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Acute Compartment Syndrome of the Thigh in a High School Soccer Player

Indications for Expedient Action

Daniel W. Golden, MD; Kyle R. Flik, MD; David A. Turner, MD; Bernard R. Bach Jr, MD; Jeffrey R. Sawyer, MD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 33 - NO. 12 - DECEMBER 2022


In Brief: Compartment syndrome in the lower leg, most commonly related to exertion, has been well documented in athletes. However, compartment syndrome resulting from trauma is rare in athletes, as in this case of a 17-year-old male goalie who sustained a direct blow to his thigh during a soccer game. He was successfully treated with early fasciotomy and delayed wound closure, and he made a full recovery.

Compartment syndrome is "a condition in which increased tissue pressure within a limited space compromises the circulation and the function of the contents of that space."1 Posttraumatic compartment syndrome is a surgical emergency that requires fasciotomy. Acute anterior compartment syndrome of the thigh without associated fracture is a rare but serious clinical condition that must be recognized and treated as quickly as possible. Typical signs and symptoms include a history of trauma to the thigh, progressive pain out of proportion to the initial injury, a markedly swollen thigh, and a progressive neurologic deficit. Morbidity varies from mild, (eg, quadriceps weakness, fatigue, myositis ossificans) to severe, with life-threatening vascular compromise.2 A high index of suspicion for this condition is necessary when evaluating athletes who have significant thigh contusions, such as in the following case of a young soccer player.

Case Report

History. A healthy 17-year-old high school soccer goalkeeper sustained a direct blow to his left thigh during a collision with an opposing player. He experienced immediate pain but was able to continue playing. Over the next 12 hours, the pain became progressively worse despite treatment with ice and rest. By the next morning, the patient could no longer ambulate because of pain.

Approximately 19 hours postinjury, the athlete underwent evaluation in the emergency department. He had no history of any medical problems, including hemorrhagic diatheses, and was not taking any medications.

Physical exam. The patient's blood pressure was 130/80 mm Hg. His left thigh was markedly swollen and 5 cm larger than his right thigh. The anterior compartment was tense, but the medial and posterior compartments were not. Two-point discrimination over the anterolateral thigh was diminished compared with the contralateral side. He was unable to perform a straight-leg raise because of pain, and he was able tolerate only 20° of passive flexion of the knee. The remainder of his neurovascular exam was normal, with palpable dorsalis pedis and posterior tibial pulses.

Imaging and tests. Radiographs of his entire left lower extremity and pelvis revealed no fractures. His hemoglobin (13.5 mg/dL) and urine myoglobin (<2 ng/mL) were normal. A coagulation profile was drawn, and his preoperative prothrombin time was 13.7 seconds, with an international normalized ratio (INR) of 1.15.

Diagnosis. Over the next 3 hours, the patient's pain markedly worsened, requiring significantly more narcotic medication. Sensation over his thigh continued to decrease as swelling of both the anterior and medial compartments increased. At that time the diagnosis of acute compartment syndrome was made.

To expedite surgery, compartment pressure monitoring was not performed, because the clinical diagnosis of an acute compartment syndrome seemed obvious. Because the patient's neurologic deficit was progressing so rapidly, we decided not to delay surgery by waiting for further imaging studies of the thigh.

Treatment and Follow-up. Approximately 22 hours after the initial trauma, the patient underwent a three-compartment fasciotomy of his thigh. The anterior compartment fascia was released first, and the vastus lateralis muscle bulged through the release site immediately (figure 1A). The muscle was purple and dusky but contractile. Approximately 50 mL of hematoma was evacuated from within the anterior compartment of the thigh. The appearance of the muscle improved during direct surgical observation. Limited posterior and medial compartment fasciotomies revealed normal muscle that was pink, healthy, nonedematous, and contractile. The incisions were thoroughly irrigated, packed, and loosely secured with retention sutures to accommodate further swelling (figure 1B). The patient was placed on intravenous antibiotics.

