Monthly Archives: September 2008

September 2008

May-Hegglin and other Platelet Dysfunctions as Complications to Compartment Syndrome: A case report
by Jason R. Miller, DPM, FACFAS, FAPWCA, Peter Moyer, DPM

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Creating the Ideal Microcosm for Rapid Incorporation of Bioengineered Alternative Tissues Using An Advanced Hydrogel Impregnated Gauze Dressing: A Case Series
by Jonathan Moore, DPM, MS

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Spontaneous Fracture of the Tibial Sesamoid: A case report
by Al Kline, DPM

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Technical Tip: A Simple Method for Proper Placement of an Intramedullary Nail Entry Point for Tibiotalocalcaneal or Tibiocalcaneal Arthrodesis
by Ronald Belczyk, DPM ,Wenjay Sung, DPM, Dane K. Wukich, MD

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Photo Quiz: Unusual pits to the bottom of the foot
by Al Kline, DPM

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Answer: Photo Quiz #6

Pitted keratolysis

ISSN 1941-6806
doi: 10.3827/faoj.2008.0109.0005

Pitted keratolysis or PK was first described in a Ceylonese patient in 1910, by Castellani as keratoma plantare sulcatum secondary to yaws. [1,2] The condition is caused by a cutaneous gram positive bacterial infection linked to both the Corynebacterium and Actinomyces species. [1,2] This disorder is characterized by keratomatous pitting of the skin usually to weightbearing regions of the foot, such as the forefoot and heels.

The condition has no age or sex predilection and can affect individuals at any age. The condition is associated with athletics and individuals who prefer going bare-footed in tropical regions. The condition may or may not be associated with underlying hyperkeratosis. It can be malodorous and pruritic in nature. It is also known to be associated with hyperhidrosis and perfuse sweating of the feet. In association with hyperhidrosis, the punched-out pits can coalesce and form white clusters. [3,6] The keratin pits associated with this condition are usually small in the diameter range of 0.5-7mm. Larger pitting and lesions are associated with a variant form called crateriform pitted keratolysis. [1] It is suggested that the pitting is caused by proteases secreted by the bacteria and alter the structure of both the corneodesmosomes and the keratohyalin granules. The corneodesmosomes at the bottom of the pits were in part cleaved leading to partial corneocyte dissociation. [4]

The differential diagnosis in our quiz included arsenical keratosis, keratosis punctata, keratosis pilaris, intractable plantar keratosis, porokeratosis plantaris discreta, hyperhidrosis and bromohidrosis.

Arsenical keratosis present as yellow-brown lesions usually seen on the sole of the feet after exposure to arsenic. [6]  It is also involves the hand. Although the brown discoloration of arsenical keratosis may appear similar to pitted keratolysis, arsenical keratosis is extremely rare and only occurs after long-term exposure to arsenic. It has been shown to cause Bowen’s disease or in-situ squamous cell carcinoma. [7]

Keratosis punctata is a dominantly inherited disorder that develops between the ages of 15 and 30. [6] The condition will last a lifetime. [6]  These lesions are more punctuate, as the name implies and will not disappear when superficially debrided as in pitted keratosis.

Keratosis pilaris is not a condition that involves the plantar surface of the foot. It is commonly associated with atopic dermatitis. [6] It is associated with kertinization of hair follicles. It is an extremely common benign condition that manifests as small, rough folliculocentric keratotic papules, often described as chicken bumps, chicken skin, or goose bumps, in characteristic areas of the body, particularly the outer-upper arms and thighs. [8]

Intractable plantar keratosis or IPK is usually an isolated hyperkeratotic lesion under a metatarsal head. These lesions are large and measure up to 20-30mm in diameter. [9]  These lesions are sometimes confused with porokeratosis plantaris discreta, however, porokeratosis is a much smaller hyperkeratotic lesion that can reach a depth of 1.5mm or more.  It can also be associated with non-weightbearing surfaces, unlike the IPK.

Hyperhidrosis is a local condition of sweaty feet or excessive perspiration. This condition can certainly lead to and is commonly associated with pitted keratolysis. Bromohidrosis is the termed used to describe the pungent odor of malodorous feet. Bromohidrosis is commonly associated with hyperhidrosis, ingestion or exposure to heavy metals such as arsenic and the odor associated with fungal and bacterial infections of the feet. [6]

Treatment of pitted keratolysis can include localized debridement of the overlying epidermis and topical drying agents with oral and topical antibiotics. Topical drying agents can include Drysol or aluminum chloride hexahydrate. Roll-on antiperspirants such as aluminum chloride have also been described. [1]  Zeasorb super absorbent powder to address the hyperhidrosis can also be useful. Oral antibiotics to treat the underlying infection are also indicated when treating PK if the condition is resistant to topical antibiotic treatments. The oral and topical antibiotic of choice is clindamycin. Antibacterial gels or creams such as clindamycin, erythromycin and mupirocin has also been described. [5]  Twice daily applications of these topicals for 2-3 weeks will usually clear the lesions. In other cases, botulinum toxin injections have been shown to be effective. The overall prognosis is excellent when properly treated.

The patient was prescribed erythromycin 2% cream for two weeks.  She was advised to keep her feet dry and use talcum powder after the application of erythromycin cream.  After having the condition for over a year, the condition resolved promptly after 2 weeks of topical treatment.


1. English, J.C.: Pitted Keratolysis eMedicine, [online], 2006
2. Singh, G., Naik, C.L.: Pitted Keratolysis Indian Journal of deratology, Venereology and leprology, 71(3), 213-215, 2005 [open access].
3. DermNet NZ: Pitted keratolysis, [online], 2008.
4. Hermanns-Le, T., et al.: Pitted keratolysis: New Ultrastructural Insight in Keratohyalin Granule and Corneodesmosome Alterations. Exogenous Dermatology, 3(3), 2004.
5. American Osteopathic College of Dermatology: Pitted Keratolysis [online], 2008.
6. Dockery, G., Crawford, M.E.: Color Atlas of Foot & Ankle Dermatology, Lippincott-Raven, 1999.
7. Chen, Chi-Shen J.: Arsenical Keratosis, eMedicine, [online], 2008.
8. Alai, N.: Keratosis Pilaris, eMedicine [online], 2008.
9. Kline, A. Keratotic Skin Lesions of the Foot, The Foot Blog, [online], 2006.

Address correspondence to: Al Kline, DPM. 3130 South Alameda, Corpus Christi, Texas 78404.

Adjunct Clinical Faculty, Barry University School of Podiatric Medicine. Private practice, Chief of Podiatry, Doctors Regional Medical Center. Corpus Christi, Texas, 78411.

© The Foot & Ankle Journal, 2008

Photo Quiz: Unusual pits to the bottom of the foot

by Al Kline, DPM 1

The Foot & Ankle Journal 1 (9): 5

ISSN 1941-6806
doi: 10.3827/faoj.2008.0109.0005

Case History

A 21 year old female presents with unusual ‘pits’ along the bottom of the forefoot. (Figs. 1) The patient states that she has had the condition for over a year. She relates to going bare-footed and wearing sandals whenever possible. There is an associated pungent odor to her feet. She relates to having to wash her feet often. The patient initially thought it was just dirt that “didn’t wash off” in the bath. She became more concerned when the lesions and dark brown pits would not go away.


Figures 1    Dark-stained appearing pits to the bottom of the forefoot.   The patient attributed this condition to her feet getting dirty while going bare-footed.   However, it appeared that the ‘dirt’ would not wash off.

The patient’s medical history is unremarkable. She is allergic to Ceclor®. She does not take any prescription or over-the-counter medications.

The lesions or pits appear to be confined to the epidermis and seem to disappear with superficial debridement. (Figs. 2)


Figures 2    Closer clinical examination reveals tiny hollow pits and small craters within the epidermis.  Simple debridement does not reveal deeper keratosis. 

Question: Based on the patient’s clinical history, which of the following is the correct diagnosis?

A. Arsenical keratosis
B. Pitted keratolysis
C. Keratosis punctata
D. Keratosis pilaris
E. Intractable plantar keratosis
F. Porokeratosis plantaris discreta
G. Hyperhidrosis
H. Bromohidrosis

Address correspondence to: Al Kline, DPM. 3130 South Alameda, Corpus Christi, Texas 78404.

1 Adjunct Clinical Faculty, Barry University School of Podiatric Medicine. Private practice, Chief of Podiatry, Doctors Regional Medical Center. Corpus Christi, Texas, 78411.

© The Foot & Ankle Journal, 2008

Technical Tip: A Simple Method for Proper Placement of an Intramedullary Nail Entry Point for Tibiotalocalcaneal or Tibiocalcaneal Arthrodesis

by Ronald Belczyk, DPM 1 , Wenjay Sung, DPM 2, Dane K. Wukich, MD 3

The Foot & Ankle Journal 1 (9): 4

The purpose of this article is to report on a technical tip when performing tibiotalocalcaneal or tibiocalcaneal arthrodesis. Technical faults of this arthrodesis may include malpositioning of the IM nail that can potentiate complications such as nonunion, delayed union, malunion, screw fracture, painful hardware, fracture of the intramedullary nail, tibial fracture, wound healing complications, and nerve damage. This article will present important information to aid the surgeon in preventing malpositioning of an IM nail and will provide a simple clinical pearl for perioperative incisional planning using image intensification.

