Tag Archives: Osteomyelitis

Staphylococcus simulans Osteomyelitis of the Foot: A case report

by Al Kline, DPM1

The Foot and Ankle Online Journal 3 (1): 4

Staphylococcus simulans, a coagulase-negative pathogen is not commonly seen in the foot. The pathogen has been isolated in chronic osteomyelitis and infected internal fixation. This case describes a 65 year-old, diabetic male with recalcitrant osteomyelitis following partial metatarsal head resection. Staphylococcus simulans was the primary pathogen isolated. This may be the first reported case of Staphylococcus simulans osteomyelitis of the foot.

Key words : Osteomyelitis, Diabetic foot infection, Staphylococcus infection.

Accepted: December, 2009
Published: January, 2010

ISSN 1941-6806
doi: 10.3827/faoj.2010.0301.0004

Staphylococcus simulans is a common, coagulase-negative (CoNS) pathogen linked to animals, including cattle. [1] The pathogen is common in normal flora and is primarily acquired through contact with domestic animals. In animals, the pathogen has been isolated and implicated in a condition called “bumble foot”. [2,4] Bumble foot, or ulcerative pododermatitis, has been described in both rats and birds. [2,3,5] In humans, the pathogen has been isolated in intravascular and indwelling catheters and conditions including urinary tract infections, septicemia, conjunctivitis, and endocarditis. [1,6,7,8] In the past 15 years, the organism has been isolated in cases of osteomyelitis, prosthetic joint infections, and infected internal fixation devices. [1,7,8] The author has found no reported cases of Staphylococcus simulans osteomyelitis of the foot. This report describes a patient who presented with a draining wound after having a previous partial metatarsal resection for acute osteomyelitis.

Case Report

A 65 year-old diabetic male presented to our office with a draining dorsal abscess of the right foot. In May 2006, he underwent a partial metatarsal resection of the 3rd right metatarsal by another podiatrist. Unfortunately, the area became infected. He states the surgery was performed through the ‘top of the foot’ and the ulcer was left to close on the bottom. He reports the dorsal incision, which was primarily closed, opened just days after surgery and began to drain. The plantar ulcer did not close. The patient reports he had a dog. It appeared that hair from the dog constantly adhered to his wound because of walking bare foot on the carpet. His treatment included antibiotic therapy and local wound care. He was on an oral Ciprofloxacin He continued on local wound care and oral antibiotics until he presented to our office in January, 2007. He has had a draining sinus for the past eight months. Radiographic evaluation revealed reactive bone changes to the base of the 3rd proximal phalanx consistent with recalcitrant osteomyelitis. (Fig. 1)

Figure 1  Radiographs of the foot revealed a previous metatarsal resection.  Reactive, osteolytic changes were seen of the 3rd proximal phalanx base consistent with chronic osteomyelitis.

Magnetic resonance imaging (MRI) was performed using high field 1.5 Tesla without contrast. Multiplanar, multisequence images were obtained through the previous partial amputation of the distal right third metatarsal bone and proximal phalanx. On T1 coronal and axial views abnormal bone marrow signal intensity was seen involving the proximal phalanx of the third toe and third metatarsal at the distal shaft. On the respective STIR coronal images and T2WI, there was diffuse high signal intensity. MRI confirmed osteomyelitis to the base of the 3rd proximal phalanx as well as the 3rd end of the remaining metatarsal stump. (Fig. 2A and 2B)


Figure 2A and 2B   MRI axial (a), coronal (b) images revealed abnormal image intensity to the base of the 3rd proximal phalanx and 3rd metatarsal bone.

The patient was admitted to the hospital and scheduled for incision and drainage of the wound with deep tissue and bone cultures with partial resection of the metatarsal stump and base of the proximal 3rd digital phalanx. At surgery, the patient had significant scarring with chronic osteomyelitis of the 3rd metatarsophalangeal joint (MPJ) space. Deep tissue cultures were performed around the base of the 3rd proximal phalanx. Bone was then resected from the base of the 3rd phalanx and 3rd metatarsal stump. Bone was then sent for culture and sensitivity. The wound was left open and packed with plain gauze and saline.

Surgical Culture Report

Surgical culture results revealed Staphylococcus simulans as the primary organism. Bone cultures were also consistent with the same organism. Culture sensitivities reported resistance to Ampicillin, Ciprofloxacin, Clindamycin, Erythromoycin, Oxacillin, Penicillin, Primaxin, Cefazolin and Ceftriaxone. The organism was susceptible to Gentamycin, Tetracylcine, Vancomycin and Bactrim.


Osteomyelitis associated with Staphylococcus simulans is rarely reported. This appears to be the first documented case of Staphylococcus simulans osteomyelitis from a chronic plantar foot ulcer. In 1985, Males, et al., documented a case of fibular, malleolar osteomyelitis after removal of a syndesmotic screw that led to Staphylococcus simulans septic ankle arthritis and septicemia. [8] Before 1985, many species of staphylococcus, including S. simulans, were not identified as a separate strain of staphylococcus and were often labeled Staphylococcus epidermidis. This may explain the lack of reported cases from this pathogen. Staphylococcus simulans is also known to produce a strong slime layer. The production of a strong slime layer and its adherence to smooth surfaces, is linked to the organisms ability to colonize, especially in prosthetic devices, shunts and catheters. [8,9,10] In cases of chronic osteomyelitis, this slime layer is also observed in grossly colonized abscesses. In this case, we also observed a mucoid, slime layer adherent to the packing material. We lavaged and repacked the wound daily. It has also been shown that the encapulated forms of Staphylococcus simulans (i.e. slime layer), as compared to unencapsulated forms of the pathogen, have a antiphagocytic effect on human PMN’s. Little phagocytosis was observed during a 2 hour incubation of PMN’s , even when the ratio of PMN’s to bacteria was increased from 1:1 to 10:1.11 This would explain the virulence of this organism and its ability to colonize wounds and prosthetic devices.


