Proactive Diabetic Foot Surgeries

  • Lientra Q. Lu, Michael B. Strauss and Anna M. Tan
  • Volume 08 - Issue 3

Commentary on our Prevention of New and Recurrent Diabetic Foot Wounds Series

This article on proactive diabetic foot surgeries for the prevention of new and recurrent diabetic foot wounds completes our five-article series on the prevention of new and recurrent diabetic foot wounds.1-4,15

In the current atmosphere of intense scrutiny and unrelenting requirements for authorizations by the payers, outcomes have become a major consideration. Outcomes relate to durability, and durability relates to the prevention of new and recurrent wounds after the healing of a wound, diabetic or otherwise. We believe our series is the most comprehensive literature available on this subject.

The current and previous articles in the series address the crucial topics for wound prevention with 1) patient education, 2) skin and toenail evaluation and management, 3) selection of appropriate protective footwear and 4) early implementation of proactive surgeries. The information from this series will become an essential component for the second edition of our MasterMinding Wounds text.

The majority of wounds, when managed appropriately, heal while the patient is hospitalized or in the controlled atmosphere of a skilled nursing facility. Problems arise when patients return to their usual and customary lifestyles. Without adherence to the four topics of our article series, new wound problems are likely to arise. Diabetic patients with healed foot wounds are a special population that need to be followed on a regular basis; their situation is detailed in the second article (i.e., patient education) in our wound-prevention series. This contrasts with the youthful patient with a traumatic wound, where once the wound is healed, follow- up is not usually necessary.

When new, recurrent or impending wounds are first noted in the vulnerable diabetic as well as other at-risk foot populations, immediate proactive interventions need to be initiated. They start with appropriate skin and toenail care, proper selection of protective footwear and debridements of hypertrophic calluses over underlying bony deformities — all of which are detailed in our wound-prevention series of articles. Remember when foot wounds are not healing as expected, three causes account for more than 90 percent of the reasons:6 1) underlying bone and soft-tissue deformities, 2) deep infection involving bone, bursa and/or cicatrix and 3) ischemia-hypoxia. Each component of the troublesome triad has appropriate interventions for management; there should be no delays in initiating such. This article will describe what should be done for the deformity component of the triad.

Remember: “To heal the wound is ideal; to prevent it from returning is sublime.” Our series of wound-prevention articles in Wound Care and Hyperbaric Medicine helps achieve the sublimity state.


Proactive diabetic foot surgeries are those done before a new or recurrent wound occurs. As a corollary, if a wound is present, surgical intervention is done before the wound worsens, makes the surgery complicated and/or necessitates a major amputation. In terms of underlying pathology of recurrent or new diabetic foot wounds, the three major indications for proactive surgeries in diabetic feet are 1) deformities (bone, bursa and/or cicatrix), 2) muscle imbalances and 3) contractures or combinations of these (Figure 1).

Perfusion and oxygenation to the “at risk” foot is always a critical consideration. Consequently, revascularization may be needed before doing the proactive surgery. Revascularization options include bypass surgery, angioplasty and stenting. The decision as to what needs to or can be done regarding  revascularization is determined by the vascular surgery, interventional cardiologist or interventional radiology consultant.

When these problems are addressed proactively, the surgeries can usually be minimally invasive (MIS) and adhere to the goal of keeping them simple and speedy (KISS). MIS and KISS surgeries typically avoid elaborate exposures and extensive dissection of tissues. This is reflected by wound closures that require only simple, removable sutures and staples to close the flaps and skin layers. In addition, the sue of internal fixation devices such as screws, plates or intramedullary rods as well as deep nonabsorbable and braided- type sutures is avoided.

FIGURE 1. Nonhealing wound due to infected bursa


Legend: Massive bursa formed over end of resected 5th metatarsal (MT) after partial 1st ray amputation. The bursa formed and became infected as a response to the prominence of the remaining end of the fifth MT shaft—obviously a mechanical/deformity problem.


Goals of Proactive MIS/KISS Surgeries

The primary goal of proactive surgeries is to prevent new or recurrent wounds by doing nonurgent surgeries. This is in contradistinction to reactive surgeries that need to be done on an urgent basis for impending toe or lower-limb- threatening diabetic foot problems.

Secondary goals include achieving plantigrade and pain-free feet. Pain is often not a consideration in this patient group, however, due to diabetic sensory neuropathies. Ability to wear protective footwear and restore mobility are tertiary goals. Rarely, the patient is left with a chronic, stable, small wound that requires minimal wound care but still allows mobility. Elimination of this type of wound with surgery could require altering foot anatomy and biomechanics to such a degree that when ambulation is resumed, worse problems develop. In these situations, the adage “the cure is worse than the disease” is applicable.

Although this article, Part 5, is directed to the surgeon, it integrates well with all the information presented in our preceding four wound-prevention articles.1-5 All wound care givers should be aware of the proactive MIS/KISS surgical options and readily refer to surgeons familiar with them for operative management. The consensus opinion risk factors for incipient new and recurrent diabetic foot wounds should be used to support the decision for referral for proactive MIS/KISS surgeries. They include 1) peripheral artery disease, 2) deformity, 3) previous wound, 4) prior amputation, and 5) neuropathy.6 As the number of risk factors increase, the likelihood of a new or recurrent diabetic foot wound increases proportionately.7

This article discusses six surgical procedures that meet the criteria for MIS/KISS surgeries for the prevention of new and recurrent diabetic foot wounds. It applies equally well, however, to patients who are not diabetic and who have one or more of the above enumerated risk factors. It is appropriate to do some of the surgical procedures in the clinic or at the bedside in the hospital or skilled nursing facility. Regardless, the knowledge of these available MIS/ KISS interventions adds an additional dimension to the comprehensive management of the diabetic foot.