Key words: Tibiotalocalcaneal fusion, tibiocalcaneal fusion, IM nail, intramedullary rod, complications

This is an Open Access article distributed under the terms of the Creative Commons Attribution License.  It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot & Ankle Journal (

Accepted: July 2008
Published: September 2008

ISSN 1941-6806
doi: 10.3827/faoj.2008.0109.0004

Several authors have reported the use of intramedullary (IM) nails in ankle and hindfoot arthrodesis with varying rates of success and complications. [1, 5, 7, 12] Since intramedullary nailing involves arthrodeses of the ankle and hindfoot, accurate entry point placement is a critical step with this procedure. Although many technical pearls of initial guide-wire placement have been described in the literature, we have nonetheless seen complications arising from malpositioning. [1-3]

This manuscript reviews potential complications associated with intramedullary nailing, in particular to malpositioning of the retrograde nail. We present two cases that presented with continued pain upon ambulation after attempted tibiotalocalcaneal fusions. Their nonunion and failure of fixation was related in part due to malpositioning of the intramedullary nail. This article further reviews several authors’ recommendations for determining the ideal entry point for the insertion of an intramedullary nail for tibiotalocalcaneal fusion. Many of these studies recommend a guide wire entry point based on anatomical landmarks and preoperative radiographic findings.

Lastly, this article will describe a simple method of perioperative incisional planning by using image intensification.

Potential complications

Potential complications associated with this type of procedure include: nonunion, delayed union, malunion, screw fracture, painful hardware, fracture of the intramedullary nail, tibial fracture, wound healing complications, and nerve damage. [4-10]  Table 1 summarizes complications encountered by several foot and ankle surgeons.

Table 1  Reported complications of IM nailing. 

In addition to those complications listed in table 1, we present two cases with improperly placed intramedullary nails. Figures 2 and 3b are calcaneal axial radiographs which reveal malpositioning of an intramedullary nail.

Case 1

A 56 year old female with hypothyroidism, diabetes, peripheral neuropathy and a significant history of tobacco use presented to our service with severe pain in the medial aspect of her foot. She had sustained an ankle fracture five years prior and underwent open reduction internal fixation, subsequently developing a valgus deformity of her ankle and Charcot neuroarthropathy. Her ankle and hindfoot deformity was treated with a tibiotalocaneal fusion using a retrograde intramedullary nail. At the time of IM nail removal, movement was seen through the subtalar joint. (Figs.1ab, Fig.2)


Figure 1a  Case 1:  Anteroposterior (AP) ankle radiographs showing an intramedullary nail for a tibiotalocalcaneal arthrodesis.

Figure 1b  Case 1:  Lateral ankle radiographs showing placement of  intramedullary nail for the tibiotalocalcaneal arthrodesis.

Figure 2  Case 1:  Calcaneal Axial radiograph demonstrating malpositioning of the IM nail through the hindfoot with the insertion site too medial.

Case 2

A 66 year old male with rheumatoid arthritis, diabetes and peripheral neuropathy presented with significant pain upon ambulation. He related a history of a talus fracture that went on to Charcot neuroarthropathy of the ankle and hindfoot. He underwent a tibiotalocalcaneal fusion with intramedullary nail two years prior to our initial consultation. Figures 3abc demonstrate the patient’s initial presenting radiographs. The radiographs reveal distal migration of the IM nail. A computerized tomography (CT) scan showed a nonunion of the tibiocalcaneal joint. Laboratory data revealed no clinical signs of infection. Revisional arthrodesis was performed using circular ring fixation and external bone stimulation.


Figure 3abc  Case 2:  AP (a), axial (b) and Lateral (c)  radiographs of the ankle demonstrate an attempted tibiocalcaneal fusion with an intramedullary nail with broken calcaneal screw and distal migration of the nail.

Recommendations for determining guide wire entry point

Accurate guide wire placement is critical prior to reaming and inserting a retrograde intramedullary nail for tibiotalocalcaneal or tibiocalcaneal fusion. The guide wire is typically placed into the central medial aspect of the calcaneus and centered in the medullary canal of the tibia. Because the longitudinal bisection of the calcaneus is lateral relative to the alignment of the tibia in a normal anatomic structure, it is usually necessary to medially translate the talus and calcaneus.

This will allow insertion of a straight nail from the calcaneus into the central portion of the tibia. [11]

The foot placement should be 90 degrees with respect to the lower leg, maintaining the heel in neutral position with 10-15 degrees of external rotation. Blunt dissection is carried down to the bone to avoid any neurovascular structures. [13]

A number of authors have described the anatomical placement of the IM nail. Table 2 summarizes several author recommendations for determining the proper entry point. The surgical approach to placement of the IM nail is described in terms of measurement from specific landmarks and anatomical structures.

Table 2  Several recommendations for determining proper IM nail entry points.

Our technique uses perioperative imaging to determine the placement of the IM nail. Using intraoperative C-arm visualization, the long axis of the tibia on lateral view is used to determine the tibial location along the plantar entry point of the foot. The IM nail is simply placed along the lateral leg just above the border of the fibula. A marking pen is then used to draw a horizontally placed line along the plantar aspect of the foot. This corresponds to the central tibial component for IM nail placement.

The IM nail should visually appear to go directly through the lateral process of the talus on lateral view.

The second vertical or longitudinal bisecting line is made with the calcaneal axial view perioperatively. The IM nail is placed directly against the plantar heel on axial view. The line corresponds to the valgus or varus rotation of the calcaneus. The marking pen is then used to draw a longitudinal bisecting line. The center of the bisecting line represents the ideal entry point for the IM nail. Here, no measurements are required, and the landmarks to determine the ideal entry point correspond to radiographic anatomical structures. Figures 4-7 show a stepwise approach for perioperative incisional planning. The entry point is based on lateral ankle and calcaneal axial views utilizing C-arm visualization.


Figure 4abc  Preoperatively, a line is made on the ankle which is consistent with a line that bisects the tibia and goes through the lateral talar process.

Figure 5  The mark on the lateral aspect of the ankle is then continued transversely on the plantar surface of the foot.  A guide-wire or metallic marker, in this case a threaded rod, is then placed against the plantar aspect of the foot along the center of the heel. 

Figure 6   Using image intensification, a calcaneal axial view is taken and a line bisecting the calcaneus is then marked on the plantar skin.

Figure 7   The center of the two intersecting lines is the ideal entry point.


In summary, ideal incisional placement permits accurate insertion, good screw purchase, and avoids neurovascular damage. (Fig. 8ab)


Figure 8 ab Lateral ankle (a), calcaneal axial (b) radiographs demonstrate a tibiotalocalcaneal fusion with a properly placed intramedullary nail.

Although fixed angled devices are being popularized as being able to purchase a greater amount of calcaneus and not having to medially translate the talus to align the tibia and calcaneus, clearly intraoperative errors can lead to postoperative complications as presented in this article. A simple, accurate, and reproducible method of determining the proper entry point as described in this article is invaluable to the foot and ankle surgeon performing tibiotalocalcaneal or tibiocalcaneal fusion with intramedullary devices. Currently there are retrograde devices approved for use that have a valgus orientation built into the nail.

The valgus nail such as the T2 Ankle arthrodesis nail (Stryker, Kalamazoo, MI) or the Hindfoot Arthrodesis Nail-EX (Synthes, West Chester, PA) can facilitate proper entry site placement, however, we recommend the above technique to guide proper placement. Proper placement of the device in the calcaneus improves fixation with the distal interlocking screws whether they be transverse or axial in nature.


