EVALUATION

Knee dislocations are typically the result of high-energy, violent trauma. Therefore, the initial evaluation should always begin in the same fashion as that for a polytrauma patient. A primary survey consisting of assessment of the patient’s airway, breathing, and circulation (ABCs) is performed first. The secondary survey seeks life-threatening injuries and conditions. Polytrauma patients require a thorough neurologic and vascular examination, followed by an assessment of the chest, abdomen, and pelvis along with a detailed musculoskeletal examination of the extremities and spine. Whenever possible, the medical history should be reviewed while the patient is assessed for common polytrauma conditions, such as hypovolemia and concussion. Once the basics of trauma care have been attended to, the injured extremity should be carefully examined.

The vascular and neurologic examinations are of utmost importance and are detailed in the following sections. Starting with visual inspection, all open injury sites should be identified and cleansed. Palpation of bony prominences, areas of soft tissue swelling, and key insertion sites provides important information. If possible, the extensor mechanism should be tested to ensure the status of the quadriceps and patellar tendon. If the patient is unconscious or cannot cooperate, these structures should be imaged by MRI followed by a physical examination, when possible. Lastly, a complete ligament examination is conducted to assess the anterior cruciate ligament (ACL), posterior cruciate ligament (PCL), fibular collateral ligament (FCL), medial collateral ligament (MCL), and posterolateral and posteromedial structures using translation and rotation testing. Stress view imaging may be helpful, but may not be appropriate in the acute setting.

CLASSIFICATION

A patient with two or more torn major ligaments may have sustained a knee dislocation.⁵⁴ This definition accounts not only for those knees that are dislocated at the time of evaluation but also for those that have spontaneously reduced. Clinically, the degree of ligament disruption can be misleading. Because ligaments can stretch and may not appear completely disrupted, especially on MRI, the severity of these injuries can be easily underestimated.

The following variables are the basis for classification and complete description of a dislocated knee: (1) direction of dislocation, (2) open or closed, (3) high- or low-energy trauma, and (4) time from dislocation.¹⁶ Schenck⁵⁰ has also recommended that the extent of ligamentous injury be included in the classification of knee dislocations (see Chapter 26, Classification of Knee Dislocations).

The direction of dislocation may be unidimensional (anterior, posterior, medial, or lateral) or a rotatory combination. If the knee has spontaneously reduced, classification is based on direction of instability.⁴⁶ Anterior dislocations caused by hyperextension of the knee are the most common, occurring in 40% according to Green and Allen’s review¹⁷ of 245 knee dislocations. Posterior dislocations, often caused by high-energy dashboard mechanisms, accounted for 33% of the cases. Medial and lateral dislocations were present in 18% and 4% of the cases, respectively.

In 1963, Kennedy’s biomechanical study²⁶ in cadavers elucidated the mechanisms for both anterior and posterior dislocations. This investigation demonstrated that by progressively hyperextending the knee, the posterior capsule ruptured followed by the PCL and the ACL. Without adequate ligamentous restraint, the knee dislocated in an anterior direction. A high posteriorly directed force on the proximal tibia in knee flexion caused a posterior dislocation.

Posterolateral dislocations are the most common type of rotatory dislocations. The flexed and non–weight-bearing knee undergoes a sudden rotatory moment that abducts and internally rotates the lower leg on the femur.⁴⁴ This causes the medial femoral condyle to “buttonhole” through the anteromedial capsule, which may be irreducible. Inspection of the knee will reveal a transverse groove in the skin along the medial joint line secondary to invagination of the medial capsule. This “dimple sign” becomes more prominent with attempted reduction and is pathognomonic of the irreducible posterolateral dislocation.^{16,38,45,48,49}

Open dislocations of the knee are emergencies that require antibiotics and urgent irrigation and débridement in the operating room. Open injuries, present in 19% to 35% of knee dislocations, are most commonly seen with anterior and posterior mechanisms.^36,55

VASCULAR INJURIES

Arterial trauma associated with knee dislocations represents limb-threatening injuries. The incidence of popliteal artery disruption during a knee dislocation is 32% to 45%.^17,24 Delay in diagnosis longer than 6 to 8 hours is associated with an increasing amputation rate.^17,24 Because of the high rate of injury and the devastating consequences associated with a delay in diagnosis, it is imperative to recognize vascular injuries early. An abnormal vascular examination should prompt an immediate vascular surgery consultation.