It is unfortunate that the risk factors are described only as present or absent without consideration for severity by this consensus group. We feel that severity needs to be factored into making the decision for referrals for MIS/KISS proactive surgeries. We propose categorizing each risk factor as insignificant, moderate or a severe problem (Table 1). With this grading system, decisions for proactive surgeries become objective. Consider the following:
One risk factor in the severe category, two in the moderate category or combinations of these deserve consideration for surgical interventions.
If the risk factors are not all present or all are minimal, rechecks should be done periodically; annually if the patient is compliant versus monthly if the patient is noncompliant.
Each diabetic patient should be educated in recognizing the risk factors and if any appear or noticeably worsen, an expedited evaluation should be done.²

Toe Tendon Tenotomies to Mitigate Deforming Forces

While toe deformities may appear to be unimportant, they can have serious consequences. This is especially the situation in patients with diabetes who have neuropathies. A small ulcer can evolve to osteomyelitis of the phalanges, septic joints of the toes, ascending tenosynovitis and progressive necrotizing soft-tissue infections.  Malperforans ulcers are invariably the consequence of underlying bone and joint deformities, and the pathology in the toes is no different than when they occur in the foot and ankle.Consequently, early attention to correction of gnarled toes is an essential proactive wound-prevention measure for the insensate foot; it has more than cosmetic ramifications. This section describes the anatomy of claw, hammer and mallet toes, explains the pathophysiology that leads to forefoot and toe wounds, and provides a dozen paradigms about tenotomies to manage the axial (that is, the toes are inline with the metatarsals) deformities of the toes.

TABLE 1. Quantifying risk factors for diabetic foot
Grade Assessment


Not Problematic


Mild to Moderate



1. Peripheral Artery Disease Palpable pulses Doppler pulses Imperceptible pulses
2. Deformity None significant Palpable or visible with or without erythema or attenuation of skin Ulcer or impending skin breakdown
3. Previous wound Normal healing Delayed healing Requiring surgery to correct or close
4. Prior amputation toes Forefoot Proximal to forefoot
5. Neuropathy None Impaired sensation, minor contractures and/or muscle weakness Insensate, major contractures, paralysis

Note: Half points may be used if the findings are mixed or intermediate between two grades.


TABLE 2. Toe deformities and their potential wound problems

Deformity Description Pathomechanics (Etiology) Wound Concerns
Mallet toe Flexion contracture at the distal interphalangeal joint Overactivity of the flexor digitorum longus muscles Ulcerations at the toe tip and over apices of the IP joint; toenail injury
Hammer toe Flexion contracture at the proximal IP joint Overactivity of the flexor digitorum brevis muscles and loss of toe intrinsic muscles Same as above
Combination of hammer and mallet toe Flexion contracture at both the IP joint levels Combinations of the mallet and hammer toe etiologies Same as above plus "kissing" lesions between phalanges
Dorsiflexed toe Hyperextension posturing of toe at the metatarsal---phalangeal joint level Overactivity of the long extensor tendons to the toe Nail matrix and dorsal distal phalanx wounds from pressure contact with the toe box of the shoe
Claw toe Hyperextension contracture at the MTP joint and flexion contractures at the PIP and DIP joints Loss of toe intrinsic muscle function plus overactivity of toe flexor and extensor muscles. MT heads displaced plantarward Wound over IP joints and tips of toes; malperforans ulcers under metatarsal head displacements

Note: * Since the hallux has only a single interphalangeal joint, a flexion deformity at this level may be named either a hammer or a mallet toe.

Abbreviations: DIP = distal interphalangeal, IP = interphalangeal, MT = metatarsophalangeal, PIP = proximal interphalangeal


FIGURE 2. Bone and joint anatomy of clawed, hammer and mallet toes

FIGURE-2Legend: Axial deformity classification of toe based on levels of joint involvement. Table 2 explains the pathophysiology causing the deformities. Red arrows indicate levels of joint contractures. Yellow oblongs indicate sites for ulcerations. The clawed toe is the cause of the malperforans ulcer under the metatarsal head—note the dorsal subluxation of the proximal phalanx, which "drives" the MT head downward.

KEY: DIP = distal interphalangeal, HE = hyperextension, MTP = metatarsal phalangeal, PIP = proximal interphalangeal joint

Classification of axial toe deformities.

The classification of axial toe deformities is straightforward (Figure 2). A hammer toe occurs with hyperextension at the metatarsophalangeal joint and flexion at the proximal interphalangeal joint with or without extension of the distal interphalangeal joint. A claw toe is present when the metatarsophalangeal joint is hyperextended and the proximal interphalangeal joint is hyperflexed with or without hyperflexion of the distal interphalangeal. In a “pure” mallet toe deformity, the metatarsophalangeal joint and proximal interphalangeal joints are unaffected, but the distal interphalangeal joint is flexed.

Pathophysiology of axial toe deformities.

The pathophysiology of the toe deformities that leads to forefoot and toe wounds results from neuropathy. The essential problem is a motor neuropathy in which fine muscle balance between flexor and extensor muscles is altered or lost. With loss of the intrinsic muscles that flex the toes at the metatarsophalangeal joints and extend the toes at the interphalangeal joints, hyperextension of the metatarsal phalangeal joints occurs due to overpull of the toe extensor muscles, while overpull of the flexor muscles cause toe interphalangeal joint flexion contractures (Table 2). Consequences of the muscle imbalances include:

  1. Clawing of the toes with inability to visualize the flexor creases of the toes, i.e. the "hidden crease" sign

  2. Retraction of the toes proximally onto the dorsum of the foot

  3. Dorsal subluxation of the proximal phalanges over the metatarsal heads

  4. Downward pressure on the metatarsal heads (from the subluxed metatarsophalangeal joints) into the forefoot fat pad with loading as occurs with standing and walking

  5. If not corrected, a malperforans ulcer develops as the plantar surface of the metatarsal head erodes from inside- to -outside with weight bearing because of the deformity (Figure 3). This often goes unnoticed because of diabetic sensory neuropathy.


FIGURE 3. Deformities and contractures causing a malperforans ulcer


Legend: Deformities and contractures generate biomechanical problems, which in turn lead to wounds—as in this example of a malperforans ulcer.


