Article review:   Bhavan KP, Marschall J, Olsen MA, et al:  The Epidemiology of hematogenous vertebral osteomyelitis: a cohort study in a tertiary care hospital.  BMC Infectious Diseases, 2010: 10: 158doi: 10.1186/1471-2334-10-158  (Published 7-7-2010).

Dr. Cierny’s comments:  this article describes the epidemiology and early management of hematogenous vertebral osteomyelitis (anatomic types I and IV) in 70 patients over a 2-year period at Barnes Hospital in Missouri (a retrospective, cohort review).  A microbiological diagnosis was made in only two-thirds the cases.  S. aureus was the most common causative organism.

Results – The mean age was 59.7 years with 54% male. Predisposing factors included: B-hosts with diabetes (43%) or renal insufficiency (24%); in the 30 days prior to admission, an indwelling catheter (30%), bacteremia (19%) or skin/soft tissue infection (17%).  Back pain was the most common symptom (87%), followed by weakness (56%) and fever (46%); seven patients presented with paraplegia.  48% had a normal WBC but 95-98% had either an elevated ESR or CRP. 

The lumbar spine was the most common anatomic location (47%): thoracic (29%); cervical (24%).  Among the 46 (66%) patients with a microbiological diagnosis, the most common organisms were MSSA (33%) and MRSA (22%).  Among the 44 (63%) patients who had a diagnostic biopsy, open biopsy was more likely to result in pathogen recovery [14 (93%) of 15 with open biopsy vs. 14 (48%) of 29 with needle biopsy; p=0.003].   Surgery was required during the initial hospitalization in 23% of patients: decompression laminectomy 14%), laminectomy /fusion (7%) and corporectomy (1%).  Treatment outcomes were not included.  

The article:  What is Osteomyelomyelitis? What Causes Osteomyelitis?” in Medical News Today: 10 Feb 2010-0:00PST

Dr. Cierny comments:

TYPES OF OSTEOMYELITIS: ‘Acute’,’ sub-acute’ and ‘chronic’ are time-related terms that parallel the fundamental principles and mechanisms  inherent to wound colonization by microorganisms.  Early in the course of infection, microorganisms are mobile (plankonic) and vulnerable to antibiotics and host defenses.   If the fracture is live and stable, the infection may resolve following adequate wound decompression, antimicrobials and the elimination of dead space (the acute wound).  After 2-3 weeks,  reactions between surface macromolecules begin forming at pathogen-substrate interfaces (sub-acute), resulting in a resilient “microzone’ of attachment in 4-6weeks that is precursor to a microbial-based, mucopolysaccharide “slime” that encompasses the entire colony.   Within the bio-slime (biofilm) microbial nutrition and growth are enhanced, protected from host defenses and the penetration /effects of antimicrobials.  The result is a profound compromise to the host: wound healing and fracture repair are impaired due to toxins produced by the pathogens and the by-products of host efforts to unsuccessfully destroy the biofilm colony. Curative treatment of such a biofilm-infection (chronic /refractory) requires both anti-microbial therapy and surgical removal of the entire biofilm burden.

WHAT ARE THE SIGNS AND SYMPTOMS OF OSTEOMYELITIS? See: http://www.osteomyelitis.com/html/osteomyelitis.html

WHAT ARE THE RISK FACTORS FOR OSTEOMYELITIS? Open fractures create “the perfect storm” for infection to complicate injury:  the initial wound is contaminated and injury to soft tissues potentiates an on going exposure to pathogens; surgical implants and dead bone fragments grant ‘safe-haven’ to proliferating microbes; ischemia, dead space and foreign bodies impede local immunity and the delivery of antibiotics; shock, injury and pre-existing health conditions compromise the host response.   The goals of treatment are three-fold: timely intervention; creation/maintenance of a clean, manageable wound; adequate and durable fracture fixation.

Surgical Site Infections (infection following elective surgery) are more common in compromised hosts,( ), long procedures (SSI) and operations where in a large surgical implant is used (substrat surfaces; see above).  OSTEOMYELITIS: CIERNY/MADER HOST STATUS  OSTEOMYELITIS: CIERNY/MADER CLASSIFICATION SYSTEM 

DIAGNOSIS OF OSTEOMYELITIS:   MALNUTRITION;   WHAT BLOOD TESTS ARE USED TO DIAGNOSE OSTEOMYELITIS?    DO POSITIVE CULTURES ALWAYS MEAN A BONE INFECTION IS PRESENT?   WHEN DO I NEED A NUCLEAR SCAN?

