In the unstable Charcot foot, the concept of beaming may help patients with diabetes attain stability and greater weightbearing. These authors discuss the pathway of Charcot neuroarthropathy and offer essential surgical pearls.
Charcot neuroarthropathy is a disease that arises secondarily in patients with diabetes mellitus and peripheral neuropathy although there are cases of Charcot in which patients may or may not have diabetes or neuropathy.1 Due to fast food diets and eating-on-the-go lifestyles, diabetes has become an epidemic across the globe.2 Charcot neuroarthropathy results in structural deformities and most commonly occurs in the foot and ankle. Bony deformities of the foot can result in the development of ulcerations in areas of high pressure. Diabetic foot ulcers are a frequent cause of foot amputations.2
Charcot neuroarthropathy disease is characterized by increased local bone resorption by osteoclasts in small weightbearing joints, particularly in the foot. Osteoclasts are among the three main cells present in bone and they resorb bone tissue.3 The elevated bone resorptive process that occurs in Charcot neuroarthropathy is a product of more than just one cellular pathway. The receptor activator of nuclear factor-kB ligand (RANKL) is an integral component in the regulation of osteoclast differentiation and activation. The RANKL activates the osteoclast membrane protein known as RANK.4
Advanced glycation end products (AGEs) regulate RANKL activation. The AGEs modify type 1 collagen and these end products are a normal result of aging but can form prematurely.5 The receptor for advanced glycation end products (RAGE) expresses continually and increases RANKL activation. The soluble receptor for AGE (sRAGE) down-regulates RANKL activation.6
Researchers have yet to determine the cellular process primarily responsible for Charcot neuroarthropathy but there are multiple pathways to consider.
Receptor activator of nuclear factor-kB ligand induces the activation and differentiation of osteoclasts by binding to the osteoclasts’ RANK.7 Both RANK and RANKL are expressed constitutively. The RANKL overproduction is a characteristic of Charcot but it is not limited to Charcot. It also occurs in many bone diseases such as psoriatic arthritis, rheumatoid arthritis and osteoporosis.1
In a study involving three patient groups, Mabilleau and colleagues compared monocyte formation into osteoclasts and osteoclastic activity in vitro with and without the addition of RANKL.8 The groups included patients with diabetic Charcot neuroarthropathy, healthy patients and patients with diabetes. Without the addition of RANKL, researchers noted a significant increase in osteoclast formation in the Charcot group in comparison with the healthy and control groups. There was also increased osteoclastic activity in the Charcot group in comparison with the others.
With the presence of RANKL, the study authors noted an increase in osteoclastic activity in all three of the groups.8 However, osteoclastic activity was considerably more aggressive in the Charcot neuroarthropathy group and was four times greater than the osteoclastic activity in the healthy group. Osteoclasts in patients with Charcot neuroarthropathy differentiate to become highly active.5
The formation of AGEs is a common consequence of aging. Increased AGE production occurs in patients with prolonged elevated blood glucose levels, frequently termed hyperglycemia. Advanced glycation end products modify N-carboxymethyl lysine of type I collagen (CML collagen).9 The post-translational modification of the CML collagen occurs by non-enzymatic glycosylation, termed glycation. This primarily occurs in tissues with a slow turnover rate, exposing collagen proteins to the extracellular environment where non-enzymatic glycosylation takes place.5
Advanced glycation end products crosslink within and around collagen fibers, and compromise their functionality.10 Type 1 collagen’s main function is to resist tension and accounts for the for rigidity in bone. Its primary locations are skin, tendon, bone and dentin.6 Collagen crosslinking within bone is known to affect bone stiffness and Young’s modulus independent of the bones’ mineralization and microarchitecture. This leads to weakening of bone strength without evidence of demineralization.11
Advanced glycation end product accumulation recruits the increased formation of the pattern recognition receptor for AGE, known as RAGE, which expresses constitutively and causes increased downstream activation of RANKL when bound. According to Macaione and colleagues, increased RANKL activation causes osteoclastogenesis.12 The soluble receptor (sRAGE) competes with RAGE to bind RANKL. The sRAGE also inhibits RAGE by binding to RAGE.13
Witzke and colleagues assessed the loss of RAGE defense as a cause of Charcot neuroarthropathy by focusing on three groups of patients.6 The three groups included healthy control patients, patients with type 2 diabetes and patients with diabetic Charcot neuroarthropathy. Researchers recorded circulating levels of sRAGE and bone stiffness for each group. The study authors noted an 86 percent decrease in sRAGE values for patients with Charcot neuroarthropathy in comparison to the healthy control population. Bone stiffness was markedly reduced in the Charcot group. The study authors concluded that RAGE did in fact increase RANKL activation and RANKL is responsible for increased osteoclastic activity. Additionally, a reduction in bone stiffness with a concomitant increase in bone density may suggest a pathologic proliferation of cross-linked collagen.