If the intrinsic muscles of the foot continue to function but there is unbalanced overpull of the extensor muscles, the toes may remain straight but be hyperextended at the metatarsal- phalangeal joints. The hammer and mallet toe deformities occur because of overpull of the flexor tendons and loss of the intrinsic muscle abilities to extend the interphalangeal joints. If the problem lies primarily with the short intrinsic flexors of the toes, the hammer toe deformity occurs and causes the toe tip to “drive” into the sole of the shoe. The consequence is a pressure sore at the tip of the toe. This typically progresses to a penetrating ulcer to the distal tuft and osteomyelitis of this structure (Figure 4). Overpull of the long flexor muscles of the toes results in mallet deformity. When the combination of the above problems occurs, the hyperflexed proximal interphalangeal (PIP) joint in association with the hyperextended metatarsophalangeal joint can cause a pressure sore over the apex of the PIP joint (Figure 5). With progression, the ulceration erodes into the joint, causing a septic joint and osteomyelitis. If unchecked, the infection can track proximally along the tendon sheaths, resulting in ascending tenosynovitis and progressive necrotizing soft-tissue infection.

FIGURE 4. Ulceration at tip of hammer toe deformity


Legend: The reason for the toe tip ulceration is obvious from the examination. The mallet toe deformity increased the contact pressure when standing and walking between the toe tip and the underlining supporting surface enough to generate a pressure sore over toe tip.

Note the flexor creases of the clawed toe are obscured because of the flexion contractures. We label this clinical finding the "hidden crease" sign.



Usually a sensory neuropathy is associated with the motor neuropathy, especially in the patient with diabetes mellitus. Other motor neuropathies, however, have hereditary causes such as Charcot-Marie-Tooth disease, acquired causes such as a result of trauma, and/  or demyelinating causes such as multiple sclerosis that may not have sensory neuropathy components to them. While a sensory neuropathy does not cause a deformity, it may delay the diagnosis of the deformity because of the absence of pain and delay the patient from seeking care until a complication arises, such as obvious infection at the deformity site or systemic sepsis. Consequently, any patient with sensory neuropathy in the feet and associated toe deformities should be informed of the need for proactive interventions anytime an impending pressure sore is observed in the forefoot and/or toes. Also, all foot- care providers should be aware of this information and counsel their patients accordingly.

FIGURE 5. Ulceration over proximal interphalangeal joint


Legend: Ulceration over proximal interphalangeal (PIP) joint secondary to hammer toe deformity. The biomechanical problem is that of the apices of hyperflexed PIP joints causing pressure concentrations with the toe box of the shoe.

Note the unhealthy long, dystrophic and fungus—infected toenails and the scaly, callus skin (at the toe tips), indicating that toenail and skin—care instructions are also needed.


Paradigms for evaluation and management of axial toe deformities.

With the above considerations and experiences with several hundred tenotomies of toe tendons (MBS) in the past dozen years, we reiterate some of the above information as well as share our “pearls” in the evaluation and management of axial toe deformities. A large review experience of toe tenotomy surgeries is found in the Tamir et al. article in Foot and Ankle International (2014).9 Whereas some of the procedures need to be done in the operating room, we do the majority of tenotomies in our outpatient wound- care programs. The following are 12 paradigms that relate to axial toe deformities and their management with tenotomies.

1. Often toes are retracted proximally the dorsum of the foot due to overactivity of the long extensor tendons. This leads to downward pressure on the metatarsal heads and is a precursor to malperforans ulcerations (Figure 5). The toe sign is an indication for toe extensor releases.

2. Manipulation of interphalangeal joint contractures should always be a component of the tendon release procedures. Occasionally, the manipulation results in avulsion of skin at flexor creases of the interphalangeal joints. All of these superficial wounds have healed without incidence.

3. In many instances, extensor tendon releases are difficult to perform in the presence of edema, scar or hidebound skin. In these cases we perform these procedures in the operating room (see text box).

Two-centimeter incisions are made and carried through the subcutaneous tissue level in the intermetatarsal spaces just proximal to the metatarsal necks. The extensor tendons are then captured with a curved hemostat brought to the skin surface and incised under direct visualization with a scalpel, scissors or electric cautery.
Much variation in the extensor tendon anatomy has been observed, often requiring release of more than one tendon for each toe. The short incisions are usually closed with small nylon sutures or staples (if already on the field from closing a wound at a different site).

4. Releases of extensor hallucis longus tendons for managing clawing of the great toes have generally not been effective in managing malperforans ulcerations of these toes. In such cases, the underlying bony deformities require sesamoid removals.

5. If the patient with a neuropathic foot is in the operating room for a foot surgery unrelated to toe deformities, then tenotomies should be recommended to the patient at the time of the preoperative evaluation. We perform our toe flexor tenotomies at the level of the metatarsal head rather than at the proximal interphalangeal joint crease levels. The additional soft-tissue padding (metatarsal head fat pad) affords more reliable healing rates compared to hidebound flexion joint creases.

6. With ankylosed interphalangeal joints, tenotomies may need to be supplemented with realignment interphalangeal joint resections. We also do this minimally invasively. Our approach negates the need for maintaining alignment of the interphalangeal joint fusion with temporary placement of a Kushner wire through the medullary canal and the potential problems it imposes, such as keeping the patient nonweight bearing, infection of the pin tract and/or breakage or bending of the pin (see text box).

An ovoid incision is made about 8 mm wide centered over the apex of the deformity with, the ends of the ovoid at about the midpoint of the medial and lateral sides of the toe. The ovoid skin incision is carried down to the bone level and the skin, extensor tendon and extensor joint hood are excised. Next precise parallel osteotomies perpendicular to the long axes of the phalanges on both sides of the joint are made. The ovoid skin is closed with small nylon sutures. The approximation of the skin edges brings the osteotomized phalangeal ends in contact with each other, straightens the toe and acts as an external splint to maintain the toe alignment.

7. Infrequently, toes straightened with tenotomies develop recurrent deformities. This should be mentioned in the preoperative orientation for the patient. If necessary, second-stage tenotomies and/or joint resections (see previous text box) are done when needed.

