Ankle dislocations without fracture occur when significant force applied to the joint results in loss of opposition of the articular surfaces. Because of the large amount of force required and the inherent stability of the tibiotalar joint, dislocation of the ankle joint is rarely seen without an associated fracture. Certain researchers argue this is due in part to the strength of the ankle joint ligaments and the relative weakness of the bones that make up the ankle.[1]
A paucity in the medical literature exists illustrating critical examination of the injury, treatment protocol, and outcomes. In 1939, Wilson, Michele, and Jacobsen discussed ankle dislocations without fracture but were limited to 2 private patient case studies and only 14 cases that had been previously reported since 1913.[2] It was this study that attempted a literature review, evaluation of the mechanism, treatment, and results. Again, in 1991, further lack of ankle dislocation research prompted Moehring et al to compile one of the larger series of open ankle dislocation.[3] Recently, most literature demonstrates isolated cases studies of pediatric and adult tibiotalar/ankle dislocations.
Some controversy exists regarding the treatment of ankle dislocations. However, the outcomes appear to be satisfactory in cases treated with immediate reduction of the joint and relief of neurovascular stress as the primary goals of treatment.[4]
Karampinas et al performed a retrospective evaluation of complete talar extrusion without associated fractures and immediate reimplantation and reported that it is important to attempt reimplantation of the talus because of good final outcomes. According to the authors, even in the case of a catastrophic complication, this technique ensures adequate bone stock for additional surgical procedures. The dislocated talus was reduced and held in place with 2 Steinmann pins placed from the inferior aspect of the calcaneus, through the talus, and into the inferior aspect of the tibia. An external fixator was used to stabilize the limb.[5]
The ankle joint is designed for a balance of stability and flexibility, particularly the former. Joint stability is provided by close articulation of the talus with the tibia and fibula. The mortise design further enhances the stability of the configuration.
The talus is trapezoidal in shape, with the greater width anteriorly and narrower posteriorly. As the joint moves into plantar flexion, the talus becomes narrower, resulting in a decrease in stability. It is important to note that this position of plantar flexion is typically in conjunction with the foot being in a supinated position. Thus, despite the foot, particularly the subtalar joint, being in a stable position with all the lesser tarsal bones stacked upon each other, the ankle remains vulnerable to inversion strain and subsequent injury. Conversely, the dorsiflexion of the talus in the ankle joint is typically accompanied by a foot being in the pronated position. Although inversion stress is greatly reduced, strain upon the syndesmotic ligament, medial malleolus, and medial deltoid ligament structures are their greatest disadvantage.[6, 7]
During normal walking, the ankle joint bears 3-5 times the body's weight. This factor increases several fold during running and jumping activities. As weight is applied on heel strike, the fibula descends to increase stability of the ankle joint.
See the image below.
View Image | Anatomy of the lateral ankle ligamentous complex and related structures. |
Associated fractures are the rule rather than the exception with ankle dislocations. Ligamentous disruption varies according to the type of dislocation. (See Ankle Injury, Soft Tissue.) Neurovascular injury is the principal concern, as with any dislocation. Vascular compromise may result in avascular compromise of the talus, permanent sensation or nerve damage, and lower extremity tissue necrosis; and gangrene may occur if not promptly reduced. Tented skin may be subject to ischemic necrosis
Children and adolescents have the most ankle dislocations. Dislocations of the ankle are seen more frequently in young males than in any other group. This presumably is related to their increased risk overall for traumatic injury.
Postmenopausal women are at higher risk for associated fractures. Increased fracture risk probably is related to osteoporotic changes in this subset of patients.
Dislocated ankles should not be expected to return to premorbid function.
The amount of force and level of capsular disruption required to dislocate the inherently stable joint results in significant injury with lasting effects. To a limited extent, prompt intervention can reduce the risk of complications.
For patient education resources, see the Breaks, Fractures, and Dislocations Center, as well as Ankle Fracture.
A detailed history regarding the mechanism of injury often helps predict the type of injuries to expect. Furthermore, an understanding of the injury mechanism aids treatment, since an opposite force is required in reduction of the joint. Because of the inherent stability of the ankle joint mortise and surrounding tendons and ligaments, dislocation is most usually caused by high-energy trauma that causes plantar flexion of the ankle combined with either inversion or eversion stress upon the foot.[1] Four types of dislocations are seen around the ankle joint: posterior, anterior, lateral, and superior:
A posterior dislocation in the most common type of ankle dislocation.[8] The talus moves in a posterior direction in relation to the distal tibia as force drives the foot backward.[9] The wider anterior talus wedges back, resulting in forced widening of the joint. This must be accompanied by either a disruption if the tibiofibular syndesmosis or a fracture if the lateral malleolus, occurring most commonly when the ankle is plantar flexed.
Anterior dislocations result from the foot being forced anteriorly at the ankle joint.
Typically, anterior dislocation occurs with the foot fixed and a posterior force applied to the tibia or with forced dorsiflexion.
Lateral dislocations result from forced inversion, eversion, or external or internal rotation of the ankle.They are associated uniformly with fractures of either (or both) the malleoli or the distal fibula.
Diastasis occurs when a force drives the talus upward into the mortise. These dislocations usually are the result of a fall from a height. In such cases, the patient should be evaluated carefully for concomitant spine injury and fracture of the calcaneus.
