaedic services because of the higher risk for non-union or for long-term disability.

Compartment syndrome results from increased pressure within a closed space that leads to tissue ischemia and death. The underlying etiology of this increased pressure may be trauma, reperfusion injury, prolonged limb compression, or exertion. Exertional compartment syndrome can be broken into acute or chronic, both of which are a result of increased muscle volume and weight secondary to increased blood flow and edema as a consequence of exercise.[9] Chronic exertional compartment syndrome is by far the most common of the two. Patients have severe pain in the affected compartment occurring with exercise and relieved with rest. Relief of pain with rest and recurrent pain help distinguish chronic exertional compartment syndrome from acute exertional compartment syndrome.[10] Acute exertional compartment syndrome has been associated with a sudden increase in activity levels in unconditioned individuals.[10] The clinical presentation of compartment syndrome has traditionally been described as the 5 Ps of pain, pallor, pulselessness, paresthesia, and paralysis. Unfortunately, most of these are late findings and signify irreversible tissue damage. Early findings in compartment syndrome are pain out of proportion to examination results, tense swollen compartment, and pain with passive stretching of the compartment.[2]

Diagnosis of compartment syndrome is typically based on clinical signs and symptoms. There are, however, confounders that may make the diagnosis more difficult, where measurement of intracompartment pressures is necessary. These include patients who are unconscious, patients at high risk who require continuous monitoring, and patients in whom there is high clinical suspicion but the presentation is atypical. Treatment of compartment syndrome is fasciotomy to allow expansion of the compartment, which decreases intracompartment pressure.

The patient described above had a sudden onset of pain following an abrupt increase in his physical activity. Once the diagnosis of severe stress fractures was made, his workup ceased because it was thought that the severity of his stress fractures was adequate to explain his pain, and a treatment regimen for his stress fractures was undertaken. Only later in his course did compartment syndrome become apparent. To the best of our knowledge, this is the only case of acute exertional compartment syndrome presenting concurrently with stress fractures reported in the literature. Reviewing the patient's history reveals a few clues that point more toward acute exertional compartment syndrome stress fractures. For instance, he denied any preceding leg pain (which is difficult to explain given the severity of his stress fractures), his pain was sudden in onset with pain out of proportion to results of examination, and his lower extremities were notably swollen. This case reinforces the importance of ruling out compartment syndrome in athletes with pain because a delay in diagnosis will result in permanent damage.