1. Paley D, Herzenberg J, Tetsworth K, McKie J, Bhave A. Deformity planning for frontal and saggittal plane corrective osteotomies. Orthop Clin N Am 25(3):425-465, 1994.
2. Roukis T. Determining the Insertion Site for Retrograde Intramedullary Nail Fixation of Tibiotalocalcaneal Arthrodesis: A Radiographic and Intraoperative Landmark Analysis. J Foot and Ankle Surgery 45(4):227-234, 2006.
3. Lamm B, Paley D. Deformity correction planning for hindfoot, ankle, and lower limb. Clin Podiatr Med Surg 21(3):305-326, 2004.
4. Buratti R, Johnson J, Buratti D. Concurrent ankle and subtalar arthrodesis. J Foot and Ankle Surgery 33(3):278-282, 1994.
5. DiDomenico L, Adams H. Intramedullary nailing for Charcot arthroplasty of the hindfoot and ankle. Philadelphia: Lippincott Williams and Wilkins Co., 2005.
6. Harvey E, Agel J, Selznick H, Chapman J, Henley M. Deleterious effect of smoking on open tibia-shaft fractures. Am J Orthop 31(9):518-521, 2002.
7. Kile T, Donnelly R, Gehrke J, Werner J, Johnson K. Tibiotalocalcaneal arthrodesis with an intramedullary device. Foot Ankle Int 15(12):669-673, 1994.
8. Perlman M, Thordarson D. Ankle fusion in a high risk population: an assessment of nonunion risk factors. Foot Ankle Int 20(8):491-496, 1999.
9. Quill G. Tibiotalocalcaneal Arthrodesis with Medullary Rod Fixation. Techniques in Foot and Ankle Surgery 2(2):135-143, 2003.
10. Thordarson D, Chang D. Stress fractures andtibial cortical hypertrophy after tibiotalocalcaneal arthrodesis with an intramedullary nail. Foot Ankle Int 20(8):497-500, 1999.
11. McGarvey WC, Trevino SG, Baxter DE, Noble PC, Schon LC. Tibiotalocalcaneal arthrodesis: anatomic and technical considerations. Foot Ankle Int 19(6):363-9, 1998.
12. Singh PJ, Perera NS, Dega R. Measurement of the dose of radiation to the surgeon during surgery to the foot and ankle. J Bone Joint Surg Br 89(8):1060-3, 2007.
13. Flock TJ, Ishikawa S, Hecht PJ, Wapner KL. Heel anatomy for retrograde tibiotalocalcaneal roddings: a roentgenographic and anatomic analysis. Foot Ankle Int 18(4):233-5, 1997.

Address correspondence to: Dane Wukich, MD. UPMC Comprehensive Foot and Ankle Center. Roesch-Taylor Bldg Ste 7300. 2100 Jane St. Pittsburgh, PA 15203. Phone: 412-586-1546 Fax: 412-586-1544

PGY-4, Fellow, Foot and Ankle Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, 15203.
Resident, Foot and Ankle Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, 15203.
Chief, Foot and Ankle Division, University of Pittsburgh Medical Center Department of Orthopedic Surgery and Assistant Professor, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, 15203.

© The Foot & Ankle Journal, 2008

Spontaneous Fracture of the Tibial Sesamoid: A case report

by Al Kline, DPM 1

The Foot & Ankle Journal 1 (9): 3

A tibial sesamoid fracture is described. A female, while walking in an airport, experiences discomfort and pain under the first metatarsal head while wearing a high-heel shoe. Clinical investigation reveals a spontaneous fracture of the tibial sesamoid. The patient also has associated hallux valgus. Conservative treatment and surgical options are presented and discussed. The patient, after failed conservative treatment, had the sesamoid removed and a simple bunionectomy performed. It appears that a centrally placed tibial sesamoid with associated hallux valgus can cause a spontaneous fracture of the tibial sesamoid under the right circumstances.

Key words: Tibial sesamoid fracture, HAV deformity, bunion

This is an Open Access article distributed under the terms of the Creative Commons Attribution License.  It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot & Ankle Journal (

Accepted: August 2008
Published: September 2008

ISSN 1941-6806
doi: 10.3827/faoj.2008.0109.0003

Tibial sesamoid fracture is common in athletes and active individuals. Usually, the incident is preceded by stress injury or acute trauma from stressed dorsiflexion or hyperextension of the hallux. The first ray will transmit about 60% of a person’s weight-bearing stress through the first metatarsophalangeal joint during the gait cycle. In acute instances, these stresses can be many times greater. Interestingly, there have been infrequent reports of tibial sesamoid fracture from non-acute injury such as walking. In non-acute injuries, many patients will present with a sharp initial pain followed by a dull ache or pain under the sesamoids. The differential diagnosis may include sesamoiditis, chondromalacia, first metatarsal joint capsulitis, flexor hallucis tendonitis and arthritis.

MRI and radiographic evaluation are the most common modalities used to differentiate injury and fracture from more subtle injuries such as sesamoiditis or capsulitis.

A clinical entity such as a bipartite sesamoid may confuse the clinician in the proper diagnosis. This condition was first described as early as 1904 by Stieda and confirmed by Dwight. [1] Bipartite sesamoids are a common finding on foot radiographs. They often look like tibial sesamoid fractures, however, close inspection of the radiograph usually reveals a well-defined, smoother partition between the two fragments. A fractured sesamoid will likely have a rough, irregular partition. Bipartite sesamoids are a normal variant when two ossification centers fail to fuse at maturity. This condition is present in about 10% of the population, and in that population, 25% are bilateral. [2] In cases of acute injury, diastasis of the bipartite sesamoid can lead to acute pain under the first metatarsal head. This has been reported in hyperextension or “turf-toe” injuries in football players. [3]

It is the author’s opinion that bipartite sesamoids can also lead to sesamoid pain. Bone scintigraphy can also differentiate sesamoid fracture from congenital partition. [4]

In non-acute injuries of the tibial sesamoid, conservative treatments are designed to de-weight the sesamoid and allow for healing. Conservative methods of treatment can include wearing a surgical shoe to prevent extension of the toe or even casting and non-weightbearing. Once the correct diagnosis is made, appropriate treatment can be initiated. Conservative care for sesamoiditis can also include wearing an accommodative insert with first metatarsal padding. The pad can be placed just behind the sesamoid in order to decrease stress through the sesamoid apparatus. Other conservative treatments include 1) NSAIDS, 2) avoiding high heels, 3) off-loading shoes and 4) steroid injection. These injections may be used along with joint taping to prevent excessive extension of the first metatarsophalangeal joint. Care must be taken in the injection of steroids to this region, especially if fracture is suspected. Injection of steroids can sometimes lead to avascular necrosis of a fractured tibial sesamoid.

In acute fracture, non-weightbearing in a cast is recommended for 6 to 8 weeks. [5,7] It appears, from experience and previous study, that the non-union rate of sesamoid fractures is high. This may be related to the vascular supply of the sesamoids and the forces placed on the bone fragments once fractured. It is theorized that the anatomical pull of soft tissue, once the sesamoid fractures, causes a distraction of the fracture line. Anatomically, the tibial sesamoid has anatomical attachments to the abductor hallucis muscle, plantar fascia, flexor hallucis brevis tendon, intersesamoidal ligament, medial metatarsal and phalangeal sesamoid ligaments. [4]

Once the tibial sesamoid fractures, these attachments tend to distract the fracture fragments. The vascularity of the tibial sesamoid is supplied by three sources: 1) the deep and superficial branches of the medial plantar artery, 2) branches from the lateral plantar artery and perforating branches of the dorsalis pedis artery, and 3) pole arteries through the length of the sesamoid. [4,6] One explanation for the high incidence of non-union is that the primary blood supply of all three sources originates from the proximal pole of the sesamoid through the tendon of the flexor hallucis brevis. [4] Since most fractures of the tibial sesamoid are transverse, once the fracture occurs, the distraction causes disruption of this vascular communication leading to non-union. Bone stimulators may also be effective in the conservative treatment of tibial sesamoid fractures. They are certainly indicated after immobilization and non-unions are suspected.

Anatomy and Sesamoid Position in its relation to Hallux Valgus

The sesamoid position may also play an important role in stresses that are directed through the metatarsophalangeal joint. Anatomically, both the tibial and fibular sesamoids act in unison during the propulsive phase of gait. The articular surfaces of both the tibial and fibular sesamoids glide along the sesamoidal groove and are separated by the central crista in its anatomical alignment. The crista is a central plantar ridge along the metatarsal head that separates the sesamoids. The glistening surfaces of the sesamoids are facet- shaped within the plantar groove of the metatarsal head. In hallux valgus, the sesamoid position is described in distinctive positions. These positions are described as positions 1-7 in the radiographic evaluation of hallux valgus. (Fig. 1.)

Figure 1  Tibial sesamoid position is radiographically described in seven positions.  Position four is described as being directly under the crista of the first metatarsal head, likely increases stress forces through the tibital sesamoid.  The fibular sesamoid (FS) will rotate even further into the first interspace between the first and second metatarsal as the hallux valgus worsens.

It is commonly understood that these positions are dictated by the movement of the metatarsal head as the entire metatarsal subluxes medially in the classic hallux abductovalgus deformity.

It is theorized that position four is the most stressful position for the tibial sesamoid and could cause tibial sesamoid fracture under the right circumstances.

This may be even more plausible in a high-heeled shoe that causes increased stress along the plantar metatarsophalangeal joint. (Fig. 2)

Figure 2   Radiographs demonstrate the increased hyperextension of the first metatarsophalangeal joint in a high-heel shoe.   It is theorized that excessive hyperextension of the joint places increased pressure through the sesamoid apparatus.

Case Report

In February 2006, a 33 year old active female began to experience episodes of pain under the tibial sesamoid. She reported walking in the airport and experiencing a pain under the first metatarsophalangeal joint while in a high heel. She initially presented to another podiatrist, who diagnosed her with ‘fractured tibial sesamoid’. He instituted conservative treatment including padding and a local steroid injection. She did well for several months , but continued to have episodes of increasing pain.