The popliteal artery is at risk of injury during a knee dislocation owing to its anatomic location (Fig. 27-1). The popliteal artery is tethered proximally by the adductor hiatus and distally by the soleus arch. The artery bifurcates into the anterior and posterior branches at the soleus arch. Collateral circulation in the form of the genicular arteries originates within the popliteal fossa. The geniculate arterial system is usually not sufficient to perfuse the limb should there be obstruction or transection of the popliteal artery.^16,40 Anterior dislocations of the knee can place significant traction on the popliteal artery, leading to extensive intimal injury and/or vasospasm (Fig. 27-2).¹⁷ Posterior dislocations can result in complete transection of the artery (Fig. 27-3).⁴¹

FIGURE 27-1 Schematic diagram of the sciatic, tibial, and common peroneal nerves and their relationship to the other structures in the popliteal fossa.

(Used with permission from Kim, T. K.; Savino, R. M.; McFarland, E. G.; Cosgarea, A. J.: Neurovascular complications of knee arthroscopy. Am J Sports Med 30:619–629, 2002.)

FIGURE 27-2 Angiogram demonstrates diffuse irregularity in the popliteal artery with intimal dissection.

FIGURE 27-3 Left, An anterior knee dislocation demonstrates a traction injury to the popliteal artery. Right, A posterior dislocation demonstrates a transaction injury to the popliteal artery.

The diagnosis of a vascular injury should be made on the assimilation of a variety of clinical and diagnostic tests including physical examination, ankle/brachial index (ABI), and arteriography. The dorsalis pedis arterial pulse is palpated on dorsum of the foot, and the posterior tibial arterial pulse is palpable posterior to the medial malleolus. The presence of these pulses with a warm foot is not a guarantee that an arterial injury is not present. There are multiple reports of vascular occlusion or intimal tears with normal distal pulses; the incidence is reported to be 5% to 15%.^1,24,33,61 In 2004, Barnes and coworkers⁴ performed a meta-analysis that included 284 multiligamentous knee injuries in seven studies. Seven of 52 patients requiring vascular surgery had normal pulses on presentation. Thirteen of 140 patients with normal pulses who underwent arteriography had nonocclusive intimal defects that were safely observed. Abnormal pulses had a sensitivity rate of 0.79 (95% confidence interval [CI], 0.64–0.89), specificity rate of 0.91 (95% CI, 0.78–0.96), positive predictive value of 0.75 (95% CI, 0.61–0.83), and a negative predictive value of 0.93 (95% CI, 0.85–0.96). The low sensitivity and specificity may be associated with hypotension in the acutely traumatized patient, as well as intimal lesions that may initially present with normal pulses.

The ABI is the second diagnostic tool to be used. ABIs are determined by measuring the systolic blood pressure for all four extremities using a Doppler probe and a standardized blood pressure cuff. For the lower extremity, the systolic pressure is measured at the posterior tibial and dorsalis pedis arteries. ABI is then calculated by dividing the highest measured pressure in the ankle or foot by the higher of the brachial arterial pressures. An ABI of less than 0.90 is considered abnormal and should prompt arteriography. In 2004, Mills and associates³⁷ demonstrated that 11 of 11 patients with ABIs less than 0.90 required a reverse saphenous vein graft for popliteal artery injury (3 popliteal artery transections, 6 popliteal artery occlusions, 1 common femoral and peroneal artery thrombosis, and 1 high-grade superficial femoral artery occlusion with intimal flap altering popliteal artery flow). None of the 27 patients with ABIs greater than 0.90 had evidence of vascular injury by serial examination or duplex ultrasonography. The sensitivity and specificity was 100%. In 1998, Cole and colleagues⁸ evaluated 70 consecutive patients with blunt trauma and found no arterial injury with ABI greater than 0.90, whereas an ABI lower than 0.90 had a positive predictive value of 88%. Lynch and Johansen³¹ studied blunt and penetrating trauma in 100 consecutive patients and found an ABI less than 0.90 predicted vascular surgery with a sensitivity of 87%, specificity of 97%, and positive predictive value of 91%.