Inspection of the ankle reveals significant edema with deformity ranging from trace to obvious. Tenting of the skin by the malleoli may be noted.
Palpation of the joint reveals tenderness along the joint line, corresponding to areas of capsular or ligamentous disruption.
In associated fractures, tenderness, deformity, or tenting proximal to the joint may be seen.
Possible risk factors that may predispose a patient to dislocation include the following: joint hyperlaxity, internal malleolar hypoplasia, peroneal muscle weakness, and a history of prior ankle sprains.[1]
Complications of ankle dislocation may include the following:
Routine radiographic examination of the ankle includes the following views:
Obtain prereduction and postreduction films.
Computed tomography (CT) may be indicated for evaluation of osseous structures, occult fractures, and alignment.
Ultrasound may be used in guiding injection of pain medicine into the ankle.[11]
In patients with obvious or complete neurovascular compromise, perform reduction prior to radiographic studies. Prompt reduction is important in reducing the risk of complications related to neurovascular compromise.
Reduction is accomplished with the knee in flexion to reduce tension on the Achilles tendon. With one hand on the heel and another on the dorsum of the foot, apply traction while maintaining countertraction at the knee. Entrapment of the tibialis posterior tendon (or of a fracture fragment within the joint space) may result in an irreducible dislocation.
Anesthesia includes Bier block, spinal block, conscious sedation with narcotics and/or benzodiazepines, or general anesthesia. Bier block is the preferred method because of its efficacy and risk profile, although time may not permit in cases of vascular compromise. One technique described is termed the hematoma block (injection of intra-articular local anesthetic into the ankle joint and associated fracture hematoma). Ross et al suggest this as an alternative to conscious sedation, avoiding the risks of seizure and/or respiratory arrest.[12]
Prehospital personnel should immobilize the joint following standard procedure for any extremity injury.
If neurovascular compromise is identified in the field by examination, revealing a cold, discolored, and pulseless or insensate foot, the joint should be realigned unless transport time is brief. This is accomplished by in-line traction with countertraction. Traction or splinting should be maintained en route to the hospital (see Splinting, Ankle).
Intravenous opioids should be administered to make the patient comfortable and especially if traction is applied to reduce the dislocation en route. If intravenous opioids are unavailable, intravenous benzodiazepine medications can be used as an alternative.
Early reduction is essential since delay may increase risk of neurovascular compromise or damage to articular cartilage. In patients with vascular compromise, perform reduction prior to radiologic examination.
Postreduction radiographs should confirm proper joint alignment. Appropriate pain management is the greatest contribution an emergency physician can make to the patient's care. Postreduction splinting is discussed below.
Dislocations of the ankle are, by definition, unstable due to accompanying disruption of the lateral or medial ligaments or the tibiofibular syndesmosis. These require an immediate orthopedic or podiatric consultation for surgical intervention that may involve the internal or external fixation of any associated fractures and repair of capsular or ligamentous tears.[13, 1]
The Ottawa Ankle Rules, originally developed by Stiell and colleagues, provides a clinical decision approach to guide the assessment of ankle injuries, particularly to determine the need for radiography in emergency departments.[14, 15]
The ACR Appropriateness Criteria for acute trauma to the ankle for adults and children older than 5 years notes that the Ottawa Ankle Rules recommend ankle radiographs if any of the following is present: (1) inability to bear weight immediately after the injury, OR (2) point tenderness over the medial malleolus, or the posterior edge or inferior tip of the lateral malleolus or talus or calcaneus, OR (3) inability to ambulate for 4 steps in the ED.[16]
Drugs used to treat the pain associated with dislocations include analgesics and anxiolytics.
Clinical Context: Narcotic analgesic with greater potency and much shorter half-life than morphine sulfate. DOC for conscious sedation analgesia. With short duration (30-60 min) and ease of titration, an excellent choice for pain management and sedation. Easily and quickly reversed by naloxone. After initial dose, subsequent doses should not be titrated more frequently than q3h or q6h.
Clinical Context: Drug combination indicated for relief of moderately severe to severe pain. DOC for aspirin-hypersensitive patients. Different strengths available.
Clinical Context: Drug combination indicated for relief of moderately severe to severe pain.
Clinical Context: Drug combination indicated for treatment of mild to moderately severe pain.
Clinical Context: DOC for analgesia due to reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Various IV doses are used; commonly titrated until desired effect obtained.
Pain control is essential for quality patient care. It ensures patient comfort, promotes pulmonary toilet, and aids physical therapy regimens. Many analgesics have sedating properties that benefit patients who have sustained injuries.
Clinical Context: Depresses all levels of CNS, including limbic and reticular formation, possibly by increasing activity of GABA, a major inhibitory neurotransmitter. Individualize dosage and increase cautiously to avoid adverse effects.
Clinical Context: Sedative hypnotic in benzodiazepine class that has short onset of effect and relatively long half-life. By increasing GABA, a major inhibitory neurotransmitter, may depress all levels of CNS, including limbic and reticular formation. When patient needs to be sedated for >1 d this medication is excellent. Monitor patient's blood pressure after administering dose and adjust as necessary.
Patients with painful injuries usually experience significant anxiety. Anxiolytics allow the clinician to administer a smaller analgesic dose to achieve the same effect.