Approximately 23.6 million people in the United States have diabetes, according to the 2007 statistics from the American Diabetes Association.1 Many of these patients have an associated comorbidity of obesity and, all too often, Achilles tendon contracture.
As we age, the tendon naturally tightens. However, diabetes exacerbates this tightening process as increased blood sugar levels deposit glucose in the collagen of the tendon, greatly reducing its elasticity. Obesity can also contribute to the tightening of the posterior muscle group, which includes the Achilles tendon. The glycation effect with the Achilles tendon also occurs in the plantar fascia and other tendinous tissues.
In one study, researchers in Brazil assessed ultrasound studies of the Achilles tendon of patients with diabetes in comparison to those of patients without diabetes. They found disorganized tendon fibers in 89 percent of patients with diabetes (62 of 70) and calcification of the tendon in 76 percent (53 of 70) of the patients with diabetes.2
The study also indicates a correlation between the duration of diabetes and tendon disorganization. The oldest patients in the study also appeared to have a greater prevalence of Achilles tendinopathy.2 
In a similar study in 2006, Orendurff, et al., revealed via electron micrographs alterations in the collagen tissue in tendons that are likely related to the non-enzymatic glycolation of the tissue by advanced glycolytic end products.3
Both of these studies demonstrate the biologic effects in the tendon, including changes in the inherent stiffness in the tendon, which subsequently leads to increased forefoot pressures.
Increased stiffness in the tissue of the Achilles tendon may result in joint contracture, causing an earlier heel off and increased pressure to the forefoot for a longer period of time.
Accordingly, the Achilles tendon plays a significant role in the formation of calluses and ulcers in the forefoot. The Achilles in some cases can act as an impediment to healing ulcers with increased forefoot load and decreased ankle dorsiflexion.
In a large multicenter prospective study involving 248 individuals with diabetes, Caselli, et al., specifically looked at the forefoot to rearfoot ratio of plantar pressures and found that both of these pressures are increased in diabetic neuropathic feet.4 
Caselli claims that while other studies had looked at forefoot pressures, this study was the first to address the increased peak pressure present at the rearfoot in patients with diabetic neuropathy in comparison to non-diabetic patients. The authors concluded that the forefoot to rearfoot peak pressure ratio is increased only in patients with severe diabetic neuropathy.4
This imbalance in the pressure distribution (forefoot to rearfoot peak pressure ratio) occurs with increasing degrees of neuropathy. Equinus and muscle weakness develop in later stages of peripheral neuropathy and forefoot ulceration may result.5
Abnormal gait biomechanics with neuropathy and intrinsic muscle loss also contribute to increased plantar forefoot pressures. When shear and vertical forces exert pressure on the skin overlying bony prominences, callus formation occurs. This callus increases pressure on underlying tissues. Removing callus under bony prominences in the forefoot can reduce plantar pressure by 26 percent.6
Achilles tendon lengthening, which is aimed at reducing mechanical loads to the plantar surface of the foot, can be beneficial for patients with diabetes. Researchers have found this procedure to be effective in reducing forefoot pressure by 27 percent.3
Additionally, the aforementioned study by Orendurff, et al., examined peak pressures of the forefoot for a period of time after lengthening of the Achilles and found that the ulcers healed 80 percent of the time. However, after eight months postoperatively, the peak pressure to the plantar forefoot returned.3
While the ulcers healed, the researchers found that patients had ankle weakness/instability due to the persistence of plantar flexor torque that persisted with gait. They did note that ankle dorsiflexion flexibility continued to improve.3
In 2005, a group of physical therapists and orthopedists compared the effects of total contact casting and tendo-Achilles lengthening (TAL) for the treatment of diabetic foot ulcers.6
Total contact casting (TCC) offers another method of treating foot ulcers by distributing plantar pressure more evenly in the foot via offloading of the ulceration and elimination of the pull from the Achilles tendon.
Researchers concluded that the Achilles lengthening group achieved more healed ulcers and for a longer period of time overall in comparison to the total contact cast group.6 These patients had substantial increases in dorsiflexion (9 to 19 degrees) and a short term reduction in peak plantar pressure of seven months.
The concentric plantarflexion peak torque decreased by 31 percent following TAL and immobilization, but returned to baseline level after eight months. The study authors suspect this may have the been the result of exercise instructions the patients received.6
One can lengthen the Achilles tendon by performing a percutaneous tendo-Achilles lengthening or a gastrocnemius recession.4 The major advantage to the gastroc recession is that the procedure leaves the soleus muscle/tendon intact. This eliminates the risk of over-correction and possible calcaneal gait. There is a recurrence rate of 15 percent for the contracture of the Achilles with gastrocnemius recession. The amount of normal dorsiflexion necessary with gait is 10 degrees past neutral.