Arteriography, developed in the 1960s, has improved outcomes and reduced the number of negative explorations. Many authors have advocated routine use of arteriography to evaluate the limb after a suspected knee dislocation.^{1,9,17,25,26,30,32,33,67} The routine use of arteriograms for suspected knee dislocations is justified by the relative low morbidity of the test, the high incidence of popliteal injury, and the devastating consequences of a delay in diagnosis.⁴⁶ However, clinicians should be aware that not all arterial trauma is detectable with arteriography. Stretch injuries of the intimal wall and small intimal flap tears may not be visualized on the arteriogram, but may subsequently clot and result in arterial occlusion. Those patients who worsen usually do so within the first 3 months, but more commonly, within a week after injury. McDonough and Wojtys³⁴ reported on three patients with normal initial arteriograms. Two patients who had loss of pulse after tourniquet release during ligament reconstruction were found to have chronic intimal flaps with thrombi at immediate revascularization. One patient developed a pseudoaneurysm, which was recognized by a second arteriorgram after there was significant postoperative swelling.³⁴

Arteriograms can be performed in the operating room if there are obviously diminished pulses or if the delay in obtaining a formal arteriogram in the angiography suite would compromise limb survival. Six to 8 hours of warm ischemic time will significantly compromise a lower extremity.¹⁷ Formal angiography is performed with a femoral artery puncture followed by insertion of a pigtail catheter. Next, a bolus of contrast is injected and an angiographic unit is used to capture images. The length of the segment to be imaged determines the number of acquisitions needed. Intraoperative arteriogram can be performed by injecting 45 mL of contrast through an 18-gauge catheter with a single film exposure³⁵ or a vascular fluoroscopic unit.

Unfortunately, arteriography is not without risks, costs, and false-negative results. The complication rate has been reported to be 1.7% and includes thrombosis, arteriovenous fistulae, bleeding, renal failure, reaction to contrast material, and pseudoaneurysm formation.^{3,27,37,61,66} The reported false-positive results have ranged from 2.4% to 7%, which could lead to unnecessary surgical intervention.^3,58,61,66 The cost of the arteriograms ranged from $750 to $1,500 per study in 1990; a more recent figure was $5,240 in 2003.^3,58,61

In addition to formal angiography, new techniques such as computed tomographic angiography (CTA) and magnetic resonance angiography (MRA) are being developed. These techniques make use of readily available imaging techniques often with a bolus of contrast to define the lower extremity arterial system. Potter and coworkers⁴³ demonstrated 100% correlation between conventional angiography and MRA in a small cohort of patients (six patients: four normal, one intimal tear, one decreased flow).

NEUROLOGIC INJURIES

Neurologic damage occurs in 16% to 40% of knee dislocations.^2,57 This may range from a stretch injury (neurapraxia) to a complete transection (neurotmesis). The peroneal nerve is most commonly injured as it is stretched over the fibular neck during a posterolateral dislocation (Fig. 27-4).^{14,47,60,62,67} A common presentation for peroneal nerve injuries is a patient with a drop foot and sensory deficit over the dorsum of the foot. Tibial nerve injury associated with a popliteal artery injury has also been reported.⁶⁷ Although difficult, a complete neurologic examination of both lower extremities should be performed both before and after any attempt at reducing a knee dislocation. Repeated examinations are recommended during the course of treatment because there is a potential for nerve compromise due to soft tissue swelling and compartment syndrome, pressure, immobilization, and/or positioning.