The patient responded well to intravenous (IV) Vancomycin during his hospital course. He remained in the hospital setting for 16 days on IV antibiotic therapy until the dorsal incision closed. This patient returned to a diabetic shoe without further complication. To date, no signs of recurrent osteomyelitis have been reported.


1. Razonable RR, Lewallen DG, Patel R, Osmon DR: Vertebral osteomyelitis and prosthetic joint infection due to staphylococcus simulans. Mayo Clinic Proc. 76 (10): 1067 – 1070, 2001.
2. McArthur J: Bumble Foot, ulcerative pododermatitis. [Online] Unable to find complete reference – the website address has been closedown.
3. McLeod L: Bumblefoot in Rats. About: Exotic Pets, [Online] Unable to find complete reference – the website address has been closedown.
4. Vorgelgt V, Pfanzelt D: Epidemiologie boviner staphylococcus epidermidis isolate: Pravalenz Virulenz-assoziierter Gene und klonale Verwandtschaft mit humanen Isolaten. Hannover, 2006 [Online] Unable to find complete reference.
5. Clauer PJ: Leg and Foot Disorders in Domestic Fowl. Small Flock Factsheet No 35. Virginia Cooperative Extension [Online] Unable to find complete reference – website unavailable.
6. Marrie TJ, Kwan C, Noble MA, West A, Duffield L: Staphylococcus saprophyticus as a cause of urinary tract infections. J Clin Microbiology 16: 427 – 431, 1987.
7. Wilson M: Microbial inhabitants of skin, their ecology and role in health and disease. Cambridge Press, November, 2004.
8. Males BM, Bartholomew WR, Amsterdam D: Staphylococcus simulans Septicemia in a Patient with Chronic Osteomyelitis and Pyarthrosis. J Clin Microbiology 21 (2): 255 – 257, 1985.
9. Byston R, Penny SR: Excessive production of mucoid substance in Staphylococcus IIA: a possible factor in colonization of Holter shunts. Dev Med Child Neurol 14 (suppl 27): 25 – 28, 1972.
10. Christensen GD, Simpson WA, Bisno AL, Beachey EH: Experimental foreign body infections in mice challenged with slime-producing staphylococcus epidermidis. Infect. Immun. 40: 407 – 410, 1982.
11. Ohshima Y, Schumacher-Perdreau F, Peters G, Quie PG, Pulverer G: Antiphagocytic effect of the capsule of staphylococcus simulans. Infection and Immunity, 58 (5), 1350 – 1354, 1990.

Address correspondence to: Al Kline, DPM
3130 South Alameda, Corpus Christi, Texas 78404.
Email: alklinedpm@gmail.com.

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

© The Foot and Ankle Online Journal, 2010

Gaenslen’s Split Heel Incision for Calcaneal Osteomyelitis: A case report

by J. Terrence Jose Jerome, MBBS, DNB (Ortho), MNAMS (Ortho)1 , Mathew Varghese, M.S. (Ortho)2 , Balu Sankaran, FRCS, FAMS3 , Simon Thomas, MBBS, DNB (Ortho), MNAMS (Ortho)4

The Foot and Ankle Online Journal 2 (4): 3

Patients who have a recurrent ulcer of the heel often have a below-the-knee amputation because durable soft tissue coverage cannot be obtained over the calcaneus. Often, even if the ulcer heals satisfactorily or the area appears to be revascularized as a result of a peripheral vascular procedure, the resulting surface is not durable and the ulcer recurs. We report a 40 year old lady who had a chronic osteomyelitis right calcaneum with a large non-healing ulcer and discharging sinus, treated by split heel incision of Gaenslen.

Key words: Calcaneal osteomyelitis, Gaenslen’s incision

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 (www.faoj.org)

Accepted: March, 2007
Published: April, 2009

ISSN 1941-6806
doi: 10.3827/faoj.2009.0204.0003

Chronic osteomyelitis of the calcaneum presents a formidable management dilemma. Split-thickness skin grafts that are placed directly over the calcaneus occasionally can be used to cover the defect, but these grafts usually cannot withstand the forces that are generated during weight bearing. Furthermore, these patients are often poor candidates for a free tissue transfer because of underlying vascular disease or diabetes. We report a case in which Gaenslen’s split-heel technique was successfully used in the management of calcaneal osteomyelitis. Gaenslen’s technique is recommended for refractory cases or patients with a draining sinus centrally located on the plantar aspect of the heel. An excellent functional result can be obtained.

Case Report

A 40 year old lady with spina bifida came to our out-patient department with a large non-healing ulcer of her right heel for 3 months duration. She had consulted various doctors for the same problem, but could not get better. Her right heel showed a circular, 4 cm diameter, non-healing ulcer with seropurulent, draining sinus. (Figs. 1) The base of the ulcer had necrotic slough and was indurated to the underlying calcaneus. The margins and edges were ill-defined. The radiograph showed a lytic lesion of the postero-inferior calcaneus with a little break in the cortex. (Fig. 2) Erythrocyte sedimentation rate was 78mm/ hour (normal <14). Her blood parameters revealed hemoglobin 11.2gms, TLC 7,500cu\mm. All other blood parameters were within normal limits.