She presented to our office in September 2006. Clinical evaluation revealed bunion pain and pain directly under the tibial sesamoid. She was ambulating and wearing shoes, but had episodes of pain and signs of non-healing of the tibial sesamoid fracture. Radiographs confirmed a tibial sesamoid fracture with a mild bunion deformity. (Fig. 3)

Figure 3  Radiographs confirm tibial sesamoid fracture.  The fracture edges are irregular and sharp, consistent with fracture instead of bi-partite sesamoid.  The tibial sesamoid is positioned directly under the crista in sesamoid position four.

We placed her on crutches with off-loading for 6 weeks and progression to a Darco™ walking shoe, then athletic sneakers with proper accommodative metatarsal padding. Despite these attempts, she continued to have pain and we decided to schedule her for simple bunionectomy and tibial sesamoid excision.

Surgical Technique

The patient was brought to the operating room and underwent simple bunionectomy and tibial sesamoid excision. A medial incision is made along the border of the first metatarsophalangeal joint. Care must be taken to identify the medial cutaneous nerve or ‘bunion’ nerve.

The medial cutaneous nerve has variable branches and may run a course more medial and inferior to the dorsomedial branch. Once the nerve is identified, a medical capsular incision is made and the fracture is identified. (Figs. 4ab) Care must also be taken when excising the tibial sesamoid. The sesamoid is encased along the capsular tissue of the first metatarsophalangeal joint. It has attachments to the abductor hallucis muscle, plantar fascia, flexor hallucis brevis tendon, intersesamoidal ligament, medial metatarsal and phalangeal sesamoid ligaments. The flexor hallucis longus tendon also glides between the two sesamoids.


Figures 4ab  (a)  A medially placed incision along the sesamoid is fashioned.  Care is taken to identify the medial cutaneous nerve.  (identified at the tip of the blade). (b) Once the capsule is incised, the fractured tibial sesamoid is identified.

Care must be taken not to cut the tendon when excising the sesamoid. A number 15 blade is used to enucleate the sesamoid from these fibrous, soft tissue attachments. Once the sesamoid is removed, suture is used to approximate the ligamentous and capsular attachments. The sesamoid should be ‘cleanly’ excised with little tissue attachment. (Fig. 5) The postoperative radiographs reveal a post-excisional tibial sesamoidectomy with simple bunionectomy. (Fig. 6).

Figure 5   After the tibial sesamoid fracture is excised, it appears as if the fracture recently occurred.  There are no signs of attempted bone healing or calcification.  This is testament to the distraction forces that keep the sesamoid fracture apart. 

Figure 6   Post-operative radiographs reveal removal of the tibial sesamoid and a simple bunionectomy performed.


Surgical excision of the entire tibial sesamoid appears to be a viable alternative of treatment to non-healing fractures of the tibial sesamoid. One of the earliest reports of tibial sesamoidectomy with relief of symptoms was described by Müller in 1911. [1] Recently, Jones et al., reported the results of tibial sesamoid excision following tibial sesamoid fracture in a softball player. After 1 year, the patient was “free of pain in all shoe types”. [5] There is only one report to date of attempting internal fixation to repair the tibial sesamoid fracture.

In 2001, Riley and Selner reported using monofilament wire to internally fixate a tibial sesamoid fracture with excellent results in a 17 year old female. [7] This approach may be more desirable in the acute fracture of young, active patients. In our case, surgical excision was more desirable since the tibial sesamoid was directly placed under the crista. Reported complications of removing the tibial sesamoid include hallux valgus, transfer pain, tendonitis, arthritis and hallux extensus. [5,7]

In this particular case, the association of hallux valgus and the placement of the tibial sesasmoid in position four appear to increase the likelihood of fracture when wearing a high-heeled shoe. The association of hallux valgus as a risk for tibial sesamoid fracture was first described in 1929, although most cases of fractures are related to direct trauma and a sudden increase in weight-bearing force, Hobart reported “an association with hallux valgus is often found”. [8] Anatomically, the central rise of the crista may explain the increased force through a sesamoid. Stressed dorsiflexion in a high heeled shoe after extensive walking could directly lead to spontaneous fracture. In this case, our surgical goals were straight forward: simple bumpectomy with sesamoid removal.

To date, the patient has returned to activity with accommodative sesamoid padding and without pain or discomfort.


The tibial sesamoid fracture is now demonstrated to be a common fracture of the foot. The diagnosis is usually made by clinical presentation, using radiographs and MRI for confirmation. Bone scans can also be used. The stresses placed through the metatarsal head during gait can be complicated. This report suggests that an abnormally placed sesamoid due to associated hallux valgus or bunion may lead to increased stress of the sesamoid and can lead to fracture. This is especially true in patients who attempt to walk for extended periods in a high-heel shoe. It is suggested that patients with hallux valgus wear a simple accommodative device, such as a dress orthotic, in an attempt to off-load the stress through the sesamoids. This case also demonstrates that if the sesamoid does fracture, total tibial sesamoidectomy is a viable procedure in cases of non-union or delayed healing.



1. Müller, G.P. Fracture of the Sesamoid Bones. Ann Surg, Read before the Philadelphia Academy of Surgery, October 2, 1911. [Online-PDF]
2. Neerajana, DODA, Wilfred, C.G. PEH Woman with possible right toe fracture: Radiology Series Asia Pacific Journal of Family Medicine, Volume 5, Issue 3, 2006. 
3. Rodeo, SA, et al Diastasis of bipartite sesamoids of the first metatsophalangeal joint. Foot Ankle, 14(8): 425-34. Oct. 1993.
4. Swierzewski, J. Acute and Chronic Injuries to the Sesamoids: Etiology and Treatment CPMA, Vol 10, No. 4, Fall 2001.
5. Jones, J.L., Losito, J.M. Tibial Sesamoid Fracture in a Softball Player JAPMA Vol. 97, No. 1 Jan/Feb 2007.
6. Banks, A.S., Downey, M.S., et al McGlamry’s Comprehensive Textbook of Foot and Ankle Surgery, 3rd ed. Lipcott and Williams, 2001.
7. Riley, J., Selner, M. Internal Fixation of a Displaced Tibial Sesamoid Fracture JAPMA, Vol. 91, No. 10, 2001.
8. Hobart, M. Fracture of Sesamoid Bones of the Foot: With Report of a Case JBJS (Am) 11:298-302, 1929.

Address correspondence to: Al Kline, DPM. 3130 South Alameda, Corpus Christi, Texas 78404.

1 Adjunct Clinical Faculty, Barry University School of Podiatric Medicine. Private practice, Chief of Podiatry, Doctors Regional Medical Center. Corpus Christi, Texas, 78411.

© The Foot & Ankle Journal, 2008

Creating the Ideal Microcosm for Rapid Incorporation of Bioengineered Alternative Tissues Using An Advanced Hydrogel Impregnated Gauze Dressing: A Case Series

by Jonathan Moore, DPM, MS1

The Foot & Ankle Journal 1 (9): 2

The purpose of this article is to demonstrate the effectiveness of a novel hydrogel impregnated gauze dressing in creating the ideal microcosm around a bioengineered alternative tissue to prevent tissue dehydration and cell death, accelerate angiogenesis, prevent infection and facilitate the interaction of growth factors with the target cells. Using the BRAIN principles along with this hydrogel impregnated gauze dressing in 50 diabetic patients with neuropathic foot ulcerations (including the six cases presented herein) resulted in substantially improved incorporation rates, increased frequency of wound closure, decreased time to achieve wound closure and a reduction in overall costs. Based on a log transformation the typical healing time is 17.8 days with a 95% confidence interval of 15.6 days to 20.2 days.

Key Words: Bioengineered alternative tissue, diabetic wounds, neuropathic wounds, Amerigel®, BRAIN principle

This is an Open Access article distributed under the terms of the Creative Commons Attribution License.  It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot & Ankle Journal (

Accepted: August, 2008
Published: September, 2008

ISSN 1941-6806
doi: 10.3827/faoj.2008.0109.0002

The efficacy of bioengineered alternative tissue (BAT) for lower extremity ulcers (diabetic and non-diabetic) is well described in the literature. [1-6] As the use of BATs continue to grow world wide, it is important that the wound care specialist consider the principles and tools that will maximize the effectiveness of these tissues to enable wounds to heal faster. Using the BRAIN principles (Table 1) will be fundamental in improving incorporation rates and maximizing the effectiveness of BATs. [7]

Table 1  The BRAIN principles to maximize BAT incorporation and wound healing.

Treating wounds in patients with diabetes is more complex than simply choosing what dressing to use. Emerging technologies over the past decade have not only helped improve our understanding of how wounds heal, but more importantly why wounds do not heal. Understanding and addressing the physiological alterations of the wound healing cycle in the diabetic patient is fundamental. As diabetic wounds become stalled in the inflammatory phase of wound repair, chronic wound fluid with elevated levels of matrix metalloproteinases (MMPs) increases proteolytic activity in the wound, which in turn inactivates growth factors.

In addition, with decreased collagen synthesis and impaired cellular activity due to hyperglycemia, there is less nitric oxide available and less endothelial cell proliferation. [8]

With this impaired wound healing physiology, it is vital for the wound care specialist to provide the wound what it lacks (i.e. growth factors, BATs, etc.) and decrease excess chronic wound fluid. Consequently, providing the wound with what it needs at the right time is imperative.