When is a percutaneous tendo-Achilles lengthening preferable? When testing ankle dorsiflexion, if the foot is in equinus with knee flexion and extension, one would opt for the percutaneous procedure. Otherwise, a gastrocnemius recession is indicated if the necessary 10 degrees of dorsiflexion are present with knee flexion.
There are several disadvantages to lengthening of the Achilles. One disadvantage is substantial weakening of the ankle as evidenced by decreased plantarflexory power that has been anecdotally reported after TAL and immobilization.
Also be advised that over-lengthening of the tendon can result in a calcaneal gait with possible sequelae of heel ulceration. There is also the possibility of Achilles tendon rupture.
When performing a transmetatarsal amputation, the surgeon often needs to address the Achilles tendon as well, since there may be a progressive development of an equinovarus type of deformity. The release of the Achilles tightness will greatly reduce pressure and possible breakdown under the fifth metatarsal.
Additionally, when it comes to Charcot arthropathy, the Achilles tendon plays a vital role in decreasing stress to the midfoot. In 2002, Armstrong and Lavery studied the Achilles tendon contracture in patients with diabetic neuropathy. They found that increased load to the forefoot with plantarflexion of the heel can result in Charcot arthropathy breakdown.
The authors theorized this occurs most often in the midfoot since it is where the foot’s superstructure is the weakest. Achilles tendon lengthening can greatly reduce stress to this area.7
It is crucial to examine and address other potential causes of increased plantar forefoot pressure such as hammertoes, long and/or plantarflexed metatarsals, fat pad atrophy or other foot positional stresses. We need to educate our patients about stretching of the Achilles tendon, using accommodative insoles and wearing proper shoe gear.
The question remains as to whether one should preventively lengthen the Achilles tendon or address the tendon after the ulceration has occurred. Achilles lengthening may serve as a beneficial method to heal and prevent neuropathic forefoot ulceration.
The Achilles lengthening or gastrocnemius recession can have a profound effect in decreasing peak plantar pressures at the forefoot and increasing ankle dorsiflexion. This can result in a greater percentage of healed diabetic foot ulcers and reduced healthcare costs.
Dr. Wilson is in practice at Kaiser Permanente Medical Center in Springfield, Va.
Dr. Steinberg is an Assistant Professor in the Department of Plastic Surgery at the Georgetown University School of Medicine in Washington, D.C. Dr. Steinberg is a Fellow of the American College of Foot and Ankle Surgeons.
For further reading, see “Tendo-Achilles Lengthening: Friend Or Foe In The Diabetic Foot?” in the November 2007 issue, “Tendon Lengthening: Is It A Viable Option For Forefoot Ulcers?” in the July 2005 issue, “Addressing Tendon Balancing Concerns In Diabetic Patients” in the March 2003 issue, “A Guide To Offloading The Diabetic Foot” in the September 2005 issue or “Offloading The Plantar Fascia: What You Should Know” in the November 2005 issue.
To check out the archives or get information on reprints, visit www.podiatrytoday.com .
1. American Diabetes Association Web site, http://www.diabetes.org/diabetes-statistics.jsp , accessed on Feb. 28, 2009.
2. Batista F, Nery C, Pinzur M, et al. Achilles tendinopathy in diabetes mellitus. Foot Ankle Int 29(5):498-501, 2008.
3. Orendurff MS, Rohr ES, Sangeorzan BJ, et al. An equinus deformity of the ankle accounts for only a small amount of the increased forefoot plantar pressure in patients with diabetes. J Bone Joint Surg (Br) 88(1):65-68, 2006.
4. Caselli A, Pham H, Giurini JM. The forefoot to rearfoot plantar pressure ratio is increased in severe diabetic neuropathy and can predict foot ulceration. Diabetes Care 25(6):1066-71, 2002.
5. Nishimoto GS, Attinger CE, Cooper PS. Lengthening the Achilles tendon for the treatment of diabetic plantar forefoot ulceration. Surg Clin North Am 83(3):707-26, 2003.
6. Salsich GB, Mueller M, Hastings MK, et al. Effect of Achilles tendon lengthening on ankle muscle performance in people with diabetes mellitus and a neuropathic plantar ulcer. Phys Ther 85(1):34-43, 2005.
7. Lavery L, Armstrong D, Boulton A. Ankle equinus deformity and its relationship to high plantar pressure in a large population with diabetes mellitus. J Am Podiatr Med Assoc 92(9):479-82, 2002.