Figures 1   The patient’s right heel showed a circular, 4 cm diameter, non-healing ulcer with seropurulent, draining sinus (A and B).

Figure 2   The radiograph showed a lytic lesion in the postero-inferior part with a little break in the cortex.

The patient was put in the prone position with a support beneath the right ankle. A longitudinal incision exactly in the midline of the heel, extending 2.5 to 4 cm from the level of the base of the fifth metatarsal posteriorly was performed to split the end of the tendocalcaneus.

The plantar fascia was incised in the plane created between the abductor digiti quinti and flexor digitorum brevis. The lateral plantar artery was retracted medially and the nerve kept in the distal aspect of the wound. The quadratus plantae muscle and plantar ligament were split longitudinally. The calcaneus was visualized. It was divided from posterior to anterior with a broad osteotome and split into two halves to expose the interior of the bone (Fig 3). Sequestra, infected material, necrotic slough, damaged cortex were removed. Thorough lavage was performed.

Figure 3   The Gaenslen approach uses a broad osteotome and splits the calcaneus into two halves to expose the interior of the bone.

The wound was closed loosely with a drain in-situ. A short leg cast was applied post-operatively with the foot in neutral position and ankle at 90 degree. A window was cut over the calcaneus to permit dressing changes. Sequential dressings were done every 4th day. Two weeks after surgery, a pressure ulcer was noted just below medial malleolus (Fig 4). Extra padding and aseptic dressing was done. After 6 weeks, the pressure sore and the surgical wound healing was remarkable (Fig 5). The heel thus developed a deeply situated surgical scar over which the surrounding tissues were laid, forming thick cushions on either side of the incision. (Fig. 6)

Figure  4   2 weeks after surgery, a small pressure ulcer developed just below the medial malleolus.

Figure 5   The surgical and pressure wounds healed without incident.

Figure 6   The heel develops a deeply situated surgical scar over which the surrounding tissues were laid, forming thick cushions on either side of the incision.


In osteomyelitis of the calcaneus, as of the other tarsal bones, the destruction of the cortex usually is not very extensive. The periosteum is firmly attached to the bone, and is usually perforated rather than elevated by purulent material; therefore the formation of involucrum is minimal. [1] Partial calcanectomy is not a new procedure. Four reports, between 1931 and 1959, discussed resection of all or part of the calcaneus for the treatment of conditions as diverse as osteomyelitis of the calcaneus, cutaneous ulceration of the heel, and fracture of the calcaneus. [2,3,4] These authors reported that all of the patients were managed successfully and maintained their functional mobility. Reports published between 1972 and 1991 also documented favorable results. [1,5,6,7]

However, partial calcanectomy has not received much attention, and it seems that surgeons are often unaware that it is an option for the management of large ulcerations of the heel or osteomyelitis of the calcaneus.

Total calcanectomy is an alternative procedure to trans-tibial amputation in patients with chronic osteomyelitis of the calcaneus. Eradication of infection and preservation of functional ambulation is achieved. [8] Assessment of ankle strength and range of motion of the surgical limb demonstrated decreased dorsiflexion and plantarflexion strength and variable range of motion compared to the contralateral limb. [8] The split-heel technique was successfully used in the management of calcaneal osteomyelitis in children.

Antibiotic therapy and debridement when necessary through medial or lateral incisions will usually eradicate the infection.

Gaenslen’s technique is recommended for refractory cases or patients with a draining sinus centrally located on the plantar aspect of the heel. In general, excision of the calcaneus for chronic osteomyelitis in children is not necessary. [9] The resultant scars usually are painless.

They are so deeply situated that the tissues on either side curl inward. Diabetic, neuropathic patients are often at risk for ulceration. Those that are temporarily or permanently limited in ambulation and restricted to a supine position are, over time, very susceptible to heel decubiti. Subtotal calcanectomy is a relatively simple procedure to perform. Aggressive debridement of all nonviable tissue, thorough antibiotic course, ankle-foot orthosis combined with a custom-molded shoe in the postoperative period made all patients who were ambulatory preoperatively to resume their function after surgery. [10] In the presence of adequate vasculature, it is a good alternative to below-the-knee amputation and the accompanying sequelae. Composite wounds of the heel with secondary osteomyelitis of the calcaneus remain a reconstructive challenge. A paucity of regional flaps has often necessitated microvascular transplantation in order to obtain wound healing. Subtotal calcanectomy, traditionally a technique of the orthopedic surgeon, can, in selected cases, eradicate infection and achieve wound closure and limb preservation. [11]

A distally based sural fascio-musculocutaneous flap including the sural nerve and a midline cuff of the gastrocnemius muscle can be useful for covering the defect. This flap is designed on the proximal half of the posterior calf and has an adequate blood supply derived from retrograde perfusion of the vascular axis of the sural nerve to the musculocutaneous perforators of the gastrocnemius muscle. The patency of the peroneal artery should be confirmed by doppler ultrasound or angiography before surgery. [12] The flap was reliable and technically simple to design and execute. This 1-stage procedure not only preserves the major arteries of the injured leg but has also proved valuable for filling bony defect and treating bony infection because it provides a well-vascularized muscle fragment.