Another potentially deleterious effect of reduction in circulating sRAGE is AGE-induced osteoblast apoptosis, which has been implicated in alterations to bone repair in the face of elevated osteocalcin.13 This may explain why Charcot fusion sites remain weak even after consolidation.
For the foot and ankle surgeon, the most important part of these biochemical studies is the finding that bone stiffness was markedly reduced in patients with Charcot neuroarthropathy.6 These findings correlate directly with studies that demonstrate decreased Young’s modulus of elasticity and tensile strength in the Achilles tendon in patients with Charcot neuroarthropathy.14
Carboxymethyl lysine of type I collagen is a major constituent of bone, tendon and the ligaments that holds bones together. There is a combination of biochemical evidence and laboratory testing evidence that shows that AGE radically alters bone and tendon.14 The best clinical treatment solution for this process would be a reversal of AGEs or a replacement of sRAGE, but these options are not feasible at this time.
The alternative for surgeons is to design methods of reconstruction that deal directly with the decrease in tissue strength. This demands an approach different from traditional fixation with plates and/or screws that count on a normal healthy arthrodesis to be the arbiter of load bearing. In fact with Charcot neuroarthropathy, even if arthrodesis occurs, there is compelling evidence to believe that the healed bones are abnormal and at risk of re-fracture.15
The concept of beaming is such a solution. In the field of engineering, beams accept loads of tension and compression. These are exactly the same types of loads that the foot experiences during weightbearing and propulsion. In the case of Charcot neuroarthropathy, beaming provides the appropriate load sharing for pathologic bone and ligament.15
Medial and lateral column beaming can clinically increase the stability of the hindfoot and arthrodesis of the Lisfranc joint in patients with Charcot neuroarthropathy. When the foot receives the axial load of weightbearing, there is maximum load at the level of the subtalar joint with the creation of bending moments posteriorly toward the calcaneus and distally toward the first metatarsal head. The dorsal surface of the foot is under compression and the plantar surface of the foot bones are under tension.
Surgeons currently perform beaming by using large diameter cannulated screws. From a surgical perspective, there are two columns to beam for Charcot. There is the medial column to include the first metatarsal, medial cuneiform, navicular and talus. There is also the lateral column to include the bases of the fourth and fifth metatarsals, the cuboid and calcaneus. From a reconstructive perspective, the two columns act independently.16 Beaming the medial column, however, will improve the function of the lateral column but the reverse is not true. A beamed lateral column is not capable of providing a stable and propulsive medial column.
In many instances, we see a unique biomechanical combination of events with Charcot neuroarthropathy. We see a collapsed medial longitudinal arch and a simultaneous ulcer laterally beneath the cuboid and a varus heel. This represents the reactive forces of weightbearing on a foot with a contracted and inelastic Achilles tendon and weakened midfoot ligaments that fail. The bases of the lesser metatarsals dislocate and sit dorsal to the cuboid, pushing the cuboid through the plantar surface of the foot. The peroneus longus and brevis tendons lose their functional pull with the cuboid altering the tendon balance. An unopposed tibialis posterior pulls the hindfoot into varus, instigating medial column collapses and an inability of the first metatarsal to bear weight, creating a rocker bottom.14 Beaming as a basic construct for reconstruction of both columns represents a surgical solution to a metabolic disease.
In a severe Charcot midfoot collapse, beaming of the columns can act as a simple solution to a complex anatomic dilemma with fracture and/or dislocation at multiple joints. Simply stated, a beam down the medial column can align the first metatarsal, medial cuneiform, navicular and talus in a rectus alignment swiftly and surely as in the radiograph image below. Since the screw is cannulated, one can use a Steinmann pin to directly align all fractures and dislocations. It is the senior author’s experience that it is sometimes easier to remove some of the most dislocated/fractured bones, allowing one to manipulate the foot more easily into a rectus alignment with a Steinmann pin, replacing the dislocated bones just prior to beam placement.
