The Journal of Foot & Ankle Surgery xxx (2014) 1–5

Contents lists available at ScienceDirect

The Journal of Foot & Ankle Surgery journal homepage:

Case Reports and Series

Infectious Spondylodiscitis, Epidural Phlegmon, and Psoas Abscess Complicating Diabetic Foot Infection: A Case Report Nicole Nicolosi, DPM, Christina Pratt, DPM Resident, Podiatric Medicine and Surgery, HealthSpan/Cleveland Clinic, Cleveland, OH

a r t i c l e i n f o

a b s t r a c t

Level of Clinical Evidence: 4

Few published case reports have cited vertebral osteomyelitis as a sequela of a diabetic foot infection. The purpose of the present report is to increase awareness of a potentially severe complication of diabetic foot ulceration: vertebral osteomyelitis and associated pathologic features. We present the case of a 63-year-old male with right calcaneal osteomyelitis who developed acute onset lower back pain with concomitant fever and chills. Magnetic resonance imaging revealed L4-L5 vertebral osteomyelitis, a T9-L1 epidural abscess, and a right psoas muscle abscess secondary to hematogenous seeding from the calcaneus. The patient underwent right partial calcanectomy, spinal and right psoas abscess incision and drainage, and direct lumbar interbody fusion of L4-L5 with a right iliac crest allograft. All bone, blood, and abscess cultures were positive for methicillin-resistant Staphylococcus aureus. After the surgery, the patient’s pain resolved in his back and hip and he regained full right lower extremity function. The 1-year follow-up examination revealed that the patient had vertebral arthritis but was able to perform his activities of daily living with a walker and cane. It is important to recognize the potential complications of diabetic foot ulcerations and be aware of the identifying symptoms and treatment options for this condition to prevent significant morbidity and mortality. Ó 2014 by the American College of Foot and Ankle Surgeons. All rights reserved.

Keywords: calcaneal osteomyelitis epidural abscess hematogenous osteomyelitis MRSA vertebral osteomyelitis

Vertebral osteomyelitis, or infectious spondylodiscitis, can present by hematogenous spread from a distant source, contiguous spread from an adjacent source, or direct inoculation during spinal procedures. Staphylococcus aureus is the most common cause of adult hematogenous vertebral osteomyelitis and methicillin-resistant S. aureus (MRSA) has been found in more than 67% of cases (1). Priest and Peacock (1) performed a retrospective review of 40 patients with S. aureus vertebral osteomyelitis and reported a 55% causal incidence after an invasive vertebral procedure. A 2008 study by Grammatico et al (2) estimated the overall incidence of vertebral osteomyelitis at less than 1%, approximately 2.4/100,000 persons. The incidence of a psoas abscess and spinal epidural abscesses has also been rare, estimated at 12 cases annually and 0.2 to 1.2/10,000 persons annually, respectively (3,4). The development of all 3 conditions is thus even rarer still. Epidural and psoas abscesses can originate from vertebral osteomyelitis, but each of these infections can also result in the development of the other (5). However, the incidence of vertebral osteomyelitis has been increasing, especially in patients with

diabetes, because of the use of indwelling catheters and injectable recreational drugs (6,7). Few studies have cited the foot as the hematogenous source of vertebral osteomyelitis, none of which specifically named the calcaneus. In 1977, Ceilley (8) published a case report of a 71-year-old diabetic female with pedal osteomyelitis whose vertebral, pedal wound, and blood cultures revealed the same organism: Corynebacterium haemolyticum (now Arcanobacterium haemolyticum). In 2013,  et al (9) reviewed 3 cases of hematogenous spread of Cechurova methicillin-sensitive S. aureus from recurrent neuropathic diabetic foot ulcers. They concluded that a sudden onset of back pain was a common fundamental symptom in their diagnosis. Our case report illustrates the development of hematogenous osteomyelitis that spread from a calcaneal origin. The purpose of the present case report is to inform podiatrists of this potentially severe pedal osteomyelitis complication. It is important to be aware of the identifying symptoms and treatment options for this condition to prevent significant morbidity and mortality. Case Report

Financial Disclosure: None reported. Conflict of Interest: None reported. Address correspondence to: Nicole Nicolosi, DPM, Podiatric Medicine and Surgery, HealthSpan/Cleveland Clinic, 9500 Euclid Avenue, NA-40, Cleveland, OH 44195. E-mail address: [email protected] (N. Nicolosi).