Our patient had a large non-healing plantar ulcer with discharging sinus along with chronic calcaneal osteomyelitis. Split heel incision of Gaenslen removed all sequestra, obviously infected matter and did little damage to the cortex.

The resultant scar was painless and was so deeply situated that the tissues on either side curl inward to form ‘cushions’. Gaenslen’s technique is recommended for refractory cases of osteomyelitis or patients with a draining sinus centrally located on the plantar aspect of the heel. An excellent functional result can be obtained.


1. Antoniou D, Conner AN: Osteomyelitis of the calcaneus and talus. J Bone Joint Surg 56A: 338, 1974.
2. Gaenslen, FJ: Split-heel approach in osteomyelitis of os calcis. J. Bone joint Surg 13A: 759 – 772, 1931.
3. Wiltse LL, Bateman J, G, Kase S: Resection of major portion of the calcaneus. Clin Orthop 13: 271 – 278, 1959.
4. WoII TS, Beals RK: Partial calcanectomy for the treatment of osteomyelitis of the calcaneus. Foot and Ankle 12: 31 – 34, 1991.
5. Crandall RC, Wagner FW Jr: Partial and total calcanectomy. A review of thirty-one consecutive cases over a ten-year period. J Bone Joint Surg 63A: 152 – 155, 1981.
6. Horwitz T: Partial resection of the os calcis and primary closure in the treatment of resistant large ulcers of the heel with or without osteomyelitis of the os calcis. Clin Orthop 84: 149 -153, 1972.
7. Martini M, Martini-Benkeddache Y, Bekhechi T, Daoud A: Treatment of chronic osteomyelitis of the calcaneus by resection of the calcaneus. A report of twenty cases. J Bone Joint Surg.. 56A: 542 – 548, 1974.
8. Baumhauer JF, Fraga CJ, Gould JS, Johnson JE: Total calcanectomy for the treatment of chronic osteomyelitis, Foot Ankle 19: 849 – 851, 1948.
9. Broudy AS, Scott RD, Watts HG: The split heel technique in the management of calcaneal osteomyelitis in children. Report of three cases. Clin Orthop Relat Res (119): 202 – 5, 1976.
10. Baravarian B, Menendez MM, Weinheimer DJ, Lowery C, Kosanovich R, Vidt L: subtotal calcanectomy for the treatment of large heel ulceration and calcaneal osteomyelitis in the diabetic patient. J Foot Ankle Surg 38(5): 373 – 4, 1999.
11. Isenberg JS, Costigan WM, Thordarson DB: Subtotal calcanectomy for osteomyelitis of the os calcis: a reasonable alternative to free tissue transfer. Ann Plast Surg 35 (6): 660 – 3, 1995.
12. Chen SL, Chen TM, Chou TD, Chang SC, Wang HJ: Distally based sural fascio musculo cutaneous flap for chronic osteomyelitis in diabetic patients. Ann Plast Surg 54 (1):44 – 8, 2005.

Address correspondence to: Dr. J. Terrence Jose Jerome, MBBS.,DNB (Ortho), MNAMS (Ortho)
Registrar in Orthopedics, Dept. of Orthopedics
St. Stephen’s Hospital, Tiz Hazari, Delhi 54, India

Registrar in Orthopedics, Department of Orthopedics, St. Stephens Hospital, Tiz Hazari, Delhi, India.
Head Professor, Department of Orthopedics, St. Stephens Hospital, Tiz Hazari, Delhi, India.
Professor Emeritus, Orthopedics, St. Stephens Hospital, Tiz Hazari, Delhi, India. E-mail: pasle@bol.net.in
Registrar in Orthopedics, Department of Orthopedics, St. Stephens Hospital, Tiz Hazari, Delhi, India. Phone: 991-23966021-27.

© The Foot and Ankle Online Journal, 2009

Vancomycin-Induced Thrombocytopenia: A case report

by Al Kline, DPM1

The Foot & Ankle Journal 1 (10): 4

Vancomycin has been implicated as a cause of thrombocytopenia since 1990. In a recent report of The New England Journal of Medicine, the BloodCenter of Wisconsin has identified Vancomycin-Dependent, Platelet-Derived antibodies to detect Vancomycin induced thrombocytopenia. In this case report, a 65-year old male was treated with Vancomycin for osteomyelitis. On the 10th day of treatment, the patient had a fever and developed a rash. Angiopathic petechiae were most pronounced on the back and arms. The platelet count dropped from 189 x 103/mm3 to 1 x 103/mm3 in 48 hours. This case report supports the use of drug-dependent antibody assays to identify and confirm the cause of thrombocytopenia in patients who show a precipitous drop in platelet levels while receiving Vancomycin.