8. Active toe flexion and extension for respective extensor and flexor tenotomies by the awake patient facilitates the releases. This makes the tendons taut like a bowstring (and sweeping the #11 scalpel) blade transversely across the tendon in a pendulum-like fashion with the 2- to 3- millimeter skin incision as the pivot point) easy to release (Figure 6). Usually audible and palpable sensations confirm the tenotomy is complete and verified by the patient being unable to actively flex or extend the toe. If the patient is insensate, as is frequently the situation in patients with diabetes mellitus, no anesthesia is needed. If sensation is present, a field block with 1% lidocaine (without epinephrine) proximal to the incision provides adequate anesthesia for the procedure.


FIGURE 6. Percutaneous transection of bowstringing extensor tendon


Legend: The contracted toe extensor tendons are easily released when they bowstring across the dorsum of the forefoot. This can be done with a #11 scalpel blade using a 2---3 mm incision. No suturing/stapling of the small incision is needed.

The contracted muscle tendon units cause hyperextension of the toes at the metatarsal phalangeal joints, retraction of the toes proximally on the dorsum of the foot and downward pressure of the proximal phalange base on the metatarsal head.


9. Anticoagulation is not contraindication to doing these minimally invasive surgeries. In the anticoagulated patients, we typically double the time we apply direct pressure to the operative site(s); i.e., 10 minutes instead of five.

10. Advanced peripheral arterial disease, even in those patients with barely perceptible Doppler pulses, has not been a contraindication for doing these minimally invasive tenotomies. After the tenotomies, we allow our patients to walk out of the office. Bandaging is minimal and done to maintain the toe in the corrected position - usually with weaving between the toes or horseshoe wrap under or over the toe, depending on the correction desired.

11. After having dealt with many toe deformities with "textbook" management (i.e., correction utilizing flexor tendon transfers and arthrodesis of the interphalangeal joints) of clawed, hammer and mallet contractures, the minimally invasive toe tenotomy procedures without question are our preferred recommendations (Figure 7).

FIGURE 7. "Textbook" versus minimally invasive surgery approaches to claw toes

FIGURE-7Legend: In the left---side photo, the patient had the more traditional (textbook) approach for dealing with her claw toe deformities, including rerouting the flexor tendons to the dorsums of the proximal phalanges, interphalangeal joint fusions and temporary percutaneous joint pinnings. Note the shortened 2nd and 3rd toes and their recurrent deformities. These toes were almost totally immobile. Thirty to 45 minutes surgical times, at best, are required to perform these procedures for each toe.

The right ---hand photo shows the photos of previously clawed toes managed with tenotomies, limited open for the extensor tendons and percutaneous for the flexor tendons. With bilateral toe deformities, the patient elected to have the procedures done at one time in the operating room versus the serial releases in the office. Although the toes are immobilize, they remain straight, at a normal length and are not prone to developing ulcers. Note the mild recurrent hammer deformity of the little toe. If the patient so elects, this can be managed with a second ---stage in---office percutaneous flexor tenotomy.


12. When patients are presented the options of living with nonfunctional deformed toes that are at risk for developing ulcerations versus straight, cosmetically pleasing, not actively mobile toes that are not prone to ulceration, the answer is invariably the straight toe choice. This option is especially recommended for the patient with comorbidities such as diabetes mellitus, peripheral artery disease and peripheral neuropathy. Percutaneous and limited open (may be required for extensor tendons) tenotomies are the minimally invasive, quick and easy solution to achieve this goal.


Our approach to managing clawed, hammer and mallet toes has been uniformly successful with almost 100 percent satisfaction in the patients. One nonanticoagulated patient did develop a hematoma at a single open extensor tenotomy site, and a couple others had minor superficial skin dehiscence that subsequently healed with minor care. No complications were associated with the solely percutaneous technique. Several patients required delayed secondary procedures such as flexor tenotomies after their extensor tenotomies. If the procedures are done in the office, clinic or at bedside, no more than two tenotomies are done at any one time. At these venues, the patients are given prophylactic oral antibiotics for a day or two.

What surgical skills are needed to perform the percutaneous tenotomies? Surgeons familiar with foot anatomy and an understanding of the pathophysiology of the axial toe deformities are the logical choices. Although obviously bowstringing tendons are easy to transect, more difficulty may be experienced with tendons “hidden” by fatty subcutaneous tissues, edema, scar tissue or hidebound skin. For such situations, the tenotomies should be performed by a foot and ankle surgeon, especially when these conditions are present on the dorsum of the foot. For easily accessible tendons, any wound care giver with suturing and debriding experience should be able to perform the minimally invasive percutaneous procedures after being suitably mentored and found to be competent in doing the tenotomies. Occasionally, a 2-3 mm incision becomes extended because of patient movement or inexperience. If this occurs and the accidental incision is large enough, it can be easily approximated with a couple of small nylon sutures.

Another advantage of our MIS and KISS approach to axial toe deformities is its cost effectiveness. When done in the clinic or bedside, the charges are a fraction of what they would be if done in the operating room. Use of the operating room may cost $5,000 to $10,000 versus the in-clinic, bedside procedure costing 1/10th to 1/20th of this. The information described above demonstrate the considerations we address when providing this effective, cosmetically pleasing and cost-effective option to our patients with clawed, hammer and/or mallet toes. 

Realignment of Metatarsal Heads to Manage Malperforans Ulcers

Malperforans ulcer (MPU) is a term used to describe an ulcer over a bony deformity. The ulcer develops from contact pressures between the overlying skin and the underlying deformity. It most frequently occurs under the metatarsal heads in the forefoot. It is typically associated with other conditions affecting the nerves causing neuropathy and often a complication in diabetes mellitus, in which case it is often referred to as a diabetic neuropathic ulcer. Conditions that predispose patients to malperforans ulcers (see previous toe deformity section) include, but are not limited to, impaired  pain perception at the skin pressure point over a bony prominence. clawed toes due to muscle imbalances, metatarsophalangeal joint subluxations/dislocations, and metatarsal heads being directed plantar ward.

In contrast to ulcers from shear forces, trauma, venous stasis disease, arterial insufficiency, vasculitis or combinations of these that have external causes, the malperforans ulcer evolves from inside to out. When the deformity with or without contact pressures exceeds the integrity of the overlying skin, an ulcer develops.
In the insensate foot, the patient may not appreciate the pressure concentrations between the deformity and the underlying skin. In the insensate foot, the pain would be analogous to walking with a pebble in the shoe.