TYPES OF BONE INFECTIONS:   There are really only three etiologic categories of bone infection, not five:  hematogenous (blood-born) osteomyelitis;  contiguous-focus osteomyelitis;  and post-traumatic osteomyelitis.  Osteomyelitis due to vascular insufficiency is a form of contiguous focus infection since the lack of oxygen leads to breakdown of the integument (skin), ulceration and eventual exposure ( and contamination) of the underlying bone (a contiguous focus).  Ischemic compromise can  occur in patients with peripheral vascular disease, disruption of major bood vessels, diabetes (foot ulcers) and patients developing bed (decubitus) ulcers.

The categorization of bone infection into etiologic types,  however, does not help with establishing a treatment strategy or prognosis.  To do this, the chronology (see above), patient’s health and anatomic localization of the infection (in the bone itself) must be brought together into a staging system similar to those used for various forms of cancer.    For example, vertebral osteomyelitis is a regional localization of infection (the spine) as opposed to an anatomic localization (configuration) of the disease in the spinal bone (s) itself.  Spine infections occur following: blood-born contamination (hematogenous) to the marrow part of the bone or to the disc between the vertebral bodies;  as a contiguous focus infection (sacral decubitus ulcers); or following trauma (ie; post-operative, surgical site infections ).   Treatment will depend on the etiology, the timing (acute, subacute, chronic) and the extent to which the infection involves the bone (on the surface, in the marrow, fracture with instability, etc.).  That is why the CIERNY/MADER Clinical Staging System (1985)  is now accepted internationally as the gold standard for classifying bone infection in adults (all types, all etiologies, all locations) as it articulates the natural history of the disease with treatment and outcomes.

The A-Host and B-Host differentiation:  In the Cierny/Mader classification system for adult osteomyelitis, the host status was added to the anatomic type of infection to articulate the biology of the disease to its treatment (see illustration)  This likens our conceptualization of infection to that of the oncologist treating musculoskeletal tumors: treatment and therapeutic outcomes are scaled to grade (biologic activity): A-hosts /low grade tumors need conservative margins and have high success rates; B-hosts /high grade cancers call for radical/wide margins and have lower success rates despite more aggressive treatment.  The difference between the two disease states (tumor vs infection) is that the genetic makeup of the tumor cell, itself, determines tumor grade (low vs high) whereas, in chronic osteomyelitis, it is the capacity of the host immune and defense systems (grade of response) that determines outcomes. Yes, there are deadly, resistant and docile bacteria but, even here, treatment and outcomes will, again, be determined more or less determined by the capacity of the host (A vs B). 

The biologic grade of the disease can be used to: 1) guide patient selection(table 1; page 4);  2) scrutinize treatment options (article);  3) bring objectivity to with holding treatment either because the patient can function safely with their disease or because treatment, if undertaken, will cause more danger/stress to the patient than no treatment, at all.  In the staging system, this later scenario defines the  C-Host.  A healthy or compromised patient can opt out of treatment to be classified a C-host  but revert to an A-host or a B-host status when and if they later become a surgical candidate.  

The Clinical Staging system is about the disease, not the healthcare provider, the type of implant, the pathogen or the antibiotic.   Yes, there are bad implants, toxic drugs /bugs and inexperienced surgeons ………..but, these, too, are circumstances for which the Staging System was designed to differentiate rather than categorize.   In this context, providers, pathogens and post-surgical risks are numerators, not denominators.

Comment:  if you now look at our recent outcomes, the discrepancies between A- and B-hosts are shrinking with each year that passes.  Why? Because we no longer offer these two cohorts the same treatment —- instead, each treatment is individualized —-  options are matched to the physiologic capacity of the host.

I agree there are degrees of compromise just as there are differences in the sweetness of grapes.   But, over the years,  I have stopped trying to sort “bad” factors from the “not so bad”.  To me, anything less than normal is a compromise worthy of an effort to counter or negate its affect(s) on wound healing ———– I know that a reversed compromise will improve outcomes (somewhere, sometime).   GC 11/19/09