Acute Exercise-induced Bilateral Thigh Compartment Syndrome

Abstract

Acute compartment syndrome of the thigh is rare due to the space’s ability to accommodate large volumes of fluid and, with the exception of the lateral septum, its thin compliant linings. This article describes a case of bilateral exercise-induced severe compartment syndrome treated with anterior and posterior fasciotomies.

A 29-year-old man was admitted to intensive care with myoglobinuria. His left thigh was evaluated 18 hours later for compartment syndrome. The patient reported that 14 hours prior to initial presentation, he had participated in a 1-hour session of vigorous basketball. He gradually developed bilateral moderately severe thigh pain and tea-colored urine. Physical examination revealed pain secondary to passive stretch of both knees at 20° flexion, plus firm anterior and posterior compartments to palpation. A handheld pressure monitor revealed the following compartment pressures: left anterior 80 mm Hg; left posterior 75 mm Hg; right anterior 45 mm Hg; and right posterior 50 mm Hg. Bilateral emergent anterior and posterior compartment fasciotomies were performed. The patient developed a significant severe distal motor and sensory neurological deficit on the left side, which recovered to 3/5 motor strength and protective sensation. At 6-month follow-up, he ambulated with the assistance of a left ankle foot orthosis.

Acute severe compartment syndrome can occur following vigorous exercise. We recommend fasciotomies after exercise-induced acute compartment syndrome rather than initial observation because of the severity of morbidity associated with undertreated compartment syndrome.

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In 1881, Richard von Volkmann^1,2 first described compartment syndrome as the neural palsies and muscular contractures which resulted from prolonged compartmental ischemia in pediatric forearm and supracondylar humeral fractures. In 1926, Jepson³ demonstrated that compartmental ischemia results from subfascial increases in pressure. In 1975, Mubarak and Owen⁴ defined compartment syndrome as “local muscle ischemia and contracture resulting from edema and increased pressure within osteofascial compartments.” They also reported the first documented case of acute compartment syndrome of the thigh as a result of prolonged limb compression.

Although exercise-induced limb ischemia resulting in fatal rhabdomyolysis was described in 1987,⁵ Kahan et al,⁶ in 1994, first reported on exercise-induced thigh compartment syndrome. We describe a case of bilateral thigh compartment syndrome treated with anterior and posterior thigh fasciotomies.

Case Report

A 29-year-old man was admitted to intensive care with myoglobinuria. His left thigh was evaluated 18 hours later for compartment syndrome. The patient reported that 14 hours prior to initial presentation, he participated in a vigorous hour-long session of basketball. Two hours later, he slipped in the shower to a squatting position while keeping both of his feet on the shower floor at all times, causing a mild stretch, but no pain, to both thighs. He gradually developed bilateral thigh pain and tea-colored urine.

On initial assessment, his vital signs were as follows: blood pressure 99/70 mm Hg; pulse 75 bpm; respirations 15 per minute; oxygen saturation 95% on room air; and body temperature 98.7°F. Physical examination demonstrated an alert and oriented man in moderate discomfort. His lower extremity examinations consisted of firm bilateral anterior and posterior thigh compartments with a soft medial compartment bilaterally. He had pain in the left thigh more than the right, with passive knee flexion to 20°. His lower leg compartments were soft. He had 1+ bilateral dorsalis pedis pulses, as well as a 1+ right posterior tibialis pulse. His left posterior tibialis pulse was not palpable, but an ultrasound signal was audible. Sensory examination was intact bilaterally about the foot. Compartment pressures obtained with a handheld pressure monitor measured 80 mm Hg and 75 mm Hg anteriorly and posteriorly, respectively, on the left and 45 mm Hg and 50 mm Hg anteriorly and posteriorly, respectively, on the right.

Emergent bilateral anterior and posterior thigh compartment fasciotomies via lateral thigh incision were performed. Anterior and posterior compartment musculature appeared viable. On postoperative day 2, a repeat irrigation and minimal debridement of superficial muscle bilaterally with a delayed primary closure of the right fasciotomy skin incision was performed. The left fasciotomy was not closable without tension and was therefore dressed with sterile rubber bands to provide continuous skin tension. There was no necrotic tissue in either wound.

On postoperative day 5, the patient returned to surgery for irrigation and debridement of minimal superficial necrotic muscle and fascia from the left anterior compartment. A delayed primary closure was performed. He remained in the intensive care unit for 7 days and was discharged on postoperative day 10.