FIGURE 27-4 A, Posterolateral view of a left lower extremity cadaveric microdissection depicts the common peroneal nerve in the distal popliteal fossa and its branches, the superficial and deep peroneal nerves. B, Lateral view of a right lower extremity cadaveric microdissection shows the deep peroneal nerve muscular branches supplying the tibialis anterior, extensor digitorum longus, extensor hallucis longus, and peroneus tertius muscles. lat., lateral; N, nerve.

(Used with permission from Kim, D. H.; Murovic, J. A.; Tiel, R. L.; Kline, D. G.: Management and outcomes in 318 operative common peroneal nerve lesions at the Louisiana State University Health Sciences Center. Neurosurgery 54:1421–1428, 2004.)

In the posterior midthigh, the sciatic nerve divides into the common peroneal nerve and the tibial nerve (Fig. 27-5).²⁹ The common peroneal nerve courses obliquely through the popliteal fossa, then traverses along the fibular neck in an exposed subcutaneous fibro-osseous tunnel.^52,60 This subcutaneous position adjacent to the fibula makes the nerve susceptible to direct contact during sports and to indirect injury during a forced varus stress as it is stretched over the fibular neck.¹⁹ The tibial nerve lies lateral to the popliteal vessels within the popliteal fossa. As it courses distally, it crosses posterior to the vessels and then lies medially. It passes between the two heads of the gastrocnemius muscle and anterior to the arch of the soleus muscle to lie in the deep posterior compartment of the lower leg. Within the popliteal fossa, the tibial nerve gives off several branches. The medial sural cutaneous nerve joins the peroneal communicating branch of the common peroneal nerve to form the sural nerve. The posterior articular branch pierces the posterior capsule to innervate the contents of the knee. Finally, there is a motor branch to the popliteus muscle.²⁹

FIGURE 27-5 Schematic diagram of the popliteal artery.

A complete neurologic examination including motor and sensory evaluation of the peroneal and tibial nerve should be well documented before and after any intervention including reductions, surgical procedures, splinting, or casting. The peroneal nerve is divided into superficial and deep branches. The superficial peroneal nerve—lumbar nerve root 5 (L5) and sacral nerve roots 1 and 2 (S1, S2)—controls the peroneal muscles of the foot, which provide foot eversion. The superficial peroneal nerve provides sensation to lateral aspect of the leg and dorsum of the foot. The deep peroneal nerve (L4, L5, and S1) controls the tibialis anterior, extensor hallucis longus, and extensor digitorum longus muscles. This function can be tested manually by having the patient perform resisted ankle dorsiflexion and great and lesser toe extension, respectively. Sensory function of the deep peroneal nerve is located primarily within the first web space on the dorsum of the foot. The tibial nerve (L5, S1, and S2) innervates the muscles of the superficial and deep posterior compartments of the leg. The gastrocnemius and soleus muscles are tested by resisted plantar flexion of the foot. The flexor hallicus longus and flexor digitorum longus are tested by having the patient curl his or her great and lesser toes respectively, then performing resisted plantar flexion. The tibialis posterior is tested by resisted plantar flexion and inversion of the foot. Sensory distribution for the tibial nerve is located on the plantar aspect of the foot.²¹

Manual muscle testing is graded on a five-point scale with 0 indicating no muscle activation; 1, muscle activation without joint movement; 2, motion observed when gravity eliminated; 3, motion against gravity; 4, resisted submaximal contraction; and 5, maximal resisted motion. As with the vascular examination, the patient should have frequent neurologic examinations that are well documented. A progressive deterioration in the neurologic examination may indicate compartment syndrome or ischemia.⁴⁶ Compartment pressure testing is indicated in this scenario.

Further neurologic studies may be indicated when a nerve deficit is noted on physical examination. These include electromyography, nerve conduction studies (NCS), ultrasonography, and MRI. MRI is more commonly used to identify ligament, meniscal, or articular cartilage injuries. Ultrasonography may be helpful, but is definitely operator-dependent. Electromyography and NCS cannot differentiate from extraneural and intraneural causes of nerve impairment, nor can they distinguish between a damaged but continuous nerve and a completely dissected nerve. These studies are usually employed in the subacute or chronic setting.