So how can we create the perfect environment for wounds to heal? What is the perfect environment to incorporate BATs into to the wound? Although there is no one right answer, we do know that creating the perfect “microcosm” around the wound will not only actively modify the physiology of the wound environment, but it will also stimulate cellular activity and growth factor release. While no perfect dressing exists for every type of wound, understanding the properties necessary to create the ideal microcosm for the BAT and the periwound area is crucial. [9] (Table 2)

Table 2  The properties of the ideal wound dressing to help incorporate BATs into the wound.

With these characteristics in mind, the AmeriGel® Hydrogel Saturated Gauze Dressing (Amerx Health Care Corp., Clearwater, FL) has, in my experience, been the product of choice in creating the ideal microcosm for both the BAT (cellular or acellular) and the periwound area.

This product utilizes a polyethylene glycol base (polyethylene glycol 400 and polyethylene glycol 3350) that has the ability to remain moist without causing maceration. Because the product is still technically a gauze dressing, it will also absorb excess wound fluid into its fibers while keeping the wound moist for up to 5-7 days.

Although there are other hydrogel impregnated gauze products on the market, such as Aquagauze TM (DeRoyal, Powell, TN), Curafil® Hydrogel Impregnated Gauze (Kendall, Mansfield, MA) and Derma Cool® (Afassco, Carson City, NV), none of these products possess the antimicrobial or antifungal properties that are in the AmeriGel® Hydrogel Saturated Gauze Dressing. [10] While most hydrogel impregnated gauze products are capable of absorbing excess fluid, the AmeriGel® Hydrogel Saturated Gauze Dressing (AmeriGel®) can effectively reduce the bioburden through not only its intrinsic antimicrobial and antifungal properties, but also through its absorptive capabilities that trap debris and bacteria in its fibers. AmeriGel® is an easy to apply, non-woven 4-ply, 2×2 inch dressing that is non-cytotoxic, nonadherent, and antimicrobial.

The antimicrobial agent is Oakin®, an oak extract containing tannins. Its mode of antimicrobial action is through its ability to inactivate microbial adhesins, enzymes, and cell envelope transport proteins. [11,12] Tannins are astringent compounds that act locally by precipitating proteins to the wound, decreasing cell membrane permeability, and exerting anti-inflammatory and bactericidal properties.

The use of AmeriGel® over the BAT application site will facilitate not only a closer adherence of the living or acellular tissue to the wound bed, it will also have an “anchoring” effect by its adherence to the surrounding tissues thus reducing the incidence of hematoma or seroma formation under the BAT.

Although some controversy exists regarding the use of certain products with or on a living skin equivalent, there is no definitive evidence that demonstrates that hydrogels (especially the one being proposed in this paper) are cytotoxic. The objective of using any adjunctive wound care product (i.e. AmeriGel® Hydrogel Saturated Gauze Dressing) with a BAT (cellular or acellular) is to enhance its incorporation into the wound while maintaining the ideal environment in and around the wound site. Using the right product is key, but putting the right product on the wound in and of itself won’t get wounds healed.

The following is a series of case reports utilizing the BRAIN principles along with the AmeriGel® Hydrogel Saturated Gauze Dressing as the product of choice for local BAT incorporation into the wound.

We utilized a variety of products for a variety of particular wound beds. Strict protocol to maintain the consistency of wound preparation and BAT application was followed. The following protocol was used for every BAT application:

1. Conservative topical wound care was performed in every case (collagen wound care products, enzymatic agents etc. ) prior to every BAT application.
2. Sharp debridements were performed regularly to prepare the wound base for the application of the chosen BAT.
3. Care was taken to assure that no active bleeding was occurring prior any BAT application
4. Wound margins were thoroughly debrided to remove any hyperkeratosis and or any undermined tissue.
5. All patients in this series were diabetic, although some wounds treated using this protocol were of venous origin.
6. The BAT was placed on the wound bed such that the entire wound was covered.
7. BATs were not applied to wounds in which tendon or bone was exposed.
8. BATs were not applied in cases of infection or active drainage.
9. BATs were not applied to arterial leg ulcers.
10. AmeriGel® was applied directly over the BAT, followed by a secondary dressing (or some cases a compressive wrap in cases of edema)
11. More than one AmeriGel® Gauze Dressings were used in cases were one did not cover the wound site entirely.
12. All wounds were appropriately offloaded according to the BRAIN principles.
13. In cases where there was lower extremity edema, compression was applied over the BAT site using either an Unna’s boot, or a ProFore® Bandage System (Smith & Nephew, Largo, FL)
14. The patient was instructed to leave the dressing intact and dry for one week after application.
15. The patients returned for follow-up no more than 10 days after application, most returned at 7 days.
16. GammaGraft® (Promethean LifeSciences, Inc., Pittsburgh, PA) was chosen in most cases for two reasons; The product has a greater than 2 year shelf life and it is easy to apply and manage.
17. AmeriGel® Gauze Dressing was used daily until wound closure in every case after BAT application.

Case 1

A 63-year-old female with diabetes and rheumatoid arthritis presented with a chronic venous ulceration (2 cm X 2.6 cm) to the dorsal aspect of the right leg. (Fig. 1A) The wound had been present for over two months despite application of compression therapy and topical agents. The GraftJacket® (Wright Medical Technology, Inc., Arlington, TX) was sutured to the wound site followed by AmeriGel® placed directly over the BAT site. (Fig. 1B)


Figures 1AB  Application of GraftJacket® and AmeriGel® Dressing over this non-healing venous ulceration. Sutures were applied to assure fixation of the BAT under a compressive wrap.

A 4” X 4” fluff and an elastic bandage were applied over the AmeriGel® for moderate compression. After one week, the initial dressing was removed (Fig. 1C) and was changed daily thereafter with AmeriGel® at home by the patient. The secondary dressing was dry sterile gauze. Four weeks after application of the GraftJacket®, the wound site along with all of the surrounding erythema was completely resolved. (Fig. 1D) It was surmised that AmeriGel® facilitated significant reduction of the erythema that had been persistent around the wound.


Figures 1CD  The wound site 1 week and 4 weeks after application of BAT. Compression and continued use of AmeriGel® played a pivotal role.

Learning points: Treating wounds on the leg in the presence of venous insufficiency will require compression in conjunction with proper local wound care. Although care must be taken not to apply too much compression such that the BAT is disrupted, no compression or too little can be equally harmful.

Tip: Size and trim the BAT prior to application to ensure the BAT is capable of covering the deepest portion of the wound without tenting.

Case 2

A 42-year-old poorly controlled diabetic male presented with a chronic interdigital ulceration (1.6 cm X .9 cm) to the right foot. (Fig. 2A) The ulcer started as a result of a severe Tinea pedis infection. After the fungal infection was cleared, the ulceration was recalcitrant to traditional topical wound care agents and regular debridements. Thus, a GammaGraft® was chosen to close the wound. The GammaGraft® was anchored securely to the surrounding tissue followed by the AmeriGel® carefully placed to serve as a spacer interdigitally as well as to cover the BAT to promote more rapid healing. (Fig. 2B) After one week, the initial dressing was removed and the patient was instructed to change the dressing daily by applying AmeriGel® over the wound site followed by dry sterile gauze as a secondary dressing. After 3 weeks and 4 days, the wound site completely closed. (Fig. 2C)


Figures 2ABC  In case 2, GammaGraft® was used with AmeriGel® to advance closure of this chronic interdigital ulcer that occurred from a long standing and ignored fungal infection.

Learning points: Desiccation of the BAT is a major concern when treating distal extremity wounds where there is often autonomic impairment common in patients with diabetes. A dressing like AmeriGel® will supplement moisture to the wound site.

Tip: Because of the previous fungal infection, the antifungal properties of AmeriGel® served well to provide the ideal environment for healing.

Case 3

A 54-year-old diabetic male with a long history of Charcot deformity presented with a plantar ulcer (2.1 cm X 2.5 cm) of greater than 6 months duration. After the patient was offloaded in a Bledsoe® Walker (Bledsoe Brace Systems, Grand Prairie, TX), a granular bed was achieved after two weeks of aggressive debridement and topical wound care agents. (Fig. 3A) A GammaGraft® was then chosen to bring total closure to the wound site. The GammaGraft® was anchored to the wound site followed by AmeriGel®. (Fig. 3B) After one week, the initial dressing was changed and the patient was instructed to apply AmeriGel® every day thereafter, using dry sterile gauze as a secondary dressing. 3 weeks and 1 day later, the patient achieved complete healing. (Fig. 3C) Patient compliance with offloading and proper use of the prescribed dressings played a major role in this patient’s quick healing time.


Figures 3ABC  In case 3, GammaGraft® was used with AmeriGel® to facilitate healing of this plantar ulcer that occurred due to Charcot deformity.

Learning points: Offloading wounds like the one above is the cornerstone to success in wound healing. Encourage patients to agree and be compliant with your treatment regimen.

Tip: Avoid using questionable cytotoxic agents over or on the BAT site.