During his hospital stay, the patient had developed left lower extremity neuropathy with 0/5 motor deficit of his toe and ankle dorsiflexors and plantarflexors. His sensory deficit consisted of decreased sensation in all distributions about the foot and lower leg. He had 2+ pulses distally and had only incisional pain with range of motion of his knee. Electrophysiologic testing of the left leg demonstrated extensive neuropathy of the thigh musculature with distal sciatic sparing. Four months postoperatively, his left leg motor deficit recovered to a 3/5 strength. He still had a persistent minor sensory deficit about the foot and lower leg.

Two and a half weeks after closure of his right thigh wound, the patient had a superficial wound infection with wound dehiscence. A 10-day course of oral cephalexin resulted in resolution of infectious signs. Three and a half months later, the right thigh wound developed a draining sinus, which required repeat irrigation and debridement with intraoperative cultures. He was diagnosed with methicillin-resistant Staphylococcus aureus pyomyositis. He was placed on a 3-week course of oral trimethoprim/sulfamethoxazole after magnetic resonance imaging of the right thigh demonstrated no osseous involvement.

At latest follow-up, 6 months after his fasciotomies, his right thigh wound was healing well. The left thigh scar had healed uneventfully. He was ambulating with the assistance of a knee–ankle–foot orthosis on the left leg. Knee range of motion examination demonstrated 0° to 135° bilaterally. Sensory examination was intact and symmetrical; however, motor examination demonstrated 3/5 with fasciculations of the left toe and ankle dorsiflexors and plantarflexors. His quadriceps muscles had 2/5 strength and hamstrings 4/5.

Discussion

In addition to exercise-induced causes, reported etiologies of acute compartment syndrome of the thigh include blunt, crushing trauma; postoperative and traumatic hematoma^7-10; femur fractures^8,11; intramedullary nailing of femur fractures⁸; prolonged tourniquet time¹²; revascularization of an ischemic limb; deep venous thrombosis^13,14; iatrogenic or traumatic vascular injury^11,15; snake bite¹⁶; external compression^4,8; and surgical positioning.^17-19 Reported associated etiologies that may increase the risk of thigh compartment syndrome in an established etiology include pneumatic antishock trousers²⁰; hypotension⁸; rapid, high-volume intravenous fluid resuscitation⁸; coagulopathy⁸; and local skin scars.²¹

The unusual occurrence of thigh compartment syndrome is believed to result from the accommodating nature of the compartments due to their larger volumes and, with the exception of the lateral intermuscular septum, thinner and more compliant borders.^8,11 Also, increased fluid volume in the thigh has the potential to extravasate into the gluteal region, according to Schwartz et al,⁸ thereby decompressing the thigh compartment syndrome.

The pathogenesis of compartment syndrome, as defined by Mubarak and Owen,⁴ is ischemia resulting from increased intracompartmental pressure. They suggested that the cause was not ischemia from absent arterial inflow, but rather obstruction of venous or lymphatic outflow resulting in poor tissue perfusion. Increased pressure in the thigh has been documented to result from external compression or increased volume. The latter can result from a fluid mass effect from intracompartmental bleeding, which can be caused by muscular or vascular injury rather than direct bleeding from the intramedullary canal of a long bone.^11,15 Similarly, Winquist et al²² had no compartment syndromes in 520 femur fractures, suggesting that fracture hematomas alone were not massive enough to jeopardize the vasculature. The increased volume can also occur from interstitial edema as a result of increased vascular permeability due to exogenous chemicals,¹⁶ ischemic necrosis of soft tissue,²³ or ischemia-induced cell hypertrophy.²⁴

The diagnosis of thigh compartment syndrome is made by clinical evaluation in the awake and compliant patient. Early physical examination findings include increased compartment pressure and pain exacerbated by passive range of motion of the intracompartmental muscles. Paresthesias and paralysis distal to the compartment result from the relative intolerance of nerves to compromised perfusion. Later, more ominous findings include skin pallor and absent or diminished pulses, representing significant increases in the compartmental pressures to obstruct venous as well as arterial flow.^25,26 In the head-injured or otherwise noncompliant patient for whom one cannot elicit painful passive range of motion or accurately assess a neurologic examination, compartment pressure measurements can confirm a suspected diagnosis. Techniques have been described elsewhere.²⁷ Although compartment pressures are frequently measured in the literature, the authors contended that they were for documentation and research purposes only and did not change the course of treatment.