Ultrasonography of the peroneal nerve is performed with the patient in the prone position and the knee flexed 20° with the ankle positioned in a cushion to allow access to the popliteal region. A 12.5-MHz and 15.7-MHz broadband linear array transducer and a silicon standoff pad are used. Gruber and associates in 2005¹⁹ demonstrated that sonography by experienced technicians reliably demonstrated the state of the nerve and the surrounding soft tissues. Specifically, the level of the lesion and any scar tissue or hematoma that was surrounding the nerve were identified. It correlated precisely with intraoperative findings. It is important to identify a treatment program for peroneal nerve injury associated with dislocation.¹³ Nerve injuries from sharp laceration should be repaired acutely, those from blunt laceration should be delayed 3 to 4 weeks to delineate proximal and distal stump damage. Most commonly, nerve injury from a knee dislocation is a stretch injury or lesion in continuity. These injuries are observed for 4 to 6 months to allow for spontaneous recovery and/or delineation of the zone of injury.²⁸ Within this time interval, splinting and dedicated therapy with nerve stimulation and reeducation should be instituted. An ankle-foot orthrosis (AFO) should be used to maintain the ankle in a neutral position and prevent contracture of the Achilles tendon. Initiating stretching exercises to correct the equinovarus foot positions may help prevent the development of contractures. Baseline electrodiagnostic studies should be performed at 6 weeks and again at 3 months if there has been no clinical evidence of tibialis anterior muscle function.⁶⁰

With ongoing absence of clinical signs of recovery, nerve exploration may be indicated.^16,60 At the time of surgery, nerve action potentials across the lesion are assessed. If conduction is demonstrated, neurolysis can be performed with 80% to 88% recovery of grade 3 muscle strength (peroneal and anterior tibial muscle contract against gravity and some resistance).^27,28 End-to-end suturing or nerve grafting is recommended when there is no conduction across the deficit. Resection and suturing of short-segment deficits with partial fibulectomies may result in 84% chance of grade 3 recovery.²⁸ Kim and colleagues²⁸ also found grade 3 functional return in 42% of grafts overall; 75% of those that were less than 6 cm in length had good outcome. The outcome depends strongly on the degree of neural damage and the surgical technique used.¹⁹ When sufficient return of function does not occur, an anterior transfer of the posterior tibial tendon or other technique can maintain neutral ankle dorsiflexion and eliminate the need for the AFO.^{12,20,23,42,56,63–65}

LIGAMENTOUS INJURIES

Dislocation of the knee results in damage to the soft tissue stabilizers of the knee. Physical examination of the soft tissue stabilizers should be performed only after the life- and limb-threatening injuries have been addressed. It should also be delayed in the case of femoral or tibial fractures. Examination in this setting may further displace the fracture, and it may make the ligamentous examination less reliable. Pain may also hinder accurate examination.

A systematic approach to the evaluation of knee stability should be undertaken. The most accurate examination for identification of ACL integrity is the Lachman test.¹¹ This is performed by applying an anteriorly directed force on the tibia with the knee in 20° to 30° of flexion. With the knee at 90°, a posterior drawer or posterior force on the tibia is used to assess the PCL. Translation and endpoint are evaluated. Evaluation of posterior sag, or the position of the medial femoral condyle with respect to the tibial plateau, is also useful to identify PCL injuries.

The MCL and FCL are evaluated by applying a valgus or varus stress, respectively, at both 0° and 30° of flexion. Increased medial or lateral joint space opening at 30° typically indicates a collateral ligament injury. A posteromedial or posterolateral complex injury can be identified with additional joint space opening at 0° of flexion. The posterolateral corner can be assessed further with the dial test. Increased external rotation of the tibia, greater than 10° to 15° side-to-side thigh-foot angle at 30° of knee flexion, indicates a posterolateral corner injury. If there is additional external rotation of the dial test at 90° of flexion, a PCL and lateral corner injury is present. Twaddle and coworkers⁶² in 2003 presented 63 dislocatable knees in 60 patients. These authors reported bicruciate ligament injuries in 71% of patients. The ACL was injured in 84%; the PCL, 87%; the MCL, 44%; and the FCL, 62%.