Similarly on the lateral column, removal of a plantar dislocated cuboid from its non-anatomic location, debriding the cuboid on the back table and replacing it in an anatomically correct position can serve to eliminate the causation of the plantar ulcer and restore peroneal tendon function. The beams need to cross multiple joints beyond the joints that were fractured or dislocated.17 This is because the underlying disease is present in all of the joints and can be progressive if load sharing does not happen.
Furthermore, in many instances of Charcot, segments of the midfoot bones are virtually destroyed. Currently, we are investigating substitutes for those bones but until those become available, we frequently simply beam across the void, packing it with bone chips, platelet rich plasma and stem cells. It is understood that the beams will support the load, share the load with the remaining diseased bones and produce a framework for stability and weightbearing.
The question arises as to whether one should lock the medial and lateral columns with fusion of the subtalar joint or with a subtalar implant. The subtalar implant is the senior author’s preference because it limits any subtalar motion that is abnormal without completely eliminating inversion and eversion. Accordingly, there can be some mobile adaptation of the foot to the supporting surface on which it ambulates and, at the same time, the two columns can now serve to support each other.
It has been the senior author’s experience that of the two columns, the medial column is vastly more important in Charcot reconstruction. If one removes the medial column beam due to infection or other complications, the loss of the Charcot correction will be inevitable unless the patient has had arthrodesis. Similarly, a broken medial column beam will result in a significant loss of correction. The lateral column beam only serves to prohibit plantar dislocation of the cuboid. If the lateral column is completely stable prior to surgery, the lateral column beam is not really necessary.
It is important to recognize that the purpose of beams is not to compress the fusion sites but only to act as support structures for the diseased ligaments and bones of the foot. Grant and coworkers clearly showed evidence that a frame with tension and compression and parallel fixation produced superior compression than other methods of fixation.14
The fluoroscope is requisite for the correct placement of beams. One can place the guide pin via a plantar approach to the first metatarsal by dorsiflexing the toe or a dorsal approach by plantarflexing the toe. One should center the tip of the pin in the metatarsal head. Drive the pin through the long shaft of the metatarsal until it exits its base centrally as one can see in the photo on the right. Similarly, the guide pin should traverse the center of the medial cuneiform, the body of the navicular and the head and neck of the talus. This may take some practice.
Generally speaking, a 115 mm cannulated screw is necessary for the medial column. It should be made out of stainless steel, not titanium, because stainless steel has a 240,000 PSI versus only 180,000 PSI for titanium. Use the largest diameter screw you can find. The heads of commercial hip screws have a tendency to be very hard on the metatarsal head so carefully countersink the screw head — whether you drill or not — to protect it from splintering and collapsing.
At this time, if one decides to place a lateral column beam, advance the guide pin. Typically, it is necessary to enter the foot just proximal to the sulcus between the third and fourth toes, and transverse the soft tissues of the forefoot with the guide pin. The guide pin should be virtually horizontal as it enters between the bases of the third and fourth metatarsals. Elevate the cuboid into its anatomically correct position as the guide pin passes through the cuboid into the body of the talus.
Place the medial column beam under direct fluoroscopic guidance. The threads of the screw at the tip are the weakest point of the screw and they are at the area of the highest bending moment. The screw threads should be as far away from the talonacivular joint as possible, buried as deep as possible in the talus. The lateral column screw should have its head interdigitating between the bases of the fourth and fifth metatarsals, and not compress through the bases. This is perhaps the best evidence that the purpose of beaming isn’t to compress segments for arthrodesis, it is to load share.
If beaming a subtalar implant or fusion of the subtalar joint appropriate for the reconstruction, do this prior to the placement of the medial and lateral beams.
Since the senior author first began using beaming procedures in 1994, the demographics of the population have significantly changed with regard to obesity. This epidemic directly correlates with the increase in diabetes and patients with Charcot neuroarthropathy. Currently manufactured orthopedic screws may provide a reasonable 2x safety factor for bending moments through the hindfoot in patients weighing 150 lbs. This is not the case for patients who exceed 300 and sometimes 400 lbs. In this population group, beam failure directly associated with the design of the current commercially available large diameter cannulated screws is a clinical concern as one can see in the radiographic images above at left. We see it as a challenge to solve this problem.
Patients with diabetes and peripheral neuropathy are predisposed to have Charcot neuroarthropathy. Damaged nerve conduction pathways from altered glucose tolerance can be a viable source for inducing Charcot neuroarthropathy due to a lack of balance and proprioception resulting in damaged bone, which stimulates osteoclastic activity.2
As surgeons, our challenge is to find solutions that address the pathologies at hand. Beaming is uniquely appropriate for Charcot neuroarthropathy in that it directly addresses issues of increased bone density, decreased bone stiffness and ligament failure with a time proven basic engineering solution. Refinement of this concept is necessary as the population of our patients with this disease become more obese.