The pressure magnitude at which a compartment syndrome is confirmed is controversial. Whitesides and Heckmann²⁶ recommended any pressure within 20 mm Hg below the patient’s diastolic blood pressure necessitates a compartment fasciotomy.Mubarak et al²⁵ reported that ischemia was probably present if the intracompartmental pressure measured >30 mm Hg. However, Matsen et al,²⁸ who continuously monitored compartment pressures in suspect patients, noted that no fasciotomies were performed and no compartment syndrome sequelae developed if the peak pressure was ≤45 mm Hg.

The differential diagnosis of acute exercise-induced compartment syndrome must include chronic exertional compartment syndrome. The examining physician can differentiate the acute compartment syndrome from chronic exertional compartment syndrome through a history and physical examination. A negative history of recurrent, insidious onset compartmental pains related to activity or recurrent injuries relieved by prolonged cessation of activity suggests an acute episode.

Once acute compartment syndrome has been diagnosed, treatment should begin immediately. Robinson et al²⁹ expressed concerns regarding wound morbidity associated with fasciotomies and therefore recommended nonoperative observation with frequent neurovascular examinations, intracompartmental pressure monitoring, and narcotic analgesia. They described the successful nonoperative treatment of 6 athletes, all of whom obtained isolated anterior compartment syndrome with an intraquadriceps hematoma with no associated fracture or other injury. The mechanism of injury was not elucidated; however, it can be assumed that the athletes sustained the injuries during low-energy contact during sport participation. The authors’ concerns regarding wound sepsis were drawn from a 1989 case series of 21 thigh compartment syndromes in 17 patients evaluated at a level I trauma facility after sustaining injuries in motor vehicle or industrial accidents.⁸ In this series, Schwartz et al⁸ cite a 67% wound infection rate (6 of 9 surviving patients), with 2 of the 9 cases having a contaminated compartment as a result of an ipsilateral open femur fracture. Due to the high-energy trauma etiology of these cases, some patients required prolonged intensive care, which increased their exposure to nosocomial infectious pathogens. After multiple surgical debridements, 100% of the wound infections resolved.

Likewise, Mithöfer et al³⁰ initially espoused nonoperative treatment of an anterior thigh compartment syndrome sustained during contact sport participation. However, after initial improvement, the compartment syndrome recurred, requiring a fasciotomy. Robinson et al²⁹ also recommended observation because of possible knee flexion impairments resulting from extensor mechanism adhesions due to the long incision. However, Schwartz et al⁸ documented no compartment sequelae in 7 of 10 cases (6 of 9 patients). Of the remaining 3 cases, only 1 patient had impaired knee range of motion. Although this case was complicated by an ipsilateral grade III open tibia fracture, the patient still had 100° of knee flexion.

In contrast, the majority of authors recommend early decompression with fasciotomies, thereby decreasing the occurrence of known acute compartment syndrome sequelae.^11,27 Several authors recommend fasciotomies after exercise-induced acute compartment syndrome rather than initial observation because of the severity of morbidity associated with undertreated compartment syndrome.^6,25 Access to the anterior and posterior compartment can be accomplished through a lateral incision anterior to the lateral intermuscular septum. After the anterior decompression, the lateral intermuscular septum is incised to allow release of the posterior compartment.¹¹ Access to the medial compartment is obtained via a separate longitudinal incision over the adductor longus (the Ludloff approach). From this incision, the 3 adductors and gracilis are decompressed.²⁵

We performed fasciotomies bilaterally in our patient despite the low-energy, exercise-induced etiology of his bilateral compartment syndromes. However, our patient still developed left leg neuropathy, probably due to the delayed nature of his surgical decompression as a result of his delayed transfer. He remained in the intensive care unit for 1 week postoperatively and, despite early closure of his right, less severely involved thigh, developed a chronic methicillin-resistant S aureus wound infection. His left wound, which received 2 irrigations and debridements prior to closure, healed uneventfully. Based on this case, we recommend an emergent fasciotomy for acute thigh compartment syndrome without regard to its etiology. Subsequent morbidities, such as infections or joint contractures, are minor compared to the missed compartment syndrome sequelae.

References

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Authors

Drs Boland and Heck are from the Department of Orthopedic Surgery, University of Kentucky College of Medicine, Lexington, Kentucky.

Drs Boland and Heck have no relevant financial relationships to disclose.

Correspondence should be addressed to: Dr Michael R. Boland, MBChB, FRCS, FRACS, Department of Orthopedic Surgery, University of Kentucky College of Medicine, 740 South Limestone St, K401, Lexington, KY 40536.