REDUCTION AND IMMOBILIZATION

Knees that are dislocated at the time of presentation should be reduced immediately. Reduction in the field by knowledgeable medical personnel is preferred. The neurovascular status of the limb must be assessed prior to reduction. The use of intravenous adjuvant medications is usually sufficient anesthesia. Reduction is accomplished by applying traction to the tibia while manipulating the proximal tibia in the appropriate direction. The presence of a dimple sign, indication of a posterolateral dislocation, may be a contraindication to closed reduction. Imaging should be pursued if possible. Reevaluation of joint congruence and neurovascular status must follow reduction.¹⁶ The limb should then be immobilized in a long-leg splint. Adequate reduction and maintenance of tibiofemoral alignment must be documented in both the anteroposterior (AP) and the lateral planes. If reduction cannot be maintained in a splint, the knee may be transfixed temporarily with cross pins (through the notch) or an external fixator until sufficient capsular healing occurs.

IMAGING

Radiographs of the knee should be obtained for all suspected knee dislocations (Fig. 27-6). Radiographs may be delayed until a clinically apparent knee dislocation has been adequately reduced. The basic knee series consists of an AP and a lateral plain radiograph. In cases in which fracture is noted or suspected, oblique views or stress views of the knee may be indicated. These views can determine the direction of dislocation as well as assess the adequacy of reduction and note any residual subluxation. In addition, the identification of fractures may direct treatment. Often, femoral and/or tibial fractures will require stabilization before the dislocation can be addressed.

FIGURE 27-6 Anteroposterior (AP) radiograph of an acute knee dislocation.

A tibial eminence fracture and lateral capsular avulsion fractures from the tibia, also known as a Segond fracture, indicate an ACL injury (Fig. 27-7).^5,10,53 The tibial eminence fractures may be complete, incorporating the entire ACL footprint, or incomplete, primarily affecting the anteromedial bundle.¹⁸ The Segond fracture, best detected on the AP projection, is indicative of detachment of the middle third of the lateral capsular ligament and is associated with anterolateral rotational instability (Fig. 27-8). The fracture originates from the lateral cortex of the proximal tibia, superior, and posterior to Gerdy’s tubercle, approximately 2 to 10 mm distal to the articular surface.¹⁵ Tears of the ACL are present in 75%⁸ to 100%¹⁵ of patients with Segond fractures.

FIGURE 27-7 A 13-year-old boy with a twisting knee injury sustained while playing basketball. Frontal (A) and lateral (B) radiographs of the knee show a large avulsion fracture of the anterior cruciate ligament (ACL; black arrows). There is a Segond fracture of the proximal tibia (white arrow). C, A three-dimensional computed tomography (CT) image shows this fracture fragment to be a large, noncomminuted fragment extending beyond the insertion area of the ACL toward, but not involving, the posterior cruciate ligament (PCL) insertion area.

(A–C, Used with permission from Griffith, J. F.; Antonio, G. E.; Tong, C. W. C.; Ming, C. K.: Cruciate ligament avulsion fractures. Arthroscopy 20:803–812, 2004.)

FIGURE 27-8 Segond fracture with characteristic arthrographic findings. Four days before presentation, this 26-year-old man fell while playing tennis. A, AP view shows a 9-mm avulsion fracture arising from lateral tibial cortex. Site of origin is 3 mm below the plateau. B, Overpenetrated cross-table lateral view during double-contrast arthrogram shows absence of normal anterior cruciate ligament (arrow). C, Arthrogram of the posterior horn of the lateral meniscus shows compression of the normal tendon sheath.