Dr. Grant is a Fellow of the American College of Foot and Ankle Surgeons, and is board-certified by the American Board of Podiatric Surgery. He is an instructor in the Department of Surgery at Eastern Virginia Medical School and is in private practice in Virginia Beach, Va.
Mr. Barbato is a graduate of James Madison University and a current applicant to colleges of podiatric medicine.
Mrs. Grant-McDonald is a fourth-year podiatric medical student at Des Moines University.
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2. Sohn M, Stuck R, Pinzur M, Lee T, Budiman-Mak E. Lower-extremity amputation risk after Charcot arthropathy and diabetic foot ulcer. Diabetes Care. 2009; 33(1):98-100.
3. Christensen T, Bulow J, Simonsen L, Holstein E, Svendsen O. Bone mineral density in diabetes mellitus patients with and without a Charcot foot. Clin Physiol Functional Imaging. 2009; 30(2):130-134.
4. McCarthy A, Etcheverry S, Bruzzone L, Lettieri G, Barrio D, Cortizo A. Non-enzymatic glycosylation of a type I collagen matrix: effects on osteoblastic development and oxidative stress. BMC Central Cell Biology. 2001; 2(16) epub Aug. 2.
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6. Witzke KA, Vinik AI, Grant LM, Grant WP, Parson HK, Pittenger GL, Burcus N. Loss of RAGE defense: A cause of Charcot neuroarthropathy? Diabetes Care. 2011; 34(7):1617-1621.
7. Jeffcoate W. Vascular calcification and osteolysis in diabetic neuropathy- is RANKL the missing link? Diabetologia. 2003; 47(9):1488-1492.
8. Mabilleau G, Petrova N, Edmonds M, Sabokbar A. Increased osteoclastic activity in acute Charcot’s osteoarthropathy: the role of receptor activator of nuclear factor-kappaB ligand. Diabetologia. 2008; 51(6):1035-1040.
9. Alikhani M, Alikhani Z, Boyd C, Maclellan C, Raptis M, Liu R, Graves D. Advanced glycation endproducts stimulate osteoblast apoptosis via the MAP kinase and cytosolic apoptotic pathways. Bone. 2007; 40(2):345-353.
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11. Saito M, Marumo K. Collagen cross-links as a determinant of bone quality: a possible explanation for bone fragility in aging, osteoporosis and diabetes mellitus. Osteoporosis Int. 2010; 21(2):195-214.
12. Macaione V, Aguennouz M, Rodolico C, Mazzeo A, Patti A, Cannistraci E, Vita G. RAGE-NF-kB pathway activation in response to oxidative stress in facioscapulohumeral muscular dystrophy. Acta Neurologica Scandinavica. 2005; 115(2):115-120.
13. Lindsey J, Cippollone F, Adullah S, Mcguire D. Receptor for advanced glycation end-products (RAGE) and soluble RAGE (sRAGE): cardiovascular implications. Diabetes Vasc Dis Res. 2009; 6(1):7-14.
14. Grant W, Rubin L, Pupp G, Vito G, Jacobus D, Jerlin E, Tam H. Mechanical testing of seven fixation methods for generation of compression across a midtarsal osteotomy: a comparison of internal and external fixation devices. J Foot Ankle Surg. 2007; 46(5):325-335.
15. Grant W, Foreman E, Wilson A, Jacobus D, Kukla R. Evaluation of Young’s Modulus in Achilles tendons with diabetic neuroarthropathy. J Am Podiatr Med Assoc. 2005; 95(3):42-246.
16. Grant W, Lavin S, Sabo R. Beaming the columns for Charcot diabetic foot reconstruction: a retrospective analysis. J Foot Ankle Surg. 2011; 50(2):182-189.
17. Sammarco J. Superconstructs in the treatment of Charcot foot deformity: plantar plating, locked plating, and axial screw fixation. Foot Ankle Clin N Am. 2009; 14(3):393-407.
For further reading, see “Limb Salvage And The Charcot Foot: What The Evidence Shows” in the March 2011 issue of Podiatry Today, “Can Scaling Theory Aid In Charcot Foot Reconstruction In Obese Patients?” in the March 2013 issue or the DPM Blog “Can ‘Beam’ Surgery Have An Impact For The Collapsed Charcot Foot?” at http://tinyurl.com/pa4ah9y  .
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