Postoperatively, the patient had an immediate decrease in pain and narcotic use. Sensation began to return to his anterolateral thigh. A coagulation test 2 hours postoperatively showed his INR was 1.27, and this normalized the following morning. Because he had significant knee effusion following a high-energy collision and we were concerned about the possibility of injury to the extensor mechanism of the knee and intra-articular injury, magnetic resonance imaging (MRI) was obtained the day after the fasciotomy. The MRI revealed massive edema and hematoma within the anterior compartment of the thigh, most notably in the vastus intermedius and vastus medialis muscles. No intra-articular pathology or damage to the knee extensor mechanism was noted (figure 2). The MRI would have been performed sooner, but the fasciotomy was deemed emergent.

Three days after the fasciotomy, the patient returned to the operating room for delayed wound closure. At that time, his muscle edema had resolved considerably, and all muscles were contractile and viable. His wounds were closed. The patient began physical therapy and was discharged 2 days later.

As an outpatient, he received additional physical therapy that emphasized knee range of motion. At 6 months postoperatively, the patient resumed all preoperative activities without pain or loss of function. He is currently being recruited to play Division I collegiate athletics.

Discussion

Acute compartment syndrome can be associated with fractures, contusions, surgery, postischemic swelling after arterial occlusion, major vascular trauma, crush injuries, burns, prolonged limb compression, infiltrated infusions into deep veins, and bleeding disorders.1 The syndrome is most frequently seen in the compartments of the lower leg and forearm and less frequently seen in the thigh, arm, hand, shoulder, buttocks, and foot.3 Anterior compartment syndrome of the thigh is a rare but important clinical entity that is usually associated with multiple injuries.4 Our case is unusual in that compartment syndrome evolved without multiple injuries.

Compartment syndrome of the thigh may be rare because the osteofascial compartments of the thigh are larger and more compliant than those of the arm and leg. This allows a greater change in volume before compartment pressure becomes pathologic.

The relative risk of developing acute compartment syndrome caused by participation in athletics depends on the level of physical contact in the sport. American football, ice hockey, and rugby are associated with an increased risk of acute compartment syndrome because of the greater likelihood of high-speed collisions affecting the thigh.5

More About Pathophysiology

Compartment syndrome is caused by an increase in intracompartmental pressure that leads to a decrease in the arteriovenous gradient within the affected compartment.1 This decreased gradient leads to decreased perfusion pressure to the tissues of the compartment and subsequent nerve and muscle ischemia.

Elevation of the limb above heart level actually lowers the arteriovenous gradient and therefore should be avoided. Matsen et al6 demonstrated that elevation of the foot above the level of the heart significantly reduces local blood flow. For this reason, it is recommended that the affected limb in acute compartment syndrome be placed at heart level to maximize the arteriovenous gradient while assisting venous drainage.

In addition, traumatized tissue requires more blood flow than normal tissue to maintain its viability.1 In our patient, the severity of the contusion may have lowered the tolerance to ischemia in the anterior thigh compartment.

Making the Diagnosis

Despite advances in pressure-monitoring equipment, the diagnosis of acute compartment syndrome remains primarily clinical. Most authors state that the clinical examination is still the gold standard for the diagnosis.

Because acute compartment syndrome is a true emergency that must be diagnosed and treated promptly, clinicians must be familiar with the presenting signs and symptoms as well as current treatment guidelines. If not recognized and treated promptly, acute compartment syndrome may lead to irreversible loss of neuromuscular function, tissue necrosis, postischemic contracture, rhabdomyolysis and possible renal failure, and, ultimately, death.3 Ideally, with prompt diagnosis and treatment, normal function is preserved.

The classic clinical signs of acute compartment syndrome are known as the seven "P's" (table 1). As these signs and symptoms become progressively apparent, damage to the muscles becomes less reversible. By the time many of the clinical findings are present, irreversible neuromuscular necrosis may have already occurred. Because compartment syndrome of the thigh is uncommon, no studies have determined the absolute pressure that the compartments can tolerate before irreversible injury occurs. The most reliable early symptom of acute compartment syndrome is pain out of proportion to the injury sustained,2,3,7 as was the case with this young man.