(A–C, Used with permission from Goldman, A. B.; Pavlov, H.; Rubenstein, D.: The Segond fracture of the proximal tibia: a small avulsion that reflects major ligamentous damage. AJR Am J Roentgenol 151:1163–1167, 1988.)

PCL and posterolateral ligament injuries can also be identified on plain radiographs (Fig. 27-9). PCL injuries may present as posterior avulsion fractures of the proximal tibia. These fractures will usually involve the entire PCL and may be comminuted or split sagitally.¹⁸ A cortical avulsion of the middle medial tibial plateau, a “reverse” Segond fracture, caused by a valgus and external rotation force, corresponds to an avulsion of the deep MCL. This is usually associated with a PCL injury and medial meniscal tear. This may be the only radiologic suggestion of a knee dislocation/multiligamentous injury.¹²

FIGURE 27-9 A 52-year-old woman involved in a high-energy motor vehicle collision. A, AP intraoperative fluoroscopic spot film of the knee shows a small avulsion fragment (arrow) adjacent to the medial joint line and evidence of cortical disruption (arrowhead) of the medial tibia. B, Proton density-weighted fast spin-echo sagittal MR image shows disruption of the PCL. Note the coronal position of the tibia that results from ligamentous instability. The distal end of the PCL (long white arrow) is intact, but the entire proximal portion (short white arrows) is disrupted. Disruption (black arrows) of the superficial medial collateral ligament (arrowhead) is shown. The deep medial collateral ligament (arrowhead) is also torn. C, AP radiograph of the knee 6 months after trauma shows avulsion fragment (white arrow), now well corticated. The black arrow indicates the medial tibial bony defect.

(A–C, Used with permission from Escobedo, E. M.; Mills, W. J.; Hunter, J. C.: The “reverse Segond” fracture: association with a tear of the posterior cruciate ligament and medial meniscus. AJR Am J Roentgenol 178:979–983, 2002.)

On the lateral side, the “arcuate sign” describes an avulsion fracture of the fibular head consisting of the FCL, popliteal fibular ligament, and fabellofibular ligament may present with this fragment. Huang and associates²² found that in addition to the injury to the posterolateral stabilizers, 13 of 13 patients with the arcuate sign had PCL disruptions (6 tibial avulsions, and 7 midsubstance) and MCL injuries (5 acutely abnormal, 8 chronic fibrous thickening). Also identified were medial and lateral meniscal tears (5 medial, 6 lateral).

After a knee dislocation has been reduced, the patient stabilized, and plain radiographs confirm reduction, MRI can be obtained subacutely (Fig. 27-10). MRI will further define soft tissue and cartilage injuries and aid in planning definitive care. Whereas the physical examination is best for determining degrees of abnormal translation and rotation, MRI can help determine the location of the injury (e.g., midsubstance tear). This information can be useful in deciding the need for repair, augmentation versus reconstruction.

FIGURE 27-10 A 21-year-old man with chronic posterolateral instability of the right knee after a motor vehicle collision. A, AP radiograph reveals avulsed bone fragment of the fibular styloid process (arrow). B, Sagittal spin-echo proton density-weighted magnetic resonance image (TR/TE, 1800/20) reveals avulsed osseous fragment (arrow) adjacent to the popliteal tendon (arrowhead). C, Coronal spin-echo proton density-weighted magnetic resonance image (1800/20) reveals disruption of the lateral collateral ligament (arrowhead) and avulsed osseous fragment (arrow) in the corresponding course of the popliteofibular ligament. D, Sagittal spin-echo proton density-weighted magnetic resonance image (1800/20) obtained medial to image B reveals a tear of the PCL (arrow)

(A–D, Used with permission from Huang, G.-S.; Yu, J. S.; Munshi, M.; et al.: Avulsion fracture of the head of the fibula [the “arcuate sign”]: MR imaging findings predictive of injuries to the posterolateral ligaments and posterior cruciate ligament. AJR Am J Roentgenol 180:381–387, 2003.)

