End stage of arthritis in the distal lower extremity has almost always dictated fusion of a joint. Until relatively recently this was the case in the ankle. However, due to its essential role in normal gait, surgeons have long sought ways to replace rather than fuse this joint. 

Replacement joints have existed for decades. Early versions were fraught with complications and required revision and conversion to fusion very often. Like many procedures, refinement in design of the implant, instrumentation, and patient selection has resulted in newer versions that have fairly decent and predictable durability. 

The ideal patient has lower functional demands, although physically active. Adequate bone stock, a lower BMI, and adherence to strict post operative protocols round out the characteristics for a patient who will likely benefit. Morbid obesity, uncontrolled systemic comorbidities, peripheral vascular disease, neuropathy, and patients who cannot follow through with strict rehab protocols will likely have less than optimal outcomes, often requiring revision or conversion early on in their recovery. 

The decision to replace rather than fuse is highly individualized. Regardless of patient health, they must understand that the likelihood of some further intervention is high. This is due to the wear characteristics of the polyethylene component and high load going through the relatively small ankle joint surface area. Despite this, maintenance of sagittal plane motion becomes a deciding factor along with age, adjacent joint health, and overall desire for a more normal gait (not entirely 'normal') for a longer period of time.

The content of this podcast is for educational and informational purposes only and does not constitute medical advice. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition.

Boradly speaking, there are three types of digital contractures or hammertoes:

Flexor Stabilization: This is the most common mechanism, often driven by overpronation (flat feet). As the foot flattens, it unlocks the midfoot, causing the flexor tendons (the muscles underneath the foot) to fire earlier and longer to stabilize the foot. These overactive flexors overpower the smaller stabilizing muscles, forcing the toe to buckle downward at the proximal interphalangeal (PIP) joint.

Extensor Substitution: Common in individuals with high arches (pes cavus), this mechanism occurs when the extensor muscles (top of the foot) overpower the lumbricals and interossei muscles. The extensor tendons "bowstring" over the toe, pulling the base of the toe upward (hyperextension) at the metatarsophalangeal (MTP) joint, which in turn forces the tip of the toe downward.

Flexor Substitution. This is the least common mechanism and usually results from calf muscle weakness or nerve issues. In this case, the deep flexor muscles take over to help the foot push off the ground, overpowering the stabilizing muscles and causing the toe to curl.

The formation of hammertoes occurs in phases, beginning with a flexible deformity with mild muscle and tendon contracture, and often primarily a functional condition seen in weight bearing and ambulating. Later the deformities become rigid, where the affected tendons and joint capsules shorten and tighten permanently. The bones in the joint can luxate, meaning the toe cannot be straightened manually. This rigid phase leads to painful corns on the top of the toe or calluses on the ball of the foot from friction against footwear.

Correction methods centers around the biomechanical cause, the rigidity of the deformity, adjacent joint stability, and likelihood of recurrence. Broadly speaking, either arthroplasty or arthrodesis is performed. For retention of flexibility arthroplasty is utilized, but for long term success more often than not arthrodesis is performed. This involves removing the articular cartilage and retention of the bone ends together through the bone healing phases. Satisfaction with these procedures approaches 90%, with the most likely complication being recurrence, especially when either arthroplasty is performed or when adjacent deformity or instability is not addressed. 

The content of this podcast is for educational and informational purposes only and does not constitute medical advice. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition.

The "Diamond Model" (or Diamond Concept) of bone healing is a theoretical framework in orthopedic surgery and regenerative medicine that outlines five interdependent factors needed for successful fracture repair and non-union treatment:

Osteogenic cells, Osteoinductive mediators, Osteoconductive scaffold, Mechanical stability, and adequate Vascularity. The first four are connected by vascularity - without blood flow no healing can occur.

When evaluating a nonunion, this framework gives us a checklist upon which to determine the cause of the nonunion. A failure in any of the pillars of the model will result in a failed fusion or fracture to heal. 

Some conditions present specific challenges to bone healing that are not obvious. For example, obesity is widely known as a risk factor for nonunion. But it is not enough to just categorize high BMI solely; the obese individual poses challenges due to mechanical stability being inadequate, chronic inflammation where adipose tissue releases pro-inflammatory cytokines creating an environment favoring osteoclastic activity, and metabolic abnormalities such as insulin resistance and vitamin D deficiency.

For me the key to a successful outcome of surgery or conservative treatment of fractures is mitigating risk factors when possible, or circumventing them altogether. However when faced with a nonunion, the surgeon has to answer the two questions - how can I improve mechanics around the nonunion site and how can I improve the tissue/organ/whole body biology? Without answering these the nonunion will likely persist leading to even further morbidity.

The content of this podcast is for educational and informational purposes only and does not constitute medical advice. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition.