The Seven 'P's' of Acute Presentation in Compartment Syndrome
Sign or Symptom Major Clinical FindingPresentation
PainPain in excess of the presenting injuryEarly
Pressure Affected compartment may be tense to palpationEarly
Pain with passive stretchPain increases with passive range of motion. (This sign is nonspecific, because it may be seen in cases of severe contusions without compartment syndrome.)Early
ParesthesiaNumbness over the cutaneous distribution of the nerve that runs through the affected compartmentMiddle
Paresis or paralysisIschemia or necrosis of the nerves or muscles develops within the affected compartmentLate
PulsesCould be absent, but frequently are palpable. Decreased pulses may be detected in arteries whose proximal course includes the affected compartmentLate
PallorSkin discoloration may be visible, caused by decreased perfusion of the distal extremity specific to the arteries that course through the affected compartment or by impaired venous drainageLate

Increased pressure within the affected compartment is the classic sign of acute compartment syndrome. Multiple techniques are used for measuring compartment pressure and determining if it is high enough to warrant a fasciotomy.7 The first step in monitoring a patient with a possible compartment syndrome is to remove any compressive dressings or casts that may be constricting the affected compartment.

Generally, in normotensive patients, compartment syndrome is diagnosed when the compartment pressure is elevated by more than 30 mm Hg or increases to within 20 mm Hg of the diastolic blood pressure.1,8 The diagnosis of acute compartment syndrome may be obvious, as in our case, making the exact measurement of pressures unnecessary.9 Treatment of acute compartment syndrome should not be delayed for tissue pressure monitoring if the clinical diagnosis has already been made.

Compartment pressure monitoring is essential when the examination is complicated by factors such as a patient's altered mental status or age.7 If a nonresponsive patient is hypotensive, we use the hypotensive guideline values.

Treatment Notes

Fasciotomy is accepted as the best treatment for compartment syndrome in the leg and forearm, but it remains somewhat controversial for the thigh. Robinson et al10 studied six patients who were treated nonoperatively and had good outcomes. A high wound infection rate (50%) and significant loss of function after fasciotomy were the reasons they chose nonoperative treatment.

Mithofer et al4 found that complications were "rare in patients with isolated thigh compartment syndrome but developed in 57% of patients with additional bony or vascular injuries." In their study, the wound complication rate was 18%, primarily in patients who had multiple injuries. The complication and mortality rate correlated with the severity of injury. They concluded that avoiding fasciotomy to prevent complications seems unwarranted.

It is likely that the higher complication rate in the Robinson et al study was due to the nature and severity of the injuries sustained. In our experience, the postfasciotomy infection rate has been low. Newer technologies, such as prophylactic antibiotics and wound vacuum systems, may decrease the risk of infection even further.

The most effective treatment of acute compartment syndrome is surgical decompression. Surgical treatment also allows for gross inspection of muscle quality and contractility, ligation of bleeding vessels, and removal of hematoma. Immediate fasciotomy should be performed as soon as a diagnosis of acute compartment syndrome is made.11

The duration of acute compartment syndrome prior to surgical decompression is the most important factor in predicting the long-term functional outcome.8 Once myoneuronal function is lost, it is not regained, because fasciotomy halts, but does not reverse, ischemic damage.9 Aggressive intravenous hydration, urine alkalinization, close monitoring of urine output, and creatine phosphokinase (CPK) monitoring can help prevent renal complications.4

At the time of fasciotomy, it can be difficult to determine the viability of muscle.8 Muscle that appears ischemic upon decompression frequently will regain its viability when the blood flow returns to normal. Depending on the clinical situation, patients may need to be brought back to the operating room for further debridement and inspection.11 During surgery, elevation of the compartment should also be avoided; the thigh should always be kept at heart level. Any hematoma that is visible should be evacuated to prevent myositis ossificans as a complication of acute compartment syndrome.2 Evacuation of the hematoma also prevents further coagulopathy caused by fibrinolytic activity of the hematoma itself, as well as possibly decreasing the risk of heterotopic ossification. Primary skin closure should be done only when the skin may be closed without tension and a minimum of swelling is anticipated.11

Physical therapy should begin immediately to help maintain and regain both muscular strength and range of motion in the knee and hip. Patients may return to sport when their strength and range of motion are equal to the unaffected side and they remain comfortable while performing sport-specific movements.

No Time to Lose

Acute posttraumatic compartment syndrome is a surgical emergency that requires prompt diagnosis. An alert clinician will recognize the symptom of disproportionate pain and the signs of swelling, pressure, and paresthesia and make an early diagnosis of acute anterior compartment syndrome of the thigh. If the clinical exam findings are ambiguous, compartment-pressure monitoring, MRI, and ultrasound may confirm the diagnosis. As more time elapses before a fasciotomy is performed, the prognosis for a full recovery diminishes. Appropriate early intervention can lead to complete return to activities, even in a high-level athlete.

Irreversible—and sometimes fatal—changes can occur if diagnosis and treatment of compartment syndrome are delayed. We strongly feel that observation as a method of treatment was inappropriate in this case. The ideal candidate for nonoperative treatment would be a young, healthy, conscious patient who has an isolated thigh contusion and is brought to a medical center where expertise in managing compartment syndrome and appropriate surgical backup are available. Although our patient and facility met these criteria, we still chose to operate. If the signs and symptoms are progressing rapidly in a patient who has sustained acute compartment syndrome, fasciotomy should be performed sooner rather than later.

References

  1. Matsen FA III: A practical approach to compartmental syndromes, part 1: definition, theory, and pathogenesis. Instr Course Lect 1983;32:88-92
  2. Klasson SC, Vander Schilden JL: Acute anterior thigh compartment syndrome complicating quadriceps hematoma: two case reports and review of the literature. Orthop Rev 1990;19(5):421-427 [Published erratum in Orthop Rev 1990;19(8):659]
  3. Perron AD, Brady WJ, Keats TE: Orthopedic pitfalls in the ED: acute compartment syndrome. Am J Emerg Med, 2001;19(5):413-416
  4. Mithofer K, Lhowe DW, Vrahas MS, et al: Clinical spectrum of acute compartment syndrome of the thigh and its relation to associated injuries. Clin Orthop Relat Res 2004;425(Aug):223-229
  5. Hutchinson MR, Ireland ML: Common compartment syndromes in athletes: treatment and rehabilitation. Sports Med 1994;17(3):200-208
  6. Matsen FA III, Wyss CR, Krugmire RB Jr, et al: The effects of limb elevation and dependency on local arteriovenous gradients in normal human limbs with particular reference to limbs with increased tissue pressure. Clin Orthop Relat Res 1980;150(Jul-Aug):187-195
  7. Mubarak SJ: A practical approach to compartmental syndromes, part 2: diagnosis. Instr Course Lect 1983;32:92-102
  8. Matsen FA III, Veith RG: Compartmental syndromes in children. J Pediatr Orthop 1981;1(1):33-41
  9. Lagerstrom CF, Reed RL II, Rowland BJ, et al: Early fasciotomy for acute clinically evident posttraumatic compartment syndrome. Am J Surg 1989;158(1):36-39
  10. Robinson D, On E, Halperin N: Anterior compartment syndrome of the thigh in athletes—indications for conservative treatment. J Trauma 1992;32(2):183-186
  11. Rorabeck CH: A practical approach to compartmental syndrome, part 3: management. Instr Course Lect 1983;32:102-113

Dr Golden is a physician in training at the University of Illinois at Chicago Medical Center in Chicago. Dr Flik is a sports medicine orthopedic surgeon at Northeast Orthopaedics, LLP, in Albany, New York. Dr Turner is chairman of the Department of Radiology and Dr Bach is the director of the Sports Medicine Program, both in the Department of Orthopaedic Surgery at Rush University Medical Center in Chicago. Dr Sawyer is an assistant professor of orthopedic surgery at the Campbell Clinic at the University of Tennessee in Germantown, Tennessee. Address correspondence to Jeffrey R. Sawyer, MD, Campbell Clinic, 1400 S Germantown Rd, Germantown, TN 38138; e-mail to [email protected].

Disclosure information: Drs Golden, Flik, Turner, Bach, and Sawyer disclose no significant relationship with any manufacturer of any commercial product mentioned in this article. No drug is mentioned in this article for an unlabeled use.


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