Ankle Equinus

Etiology

Ankle equinus can result from osseous limitations, neuromuscular disorders, or contractures of the gastrocnemius complex or surrounding soft tissues.[5][6] In the setting of posttraumatic arthritis or advanced degenerative arthritis, anterior ankle impingement that restricts tibiotalar motion and reduces dorsiflexion can lead to an equinus contracture. In patients with neuromuscular disorders such as cerebral palsy, excessive spasticity of the gastrocnemius-soleus complex can lead to an equinus contracture, which is the most common impairment in these patients.[7]

Non-neuromuscular etiologies for equinus contracture can be grouped into 3 categories as described by Feraru et al:[8]

• Acquired: Trauma, neoplasm, infection, burn, and compartment syndrome.
• Congenital: Hemimelia, phocomelia, and intrauterine stroke.
• Idiopathic: Sensory integration issues and autism.

Epidemiology

A documented increase in the prevalence of ankle equinus has not been observed due to acquired or congenital reasons. However, there is a higher incidence of idiopathic toe walking, an idiopathic cause of ankle equinus, in children with neuropsychiatric or developmental delays, with a slight male predominance in this subgroup. In children aged 5.5, toe walking was observed in 2% of normally developing children and 41% of those with neuropsychiatric or developmental delays.[9][10]

Pathophysiology

Ankle equinus is characterized by restricted dorsiflexion of the ankle joint, often due to tightness or contracture of the gastrocnemius-soleus complex. This tightness causes an overpull of the Achilles tendon, limiting the ankle's upward movement toward the shin. The reduced dorsiflexion alters normal gait mechanics, leading to compensatory movements that place additional stress on the foot, ankle, and other joints. Over time, these altered biomechanics can result in pain, deformities, and other musculoskeletal issues.

History and Physical

An ankle equinus contracture diagnosis can be made solely on a physical examination. However, a thorough medical history and comprehensive physical examination are essential to determine the underlying cause and appropriate treatment options for a patient with an ankle equinus contracture. Special attention should be given to any history of neuromuscular or neuropsychiatric disorders, trauma, or diabetes, along with an assessment of the patient's activity level.

Many patients with an ankle equinus contracture initially present in childhood due to parental concerns about toe walking or downward-pointing toes. The most common causes of an ankle equinus deformity in pediatric patients are cerebral palsy and idiopathic toe walking. A history of cerebral palsy, congenital or intrauterine abnormalities, autism, or neuropsychiatric disorders should be noted. An increased incidence of idiopathic toe walking is more common in patients with neuropsychiatric diagnoses, making this an important aspect of the medical history.[11] A history of foot or ankle trauma can lead to posttraumatic arthritis or an osseous block to dorsiflexion, contributing to an ankle equinus deformity. Following such trauma, patients are often immobilized, and if immobilized in a plantarflexed position, this may result in contracture of the gastrocnemius-soleus complex, causing an equinus deformity.[12]

Patients with diabetes are at risk for diabetic neuropathy, which can lead to neuropathy of the lower extremities, subsequently leading to atrophy of the peroneal nerve, which is responsible for innervating the ankle dorsiflexor muscles. This atrophy causes an imbalance in the pull between the posterior and anterior ankle musculature, resulting in an equinus deformity.[5][13]

A thorough orthopedic physical examination should be conducted in patients with ankle equinus, with particular attention to the below-mentioned factors.

• Inspection: The lower extremity, from the pelvis to the toes, should be examined for any contractures, deformities, or signs of previous trauma that may be contributing to the ankle contracture.
  • Hair loss or glossed-over skin patches should be noted, which may indicate diabetic neuropathy, autonomic dysreflexia, or vascular insufficiency. 

• Palpation: Pulses should be assessed for signs of vascular insufficiency. 
  • If the sensation is compromised, Semmes-Weinstein monofilament testing should be performed.[14]
  • Limb length should be evaluated, and the examiner should check for symmetric iliac crests and popliteal creases. If a limb length discrepancy is suspected, the examiner should measure from the anterior superior iliac spine to the medial malleolus on each extremity. 