Case 4

A 68-year-old diabetic female on dialysis presented with a chronic right heel ulcer (3.4 cm X 3.1 cm) of greater than 3 months duration. After thorough wound bed preparation over the course of 2 weeks (Fig. 4A), GammaGraft® and AmeriGel® was chosen to bring closure to the wound site. (Fig. 4B) The patient’s dressing was changed at one week followed by daily applications of AmeriGel®, using dry sterile gauze as a secondary dressing. After 5 weeks and 3 days, the patient achieved total healing. (Fig. 4C)


Figures 4ABC  GammaGraft® and  AmeriGel® were used to together to facilitate closure of this chronic heel ulceration that occurred as a result of dyshidrosis and neuropathy. 

Learning points: Initial dressing changes after application of a BAT should occur between 5-7 days. This may vary depending on the presence of drainage or infection.

Tip: The heel can be a very difficult place to heal a chronic wound for many reasons. Hydration was really the key to healing this wound as this patient developed the wound initially from excess dryness, cracking and fissuring.

Case 5

A 71-year-old diabetic male smoker with severe peripheral arterial disease presented with a dorsal foot ulceration (2.5 cm X 2.4cm) that had been chronically open for nearly 2 years. After months of treatment at 2 different wound care centers and several interventions by local vascular specialists, the patient was referred for consultation. After 2 weeks of aggressive wound debridements and the use of a collagen topical dressing, the wound bed improved to the point of accepting a BAT. (Fig. 5A) The GammaGraft® was anchored to the surrounding tissues with Steri-Strips™ (3M, St Paul, MN) (Fig. 5B) and covered with AmeriGel®. (Fig. 5C) After one week, the initial dressing was changed and daily applications of the AmeriGel® was performed using dry sterile gauze as a secondary dressing. The patient achieved complete healing in 6 weeks. (Fig. 5D)


Figures 5AB  Application of GraftJacket® and AmeriGel® in the presence of vascular disease.


Figures 5CD  Despite poor vascular status, early intervention and rigorous wound care helped heal this longstanding foot ulceration.

Learning points: This patient’s ABI demonstrated dismal PVR’s, yet despite this, a rigorous wound care regimen was instituted that eventually led to complete healing.

Tip: Thoroughly assessing vascular status with each and every wound care patient is not only good practice; it can prevent limb loss with timely intervention.

Case 6

A 47-year-old diabetic patient with profound peripheral neuropathy developed a blister on the plantar aspect of her right heel that became recalcitrant to conservative treatment. The patient’s wound was debrided weekly and had Promogran™ (Johnson & Johnson Wound Management, Somerville, NJ) applied to the site until the wound developed a healthy granular base.  Apligraf® (Organogenesis, Inc., Canton, MA) was chosen to close the wound. It was secured in place with Steri-Strips™ and covered with AmeriGel®, along with the use of a Bledsoe® boot and wheel chair.

Due to the patient’s severe neuropathy, among other balance concerns, the patient could not use crutches. (Fig. 6A) One week post application, the absorptive capability of the AmeriGel® was evident (Fig. 6B) as well as its ability to maintain a moist, healthy wound base. (Fig. 6C) At 4 weeks and 4 days, after daily applications of AmeriGel® and dry sterile gauze as the secondary dressing, the wound was healed. (Fig. 6DE)


Figures 6ABC  After regular debridements,  aggressive offloading and conservative treatments including the use of collagen dressings, Apligraf® was chosen for closure along with AmeriGel® per the BRAIN principals.  Excellent incorporation was noted as early as one week (Fig. C). 


Figures 6DE At two weeks, the wound size had been reduced by half and following daily applications of AmeriGel®.  The wound was closed 4 weeks and 4 days after the BAT was applied. 

Learning points: The above case illustrates well the concept of meeting the needs of the wound through the use of more than one product. Aside from regular wound debridements, collagen dressings were initially used to promote a healthy wound base followed by the Apligraf® and AmeriGel®.

Tip: Do NOT mechanically debride the wound bed for at least 4-6 weeks after applying a BAT [this may vary depending on the type of BAT being utilized (i.e. GammaGraft®)] unless the presence of significant exudate and colonization is present.


Since using the BRAIN principles in my own clinics, successful incorporation rates have substantially improved when compared to conventional protocols used previously (i.e. petrolatum impregnated gauze, 4X4’s and roll gauze). Over the past two years, 50 diabetic patients with similar ulcerations were treated using the BRAIN principles along with AmeriGel®. Approximately 90% of those patients had allograft tissue (GammaGraft® and GraftJacket®) applied while the other 10% had Apligraf® applied. To date, only two of the 50 patients have demonstrated BAT failure (non-healing of the wound). Failure in these two patients was attributed to peripheral vascular disease in one and non-compliance in the other.

BATs applied to the legs healed quicker clinically than those applied to the foot. The legs being better vascularized in most cases constitute a viable reason for the comparably faster healing times. For chronic venous insufficiency ulcer patients, compression and a BAT covered by AmeriGel® allowed for healing in the majority of cases within two to three weeks. In some cases wounds were healed at one week. (Graph 1)

Graph 1 This histogram shows that, with the exception of the extreme value (55 days to healing), healing times are reasonably normally distributed, represented by the dashed curve. Based on a log transformation the typical healing time is 17.8 days with a 95% confidence interval of 15.6 days to 20.2 days.

In all cases, only one BAT was used during the entire course of treatment, which certainly reduced costs. After application of the BAT, AmeriGel® continued to be employed as the primary dressing over the wound until closure.


Successfully combining BAT application along with other adjunctive therapies is not a new concept. Armstrong combined Dermagraft® (Advanced BioHealing, Inc., La Jolla, CA) with a vacuum-assisted closure system demonstrating quicker healing rates. [13]

One may also combine BAT’s with hyperbaric oxygen treatment in wounds with local ischemia in turn improving the likelihood of BAT incorporation. [14] Furthermore, venous ulcerations in patients with edema may benefit from compression bandages in turn reducing healing times.

Clinical protocols incorporating the BRAIN principles will not only improve outcomes, but will also improve efficacy and patient satisfaction. No matter what your BAT of choice is, using the BRAIN principles to maximize the incorporation or transfer of the contents in the tissue to the wound will improve outcomes. [7] It has been evident in my patient population that the AmeriGel® gauze significantly helped to provide the ideal microcosm for the BAT after application. Reducing healing times will decrease wound infection rates and lowers the risk of amputation. When patients have faster healing wounds, the necessity for adjunctive diagnostic studies diminishes and patients may return more quickly to normal function thus reducing the costs associated with the increased number of supplies and physician office visits. [15]


This study was retrospective and conducted out of a single multi-office practice. Furthermore, this study did not ascertain the impact of age, length of time the ulcer was present, nor previous treatment modalities. Although this case series is small, the results suggest that this protocol may be beneficial in ulcers from multiple causes, including those of diabetic and venous origin. Future studies may determine efficacy of this protocol as compared to a placebo group with traditional application of the BAT alone. The rapid healing noted in this study can be attributed not only to the use of the BRAIN principles, but also to the meticulous wound bed preparation and proper offloading that took place in every case prior to and after the BAT application.


1. Kim PJ, Dybowski KS, Steinberg JS. A Closer Look at Bioengineered Alternative Tissues. Podiatry Today – ISSN: 1045-7860 – Volume 19 – Issue 7: Pages: 38 – 55, July 2006.
2. Pham HT, Rich J, Veves A, Using Living Skin Equivalents for Diabetic Foot Ulceration: Lower Extremity Wound 1(1); 27-32, 2002.
3. Falanga V, Sabolinski M. A bilayered living skin equivalent construct (Apligraf) accelerates complete closure of hard to heal venous ulcers. Wound Repair Regen 7:201-7, 1999.
4. Bello YM, Falabella AF, Eaglstein WH. Tissue-engineered skin, current status in wound healing. Am J. Clin Dermatol 2(5):303-313, 2001.
5. Claxton MJ, Armstrong DG, Boulton AJM. Healing the diabetic wound and keeping it healed: modalities for the early 21st century. Cur Diab Rep. 2(6):510-8, December 2002.
6. Lee KH. Tissue-engineered human skin substitutes; development and clinical application. Yonsei Medical Journal 41(6):774-779, 2000.
7. Moore, J. The BRAIN Principle: Managing Wounds After Application of Bioengineered Alternative Tissues to Maximize Incorporation and Wound Healing, doi: 10.3827/faoj.2008.0105.0003, The Foot & Ankle Journal, 1(5):3, 2008
8. Loots MA, Lamme EN, Zeegelaar J, et al. Differences in cellular infiltrate and extracellular matrix of chronic diabetic and venous ulcers versus acute wounds. J Invest Dermatol 111:850–7, 1998.
9. Dinh T, Pham H, Veves A. Emerging Treatments in Diabetic Wound Care. Wounds 14(1) 2-10, 2002.
10. Eisenbud D, Hunter H, Kessler L, et al. Hydrogel Wound Dressings: Where Do We Stand in 2003. Ostomy/Wound Management 49(10) 52-57, 2003
11. Akiyama, H., Kazuyasu, F., Yamasaki, O., Oono, T., Iwatsuki, K., Antibacterial action of several tannins against staphylococcus aureus, Journal of Antimicrobial Chemotherapy 48: 487-491, 2001.
12. Cowan, MM: Plant Products as Antimicrobial Agents; Clinical Microbiology Reviews, 12(4) 564-582, 1999.
13. Espensen EH, Nixon BP, Lavery LA, Armstrong, DG.  Use of subatmospheric (VAC) therapy to improve bioengineered tissue grafting in diabetic foot wounds. Journal of the American Podiatric Medical Association. 92(7): 395-401, 2002.
14. Hopf HW, Humphrey LM, Puzziferri N, et al. Adjuncts to preparing wounds for closure hyperbaric oxygen, growth factors, skin substitutes, negative pressure wound therapy (vacuum-assisted closure). Foot and Ankle Clinics. 6: 661-682, 2001.
15. Harold Brem, MD; Jeroen Balledux, MD et al. Healing of Diabetic Foot Ulcers and Pressure Ulcers With Human Skin Equivalent, A New Paradigm in Wound Healing, Arch Surg. 135:627-634, 2000.