Key words: Vancomycin, thrombocytopenia, osteomyelitis

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 (www.faoj.org)

Accepted: September, 2008
Published: October, 2008

ISSN 1941-6806
doi: 10.3827/faoj.2008.0110.0004

Vancomycin is an antibiotic frequently used in the treatment of MRSA (Methacillin resistant Staphylococcus aureus). In podiatry and orthopaedics, Vancomycin is the most commonly used intravenous antibiotic for the treatment of MRSA soft tissue infections and MRSA osteomyelitis. The most recent studies have suggested a 10 to 20-fold increase in the use of Vancomycin in the past 25 years. [1,2] There are a number of drugs that can cause thrombocytopenia. [3] Very often, patients who are on prolonged IV antibiotic treatment are also placed on Heparin to prevent DVT (deep vein thrombosis) and pulmonary embolism. Heparin, or Lovanox®, has been implicated in causing thrombocytopenia in such cases. [4]

In this setting, thrombocytopenia is characterized by an acute drop in the platelet count. In the combined use of Vancomycin and Heparin, it is often difficult to determine whether the thrombocytopenia is caused by Vancomycin-induced immune antibodies or a Heparin-induced response.

In a recent study of The New England Journal of Medicine, Von Drygalski, et al., have correlated IgG and IgM antibody levels in thrombocytopenia caused by an immune response to intravenous Vancomycin. More importantly, there now appears to be a valuable test available that can detect Vancomycin-Dependent, Platelet-Reactive Antibodies in patients who develop thrombocytopenia while on Vancomycin. [5] This case report describes the clinical presentation and treatment course of a patient who developed thrombocytopenia during a course of Vancomycin.

Case Report

A 65-year old diabetic male was treated with Vancomycin for osteomyelitis of the foot. The patient underwent surgery for osteomyelitis of the foot on February 19th, 2007. He was placed on Vancomycin on February 21st, 2007 after sensitivity reports revealed organisms susceptibility to Vancomycin. The patient had a history of diabetes mellitus, gout, chronic kidney disease, congestive heart failure, hypertension and hypercholesterolemia.

The patient’s medication list was extensive. The patient was on Coreg 25mg, Lasix 40mg , Digitek 0.125mg, Avandia 4mg, Lisinopril 5mg, Glyburide 5mg, KCl 20 meq, Allopurinol 300mg, Welchol 650mg, Zetia 10mg, Indomethacin 25mg prn for gout, Prevacid 30mg, Aspirin 81mg, Quinine 325mg prn for leg cramps, Viagra 100mg, Calcium 600mg and Glucosamine/Chondritin 500/400.

The patient did not take any Glucosamine or Chondritin while in hospital. Vancomycin peaks and troughs were run on two separate days. Peaks were 28.5 and 36.6 mcg/m and troughs were 17.3 and 13.4 mcg/ml. The infection cleared after surgery; however, on the 10th day of treatment, he began to loose his appetite and developed spiking fevers. His fever peaked to 102.5 Fahrenheit with ensuing petechiael rash of his back and arms. (Fig. 1)


Figure 1  Acute thrombocytopenic purpura was seen on the patient’s back and arms.  Microangiopathic petechiae were evident with purpura and ecchymosis of the flexor region of both arms.

The platelets showed a precipitous drop from 189 x 103/mm3 to 1 x 103/mm3 in 48 hours. The Lovanox® and Vancomycin were immediately stopped. Blood Testing was performed including PF4 Elisa test, IgG and IgM assays and detection of Vancomycin-Dependent, Platelet-Reactive Antibodies. This last test required 5mL of serum plasma from the patient.

At this writing, there is only one laboratory in the country that can test for this antibody at this writing. The plasma was sent to the BloodCenter of Wisconsin. He was given 10 units of platelets without response. After the second day, the patient’s platelets only increased to 3 x 103/mm3. He also developed a nose-bleed, which was stopped by local packing. He was then given IV dexamethasone, Immunoglobulins and Epogen. After the fourth day, his platelets increased to 15 x 103/mm3. By the end of the week, the patient’s platelet count was over 100 x 103/mm3 .

Laboratory Assay

The Laboratory tested for both IgG and IgM in the patient’s serum with and without Vancomycin present. (Table 1)

Table 1  Although there is a negative IgM assay in the presence of Vancomycin, a positive IgG assay by flow cytometry indicates the presence of vancomycin-dependent, platelet-reactive antibodies supporting the diagnosis of immune thrombocytopenia.

The BloodCenter of Wisconsin certified a positive reaction detected in the patient’s serum by flow cytometry in the presence of Vancomycin. These results indicated the presence of Vancomycin-dependent, platelet-reactive antibodies. This supports a diagnosis of vancomycin-induced, immune thrombocytopenia. At this writing, the test is not cleared or approved by the FDA (Federal Drug Administration, USA). The Laboratory claims the FDA has determined that such clearance or approval is not necessary. The test has been validated in house and is used for clinical purposes. It should not be regarded as investigational or for research. The laboratory is certified under the Clinical Laboratory Improvement Amendments of 1988 (CLIA) as qualified to perform high complexity clinical laboratory testing. [8]


Normal platelet counts range from 150 x 103/mm3 to 450 x 103/mm. [7]  Vancomycin- induced thrombocytopenia has rarely been reported in the literature. This appears to be the first report of Vancomycin-induced thrombocytopenia in the podiatry literature. The mechanism of drug-induced thrombocytopenia is one of immunological platelet destruction. The drug will bind to the fragment antigen binding (FAB) portion of an antibody.

The antibodies will then attach to the drug-platelet complex and cause platelet destruction through complement activation. [5,6,7] In Vancomycin-induced thrombocytopenia, the immunologic response is through hapten formation.