• Range of motion: The active and passive range of motion of the knee, ankle, and subtalar joints should be assessed.
  • A Silverskiold test should also be performed.[15] In this test, the examiner assesses ankle dorsiflexion with the knee in both flexed and extended positions. If dorsiflexion is restricted when the knee is flexed, it indicates a tight "heel cord" or Achilles tendon/soleus complex. With the knee flexed, the gastrocnemius is relaxed and should not contribute to the limitation in dorsiflexion. When the knee is extended, the entire gastrocnemius-soleus complex is under tension. The gastrocnemius is at least partially responsible if the ankle cannot be dorsiflexed in this position. Notably, holding the hindfoot, midfoot, and forefoot in a neutral position is important to isolate motion at the tibiotalar joint.[16]
  • Although there is no single defined metric for diagnosing ankle equinus, it is generally accepted that if a patient has less than 5° of dorsiflexion with the knee extended and more than 10° with the knee flexed, this indicates a tight gastrocnemius.[17] If the patient has less than 10° of dorsiflexion with the knee flexed, the entire gastrocnemius-soleus complex is tight. These conditions are sometimes referred to in the literature as gastrocnemius equinus and gastrocnemius-soleus equinus, respectively.[8]

Evaluation

In pediatric patients, imaging is generally unnecessary if idiopathic toe walking is suspected. Imaging may be considered if an equinus contracture is unresponsive to initial conservative management, although further imaging beyond an x-ray is rarely required. 

If osseous involvement is suspected, an ankle x-ray should be ordered to evaluate the bony architecture and identify potential areas of impingement. A full-length standing lower extremity x-ray can be obtained to assess limb length if there is concern about a limb length discrepancy. If developmental delay is documented or abnormal neurological findings are observed during the examination, magnetic resonance imaging (MRI) of the brain or entire spine should be considered to rule out an upper motor neuron etiology. 

Treatment / Management

Effective treatment of ankle equinus necessitates a comprehensive approach tailored to the underlying cause and severity. Therapeutic options include conservative management and surgical interventions, all aimed at restoring normal ankle function and alleviating symptoms.

Conservative Management

Conservative management is nonoperative, and treatment continues until the patient can ambulate with a heel-toe gait pattern, maintain adequate balance, and achieve sufficient ankle dorsiflexion. Key components of conservative therapy include:

• Physical therapy with an emphasis on stretching, strengthening, gait training, and home exercise.

• Serial casting and ankle-foot orthoses, which are primarily used in pediatric patients with ankle equinus. 
  • The goal of casting is to achieve at least 5° of ankle dorsiflexion, after which casting can be discontinued, and a physical therapy and home stretching program should be initiated.
  • For idiopathic toe walking ankle equinus, it is crucial to coordinate physical therapy after the completion of casting to help the patient regain strength that may have diminished during the casting process.[9] 
(B3)

• Botulinum toxin A injections are used to treat patients with increased spasticity and equinus contractures, particularly in those with cerebral palsy.
  • These injections are typically administered every 4 to 6 months or until they become ineffective.
  • They are most commonly combined with casting or bracing.
  • These injections work by reducing the spastic overpull of the gastrocnemius-soleus complex relative to the anterior leg compartment musculature.

• Idiopathic Toe Walking
  • Cincinnati Care Guidelines should be referred for the complete treatment algorithm.[9][8]
(B3)

Operative Management

Operative management should generally be considered only when conservative options have been exhausted, and the ankle equinus deformity remains refractory to these interventions. This typically involves a soft tissue release of one or more structures, including the Achilles tendon, the gastrocnemius-soleus complex, and/or the posterior ankle capsule. The Silverskiold test, as described previously, helps determine which structure should be released.

The possible zones of lengthening are described by Firth et al.[18] Zone 1 encompasses the proximal femoral origin of the gastrocnemius to the most distal portion of the medial gastrocnemius muscle belly. Zone 2 is described as being from the distal extent of the medial gastrocnemius muscle belly to the distal end of the soleus muscle. This zone 2 region is commonly defined as the gastrocnemius-aponeurosis soleus fascial complex.[19] Zone 3 is described as the distal aspect of the soleus muscle to the calcaneal tuberosity at the site of the Achilles tendon insertion. 