EMERGENT SURGERY

Whereas the rationale for determining the type of treatment (surgical or nonsurgical) most appropriate for a patient with a dislocated knee is beyond the scope of this chapter, the timing of surgical procedures is dependent on the postinjury physical examination and associated injuries.

Emergent surgery is indicated for vascular injury, compartment syndrome, open injury, or irreducible dislocations.⁴⁶ Vascular reconstruction, often performed with reverse saphenous vein grafts, should be performed within 6 hours to minimize ischemia to the muscles and increase the chances for limb survival. The orthopaedic surgeon may need to stabilize the limb with an external fixator to allow access to the limb during reconstruction and for postoperative wound management. Fasciotomies are often required after revascularization to prevent compartment syndrome.

Acute compartment syndrome is a condition in which the pressure within a fascial compartment rises to a level that decreases tissue perfusion leading to cellular anoxia, muscle ischemia, and death. Diagnosis is primarily clinical with supplementation by compartment pressure measurements. Clinical signs of compartment syndrome include pain out of proportion, pain aggravated by passive stretch, paresthesias, and late signs that include pulselessness, paralysis, and pallor. Compartment pressure measurements of 20 mm Hg below diastolic pressure or 30 mm Hg below the mean arterial blood pressure suggest muscle ischemia. Urgent restoration of perfusion and normalization of compartment pressures is accomplished by complete fasciotomy of all compartments.³⁹

When open knee dislocations are encountered, wound management principles should be employed. Irrigation and débridement of the open wound should be performed urgently. The patient should be started on appropriate antibiotics. Acute ligament reconstruction is contraindicated in the face of an open wound. Soft tissue issues may delay reconstruction for several months.⁴⁶

Irreducible dislocations, most commonly posterolateral dislocations with a dimple sign, require surgical reduction to avoid neurovascular compromise. Although possible, ligament reconstruction should be delayed until adequate imaging of the knee and appropriate resources for reconstruction have been assembled.

DEFINITIVE MANAGEMENT

Most, if not all, surgeons would agree that soft tissue dissection, ligament, and capsular repairs are easier in the acute setting, less than 2 weeks after the injury. Unfortunately, this is when the knee is usually swollen and range of motion is poor with decreased or absent muscle control of the limb. All of these factors can increase the risk of a permanently stiff knee. Even in the environment of a high-volume knee trauma center,^6,59 loss of motion with a multiple ligament reconstruction is difficult to prevent. Therefore, these decisions must take into account this risk of stiffness along with other patient factors such as complicating injuries, medical comorbidities, participation in rehabilitation efforts, ability to maintain knee reduction, soft tissue coverage and skin condition, and patient expectations. Fortunately, reconstructive options today surpass those available even a few years ago, thereby decreasing the need for acute repair. For patients with high physical demands, optimizing the condition of the knee (muscle function, range of motion, and swelling) and relying on reconstruction rather than acute repair may yield a superior functional result. Although time from injury dictates options such as repair versus reconstruction, it is the condition of the knee that may ultimately determine stiffness and functional results.

Arthroscopically assisted surgery should usually be delayed a minimum of 10 to 14 days after the injury to allow the joint capsule to heal and therefore minimize the risk of fluid extravasation and subsequent compartment syndrome.⁵¹ In addition, this delay allows for monitoring of the vascular status, decreased swelling, improvement in quadriceps tone, and range of motion.⁷

Shelbourne and colleagues⁵⁴ in 1991 demonstrated a significantly increased incidence of arthrofibrosis in patients undergoing ACL reconstruction within 1 week of injury compared with those delayed 21 days or more. These authors also believed that delayed surgery gave the patient the opportunity to ask questions, as well as improve her or his psychological outlook on the injury and rehabilitation. Stannard and coworkers⁵⁹ compared acute repair (within 3 wk) of the posterolateral corner with reconstruction. These investigators found significantly inferior results of repair (37% failure) to reconstruction (9% failure) in 56 patients with 57 posterolateral corner injuries at 2 years.