There is now compelling evidence that patients who develop Vancomycin-induced thrombocytopenia have Vancomycin-dependent antibodies. [5,6]

As late as 2003, Vancomycin-induced thrombocytopenia was confirmed by rechallenge of the medication or when heparin-induced thrombocytopenia was ruled out. [4,5,6]. Heparin induced thrombocytopenia is associated with a strongly positive human platelet factor 4 (PF4). This can be tested by ELISA (Enzyme-Linked ImmunoSorbent Assay) and often returns to normal after the Heparin is stopped. [5] Many times, Vancomycin and Heparin are given concurrently in cardiac patients or patients who may require prolonged bed rest. In this case report, both Lovanox® and Vancomycin is discontinued. Platelets were initially transfused during the acute phase in an attempt to increase platelet levels. This did not seem to cause any rise in platelet levels. Von Drygalski, et al., reported similar results in 11 of 14 patients who received platelet transfusions. [5] It could be theorized that circulating antibodies will continue to support a platelet destructive affect making platelet transfusions ineffective in the acute phase of thrombocytopenia. Antibodies can also persist for many months after exposure to Vancomycin. [5] Once the Vancomycin is stopped, in most circumstances, the platelet levels will normalize within 7 days. [6]

This case confirms similar results reported by Von Drygalski, et al. It is also conclude that the use of drug-dependent antibody assays can identify and confirm the cause of thrombocytopenia in patients who show a precipitous drop in platelet levels while receiving Vancomycin.


1. Kirst HA, Thompson DG, Nicas TI: Historical Yearly Usage of Vancomycinn (letter). Antimicrob Agents Chemother. 42(5): 1303-1304, May 1998.
2. Ena J, Dick RW, Jones RN et al: The epidemiology of intravenous Vancomycin usage in a university hospital. A 10-year study. JAMA; 269 (5): 598-602, February, 1993.
3. Medicine World: Drugs causing thrombocytopenia or low platelet count. [Online].
4. Davoren A, Aster, R.H.: Heparin-induced thrombocytopenia and thrombosis. Am J Hematology 81:36-44. 2006.
5. Von Drygalski A, Curtis BR, Daniel MS et al: Vancomycin-Induced Immune Thrombocytopenia. N Engl J Med 356 (9): 904 – 910, March, 2007.
6. Marraffa J, Guharoy R, Duggan D et al: Vancomycin-Induced Thrombocytopenia: A Case Proven With Rechallenge. Pharmacotherapy 23 (9): 1195-1198, 2003.
7. Wikipedia: Thrombocytopenia, [Online], 2007.
8. Correspondence Dr. Brian Curtis, Ms MT (ASCP) SBB, Technical Director, Janice McFarland, MD, Medical Director: The BloodCenter of Wisconsin,Inc., 638 N 18th Street, Milwaukee, WI. 53233-2121. (800-245-3117).

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

1Adjunct 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

An Unusual Case Report of Two Bone Osteomyelitis With Long-Term Follow-up

by Brian Carpenter, DPM, FACFAS1, Jeffrey Taylor, DPM2, Travis Motley, DPM, FACFAS3, Jason Smith, DPM4

The Foot & Ankle Journal 1 (4): 1

A 49 year-old patient, with a history of rheumatoid arthritis, presents with suspected septic arthritis of the ankle and subtalar joints. The patient was found to have osteomyelitis of both the talus and calcaneus. The patient was treated by debridement, antibiotic impregnated PMMA beads, and ultimately, a subtalar joint fusion. This case illustrates the importance of the early recognition and diagnosis, the possible sequelae, and the need for aggressive treatment of a septic joint.

Key words: Osteomyelitis, rheumatoid arthritis, subtalar joint, PMMA beads

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 (www.faoj.org 

Published Online: April 1, 2008

ISSN 1941-6806
doi: 10.3827/faoj.2008.0104.0001

Osteomyelitis is traditionally subdivided into three categories based on etiology. The first type is hematogenous osteomyelitis. This form is commonly monomicrobial, with staphylococcal organisms isolated most frequently. [7] The second type is direct extension osteomyelitis. It is usually polymicrobial in origin and seen more frequently in the general population. [6] Sources of direct extension osteomyelitis include puncture wounds, surgery, implants, contiguous ulcerations, and septic arthritis.

The third type is osteomyelitis secondary to vascular insufficiency. It is also polymicrobial in origin and seen mostly in those over 55 years of age as the result of tissue hypoxia. [1]

Septic arthritis is the most destructive form of arthritis. It is classified by its offending pathogen or etiology. Neisseria gonorrhea is commonly isolated from sexually active adults with associated superficial lesions. [8] Haemophilus influenza is commonly isolated from children under the age of two. [8] Staphylococcus and Streptococcus species, which are the most common offending pathogens overall, are seen in children over the age of two and in adults. [8] The etiologies are very similar to osteomyelitis.

Hematogenous septic arthritis may be secondary to upper respiratory and skin infections, most frequently encountered with gram-positive organisms. [8]

A joint is susceptible to infection because of the profound vascular supply within the synovial joint lining. The joint may be even more prone to an infective process given an existing arthritide, such as rheumatoid arthritis.

Arthritis not only causes direct damage to the joint, but may also be treated with repeated corticosteroid injections that can decrease the joint’s immunocompetence.