Address correspondence to: Jonathan Moore, DPM, MS. Cumberland Foot & Ankle Center.
117 Tradepark Drive, Somerset, KY 42503

1Cumberland Foot & Ankle Center. 117 Tradepark Drive, Somerset, KY 42503.

© The Foot & Ankle Journal, 2008

May-Hegglin and other Platelet Dysfunctions as Complications to Compartment Syndrome: A case report

by Jason R. Miller, FACFAS, FAPWCA1, Peter Moyer, DPM2

The Foot & Ankle Journal 1 (9): 1

Compartment syndrome is a well known surgical emergency encountered by physicians on trauma call. When compounded by platelet dysfunction, the management of a compartment syndrome becomes exponentially more difficult for the surgeon. The following case describes a twenty-four year old male who sustained multiple comminuted tarsal and metatarsal fractures after a crush injury that was further complicated by an existing platelet dysfunction known as May-Hegglin anomaly (MHA). This article reviews May-Hegglin and other rare hematological conditions that often obscure otherwise straightforward surgical cases.

Key words: May-Hegglin, MHA, compartment syndrome, external fixation, foot fractures

This is an Open Access article distributed under the terms of the Creative Commons Attribution License.  It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot & Ankle Journal (

Accepted: August, 2008
Published: September, 2008

ISSN 1941-6806
doi: 10.3827/faoj.2008.0109.0001

May-Hegglin anomaly (MHA) is a familial disorder that is a rare type of autosomal dominant platelet disorder. From 2000-2005, only 85 families with MHA were reported. [6] It is associated with thrombocytopenia with varying degrees of purpura, bleeding, giant platelets, and cytoplasmic inclusion bodies that resemble Döhle bodies in the granulocytes (neutrophils, eosinophils, monocytes). [4,6] In these patients, neutrophil and platelet function is considered to be normal. Thrombocytopenia occurs in almost all patients and severe bleeding is rare but has been reported.

These patients may have a range of symptoms from asymptomatic to recurrent epistaxis, gingival bleeding, easily bruising to menorrhagia. MHA has not been associated with higher rates of infection. [4]

In 1909, German physician May described a young female patient who had leukocytic inclusions, who was asymptomatic. [6] In 1945, Swiss doctor Hegglin described a father and his two sons who had a triad of thrombocytopenia, giant platelets, and leukocytic inclusions. [6]

These patients have a mutation of the MYH9 gene, encoding non-muscle myosin heavy chain IIA, present in chromosomal region 22q12-13. [4,6] This mutation results in disordered production of non-muscle myosin heavy-chain type IIA.

The result is macrothrombocytopenia, secondary to defective megakaryocyte maturation and fragmentation. Other associated syndromes are Sebastian, Fechtner, or Epstein syndromes. Differential diagnosis associated with thrombocytopenia and large platelets include Alport syndrome, Bernard-Soulier syndrome, Montreal platelet syndrome, immune thrombocytopenia, and gray-platelet syndrome. [6] The differential diagnosis for leukocytic inclusions includes septicemia, myeloproliferative disorders, and pregnancy.

A case report describes a twenty-four year old male who sustained multiple comminuted tarsal and metatarsal fractures after a crush injury that was further complicated by an existing platelet dysfunction known as May-Hegglin anomaly (MHA).

Case Report

A twenty-four year old deaf man was transported from a local hospital to our Level 1 trauma center for evaluation. He was at work when a steel industrial loading dock door came crashing down and landed across his left foot. (Fig. 1)

Figure 1 Initial presentation after crush injury of the left foot. 

Initial evaluation in the trauma bay was significant for left foot swelling, pain, and mottled skin. His sensory function was compromised while gross motor function remained intact. He presented with stable vital signs.

His past medical history was positive for the May-Hegglin anomaly. He reported living with his parents, denied allergies, and had an otherwise unremarkable review of systems. A full physical exam was normal with the exception of his left lower extremity.

The lower extremity exam was positive for: diminished pulses, exquisite pain on palpation of the mid-foot area, pain with range of motion of digits 1,2,3 and 4, decreased temperature, color changes, and swelling. Arterial line pressure monitoring revealed compartment pressures between 75 mmHg and 100 mmHg in the foot, therefore the operating room was called and prepared for emergent surgery.

Plain film and CT scan revealed the following fractures: comminuted intra-articular fracture of the calcaneus, comminuted fractures of the navicular, cuboid, proximal portions of the cuneiforms and fractures at the base of the second and third metatarsals. (Figs. 2,3)

Figure 2 Radiograph reveals first and second metatarsal crush fracture. 

Figure 3  Sagittal CT view of crush injury.  Displaced metatarsal, calcaneal, and cuneiform fractures are evident. 

Stat labs revealed the following abnormalities: WBC 4.9, HgB 8.6, HCT 25.9 and platelets were 39,000mm3. He was then typed and crossed for surgery.

Surgical Procedure

In the operating room, general anesthesia was administered and an emergent fasciotomy was preformed following typical sterile preparation. His left foot was noted to be severely cyanotic, mottled, and cool to touch. An 8-10 cm medial incision was made to the level of the deep fascia.

After the deep fascia was penetrated via blunt dissection, copious amounts of dark, non-coagulated blood flowed from the incision site. (Fig. 4)

Figure 4  Surgical exploration shows dark, non-coagulated blood and hematoma associated with the compartment syndrome. 

Both the medial and plantar compartments were explored through this incision. Approximately one to two minutes after initial incision was made, the hallux changed from a mottled, blanched, cyanotic color to a healthy pink hue with appropriate capillary refill time. A second incision was then made between the shafts of the second and third metatarsals. Blunt dissections in to the deep fascia revealed additional copious amounts of dark blood that was evacuated from the compartment. A third incision was placed between the fourth and fifth metatarsals, and again this compartment was relieved of congestion. Within five minutes after initial incision, the entire foot was pink and warm with a dramatic decrease in the swelling. Further evaluation noted that the rear-foot remained mottled and cyanotic. At that point a fourth incision was made anterior to the Achilles tendon into the deep fascia, and approximately 5 cc of dark blood was evacuated from the calcaneal compartment. The incisions were flushed and packed with saline soaked nu-gauze packing. Attention was then paid to the medial aspect of the calcaneus where a closed reduction of the sustentacular fragment was performed under fluoroscopy.

An external fixator device was placed in triangular fashion under fluoroscopy to maintain proper alignment of the destabilized midfoot and forefoot fractures.

Post-operatively, a posterior splint with a mild compressive dressing was applied and CBC was collected. Medical and hematology consults were activated, neurovascular evaluations were ordered every two hours, cefazolin 1g every 8 hours was started, and repeat radiographs and CT scans were performed.

On post-operative day number one (POD #1), hematology recommended transfusions of both platelets and packed red blood cells prior to the surgical procedure scheduled for POD #5. While they recommend the use of SCD’s, compression stockings, and out of bed to chair three times per day, they discouraged the use of heparin or enoxaparin for DVT prophylaxis. Hematology also recommended that in monitoring the patient for active bleeding, the hemoglobin, hematocrit and platelet count should be drawn every 12 hours and to consider desmopression (DDAVP) if the labs worsened.

On POD #4, he was transfused with four units of platelets, two units of packed red blood cells, and was given prophylactic diphenhydramine.

The patient tolerated the transfusion well with no evidence of reaction. On POD # 5, he was taken back to the operating room for a successful wash out, minor debridement and primary delayed closure. The patient was discharged on POD #6 after two normal CBC evaluations.