Progression of problems from MPUs.

MPUs may initially appear benign, but if left untreated, they can evolve to more serious problems and even limb-threatening conditions. If the surface of the MPU seals with a crust or fibrous tissue, an abscess can form in the subcutaneous tissue layer and lead to sepsis in the foot. As the abscess enlarges, the infection can spread into the surrounding tissues and proximally along tendon sheaths. If the wound is infected with group A Streptococcus, commonly known as “flesh-eating bacteria,” or other tissue toxic bacteria, it can rapidly destroy skin, fat and the tissue covering the muscles. When this occurs, the problem can lead to a limb- threatening necrotizing fasciitis.

Total contact casting (TCC) is the most- often-utilized treatment for forefoot malperforans ulcers; however, it is not the most effective. During TCC treatment, the leg is casted to offload pressure to the forefoot. The patient may need to have serial casting for as long as six months with biweekly recasting to achieve healing of the MPU. This method does not provide access for wound care during those biweekly intervals. The trapping of moisture and sweat promotes bacterial growth inside the cast and can cause dermatitis and secondary wounds. The recurrence rate is also greater than 50 percent because the underlying bony deformity is not addressed.10 When the cast is removed, the patient is likely to walk on the same pressure points with recurrence of ulcers even with protective footwear.

Management of the MPU.

We recommend management of MPUs according to their stages of progression (Table 3, Figure 8). We utilize percutaneous drilling and closed osteoclasis of the metatarsal heads for management of other than superficial MPUs  when neither osteomyelitis of the metatarsal head nor sepsis is present in the foot. If not done, previously toe tendon tenotomies are done in conjunction with the metatarsal head realignment surgery. Drilling and osteoclasis needs to be done in a sterile environment. With local anesthesia, typically a foot block, the metatarsal neck is scored with a 1-millimeter- wide puncture wound using a 0.62 mm Kushner wire. The bone is then broken (osteoclasis) at the drilling site and the metatarsal head redirected upward so that it is no longer deformed downward.

TABLE 3. Management of malperforans ulcers
Stage Findings Management
1 Callus formation under bony prominences Debride calluses, protective footwear
2 Superficial ulcer (skin only) Toe tendon tenotomies (possible Achielles tendon lengthening) plus management methods for Stage 1
3 Deep penetrating ulcer (but soft tissue coverage over bone) Realign metatarsal (MT) head with drilling and osteoclasis of MT neck
4 Metatarsal head osteomyelitis, abscess, ascending sepsis Exploration and debridement including bone and soft tissue

FIGURE 8. Staging and management of the malperforans ulcer

FIGURE-8Legend: Staging and management of the forefoot malperforans ulcer is simplified using the above system. If the stage 4 ulcer seals off, ascending tenosynovitis and necrotizing soft tissue infection may occur.


The foot is wrapped with elastic bandage without a splint or a cast. The patient can fully weight-bear and walk out of the surgery site with postop shoe. With the bandage, the newly redirected metatarsal head can load-share with adjacent heads. Prophylactic antibiotics are used perioperatively. With this technique, the malperforans ulcer typically heals within two or three weeks, as opposed to many months’ duration with total contact casting. Due to the sensory neuropathy, patients experience no pain during the fracture healing process, which may take six weeks to three months.

Scoring of the bone is analogous to cutting a board into two pieces with only a drill being available. With the drill, a series of drill holes are made in a straight line across the board. With sufficient drill holes, the board can then be easily broken (i.e.. the bone equivalent of osteoclasis of the metatarsal neck) along the line of (i.e., scored) drill holes.

Clinical observations with the drilling and osteoclasis technique.

With more than 200 cases from Long Beach Memorial Medical Center and Harbor-UCLA Medical Center, we have had uniformly good outcomes: one infection, a couple of cases of slow healing, and almost no transfer lesions.

The contraindication for drilling and osteoclasis is if the metatarsal head is infected (i.e., osteomyelitis is present) and/or the foot is septic. In such situations, formal exploration, debridement and ray resection are required.

Forefoot Narrowing for Cleft Wounds

This condition refers to diabetic and vasculopathic patients with a nonhealing/slow-healing ischemic wound after middle metatarsal resection. The cavity usually persists without evidence of filling in. Surgeons are often reluctant to place a skin graft in the cleft. The challenge is how to maintain a “mechanically sound” foot and achieve wound healing.

Multiple options are available to manage cavitary wounds, but there is a hierarchy from low oxygen and perfusion demands to high oxygen perfusion demands (Figure 9). A split-thickness skin graft (STSG) often results in partial take with sloughing in the depths of the cavity. The STSG, however, has relatively low metabolic demands compared to other techniques to manage cavitary wound. A transmetatarsal amputation can be performed to eliminate the wound, but this shortens the lever arm of the forefoot. Ischemia and higher metabolic demands to heal a full-thickness flap, however, may result in the flaps failing, sloughing and/or dehiscing. This, of course, leads to new wound problems. A below-knee amputation will lead to less mobility for the patient and require a prosthesis for walking. If there is muscle weakness or balance problems, the patient may become wheelchair bound. Narrowing of the forefoot can obliterate the wound. Elastic wraps or casting to maintain the narrowed position, however, can lead to pressure necrosis. Narrowing of the forefoot by compression with external fixation mitigates these problems.

FIGURE 9. Perfusion and oxygen needs hierarchy for healing of various wound types

FIGURE-9Legend: The cavitary wound has the greatest metabolic demand for healing. By obliterating the cavity with forefoot narrowing (or partial wound approximations), the wound can be converted to a less—demanding one for healing, healing by secondary intentions or split—thickness skin graft (STSG).

Note: TCOM = Transcutaneous oxygen measurement, HBO = Hyperbaric oxygen


Technique for fixator application.

