April 22, 2010

BONE INFECTION: treatment(types of surgery)

George Cierny, MD; REOrthopaedics in San Diego

In acute pediatric osteomyelitis  and osteomyelitis of the spine (verbetral osteomyelitis; sacroiliitis) in all ages,  surgery is not always necessary to affect cure.  In other forms of acute osteomyelitis  (infection following open fracture; surgical site infections following trauma or reconstructive surgery) and nearly all forms of the chronic disease, treatment will have to combine various aspects of surgery (with antibiotics) to result in cure .
The treatment of a refractory (chronic) osteomyelitis is governed by its pathophysiolgy —– it is a ‘biofilm disease’.    Unlike the mobile (planktonic), environmentally sensitive microbes found in an acute infection, chronic wound pathogens are sessile and resilient, transformed into colony-forming units by environmental triggers (quorum-sensing) and the successful attachment to ‘unprotected’ surfaces within the wound (inert materials; non-viable tissues or organisms, etc.).    Thereafter, individual cells become colony-forming units that mature (2-4 weeks) to secrete and maintain a mucopolysaccharide “slime” that protects them from host defenses and the penetration of most antimicrobial agents .   To cure this biofilm infection, a LIVE, CLEAN WOUND is paramount: the biofilm-colony its attachment surfaces must be completely excised.

The type of surgery will depend on the duration of the infection (acute or chronic), the contents of the wound (extent of necrosis; substrate surfaces), the anatomic site, the health and well-being (impairment) of the host, and the experience of the healthcare team.

However, surgery, as a form of treatment, is not available to everyone. Patients who are very ill may not be able to endure the extensive surgery and recovery. In these cases, doctors may use antibiotics for long periods in an attempt to suppress (rather than cure) the infection.  Then, if the infection persists and, again, threatens the patient’s well-being, lesser morbid procedures, such as amputation of all or part of an infected limb, may be necessary.  

Surgical treatment options  – Drain the infected area: Opening up the area around the infected bone allows the surgeon to drain any pus or fluid that has accumulated in response to the infection.  This is usually applied in the acute setting to decrease strain on host defenses and amplify the effects of antibiotics.  Remove the attached, biofilm-colony:  In a procedure called debridement, the surgeon removes the diseased bone and tissue. In some cases, foreign objects, such as surgical plates or screws, used in previous surgeries, may also be removed. Restore the bone and soft-tissue envelope: Your surgeon may fill any empty space left by the debridement procedure with a piece of bone or other tissue, such as skin or muscle, from another part of your body. Sometimes temporary fillers containing antibiotics (antibiotic depots) are placed in the space until the infection is cured and the patient is healthy enough to undergo a definitive reconstruction. Bone grafts and tissue flaps help the body recruit new blood vessels into the site and form new bone.  Protect against instability: Immediately following debridement, the surgeon may use an external fixatation device (external fixator) to hold and protect the bone from further injury.  This method limits the amount of implanted, foreign material (metal) in the still-contaminated wound by attaching thin wires or pins (that pass through the limb) to a frame positioned around the limb (outside the skin).  The fixator can be the only method used throughout treatment or, after a course of local antibiotic therapy, replaced with internal methods of fixation such as metal plates, rods or screws.

February 16, 2010

WHAT IS and WHAT CAUSES OSTEOMYELITIS? Dr. Cierny comments on the recent article in Medical News Today: 10 Feb 2010-0:00PST

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.

February 7, 2010

INFECTION FOLLOWING OPEN FRACTURE: G. Cierny III, MD

Fx Mono  Fx Mono Chpt 

Contents: 1) Management of Bone Loss; 2) Common Decision-Making Errors in Limb Salvage; 3) Chrnic Neuropathic Pain Following Open Fractures; 4) Management of Soft-Tissue Loss After Trauma; 5) Malunions and Nonunions in the Lower Exdtremity; 7) Infection Following Open FractureGeorge Cierny III, MD  pp71- 87.  In Complications in Orthopaedics: Open Fractures; Levin, L.S. (ed).   AAOS monograph Series; Amer. Acad. Orthop Surg, Rosemont, IL, 2010.  Here, Dr. Cierny presents his classification systems and treatment algorithms which are among  the principal advances in the management of infection following open fractures – osteomyelitis with micro-necrosis; osteomyelitis with macro-necrosis; fixation strategies; chronic_infection; staged treatment options.

November 21, 2009

OSTEOMYELITIS: PATIENT SELECTION

Posted under: Clinical Staging / Classification, Treatment Outcomes— George Cierny @ 10:49 am

Patient Selection: The treatment of adult, chronic osteomyelitis is directed by the careful consideration of anatomic, physiologic and socioeconomic parameters: the site and extent of involvement, the degree of functional impairment caused by disease, the condition of the host, physician experience and institutional resources.         ( CLICK ON IMAGE TO ENLARGE )

  CLICK ON IMAGE TO ENLARGEThe complex interplay of these factors will  determine treatment to be palliative or curative, simple or complex, limb-sparing or ablative.

November 20, 2009

OSTEOMYELITIS: CIERNY/MADER HOST STATUS

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 host rxntreatment (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

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