Instead of understanding a flexible flatfoot as a single condition, it should be understood that it is in fact multiple simultaneously occurring conditions resulting in mechanical failure. And since there are multiple components:

The surgeon should ask themselves "What component of the deformity am I correcting?"

Every operation has a purpose. Every procedure corrects a different deforming force.

That framework helps both patients and residents understand why flatfoot reconstruction is often a combination of several procedures rather than a single operation. And for patients, why they emerge from an operating room with incisions on the medial and lateral sides of their foot along with the back of their leg thinking I am just "giving them an arch."

Careful assessment of the dominant planes of deformity clue the surgeon into where the pathology lies. For example, strictly sagittal plane dominance may be a result of spasticity in the heel cord only. This is often the case in pediatric presentations. Likewise, frontal plane dominance may occur in the forefoot, the hind foot, or both. Consequently procedures designed to correct on these planes may be required at one or both levels depending on extent of deformity. 

Some procedures have a powerful impact in multiple planes. For example the Evans osteotomy will effect transverse plane (forefoot abduction) and frontal plane (forefoot supinatus) simultaneously. This is why we often use these procedures to complete a correction, so as to minimize the total surgical disruption and recovery time. 

It should also be noted that correcting a flatfoot is not necessarily about arch restoration, which is an obvious external sign of success. It's about creating a mechanically stable propulsive foot that is pain free. We can't make someone an olympic-level runner simply by raising an arch, but we can improve the mechanics that lead to a failure of the arch mechanism. 

The content of this podcast is for educational and informational purposes only and does not constitute medical advice. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition.

There are three types of cartilage in the human body, although the one we most commonly pay attention to is hyaline cartilage since this makes up the articulation between bones. The gliding and shock absorbing function of type 2 collagen makes hyaline cartilage particularly suited for absorbing force. It is arranged in a very specific manner to absorb forces and maintain structural integrity under load. When damage occurs to this tissue, the integrity becomes compromised, and similar to the laminated structure of a car tire, begins a disintegration process. 

Delamination will occur in phases, and often correlates to the radiographic and clinical findings a patient will present with. As a surgeon, my job is to determine the origin of the degradation (whether normal age related or traumatically induced) and assume certain prognostic factors, like stage and rate of degradation that is likely and secondary or collateral effects of this degenerative process. There is no one-size-fits-all approach to joint degeneration. Since this is a slow process in most cases there is time for decisions related to interventions, whether conservative or surgical. When surgery is considered, there are joint sparing and joint eliminating procedures, the choice of which is highly dependent on the knowledge and skillset of the surgeon evaluating the condition. 

The content of this podcast is for educational and informational purposes only and does not constitute medical advice. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition.

Symptomatic OLTs represent one of the most common causes of persistent pain following ankle injury. The condition is often missed due to the volume of ankle sprains seen in clinics that are routinely imaged with plain film X-ray only. These lesions not only do not appear on xray unless there is obvious bone involvement but sometimes evolve over time after the initial insult. Therefore the foot and ankle surgeon must keep this pathology in mind when pain persists beyond a reasonable amount of time in recovery. 

Lesion patterns sometimes can correlate with the mechanism of injury. Inversion sprains which are the most common type of injury, tend to produce more shallow, anterior located lesions if there is a dorsiflexion component, while deeper posteromedial lesions occur if the foot is plantarflexed at the time of injury. 

Cartilage damage is particularly challenging in that the body does not have a capacity to heal hyaline cartilage. Thus when damage occurs it can lead to symptomatology that persists well beyond the bodies repair of the surrounding tissues. This is why careful attention to the timeline after injury is so important. There is no universal clinical presentation for these lesions. Therefore MRI is essential when OLT is suspected. 

Larger lesions almost always require some type of intervention, especially with cartilage or cartilage-bone displacement. These tend to be more challenging, both in the type of repair required and the access to the joint to repair properly. Malleolar osteotomy is occasionally performed for access since direct cartilage replacement is likely the procedure of choice. 

Smaller lesions can often be treated either arthroscopically or in retrograde manner, tunneling to the lesion from underneath and performing a repair in a way that does not introduce larger injury to the joint surface. 

The content of this podcast is for educational and informational purposes only and does not constitute medical advice. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition.

The lateral collateral complex is made up of the ATFL, CFL and PTFL. The ATFL is probably one of the most commonly injured ligaments in the human body, due to the relative weak nature of the ligament and anatomic position on the outside of the ankle joint. Along with the CFL they are poor resistors of inversion since the torque of the body over these small structures can easily overwhelm their ability to contain movement beyond a certain point. Consider this an 'evolutionary weak point.' 