His uneventful postoperative course was interrupted on his second office visit when it was noticed that there was some displacement at the comminuted first metatarsal-cuneiform joint. He was taken back to the operating room for a possible fusion or re-manipulation/stabilization procedure. Intra-operatively, the joint was easily manipulated back into place, and small Steinman pins were introduced for stability. Additionally, the sustentacular fragment of the calcaneal fracture was definitively fixated with 4.0mm cannulated screw fixation under fluoroscopy by percutaneous technique. The fixation pins and external fixator were removed six weeks later and he has since returned to regular employment approximately 8 months following this injury. He reports no residual deformity or pain and is able to ambulate freely in regular shoegear. (Fig. 5)

Figure 5 Patient post reduction with functional left foot and no residual pain or deformity.


It is important to note that platelets play a central role in normal hemostasis and thrombosis. Platelets originate from pluripotent stem cells that undergo differentiation to the megakaryoblast and then to platelets. Normal platelet counts are between 150,000 to 300,000mm3, with thrombocytopenia being defined as a platelet count less than 100,000mm3. Spontaneous bleeding typically becomes evident after counts drop below 20,000mm3 (spontaneous head bleeds < 5,000mm3). [6]

In the circulating form, platelets appear as a smooth discs enclosed within a plasma membrane. This membrane contains a number of receptor glycoproteins that are responsible for platelet function. Within the platelet are two specific types of granules.

The first, alpha granules contain fibrinogen, fibronectin, factors V and VIII, platelet factor 4 and platelet-derived growth factor and transforming growth factor beta. The second type of granule is for non-metabolic pool adenine nucleotides (ADP & ATP), ionized calcium, histamine, serotonin, and epinephrine.6 When a vessel wall is damaged, platelets undergo three reactions: (1) adhesion and shape change, (2) secretion, and (3) aggregation collectively referred to as platelet activation. [4] (Fig. 6)

From May-Hegglin Anomaly, eMedicine, 2008.

Figure 6 2000x blood smear of a MHA patient demonstrating a typical giant platelet with ill defined granulation.  A normal sized platelet is also seen here.  The cytoplasmic inclusion body represents a Dohle body.


A cell blood count is essential in starting a workup in these patients. The platelet count is decreased, usually between 40,000-80,000mm3. The platelets are enlarged up to 15mm3 in diameter, with normal morphology. [4] Evaluation at the electron microscopy level reveals normal cell organelles with an increased amount of disorganized microtubuli.

The Wright-stained peripheral blood smear shows cytoplasmic inclusion bodies, most dominant in the neutrophils, but some are present in the eosinphils, monocytes, and basophils.

The inclusions are up to 5µm in size, they are spindle shaped, pale, blue-staining bodies that consist of ribosomes, endoplasmic reticulum, and microfilaments. [4] The inclusions are similar to Döhle bodies and are found in the periphery of the cytoplasm. [4] Bleeding time is typically prolonged in concordance with the degree of thrombocytopenia.

Since patients with MHA do not have significant bleeding problems, treatment should be based on clinical evaluation, laboratory evaluation and following recommendations from a hematologist pre- and post operatively. Though it is rare for a MHA patient to develop severe bleeding intra- and post operatively, the skilled foot and ankle surgeon should be aware of the risk of bleeding requiring transfusions. [5]

Desmopressin acetate (DDAVP), is a synthetic vasopressin analogue that has been used peri-operatively in patients with MHA. It is an altered form of vasopressin in which deamination of hemicysteine at position 1 and substitution of D-arginine for L-arginine at position 8 has occurred. [2] Desmopressin binds to the V2 receptor in renal collecting ducts, increasing water resorption. It also stimulates release of factor VIII from endothelial cells due to stimulation of the V1a receptor. [2] This change in stereochemistry eliminates vasopressor (V1) receptor agonist activity and enhances the antidiuretic (V2) receptor agonist action and prolongs duration of action from 2-6 hours to 6-24 hours. [2]

Desmopressin stimulates the endothelial release of factor VIII and von Willebrand factor into the plasma (V2 receptor effect).

After a slow infusion of 0.3mcg/kg, plasma concentrations of factor VIII and von Willebrand factor is 2-4x greater. [2]  Although it can be unpredictable, desmopressin has been shown to shorten bleeding time in a variety of platelet dysfunctional diseases.

DDAVP has become the drug of choice for prevention and treatment of bleeding in patients with mild hemophilia A and von Willebrand’s disease because of the increase in factor VIII and von Willebrand factor, but its mechanism in platelet disorders is still one of debate. [5]

Sehbai, et al., reported a case where 34-year old woman with known MHA underwent a craniotomy secondary to an intractable seizure disorder since childhood. [5] After an extensive family history, past medical history of the patient, and extensive workup which included; magnetic resonance imaging (MRI) of the brain, positron emission tomography (PET) scan, and 24 hour video EEG, the woman underwent craniotomy and resection of the temporal lobe foci of seizure activity. She was admitted one day prior to surgery and transfused with 6 units of platelets, and one hour before surgery was given DDAVP. Platelets were on standby if needed intra or post operatively. Her postoperative course was uneventful except for mild hyponatremia secondary to the DDAVP. [5]

Chabane, et al., reported a 24 year old female that was diagnosed with severe thrombocytopenia after giving birth. She was later diagnosed with MHA. She later went on to have a second and third child via cesarean section, and she did not receive platelets for either. The third child was affected by the MHA with a platelet count of 49,000mm3 as well as inclusion bodies on blood smear. [1]

Matzdorff, et al., reported on a patient with Fechtner syndrome that underwent a tonsillectomy and was given DDAVP pre-operatively. [3]

The patient was a 24 year old woman with a past medical history of thrombocytopenia and bruised easily in childhood. She had been diagnosed with Sebastian platelet syndrome, had also noted a impairment with her hearing as well as mild hematuria. After a detailed family history it was noted that some relatives had thrombocytopenia and hearing impairment. At the time, a blood smear was obtained and evaluated with electron-microscope, which confirmed that the inclusions were consistent with Fechtner syndrome. The woman underwent extensive laboratory evaluation: modified Ivy bleeding test, platelet aggregation studies with ADP, collagen, and ristocentin, and standard coagulation test. The patient also had a bone marrow biopsy. The pertinent test in this case was the bleeding test which was greater than thirty minutes, normal being 5-8 minutes. [3] The test was repeated after DDAVP was given, and her bleeding time normalized to 7 minutes 30 seconds, and her von Willebrand factor (her base line was above average) antigen had increased from 150% to 282%. On the day of surgery the women received DDAVP 0.4 µg/kg over 30 minutes 1 hour before the start time, and the surgery went uneventful. [3]


May-Hegglin is a rare platelet disorder associated with macrothrombocytopenia, leukocyte inclusions, deafness and nephritis. Patients may experience easy bruising, recurrent epistaxis, gingival bleeding, menorrhagia, and excessive bleeding associated with surgical procedures. A patient that presents with MHA and an un-witnessed fall should get a CT scan to rule out intracranial hemorrhage and internal bleeding. Patients that present with MHA should be evaluated by a hematologist to recommend DDAVP and platelet transfusions when necessary. In this case, MHA likely played a compounding role in the rapid development of the foot compartment syndrome encountered and could have certainly compounded the post-operative course.

This case demonstrates the need for a multi-disciplinary approach to patients exhibiting May Hegglin anomaly and expeditious surgical intervention when this rare patient population experiences a traumatic event. Additionally, it demonstrates the need to take a thorough history to reveal rare disorders, like this one, in an elective surgery population. A lack of proper treatment in patients with rare platelet disorders can certainly lead to devastating complications. It is our sincere hope that this article will serve to guide the foot and ankle surgeon to appropriately recognize and treat complicating disease processes when they present.


1. Chabane H, Gallais Y, Pathier D, Tchernia G, Gaussem P. Delivery management in a woman with thrombocytopenia of the May-Hegglin anomaly type. Eur J Obstet Gynecol and Reproduction Bio 99:124-25, 2001.
2. Mahdy A.M., Webster N.R. Perioperative systemic haemostatic agents. British J Anaesthesia 93(6):842-58, 2004.
3. Matzdorff AC, White JG, Malzahn K, Greinacher A. Perioperative management of a patient with Fechtner syndrome. Ann Hematol 80:436-439, 2001.
4. Noris P, Spedini P, Belletti S, Magrini U, Balduini C. Thrombocytopenia, giant platelets, and leukocyte inclusion bodies (May-Hegglin anomaly): clinical and laboratory findings. Am J Med 104:355-60, 1998.
5. Sehbai A, Abraham J, Brown V. Perioperative management of a patient with May-Hegglin anomaly requiring craniotomy. Am J Hematol 79:303-08, 2005.
6. Shafer FE. May-Hegglin Anomaly. eMed J [online], 2003.

Address correspondence to: Jason R. Miller, FACFAS, FAPWCA
Chief, Foot and Ankle Surgery, Pennsylvania Orthopaedic Center
Adjunct Associate Professor, Dept. of Surgery, TUSPM
Office: 215-644-6900 , FAX: 215-644-7160

1Chief, Foot and Ankle Surgery, PA Orthopaedic Center. Adjunct Associate Professor, Dept. of Surgery, TUSPM, Philadelphia, Pa. 19107.
2PGY-4, Foot and Ankle Surgery, Temple University Hospital, Philadelphia, PA, 19140.

© The Foot & Ankle Journal, 2008