Direct extension septic arthritis shares its etiologies with direct extension osteomyelitis, but septic arthritis may also originate from an adjacent osteomyelitis. [1]

The following case report describes a middle-aged female with a history of rheumatoid arthritis, who developed osteomyelitis of the talus and calcaneus. The joints were never proven to be septic by joint aspiration and culture. The ensuing destructive sequelae raises many questions about the origin and the development of the infective process. [1]

Case Report

A 49 year-old white female with a past medical history of long term rheumatoid arthritis and a sedentary lifestyle, presented to the clinic complaining of a painful left ankle. The ankle became painful, erythematous, and edematous three months prior, and was accompanied by fever and chills. The patient did not initially seek treatment. Ten to fourteen days later, with rest and a decrease in activity, the erythema and edema subsided without the use of antibiotics, however, the pain persisted. The patient then went to see her rheumatologist, who treated her with physical therapy, an NSAID, and a steroid injection of the left ankle. The patient denied trauma, but did note a superficial cat scratch to the anterior aspect of her left lower leg one to two weeks prior to the onset of pain, which she treated with a topical antibiotic.

On initial physical examination significant findings revealed a globally edematous left ankle. The swelling was markedly more edematous on the lateral aspect of the ankle. There was pain on palpation of the anterior, lateral, and posterior aspect of the ankle joint. Pain was elicited with eversion and dorsiflexion of the ankle and there was no pain of the subtalar joint with range of motion. The neurovascular status of both extremities was intact.

Plain films of the left foot and ankle, taken on a previous presentation did not reveal a fracture or dislocation, although there was significant degenerative joint disease of the left ankle joint.

The patient returned to the clinic two weeks later with an additional complaint of a painful left heel on weightbearing. Physical exam revealed severe pain with compression to the body of the left calcaneus. There was no apparent cellulitis of the left foot or ankle. Computerized tomography (CT) scan findings of the left foot and ankle revealed degenerative joint disease of the subtalar joint with an irregular calcaneal-cuboid joint that includes significant destruction of bone. A large lytic lesion in the posterior inferior aspect of the calcaneus is seen with a small lytic lesion of the medial talar dome. There were trabecular changes of the lateral talar body with surrounding soft tissue inflammation. (Fig. 1)

Figure 1  CT scan revealed joint narrowing consistent with degenerative arthritis.  A large area of bone lysis is seen in the body of the os calcis.

Plain films, taken shortly after that time, corresponded with the CT findings. We concluded that degenerative changes of the talus, calcaneus, and subtalar joint were probably the result of an infective process.

Five days later, surgical debridement of osteomyelitic bone of the left talus and calcaneus was performed to an intra-operative viable periphery. Tobramycin impregnated beads were inserted into the dead space, and the patient was placed on cephazolin 2 gm IV every 8 hours. (Fig. 2)

Figure 2  Following surgical debridement of osteomyelitic bone, antibiotic impregnated PMMA beads were inserted.  Cultures revealed staphylococcus aureus osteomyelitis.

The wound was closed over the implanted beads with a drain in place. Bone biopsy of debrided bone was positive for osteomyelitis, and biopsy of peripheral bone and residual bone was negative. Cultures of the debrided necrotic bone were positive for Staphylococcus aureus. The postoperative period was unremarkable. A Ceretec WBC-labeled bone scan performed six weeks after the initial debridement. This was negative for osteomyelitis (Fig. 3)

Figure 3  Ceretec white blood cell bone scans performed six weeks after insertion of PMMA beads were negative for any signs of active osteomyelitis.

Ten weeks after debridement of the left talus and calcaneus, the beads were removed. The residual bone of the talus and calcaneus were clinically viable, and a subtalar joint fusion with talar and calcaneal reconstruction using autogenic iliac bone graft was performed. The patient was placed in a below-the-knee cast. Plain film findings two weeks after STJ fusion demonstrated intact internal fixation from anterior dorsal to plantar posterior with good placement and joint alignment. A portion of increased density of both the talus and calcaneus corresponded to generalized osteopenia of the bone grafts. (Fig. 4)

Figure 4 Iliac bone graft is used with a single cannulated cancellous screw to fuse the subtalar joint.

Intravenous antibiotics were discontinued and the patient was put on a two-week course of oral cephalexin.

The postoperative course involved a non-weightbearing, below-the-knee cast for eight weeks with progression to a non-weightbearing removable cast walker (RCW) for three weeks. The patient was then placed in a weightbearing RCW for another three weeks. Proper foot orthoses and ankle brace was fitted when the patient progressed to her shoes.

After casting, the patient underwent eight weeks of physical therapy to increase range of motion, proprioception, and strength. The patient was pain free six months after fusion. The plain films demonstrated approximately 90% fusion of the left subtalar joint with the heel in rectus position. (Fig. 5)

Figure 5 Six months after fusion, the subtalar joint is stable and without pain on ankle and foot range of motion. 

The patient is now ten years post surgery. She is enjoying a healthy lifestyle that includes jogging without pain.


There are many questions that arise from this case report and should be addressed to make any pertinent conclusions.