Considerations for lengthening procedures of the particular zones include the following:

• Zone 1: Lengthening at this level focuses on the intramuscular lengthening of the gastrocnemius and soleus musculature, as described by Baumman and Koch.[20] This is typically performed within the fascial interval between the gastrocnemius and soleus muscles.

• Zone 2: At this level, the gastrocnemius fascia condenses into a broad aponeurotic band that lies superficial to the soleus muscle fascia. Due to the intimate relationship of these 2 layers, differential lengthening of only 1 of these structures is not considered possible.[21] However, proximal to zone 2, at the junction of zones 1 and 2, differential lengthening of the gastrocnemius or soleus fascia is possible, as described by Strayer.[22]

• Zone 3: Tendo-Achilles lengthening is indicated for refractory ankle equinus when the Achilles tendon is identified as the causative structure. This can be performed through 2 or 3 hemitransections of the Achilles tendon, as initially described by Hoke and White.[23] This procedure can be performed percutaneously or via an open approach. Alternatively, open Z-lengthening of the Achilles tendon is another option.

In addition to the commonly performed procedures, using a multiplanar external fixator is an option for more complex deformities. This treatment option involves applying an external frame that spans the ankle joint and gradually correcting the deformity with the aid of a computer software program. Typically, this is performed with a hexapod frame with 6 struts, which are elongated and shortened to correct a deformity over weeks to months gradually.[24][25]

Differential Diagnosis

The differential diagnosis of ankle equinus involves distinguishing it from other conditions with similar symptoms of limited ankle dorsiflexion and altered gait. Posterior ankle impingement syndrome and tightness of the gastrocnemius-soleus muscle should be evaluated, as both can restrict ankle dorsiflexion. Structural abnormalities, such as talar dome lesions or congenital foot deformities, may also mimic or contribute to the presentation of ankle equinus.

If there is a history of trauma, the skeletal structure of the ankle and hindfoot should be assessed to rule out any structural causes of the equinus contracture. Additionally, deficiencies in the range of motion of the hip or knee, or any limb length discrepancy, should be evaluated to ensure they are not contributing to the ankle equinus deformity. The presence of its counterpart, calcaneus deformity, should also be ruled out. Calcaneus gait is characterized by the inverse of ankle equinus, where the triceps surae has decreased power and an inability or reduced ability to plantar flex the ankle.[26] 

Prognosis

The prognosis of ankle equinus depends on the causative etiology. In cases of flexible ankle equinus, physical therapy and home stretching programs are often all that is needed to resolve the issue.

In cases refractory to conservative management, where operative intervention is required, recurrence is documented. Recurrence rates following gastrocnemius recession range from 10% to 35%.[27][28][29][30] Recurrence rates differ between patients with neuromuscular etiology and those without. Patients with neuromuscular disorders generally have higher recurrence rates. For instance, among those who underwent zone 1 lengthening (Baumann procedure), recurrence of ankle equinus was 24% for patients with a neuromuscular disorder compared to 10% for those without.[29][31]

Complications

Complications related to ankle equinus can be categorized into 2 groups based on the type of treatment.

Conservative Treatment Complications

Conservative treatment for ankle equinus, while generally effective, can be associated with specific complications, as listed below.

• Serial casting: Pressure sores or ulcer creation.

• Botulinum toxin A: Overall low complication rate, with an adverse event rate comparable to serial casting.[32]

Operative Treatment Complications

Operative treatment for ankle equinus can lead to several complications, as mentioned below.

• Achilles tendon lengthening: Loss of plantar flexion strength.

• Gastrocnemius-soleus lengthening: Injuries to the lesser saphenous vein and sural nerve and loss of plantar flexion strength.

One of the most significant complications of any lengthening procedure for ankle equinus is the development of calcaneus gait and weakness of the gastrocnemius-soleus complex. While a secondary lengthening procedure can address some issues, correcting a weakened ankle plantar flexor complex remains challenging.[18] Evidence suggests that zone 2 or zone 3 lengthening procedures (eg, Strayer procedure or Achilles tendon lengthening) may result in greater postoperative dorsiflexion but are associated with a higher incidence of calf muscle weakness compared to zone 1 lengthening procedures (eg, Baumann procedure).[33]