April 22, 2010

Eric Wickre’s Hoka Hey Motorcycle Challenge

Meet Eric Wickre (the original, Alaskan Viking Cowboy), treated at our center December 2008 for Stage IA osteomyelitis of his left tibia, a con-sequence of an open fracture suffered in 1981.   His (and others’) entire medical case portfolio will be posted  at http://www.osteomyelitis.com/html/news.html#featured-case .  After successful treatment at our treatment center in  San Diego, Eric is now back to his rough-and-ready cowboy ways, having just been selected to be one of 1000 motorcyclists from around the globe to compete in The Hoka Hey Motorcycle Challenge —– also known as the “Iditarod of Harley Davidson, 2010”.

 CLICK TO ENLARGE

CLICK TO ENLARGE

The Challenge is a grueling, 7,000 mile race from Key West, FL to the Kenai Peninsula, Alaska where “winner takes all” …one half million dollarsin Alaskan gold!  It starts June 20th and ends in Homer, AK on July 4th.  The secret route will initially head 1,000 miles into Mississippi. There, riders will get a map for the next leg of the ride: traveling the back roads, highways and byways; enduring hail storms, heat waves and scorpions; sleeping along side their bikes every night for the entire journey.

Join us as we follow Eric’s epic journey through the Americas on  OSTEOMYELITIS  BLOG.                                           Good luck, Eric!!

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 24, 2010

PREVENTING OSTEOMYELITIS AFTER OPEN FRACTURE: G. Cierny, MD; part III.

Posted under: ANTIBIOTIC DEPOTS, OPEN FRACTURES, PUBLICATIONS, Surgical site Infections— George Cierny @ 8:47 pm

Article:

EARLIER DEBRIDEMENT AND ANTIBIOTIC ADMINISTRATION DECREASE INFECTION:   Maj. Brown KV, Walker JA, Cortz DS et al.  J. Surg. Ortho.p Advances, 2010;  Vol 19(1): 18-22.    Goals: ascertain the effects of 1) earlier debridement (debridement alone or in combination with locally delivered antibiotics) and 2) the use of local antibiotic-depots on bacterial load following contamination of open fractures.  A contaminated, critical sized, rat femur, defect model was used.  Results: early debridement and early administration of local antibiotics resulted in lower bacterial loads in bone.  There was a significant increase in the rate of infection between 2 and 6 hours and a further increase between 6 and 24 hours when treatment was limited to debridement (alone) as well as when debridement was combined with local antibiotics.  Treatment with local antibiotics resulted in a significant reduction in infection at 2 and 6 h hours compared to debridement, alone.          

Dr. Cierny’S  comments:  Surgical antibiotic prophylaxis refers to the administration of antibiotics to patients without clinical evidence of infection in the operative field.  The objectives of prophylaxis are to prevent naturally occurring organisms in one site from proliferation in a normally sterile site; to prevent organisms contaminating a normally sterile site from producing diseases; and to prevent infection by exogenous organism.  In order to achieve this goal, the surgeon must recognize the high-risk patient, operate in an effective and efficient manner, and keep abreast of local hospital flora and sensitivity patterns.  Antibiotic prophylaxis is indicated in the surgical patient when there is an unacceptable incidence of infection or when the incidence of infection is low but such an infection would be devastating or lethal.  Prophylaxis accounts for approximately 30% of the antibiotic administration on surgical services in the United States.  In most instances, these antibiotics are not justified and may lead to multiple problems, including the selection of resistant organisms.  However, when the theory and practice of surgical antibiotic prophylaxis are correctly applied, the patient benefits.

            The pathogenesis of a surgical wound infection lends itself to a rational approach to surgical antibiotic prophylaxis.  The first step is bacterial contamination of surgically manipulated tissue.  Bacterial contamination, a component of every surgical wound, arises from two sources: exogenous contamination from the operative theater; or endogenous contamination from the skin, respiratory, or urogenital tracts of the patient.  Whether or not the bacterial contamination produces infection depends on the number and the virulence of the organisms, the adequacy of the patient’s defenses, and the condition of the disrupted (injured) tissue.