In February 2013, a 63-year-old male was transferred to the Cleveland Clinic from an outside hospital for treatment. A magnetic resonance imaging (MRI) scan from the outside hospital revealed an epidural abscess at the T9-L1 level, a ventral fluid collection at L4-L5,

1067-2516/$ - see front matter Ó 2014 by the American College of Foot and Ankle Surgeons. All rights reserved.


N. Nicolosi, C. Pratt / The Journal of Foot & Ankle Surgery xxx (2014) 1–5

Fig. 1. T2-weighted sagittal right foot magnetic resonance imaging scan before the right partial calcanectomy. The increased signal intensity in the calcaneus is suggestive of calcaneal osteomyelitis.

S1, with extension into the paraspinous muscle, a right psoas muscle abscess, and vertebral osteomyelitis of L4-L5. The patient’s medical history included type 2 diabetes mellitus, atrial fibrillation, hypertension, peripheral vascular disease, hyperlipidemia, chronic renal disease, renal calculi, sciatica, and a recent cessation of tobacco smoking, with a 30 pack-year history. The patient was not being treated for any spinal condition other than noninvasive therapy for sciatica. The patient’s most recent hemoglobin A1c value was 9.0%.

Fig. 2. Non-weightbearing medial oblique right foot and ankle radiograph after right partial calcanectomy.

Five months before his presentation, the patient had developed a right heel, plantar ulceration secondary to a blister. Wound care treatment under the guidance of a local podiatrist included wetto-dry dressings with saline and ambulation in an athletic shoe. The frequency of visits and whether debridement was performed remained unknown. The ulceration progressed in size within 1.5 months to measure approximately 4.0 cm  3.0 cm  2.0 cm. The patient subsequently developed right lower extremity cellulitis and edema, and the calcaneus became visible within the ulceration. The patient was admitted to an outside hospital with a diagnosis of calcaneal osteomyelitis, and wound cultures revealed the presence of MRSA in the calcaneus. The patient was treated with 1.5 g of intravenous (IV) vancomycin every 12 hours for 4 days and was discharged with 1.0 g of intravenous cefepime for 4 weeks followed by a 10-day course of oral ciprofloxacin 500 mg every 12 hours. The patient was without antibiotics for 1 week subsequent to the aforementioned treatment, when he was admitted to an outside hospital because of a sudden onset of severe back pain, fever, and chills. A delay resulted in obtaining spinal MRI scans because the patient could not tolerate lying in a supine position secondary to his back pain. Both blood and a calcaneal wound swab culture at that admission revealed MRSA. The findings from transesophageal echocardiography and transthoracic echocardiography were negative for vegetations. The patient’s hospital course was complicated by Clostridium difficile, for which the patient was treated with oral 7.5 mg/kg metronidazole every 6 hours. The patient then underwent a partial calcanectomy and was given 6 mg/kg of IV daptomycin every 24 hours after the calcaneus revealed MRSA in the intraoperative bone specimen (Figs. 1 to 3). On the ninth day of admission, the patient was placed under general anesthesia to obtain spinal MRI scans. After the images had been read, the patient was transferred to the Cleveland Clinic for additional treatment (Figs. 4 and 5). On arrival, the patient was given 1.5 g of IV vancomycin every 12 hours and 3.375 g of IV piperacillin and tazobactam (ZosynÒ, Wyeth Pharmaceuticals, Inc., a Division of Pfizer, Inc., Philadelphia, PA) every 6 hours. The physical examination revealed spinal tenderness around the mid-thoracic level to the lower lumbar spine and superior anterior right thigh. The patient was unable to perform hip flexion on the right secondary to pain. Laboratory testing revealed a white blood cell count of 13.86 k/mL and an elevated blood glucose level of 380 mg/dL. The patient underwent spinal and right psoas abscess incision and drainage, followed by direct lumbar interbody fusion of lumbar vertebrae 4 and 5 with a right iliac crest allograft. The bone and abscess cultures were positive for MRSA. Postoperatively, the patient’s pain resolved in his back and hip, and he regained full right lower extremity function. Repeat vertebral MRI scans revealed complete resolution of the psoas abscess and stable epidural phlegmon dorsal

Fig. 3. Non-weightbearing lateral right foot radiograph after right partial calcanectomy.

N. Nicolosi, C. Pratt / The Journal of Foot & Ankle Surgery xxx (2014) 1–5


12 hours and at the last follow-up visit was continuing lifetime 100 mg of oral minocycline every 12 hours suppression therapy for MRSA. A 1-year follow-up examination was conducted, and the patient reported being fully functional with a walker and cane. He displayed no evidence of pedal ulceration and denied any interval hospitalizations. However, the patient was experiencing vertebral arthritis pain and was pursuing conservative therapy for the condition. Discussion It is reasonable to assume that the source of our patient’s lumbar spine osteomyelitis and psoas abscess was the calcaneal osteomyelitis. The calcaneal ulceration and osteomyelitis predated the patient’s back pain, and he had no history of a contiguous vertebral infectious source. The initial microbiologic isolate from the heel ulceration was the same as that of the second admission isolate cultured from the patient’s blood, calcaneal wound, vertebral bone, and abscess specimens (i.e., MSRA).

Fig. 4. T2-weighted sagittal lumbar magnetic resonance imaging scan at admission to the Cleveland Clinic. The increased signal intensity ventral to the L4 vertebra is suggestive of a prevertebral abscess. The increased signal intensity dorsal to vertebrae T12-S2 is suggestive of an epidural abscess. The increased signal in the L4 vertebral body is suggestive of vertebral osteomyelitis. The increased signal in the L4-L5 and L5-S1 intervertebral disc spaces is suggestive of discitis.

to the L4 vertebra, which measured 0.5 cm  0.7 cm  2.5 cm, and continued osteomyelitis of the L4 and L5 vertebrae (Figs. 6 and 7). The patient was given a 3-month course of 1.5 g of IV vancomycin every

Fig. 5. T1-weighted transverse lumbar magnetic resonance imaging scan at admission to the Cleveland Clinic hospital. The right psoas major muscle is enlarged compared with the contralateral side. The decreased signal intensity located within the right psoas major muscle is suggestive of an abscess.

Fig. 6. T2-weighted sagittal lumbar magnetic resonance imaging scan after intervention showing cortical disruption of the superior endplate of L5, indicative of a fracture.


N. Nicolosi, C. Pratt / The Journal of Foot & Ankle Surgery xxx (2014) 1–5

Fig. 7. T1-weighted transverse lumbar magnetic resonance imaging scan after intervention. Note the right psoas major muscle has decreased in size and is comparable in size to the left psoas major muscle.

Hematogenous osteomyelitis is the infectious spread from 1 osseous site to another through the bloodstream and is usually caused by a single organism (10). The incidence of calcaneal osteomyelitis seeding to the spine is unknown. The most common clinical presentation of vertebral osteomyelitis is back pain, cited to occur in approximately 86% of patients (11). It occurs most frequently in the lumbar vertebrae (58%), followed by the thoracic (30%) and the cervical spine (11%). Approximately one third of patients will present with neurologic symptoms, such as sensory deficits and weakness of the ipsilateral limb, and the presence of severe, sharp back pain suggests the presence of an epidural abscess (11). The diagnosis of vertebral osteomyelitis is made by positive bone cultures. However, Zimmerli (11), in his review of vertebral osteomyelitis, proposed that the clinical suspicion of vertebral osteomyelitis and 2 positive blood cultures corresponds to a “probable” diagnosis. He also noted that MRI with gadolinium was more sensitive than computed tomography for diagnosing spinal osteomyelitis (11). Finally, Zimmerli (11) advised that treatment include 6 weeks to 3 months of parenteral antibiotics followed by 3 to 6 months of oral therapy. Also, repeat MRI scans should be performed after treatment initiation if no clinical improvement has occurred by 4 weeks (11). S. aureus is the most common isolated pathogen in vertebral osteomyelitis, and this microbe has a plethora of virulence capabilities, including glycocalyx secretion, biofilm production, and antibiotic resistance (10). A biofilm is a “coherent cluster of bacterial cells imbedded in a matrix,” which provides a protective barrier against mechanical influences, reducing antibiotic and host defense penetrance. Also, the bacteria within a biofilm have a reduced metabolic rate that reduces their sensitivity to antibiotics by 1,000-fold (12). This enables the bacteria to resume their metabolic activity and develop resistance to the originally administered antibiotic (12). Because of biofilms, relapses of osteomyelitis have been described up to 80 years after the initial presentation (13). For these reasons, reliable treatment requires surgical removal of the area that possesses the biofilm (12). Biofilms are commonly found in necrotic bone, retained hardware, prosthetic joints, and chronic osteomyelitis (12,14).

The selection of an effective antibiotic is essential for successful treatment. MRSA is commonly treated with parenteral vancomycin; resistance to vancomycin is still quite rare and can be effectively treated with linezolid and daptomycin (10). b-Lactam antibiotics, such as penicillins, cephalosporins, and carbapenems, penetrate infected bone more than uninfected bone, although the penetration will be markedly decreased in patients with peripheral vascular disease and is likely low in osteomyelitis sequestra (10). Clindamycin displays excellent bone penetration, and rifampin has been shown to penetrate biofilms and kill inactive bacteria (10). However, because rifampin has a predisposition to resistance development, it should only be used in combination with another MRSA-active antibiotic, such as vancomycin, sulfa, or 1 of the fluoroquinolone antibiotics. The rationale behind the use of a 3- to 4-week duration of parenteral antibiotic therapy has been based on the theory that it takes that long for the infected bone to vascularize (13). It has been suggested that no clinical studies are available to support the superiority of a 4- to 6-week course of antibiotic therapy in treating osteomyelitis (13,15). Spellberg and Lipsky (13) proposed that oral antibiotic therapy with highly bioavailable agents would be an acceptable alternative to parenteral therapy and suggested that the preference for parenteral therapy for chronic osteomyelitis has been based on custom rather than evidence. In their review of the published data, the success rates were similar for both oral and IV routes of antibiotic administration (13). They recommended fluoroquinolones or trimethoprim-sulfamethoxazole for 8 to 16 weeks combined with surgical debridement for osteomyelitis (13). However, for gram-positive cocci, they recommended the combination of trimethoprim-sulfamethoxazole and clindamycin, because fluoroquinolones are predisposed to the development of resistant bacteria (13). Many patients will eventually require debridement or amputation to completely eradicate the infection, particularly when bone has become infected. Surgical debridement should aim to remove all nonviable material, reduce the bacterial load, and achieve “clear” margins to prevent any nidus for recurrence. Insufficient debridement has been associated with a high incidence of infection recurrence (15–17). Atway et al (16) found residual osteomyelitis in 40.7% of their patients after clear margins, which were defined as no evidence of bacteria identified (Gram stain and culture) at the margin of the bone procured by surgery after amputation and irrigation. Kowalski et al (17) reported similar findings, with 35.14% (39 of 111) of their patients having residual osteomyelitis after obtaining clear margins. Simpson et al (18) showed that a margin greater than 5 mm resulted in 0% recurrence of osteomyelitis compared with marginal resections of less than 5 mm, which resulted in a 28% incidence of osteomyelitis recurrence. The Infectious Diseases Society of America guidelines for diabetic bone infections state that if no infected tissue remains after surgery, 2 to 5 days of antibiotics are required; however, if infected tissue remains present, more than 4 weeks of organism-specific antibiotics are recommended (19–20). For antibiotic delivery to effectively penetrate bone, the serum concentration must exceed the minimum inhibitory concentration of the organism (10). Thus, surgeons must remember that the local serum concentration of an antibiotic, or that which is available at the site of infection, can be limited by the amount of blood flow to the infected area. Therefore, the blood supply to the site of the infection should be assessed (e.g., peripheral vascular resistance testing, transcutaneous oxygen testing, arteriograms, and clinical assessments), and any vascular intervention that could be considered helpful should be undertaken. In conclusion, it is important to be aware of the many potential complications of diabetic foot ulcerations. As we learned first hand during the care of the present patient, a distant site, specifically the vertebral column and adjacent musculature, can be the site of

N. Nicolosi, C. Pratt / The Journal of Foot & Ankle Surgery xxx (2014) 1–5

We express our appreciation to Maja Babic, MD (Division of Infectious Diseases, Cleveland Clinic Foundation), for her expertise, insight, and guidance related to the care of our patient. References 1. Priest D, Peacock J. Hematogenous vertebral osteomyelitis due to Staphylococcus aureus in the adult: clinical features and therapeutic outcomes. South Med J 98:854–862, 2005. 2. Grammatico L, Baron S, Rusch E, Lepage B, Surer N, Desenclos JC, Besneir JM. Epidemiology of vertebral osteomyelitis (VO) in France: analysis of hospitaldischarge data 2002-2003. Epidemiol Infect 136:653–660, 2008. 3. Garner JP, Meiring PD, Ravi K, Gupta R. Psoas abscessdnot as rare as we think? Colorectal Dis 9:269–274, 2007. 4. Baker AS, Ojemann RG, Swartz MN, Richardson EP Jr. Spinal epidural abscess. N Engl J Med 293:463–468, 1975. € ckley T, Schu € tz T, Kirschner M, Potulski M, Hofmann G, Bu € hren V. Psoas ab5. Mu scess: the spine as a primary source of infection. Spine 28:E106–E113, 2003. 6. Sendi P, Bregenzer T, Zimmerli W. Spinal epidural abscess in clinical practise. Q J Med 101:1–12, 2008.



7. Cottle L, Riordan T. Infectious spondylodiscitis. J Infect 56:401–412, 2008. 8. Ceilley R. Foot ulceration and vertebral osteomyelitis with Corynebacterium haemolyticum. Arch Dermatol 113:646–647, 1977.  D, Lacigova  S, Zourek M, Gruberova  J, Haladova  I, Tomesova  J, Rusavy Z. 9. Cechurova Spondylodiscitis and epidural empyema as a complication of diabetic foot. Vnitr Lek 59:412–415, 2013. 10. Rao N, Ziran BH, Lipsky BA. Treating osteomyelitis: antibiotics and surgery. Plast Reconstr Surg 127(1 suppl):177–187S, 2011. 11. Zimmerli W. Vertebral osteomyelitis. N Engl J Med 362:1022–1029, 2010. 12. Walter G, Kemmerer M, Kappler C, Hoffmann R. Treatment algorithms for chronic osteomyelitis. Dtsch Arztebl Int 109:257–264, 2012. 13. Spellberg B, Lipsky BA. Systemic antibiotic therapy for chronic osteomyelitis in adults. Clin Infect Dis 54:393–407, 2012. pez R. Pneumococcal biofilms. Int Microbiol 12:77–85, 14. Moscoso M, Garcıa E, Lo 2009. 15. Haidar R, Der Boghossian A, Atiyeh B. Duration of post-surgical antibiotics in chronic osteomyelitis: empiric or evidence-based? Int J Infect Dis 14:752–758, 2010. 16. Atway S, Nerone VS, Springer KD, Woodruff DM. Rate of residual osteomyelitis after partial foot amputation in diabetic patients: a standardized method for evaluating bone margins with intraoperative culture. J Foot Ankle Surg 51:749– 752, 2012. 17. Kowalski TJ, Matsuda M, Sorenson MD, Gundrum JD, Agger WA. The effect of residual osteomyelitis at the resection margin in patients with surgically treated diabetic foot infection. J Foot Ankle Surg 50:171–175, 2011. 18. Simpson AH, Deakin M, Latham JM. Chronic osteomyelitis: the effect of the extent of surgical resection on free survival. J Bone Joint Surg Br 83B:403–407, 2001. 19. Lipsky BA, Berendt AR, Cornia PB, Pile JC, Peters EJ, Armstrong DG, Deery HG, Embil JM, Joseph WS, Karchmer AW, Pinzur MS, Senneville E; Infectious Diseases Society of America. 2012 Infectious Diseases Society of America Clinical Practice Guidelines for the diagnosis and treatment of diabetic foot infections. Clin Infect Dis 54:132–173, 2012. 20. Jeffcoate WJ, Lipsky BA. Controversies in diagnosing and treatment of diabetic foot infections. Clin Infect Dis 39:885–910, 2004. ˇ

infection seeding from the calcaneus. The present case has also demonstrated the virulence of MRSA in a diabetic patient who had only recently discontinued cigarette smoking. The combination of adequate surgical debridement and IV antibiotic therapy seemed to have resolved the infection in the present patient, although ongoing clinical surveillance remains in effect.


Infectious Spondylodiscitis, Epidural Phlegmon, and Psoas Abscess Complicating Diabetic Foot Infection: A Case Report.

Few published case reports have cited vertebral osteomyelitis as a sequela of a diabetic foot infection. The purpose of the present report is to incre...
1MB Sizes 3 Downloads 19 Views