A patient with an ischemic foot and nonhealing wound after middle metatarsal resection requires a debridement to achieve a healthy vascular base before placement of the external fixator. When this is achieved, the patient is brought to the operating room. Two pins are each placed in the first and fifth metatarsal shafts. Palpation of bony landmarks eliminates the need for imaging (fluoroscopy) methods. The cleft is obliterated with narrowing of the foot and holding the narrowed position with a cathedral configuration using pin grippers, clamps and rods (Figure 10). Once the cleft is obliterated and a superficial wound remains, it can be skin grafted or healed by secondary intention. The skin graft markedly reduces metabolic requirements to heal as compared to healing of the cavitary wound.

FIGURE 10. Forefoot narrowing with temporary external fixation

FIGURE-10Legend: Nonhealing cavitary wound obliterated with forefoot narrowing and temporary external fixations followed by a split—thickness skin graft.



Literature substantiation.

In 2002 Strauss et al. reported using forefoot narrowing with external fixation on 15 patients.11 Twelve patients (80 percent of the study population) completely healed and resumed their previous levels of activity.

Percutaneous Achilles Tendon Lengthening for Equinus Deformities

The indication for Achilles tendon lengthenings is any forefoot surgery where the forefoot cannot be easily dorsiflexed beyond the neutral ankle positions (e.g., equinus contracture).12,13  A “softer” indication for lengthenings is a foot surgery in which hindfoot varus is contributing to a varus deformity of the hindfoot. With reduced pressure on the forefoot when standing and walking, the likelihood of new or recurrent malperforans ulcers at this site is lessened.


The surgery is usually done in the supine position under anesthesia. A #11 scalpel blade is used to make three hemisections (Hoke technique) of the tendon (Figures 11a and 11b). The first hemisection is on the medial half of the Achilles tendon at its insertion on the calcaneus to counteract hindfoot varus. The second incision is at 2 cm proximal to the first incision, and the hemisection is done on the lateral half of the tendon. The third incision is done 2 cm proximal to the second incision. After that, forceful upward (dorsiflexion direction) pressure is applied to the plantar aspect of the forefoot while the leg is stabilized. Signs of a successful lengthening include audible and palpable sensations that confirm the tendon release, easily being able to dorsiflexed the foot beyond neutral position, and palpable gaps in the tendon at the hemisection sites.

FIGURE 11a. Percutaneous tri hemisection Achilles tendon lengthening

FIGURE-11ALegend: There are 4 steps in the minimally invasive tri hemisection Achilles tendon lengthening procedure. Notice the small incisions are made in the axial direction. Then the #11 scalpel blade is rotated 90° to hemi-sect the tendon (dotted red lines). By releasing the medical portion of the tendon at its insertion on the calcaneus, hindfoot varus can be mitigated.

FIGURE 11b. End results of tri hemisection Achilles tendon lengthening

FIGURE-11BLegend: With the tri hemisections, gaps are created in the tendon when forefoot pressure is applied in a dorsal ward direction. Often the gaps can be palpated through the skin, further signifying that hemisections were effective.


Typically, the corrected ankle condition is maintained in a cast for a six-week period. For severe contractures, external fixation is used to stabilize the foot and serial adjustments of the fixator are done to stretch out the tight posterior capsule structures and achieve a plantigrade foot (Figure 12).

FIGURE 12. External fixation as an adjunct to Achilles tendon

FIGURE-12Legend: The external fixator is an adjunct to managing severe, rigid equinus contractures. With readjustments of the fixator, additional correction of the contracture can be achieved. This occurs as a consequence of stretching the posterior capsule with its viscoelastic (strength---relaxation) properties.


Other considerations.

Additional applications of tendo-Achilles lengthening (TAL) include club foot (Ponsetti technique), cerebral palsy, Charcot-Marie-Tooth disorder, and Charcot neuroarthropathy. Options other than the tri hemisection technique include incising the gastrocnemius tendon, muscle  and/ or fascia at the proximal (Silfverskiold, Baumann), middle (Strayer), distal third portions (Vulpius), or open step-cutting the tendon. These techniques are usually effective if the ankle can be brought to the neutral position when the knee is flexed to the 90-degree position (i.e., Silfverskiold test). For quickness, minimal complications and regardless of the Silfverskiold test, the distal tri hemisection of the tendon is our procedure of choice for the TAL. In addition, the TAL can be done with a local anesthesia without a tourniquet, especially in the patient with sensory neuropathy.

Ostectomies, Bursectomies, Cicatrixectomies for Underlying Deformities

Abnormal callus, bursa and cicatrix formations represent the body’s attempts to generate a protective barrier between the underlying bony deformity and the overlying skin (Figure 13).14 This is often self-defeating in as much as these responses increase the magnitude of the deformity and at a certain point overwhelm the elasticity of the skin. The result is skin ulceration and the ensuing complications that can arise from the loss of skin integrity such as cellulitis, sepsis, ascending infection and necrotizing soft-tissue infection. Underlying deformity bone bursa, or cicatrix is one component of the “troublesome triad” that also includes deep infection and ischemia- hypoxia.Of the three components of the “troublesome triad,” the underlying deformity component is the easiest to address with MIS and KISS surgeries.


FIGURE 13. Tissue responses to underlying deformities


Legend: The body tries to mitigate pressure buildups over deformities by developing padding---type tissues.

While initially they may serve a protective role, with continuing enlargement they add to the deformity and lead to complications themselves such as ulcers, infection (see Figure 1) and interference with wound healing.


Ostectomies and calluses.

Ostectomies address underlying deformities and the abnormal biomechanics resulting from them. Deformities may be spurs, osteophytes, eburnations, posttraumatic defects/malunions, and Charcot neuroarthropathies. Often, however, the bony prominent is minimal; the “real” pathology is in the callus, bursa, and/or cicatrix overlying the deformity. These are the body’s responses, as stated above, to build up protective padding over the underlying bone deformity. A callus is a variant of normal skin that hypertrophies and becomes excessively keratinized. It is a toughened area of the horny layer of the skin, which can become extremely thick and hard in response to repeated friction, pressure, or irritation. Callus offers protection to the underlying epithelium and related skin structures. With pathological callus, the underlying etiology is invariably a bony deformity. Repetitive stress over the deformity, usually from contact pressure from loading and/or improper footwear, causes the overlying skin to thicken in an attempt to prevent loss of its integrity. When this is overwhelmed, there is skin breakdown and ulceration. Three permutations to callus responses to underlying deformity and ways to manage them include (Figure 14):

  • Benign calluses are thin, dry crusts with grape-seed-size underlying ulcers at the pressure sites. Appropriate management at the insipient stage is first paring down the callus to soft pliable skin. The skin under the callus after debridement should have the same pliability and texture as the adjacent skin; the second step is the use of protective footwear to offload the mitigate and mitigate the abnormal biomechanics.

  • Worrisome calluses are dry, firm callus circumscribing malperforans ulcer. They usually improve with the same interventions plus optimal wound management possibly using bioengineered skin substitutes.

  • Alarming calluses are white and typically surround a biofilm over infected bone. They often signal underlying bone or bursa and require exploration and debridement of the infected material. Moist callus may also be from edema fluid from the wound oozing onto the adjacent tissue and should be removed with simple paring.

FIGURE 14. Types of callus responses in the foot

FIGURE-14Legend: Benign calluses can be managed with serial debridements and offloading. Worrisome callus often improve with optimal management as use for benign calluses plus biologic dressings. Alarming calluses require ostectomies or ray resections of bone deformities.



A bursa is a tissue sac lined with synovial cells and filled with synovial fluids. It allows soft tissue to glide over bony prominences or tendons in a nearly frictionless manner. Analogous to the callus, the thickened bursa adds to the thickness of the soft-tissue deformity and contributes to ulceration. With continued loading, the bursa hypertrophies and converts via metaplasia to a firm, relatively avascular cicatrix-bursa combination (Figure 1). With ulceration, bacteria inoculate the pathological bursa tissues, proliferate, and become a source of chronic infection. If the ulcer seals off, the infection process can proceed to deeper tissues, leading to abscess, osteomyelitis, ascending suppurative tenosynovitis, and necrotizing fasciitis.


To manage the deformity, the first step is to offload the deformity site by removing or relieving pressure areas in the insole and shoe linings or increasing paddings of the surrounding area. The second step is serial debridements of the callus in the clinic. If skin integrity is threatened and/or a wound is already present, exploration and debridement of the bursa and cicatrix in the operating room is needed. Finally, ostectomy (often the minor part of the surgery versus the bursectomy and cicatrix removal), osteotomy and realignment of the affected bones (often guided by imagine studies) and/or amputation for more severe deformities are needed.

Alignment Correction and External Fixation for Configuration Problems

Malaligned feet lead to pressure concentrations bursa formation, ulcerations, infections, and often major amputations. Foot alignment problems include forefoot abduction/adduction, foot and ankle inversion (varus/ eversion (valgus), equinus contractures, and combinations of these.


While proactive surgical correction may, at first inspection, appear to be a major undertaking for these problems, surprisingly minimally invasive, KISS (keep it simple and speedy) surgical procedures can prevent these problems from becoming limb threatening (Figure 15). The first step in the surgery is the release of all dynamic deforming forces. It only takes a few minutes to do percutaneous and/or limited open tenotomies.

FIGURE 15. Minimally invasive, keep it simple and speedy surgery with external fixator to manage severe deformities

FIGURE-15Legend: Severe deformities managed with debridement, osteotomies (with debridement of the bones distal to the osteotomy) and maintenance of alignment with temporary external fixation make it possible to salvage the severest of diabetic foot deformities with MIS/KISS interventions.


Next, the bony deformity is removed, again a relatively short procedure since what needs to be done is obvious and often associated with a wound, which directs what dissection is needed. Step three is single- or dual-plan osteotomies to axially align the foot with the leg and put it in a plantigrade position. This is the most demanding of the four-step corrective procedure and requires experience in doing such. The last step is to maintain the alignment with temporary external fixation. The spanning external fixator across the foot and ankle can be applied in 15 to 20 minutes.

Dynamic forces are executed through muscle contractions. With muscle imbalances, as is typically associated with motor neuropathies, muscle contractions often initiate the deformities. With persistence, the bones of the foot and ankle remodel in response to the deforming forces. Once this occurs, the deformity becomes rigid rather than passively correctable. Consequently, not only are tenotomies required to mitigate the dynamic forces, but bone realignment (osteotomy) becomes necessary to achieve satisfactory foot alignment.

Dynamic deforming forces from muscle contractions must be differentiated from static deforming forces from ligaments, and joint capsules. These structures will stretch out with time if maintained in the corrected position due to their viscoelastic properties.

Viscoelastic is a property of connective tissues. In simplified terms, it means these tissues elongate with time or change from an elastic deforming state (e.g., stretching a rubber band and then releasing it to return to its original length) to a plastic deforming state (e.g., stretching a stick of licorice), which maintains the new elongated state.

Fascia does not appear to have the same viscoelastic properties as the other connective tissues mentioned above. Hence, fasciotomies may be required for the plantar fascia in associated with foot deformities. Another situation in which fasciotomies are needed is with chronic exertional compartment syndromes.


The spanning external fixator is applied by placing two traversing (center-threaded) pins in the foot. The first is placed from medial to lateral (to lessen the chances of injury to the neurovascular structures passing nearby). The second pin is placed through the forefoot again from medial to lateral, with the goal of centering the pin in the first metatarsal and passing through as many other metatarsals as possible. Two half-pins placed at slightly diverging angles are placed from the anterior medial and anterior lateral directions in the distal third of the leg. With the use of bone landmarks, no imaging techniques (such as fluoroscopy) are needed for pin placements.


Compliance considerations.

If the management is to be successful, utmost compliance to postoperative care must be done. This includes cleansing the pin-skin interfaces with hydrogen peroxide or normal saline to remove debris and wrapping the interfaces snuggly with gauze to prevent edema, oozing and secondary infection around the pin tracts. The patient should be nonweight bearing with the external fixator. The goal is to maintain the fixator for a minimum of six weeks to allow the soft tissues and bone (if osteotomies are done) to accommodate to the corrected position. After this, a walking leg cast is applied for a six-week duration. Finally, protective footwear from quality shoes to Charcot restraint orthotic walker (CROW) is prescribed depending on the residual appearance of the foot and ankle.