When inversion injuries occur, a square bone is turned or rotated inside of a square recess - not a good scenario. The shoulders of the ankle bone wedge the fibula outward, causing tension on the ligaments which will ultimately tear. In addition the cartilage and surrounding structures (capsule, tendons, and muscles) also sustain damage. 

Surgical repair involves inventory of all of these structures, including the syndesmosis that holds the tibia and fibula together. In this episode I focused on the direct repair or augmentation of the most common situations. In the next episode I will dive into more detail on osteochondral defects, and later on the high ankle sprain and more occult injuries that are commonly missed even by astute practitioners. 

The content of this podcast is for educational and informational purposes only and does not constitute medical advice. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition.

Achilles tendon rupture is a potentially catastrophic injury. However modern repair methods can restore the integrity of the tendon complex regardless of age or extent of injury. It is the rehabilitation protocols afterwards that are the best predictors of complete recovery, not the ability to put the tendon back together. 

I have repaired tendons on relatively sedentary patients, weekend warriors, and elite athletes - and everything in between. The factor that is most important for all of these patients to succeed is understanding the quality of the repair and gearing post operative rehabilitation accordingly. No two injuries and no two repairs are identical. Each has its own nuance, from the mechanism of injury, the patient's functional demands, the patients ability to comply with rehab directions, and the social safety system (home assistance) they employ. This is why a "one size fits all" repair method or rehabilitation program is destined to produce erratic results. 

If you understand the biologic processes and their required time to progress, you can understand the length of time these tendons need to fully heal. And the tendon is only one factor - the calf muscle strength suffers tremendously as well. Rehab programs must be designed to improve tendon elasticity while not over lengthening and coupled with strengthening to limit atrophy. This is a delicate balance. 

One other factor clinicians often forget is the psychological recovery. First is prolonged guarding, which can lead to prolonged recovery. Surgeons should appreciate that the longer they immobilize a patient the longer they have to become apprehensive about return to function. This must be monitored since patient engagement with rehab is essential to successful functional recovery. 

The content of this podcast is for educational and informational purposes only and does not constitute medical advice. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition.

There is debate among orthopedic and podiatric surgeons regarding operative and no operative repair of ruptured Achilles tendons. Why the debate? Because outcome studies have shown satisfactory results when comparing each treatment. These studies focus on strength restoration, pain scores, and quality of life. Unfortunately, we cannot directly compare individual patient outcomes, since a patient can only have been treated one way or the other. 

In my experience surgical repair is generally preferred for this injury unless there is compelling reasons to treat conservatively. This would include excessive smoking, uncontrolled systemic conditions like diabetes, demonstration of non compliance with physician direction, or extremes of age. Otherwise, this tendon can be repaired in a way that matches the contralateral limb in function and power and can be restored to its pre injury state predictably with surgical methods. That goes for chronic and delayed repairs as well. 

I trained in an era before percutaneous techniques emerged. Open repair is the gold standard for surgical treatment. This method allows complete visualization of the injury, direct reapproximation of the tendon ends, and the ability to match the injury to the mechanical construct required for repair. Without visualization, the surgeon cannot adequately assess the integrity of the ruptured ends, instead relying on the instrumentation that employs a "one size fits all" approach. Coupled with a higher incidence of sural nerve injury, there is little benefit in my mind to not simply opening the injury and fixing it. 

The content of this podcast is for educational and informational purposes only and does not constitute medical advice. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition.

Hallux limitus and rigidus are a spectrum of a disease involving progressive degeneration of the first metatarsophalangeal joint (MTPJ). There are multiple causes known to cause this condition, from biomechanical (elevated first metatarsal, elongated first metatarsal, etc.) to medical (gout, rheumatoid arthritis, infections, etc.) 

As a surgeon, I have to determine the condition of the joint at the time of presentation and the symptoms patients relate. Not all radiographically destroyed joints are symptomatic, and not all radiographically normal joints have mild symptoms. There is a spectrum of disease that has to be carefully evaluated against the conservative and surgical options available. 

Simple procedures like cheilectomy can buy time. Decompression osteotomies can do the same thing. However, if the joint degeneration is fairly advanced, the only likely outcome is secondary procedures. This is because the surgeon chose a procedure that increases painful motion. 

If a joint has undergone degeneration 'past the point of no return,' joint destructive procedures must be employed. This includes arthroplasty and arthrodesis. The former involves removing part of the joint, the latter meaning fusion or permanent removal and stiffening of the joint. 

In my experience, preservation of sagittal plane dominant joints (first MTPJ, ankle, knee) is critical to undisturbed gait. Therefore all measures should be explored before fusing these joints. Many patient have been referred in because they were given the only option of fusing the great toe joint. This is often not necessary, as implant arthroplasty has excellent long term survival rates in the right population and if performed technically well. 

The content of this podcast is for educational and informational purposes only and does not constitute medical advice. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition.