Letter to the Editor: Was osteomyelitis the culprit?

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Regarding Vair A, Keast D, LeMesurier A. The prevalence of anemia of chronic disease in patients with spinal cord injuries and pressure ulcers and the impact of erythropoietin supplementation on wound healing: a descriptive pilot study. Ostomy Wound Manage. 2015;61(6):16-26: Although the intervention mentioned seems to have great potential to provide improved outcomes for this population, certain information appears to have been omitted.

The hematological picture provided in this article screams of underlying chronic     osteomyelitis that must be addressed to achieve and maintain wound closure. In my practice, an MRI or gallium scan to rule out sequestra and surgical revision of sequestra is pivotal to treating this group. C-reactive protein (CRP) levels, albumin, and red cell distribution width will not return to pretreatment levels unless sequestra is removed; wound closure will not be achieved or maintained. Sequestra provide a nidus for bacteria and ongoing inflammation, sinus tract formation, and wound recurrence.

Although I cannot submit research as well structured as the authors’, I can tell you with a rare exception these patients will have sequestra in situ. Often recurrence or flap failure is blamed on poor offloading, inadequate surfaces, or poor nutrition (to name a few), but in my opinion the culprit is chronic osteomyelitis. Because bone is highly metabolic, it succumbs to pressure injury when nutrient channels are interrupted by pressure. Just as we would not expect a wound to close with necrotic soft tissue in situ, we should not expect to close a pressure injury with necrotic bone in situ.

Brenda Beath, RN, BScN, GNC(C), CHPCN(C), ETN



Osteomyelitis is an important complication of chronic pressure ulcers in spinal cord-injured persons; prevalence has been estimated at up to 30%. Unfortunately, there is no simple, noninvasive way to diagnose osteomyelitis. Diagnosis is confounded by overlying soft tissue inflammation and reactive bone formation. Even needle biopsies may be contaminated by bacteria in the adjacent soft tissues. A negative bone scan rules out osteomyelitis, but a positive scan is not diagnostic. Melkun et al1 compared labeled white cell scans with surgical ostectomy specimens from 11 patients who underwent surgical reconstruction. The sensitivity and specificity were 100% and 50%, respectively. Darouiche et al2 found 6 of 36 (17%) spinal cord-injured patients with pressure ulcers had osteomyelitis diagnosed by pathologic examination of bone; quantitative bone cultures were unable to distinguish osteomyelitis from infection of adjacent soft tissues. The combination of white blood cell count, erythrocyte sedimentation rate, and plain X-ray has demonstrated 89% sensitivity and 88% specificity.3 An MRI may be useful in showing bone necrosis. Lopez de Heredia et al4 demonstrated cortical bone erosion and abnormal marrow edema most strongly correlated with osteomyelitis on MRI imaging. Ruan et al5 conducted a retrospective analysis of 12 patients who had MRI examinations prior to (7) or after reconstructive surgery (5). Three (3) patients had osteomyelitis (25%). The authors found patients who had poor healing or recurrent breakdown tended to have concurrent issues such as poor self-care, increased age, increased time since spinal cord injury, poor nutrition, and other comorbid conditions.

Appropriate debridement and surgical technique plus a short course of antibiotics can successfully treat chronic osteomyelitis associated with pressure ulcers. Marriott and Rubayi6 performed a retrospective analysis of 157 people with pressure ulcers. Participants were divided into groups according to pathologic diagnosis: acute osteomyelitis, chronic osteomyelitis, and negative osteomyelitis. Shallow bone shavings were taken for histologic diagnosis and deep shavings were taken for microbiologic analysis. After debridement, ulcers were closed with muscle or musculocutaneous flaps. People with negative or chronic osteomyelitis received a 5- to 7-day course of intravenous antibiotics. People with acute osteomyelitis received 4 to 6 weeks of antibiotic therapy according to bone culture and sensitivity results. Postoperative length of stay, wound breakdown, and pressure ulcer recurrence did not differ between the groups.

Ms. Beath is concerned the laboratory data presented strongly suggest the presence of osteomyelitis. A thorough search of the literature was unable to find any reported associations between low serum prealbumin, low hemoglobins, low absolute lymphocyte counts, iron studies, creatinine, and electrolytes and osteomyelitis. The CRP was elevated, but this is a marker of inflammation that does not pinpoint the source of the inflammation. Considerations in addition to osteomyelitis may include osteoarthritis and bladder and soft tissue infections. In our experience, all spinal cord-injured patients with pressure ulcers have elevated CRP levels, making this an unreliable diagnostic indicator of osteomyelitis. The low creatinine is consistent with the reduced muscle mass in spinal cord-injured patients, and the low prealbumin and absolute lymphocyte counts point to the poor nutritional status of community-dwelling spinal cord-injured patients with pressure ulcers.

The full differential associated with the complete blood count was not reported due to limitations of space. Leukocyte counts ranged between 4.3 and 13.1 (mean 8.7); the value 13.1 was related to an intercurrent bladder infection. The white cell differential was normal. Consistently normal white cell counts make a diagnosis of osteomyelitis less likely.

Ms. Beath also seems to suggest improper pressure offloading, poor seating, poor support surfaces, poor transfers, and poor nutrition are not important factors in pressure ulcer recurrence or flap failure. This is not borne out by the weight of the literature. The Canadian Best Practice Guidelines (2013) (available at: www.onf.org) provide a recent and thorough review of the literature.

I encourage Ms. Beath to conduct a retrospective review of all her cases over a stated timeframe and submit them for publication. Clinical experience is a very important source of new evidence to inform practice. [Editor’s note: We concur!]

David H. Keast BSc, MSc, DipEd, MD, CCFP, FCFP


1.         Melkun ET, Lewis VL Jr. Evaluation of (111) indium-labeled autologous leukocyte scintigraphy for the diagnosis of chronic osteomyelitis in patients with grade IV pressure ulcers, as compared with a standard diagnostic protocol. Ann Plast Surg. 2005;54(6):633–636.

2.         Darouche RO. Landon GC, Klima M, Musher DM, Markowski J. Osteomyelitis associated with pressure ulcers. Arch Intern Med. 1994;11;154(7):753–758.

3.         Houghton PE, Campbell KC, and CPG Panel. Canadian Best Practice Guidelines for the Prevention and Management of Pressure Ulcers in People with Spinal Cord Injury: A Resource Handbook for Clinicians. Available at: www.onf.org. August 15, 2015.

4.         Lopez de Heredia L, Hauptfleisch J, Hughes R, Graham A, Meagher TMM. Magnetic resonance imaging of pressure sores in spinal cord injured patients: accuracy in predicting osteomyelitis. Top Spinal Cord Inf Rehabil. 2012;18(2):146–148.

5.         Ruan CM, Escobedo E, Harrison S, Goldstein B. Magnetic resonance imaging of non-healing pressure ulcers and myocutaneous flaps.  Arch Phys Med Rehabil. 1998;79(9):1080–1088.

6.         Marriott R, Rubayi S. Successful truncated osteomyelitis treatment for chronic osteomyelitis secondary to pressure ulcers in spinal cord injury patients. Ann Plast Surg. 2008;61(4):425–429.


In A Clinical Minute in the August 2015 issue of Ostomy Wound Management, the author’s affiliation was misstated. The author’s affiliation should read, Multidisciplinary Diabetic Foot and Wound Center, Baltimore, MD. The Editors apologize for any confusion.


The opinions contained herein are exclusively those of the authors and may not represent the opinions of their affiliations. This article was not subject to the Ostomy Wound Management peer-review process.