As an aside, a coauthor (MBS) used the same principles and techniques in managing severely deformed, neglected club feet with wounds and/ or massive bursa during a recent orthopaedic humanitarian mission to Vietnam. With soft-tissue releases plus osteotomies and initial corrections maintained with external fixators, remarkable corrections were achieved. The patients are now transitioning from casts with plantigrade, axially aligned feet to protective footwear.



Even though this information is oriented toward the surgical perspective, it is essential that all wound-care providers be aware of the surgical alternatives that exist for preventing new and recurrent diabetic foot wounds as well as wounds in nondiabetics. When the deformity component of the “troublesome triad” (deformity, deep infection — including bone, bursa and cicatrix — and ischemia-hypoxia) is present and there is risk of a wound developing, we strongly recommend early attention to proactive surgeries.

It behooves nonsurgically trained wound-care providers to have a cadre of surgeons available who are comfortable with the surgeries described in this article and, if not, the information in this article with its associated references be made available to them. In the insipient stages, new or recurrent diabetic foot wounds with underlying deformities can be managed with the minimally invasive, keep it simple and speedy surgeries with the techniques herein described.



  1. Strauss MB, AM, of new and recurrent foot wounds, part 1: introduction and misconceptions. Care & Hyperbaric Medicine. 7(2):30-37, 2016.

  2. Strauss MB, AM, Prevention of new and recurrent foot wounds,pPart 2: education. Care & Medicine. 7(3):16-27,2016.

  3. Lu LQ, Strauss MB, Tan AM. Evaluation and management of foot skin and toenails. Wound Care & Hyperbaric Medicine. 7(4):28-42, 2016.

  4. Tan AM, Strauss MB, Lu LQ. Protective footwear, part 4A. Wound Care & Hyperbaric Medicine. 8(1):32-39, 2017.

  5. Tan AM, Strauss MB, Lu LQ. Protective footwear, part 4B. Wound Care & Hyperbaric Medicine. 8(2):23-31, 2017.

  6. Apelqvist Bakker K, WH, Nabuurs-Fransen MH, Schaper NC: International consensus on the diabetic foot. In The International Consensus on the Diabetic Foot by the International on the Diabetic Foot. Amsterdam,InternationalDiabetesFederation.P96,1999.

  7. Strauss MB, Aksenov Miller SS. Masterminding P 447-448, 2010.

  8. Tan AM, Strauss MB, Lu LQ. The troublesome triads of diabetic ulcer healing. Lower Extremity Review. April 2017.

  9. Tamir E, Vigler M., Avisar E, Finestone AS. (2014). Percutaneous tenotomy for the treatment of diabetic toe ulcer. Foot and Ankle International, 35(1), 38-43.

  10. Frigg A, Pagenstert G, Schafer et al. Recurrence and prevention of diabetic foot ulcers after total contact casting. Foot Ankle International. 28(1):64-69,2007.

  11. Strauss MB, Bryant BJ. Forefoot narrowing with external fixation for problem cleft wounds. Foot & Ankle International. 23(5):433-439, 2002.

  12. Holstein P, Lohmann M, Bitsch M, and Jørgensen B. Achilles tendon lengthening, the panacea for plantar forefoot ulceration? Diabetes Metab. Res. Rev. 20: S37–S40, 2004.

  13. Nishimoto G, Attinger C, Cooper Lengthening the Achilles tendon for the treatment of diabetic plantar forefoot ulceration. Surgical Clinics of North America. 83(3):707-726,2003.

  14. Strauss MB, Manji KA, Miller SS, Manji AA. Bursa and callus: friend or foe. Care & Hyperbaric Medicine.4(2):19-28, 2013.

  15. Strauss MB, Moon H, La S, Craig A, Miller SS. incidence of confounding factors in patients with diabetes mellitus hospitalized for diabetic foot ulcers. 28(8):287-294, 2016.

About the Author


MICHAEL STRAUSS, M.D., an orthopaedic surgeon, is the retired medical director of the Hyperbaric Medicine Program at Long Beach Memorial Medical Center in Long Beach, California. He continues to be clinically active in the program and focuses his orthopaedic surgical practice on evaluation, management and prevention of challenging wounds. Dr. Strauss is a clinical professor of orthopaedic surgery at the University of California, Irvine, and the orthopaedic consultant for the Prevention- Amputation Veterans Everywhere (PAVE) Problem Wound Clinic at the VA Medical Center in Long Beach. He is well known to readers of WCHM from his multiple articles related to wounds and diving medicine published in previous editions of the journal. In addition, he has authored two highly acclaimed texts, Diving Science and MasterMinding Wounds. Dr. Strauss is actively studying the reliability and validity of the innovative, user-friendly Long Beach Wound Score, for which he already has authored a number of publications.


ANNA M. TAN, DPM, is the chief resident of podiatric medicine and surgery at Long Beach Memorial Medical Center. She graduated cum laude from the University of Southern California in 2006 and received the Dean’s Award for her undergraduate research on netrin-1, a protein involved in axonal guidance. Subsequently, she attended the California School of Podiatric Medicine at Samuel Merritt University in Oakland, California, receiving her doctor of podiatric medicine degree in 2014. Dr. Tan has special interests in surgical management of problem wounds and limb salvage. In her spare time, she enjoys Bikram yoga, cooking and traveling.


LIENTRA LU is a research coordinator at the VA Medical Center in Long Beach, California, under the guidance of Dr. Ian Gordon, a vascular surgeon, and Dr. Michael Strauss. She is also an administrative assistant in the accounting department of the Southern California Institute for Research and Education (SCIRE). She received a bachelor of science degree in chemical biology at the University of California, Berkeley, in 2015 and subsequently has taken medically related courses at the University of California, Los Angeles. Miss Lu is helping with diabetic foot and venous leg ulcer studies at the VA Medical Center while also serving as an assistant in patient care at the PAVE Clinic there. She also works with the American Red Cross in her other interest, disaster preparedness.





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