The patient’s history suggests clinical sepsis prior to presenting and the etiology remains unclear. First of all, the cat scratch she reported was probably not the cause. We were unable to isolate the most common organism isolated from cat scratches or bites, Pasteurella multiocida. [2] Also, the location and depth of the laceration are not consistent with an infectious introduction of the ankle or subtalar joint. Secondly, a steroid injection, which has been demonstrated as a source of joint sepsis in the literature, was administered to the patient early in the presentation. Injections of corticosteroid into a septic joint may increase the propagation of the infectious process, but cannot be labeled as the cause due to the onset of symptoms prior to the injection. [3,4] Finally, the patient’s long term rheumatoid arthritis must be recognized as a significant factor as to increased risk of joint sepsis, but cannot be labeled as a cause. [5,6] Given the exclusion of these three factors and the absence of other complicating trauma, although rarely seen in middle aged adults, we hypothesize the septic arthritis must be attributed to a hematogenous route. [5,6]

Assuming bacteremia one must decide on the location of the infection. Given the patient’s report, it is easy to assume ankle joint sepsis. The suspicion is heightened by the possible propagating of infection by a local joint injection to the ankle joint. The clinical and radiographic findings also suggest extra-tibiotalar sepsis. An effusion of the subtalar joint may present with ankle joint swelling that is more prominent below the lateral malleolus, given the communicating lateral anatomy of the subtalar and ankle joints. [7] Computerized tomography of the foot and ankle further supports the hypothesis of subtalar sepsis by displaying adjacent boney lesions located in the inferior talus and superior calcaneus.

Therefore, the original septic joint may have been the subtalar joint in isolation or in combination with the ankle joint. It appears the detrimental sequelae of osteomyelitis developed only in the subtalar joint.

Sequelae of septic arthritis may include persistence of the infection secondary to inadequate drainage. It can also be caused by damage to the articular cartilage, tenosynovitis, and secondary osteomyelitis. As intra-articular exudate increases, the joint attempts to accommodate its increased volume through posture, which causes more pain and stiffness. When the joint can no longer handle the intra-articular pressure, the corresponding cartilage is compressed, synovial blood supply is compromised, capsular erosions and sinus tracts form, and contiguous spread to underlying bone results. [5]

When osteomyelitis is recognized secondary to joint sepsis, joint resection arthroplasty, staged arthrodesis, or even amputation can be performed to alleviate the patient’s symptoms and stop further spread of the infection. [5] Surgical debridement of all necrotic bone must be performed. In this case, it was followed by implantation of PMMA antibiotic beads for the treatment of existing infection and prophylaxis of further infection in the anatomical dead space. The use of antibiotic laden beads is efficacious in the treatment of acute and chronic osteomyelitis. [8] PMMA beads have been in use for over 30 years. The beads are typically left in the wound for 5 to 14 days after debridement or until soft tissure coverage or primary closure can be achieved. [13] Studies have shown that minimum inhibitory concentration of antibiotics are released from PMMA beads from the first 2 days after implantation up to multiple weeks. [12] Following proper debridement and antibiotic prophylaxis, a Ceretec bone scan, which is a sensitive and specific for osteomyelitis, can be utilized to confirm the absence of infection or persistent infection. An isolated talocalcaneal arthrodesis, employing an iliac crest bone graft, has been described by many authors as an excellent way to treat various degenerative processes of the subtalar joint, and has proven to be a more functional alternative to a pan-talar fusion. [9,10]

This patient most likely developed subtalar septic arthritis from an uncommon hematogenous route. The infection was not drained and may have been even propagated with a corticosteroid injection and spread contiguously to the talus and calcaneus. Once recognized, the osteomyelitis was aggressively treated with surgery and appropriate intravenous antibiotic therapy. The case illustrates three important points about the septic joint. First, the suspicion of a septic joint must be diagnosed and treated appropriately and aggressively by joint aspiration, if possible, and proper cultures and definitive antibiotics. Secondly, early intervention in these cases is paramount, as demonstrated graphically by this case. Finally, if complications, such as osteomyelitis, do occur, proper aggressive surgical treatment must be performed promptly.


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4. Kothari, T. et al. : Pseudomonas cepacia Septic Arthritis due to Intra-articular Injections of Methylprednisolone. Canadian Medical Association Journal. 116(11): 1230, 1232, 1235, June 1977.
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8. Sternbach, G., Baker, F. : The Emergency joint: Arthrocentesis and Synovial Fluid Analysis. JACEP 5: 787-792, October 1976.
9. Calhoun, J., Mader, J. : Antibiotic Beads in the Management of Surgical Infections. American Journal of Surgery 157: 443-449, April 1989.
10. Russotti, G. et al. : Isolated Talocalcaneal Arthrodesis. Journal of Bone and Joint Surgery 79-A: 1472-1478, December 1988.
11. Thomas, F. : Arthrodesis of the Subtalar Joint. Journal of Bone and Joint Surgery 49-B: 93-97, February 1967.
12. Perry, A. et al : Antimicrobial Realease Kinetics From Polymethylmethacrylate in a Novel Continous Flow Chamber. Clinical Orthopaedics and Related Research 403, pp. 49-53 2002.
13. Walenkamp, G. et al : Osteomyelitis Treated With Gentamicin-PMMA Beads. Acta Orthop Scand 69 (5): 518-522, 1998.

1Director of Residency Training, Associate Professor, University of North Texas Health Science Center, John Peter Smith Hospital, Department of Orthopaedics, 1500 South Main Street, Ft.Worth, Texas 76104.

2Private Practice; North Texas Podiatry, 401 Westpark Way, Euless. Texas

3Staff Physician, Assistant Professor, University of North Texas Health Science Center, Department of Orthopaedics. 1500 South Main Street, Ft. Worth, Texas 76104.

4Resident, PGY-2,John Peter Smith Hospital, Department of Orthopaedics. 1500 South Main Street, Ft. Worth, Texas 76104

© The Foot & Ankle Journal, 2008

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