The first response to surgical injury and subsequent bacterial contamination is local inflammation.  Small vessels leak plasma, and leukocytes emerge in response to local leukotactic substances, migrate into the contaminated area, and begin phagocytosis.  Inflammation continues, wound induration develops, local macrophages and vascular components proliferate, and the stage is set for wound maturation.  The early local inflammatory phase is virtually identical to what is called the “decisive period” as defined by Burke (see below).  If inflammation is not appropriate and phagocytosis is overwhelmed, the patient will develop an infection.  Necrosis, ischemia, hemorrhage, and the presence of debris and/or foreign bodies impair the local host-defense mechanisms and decrease the number of bacterial organisms required to cure infection. The overall integrity of the host is important because a compromised host is at increased risk for infection. 

If an appropriate antimicrobial agent is present in adequate concentrations, a wound infection in the contaminated tissue is less likely.  The antibiotics must be in the tissues during the early, “decisive period” to effectively present bacterial invasion and proliferation.  If given later, when the bacteria are well established, the antibiotics will have no prophylactic effect.  Similarly, if the compromised host can be protected with prophylactic antibiotics until the local defense mechanisms are capable of eradication local bacterial invasion, the subsequent stages of wound healing can proceed normally.

The concept of a “decisive period” was first recognized when Burke (1961) administered an anti-Staphylococcal antibiotic one to three hours after inoculation of S. aureus into the dermis of a guinea pig model …. early antibiotic administration would reduce the size of the lesion.  However, if the anti-Staphylococcal antibiotic was given three hours after dermal infection, the antibiotic was less effective in reducing the size of the lesion.  Clinical studies have subsequently demonstrated, conclusively,  that antibiotic administered one hour before the surgery significantly decreases the incidence of postoperative infection when compared to placebo.  However, if the antibiotic is begun one to four hours after the operation, there is no reduction in the postoperative infection rate.

The correlation between the frequency of infection and the density of microorganisms present in a homogenized sample taken from the wound closure site has been established. Since it is not immediately possible to determine the microbial density of every surgical wound, a system for categorizing a surgical wound based on the probability and degree of microbiologic contamination has been developed.  The accuracy with which this clinical classification predicts the incidence of wound infection for general and orthopaedic surgery is well established.

Clean surgical procedures account for 75% of all operations.  These procedures are performed under ideal and sterile operating room conditions.  The procedures are generally elective and no entry is made into the oropharyngeal cavity or the lumen of the respiratory, alimentary, or genitourinary tract.  Inflammation is not encountered and no break in surgical technique occurs.  The incidence of wound infection in clean procures is less than 5%.

Clean-contaminated surgical procedures involve entry into the oropharyngeal cavity or the lumen of the respiratory, alimentary, or genitourinary tract without significant contamination from these sites.  Clean wounds are included in this category when there is a major break in the surgical technique. Clean- contaminated surgical procures occur in approximately 15% of all surgical operations and wound infection is reported in approximately 10% of these cases.  Since the mucosa of the oropharyngeal , respiratory, alimentary and genitourinary tracts harbor diffuse and dense microbiologic flora, some contamination of the wound is e inevitable.  Antibiotic prophylaxis is indicated in these patients and should be appropriately tailored to the flora expected in the particular region of surgery.  Clean surgery on a compromised host ( ) or transoral fixation of lesions involving the first and second cervical vertebra are examples of clean-contaminated procedures.

Contaminated-dirty surgery includes surgery through traumatic wounds, operative procedures with a major break in sterile technique and operations into a site of active infection.  The infection rate is between 20% and 40% in surgery involving these patients.  Antibiotic “prophylaxis”, in these circumstances, is directed at the prevention of infection in the soft-tissue planes and wounds previously uncontaminated by bacteria.  As such, the antibiotic(s) used  may be modified by the preoperative Gram stain or culture results stemming from biopsies of exposed granulating surfaces and/or wounds, themselves.  Surgery of open fractures is an example of contaminated-dirty surgery.  The risk of subsequent infection increases with the amount of tissue devitalization, the extent of contamination and the systemic compromise of the host. 

Final comment:  There are few controlled trials to scientifically support a practice mandating emergency-debridement of all open fractures  (< 6hrs). However, it is in agreement that 1) all open fractures require immediate, systemic antibiotic coverage and 2) that additional coverage with a local antibiotic-depot (antibiotic beads ) will reduce the incidence even further when treating  severe open injuries (Seligson D, Henry SL) when used in conjunction with systemic coverage.   BEST PRACTICE:  all methods of treatment should impact outcomes within the  “decisive period”:  immediate antibiotic coverage; host resuscitation; the earliest possible debridement; avoidance of large surgical implants; adequate (and safe) methods of stabilization; soft-tissue coverage within 7 days of injury –  Primary_versus_Delayed_Soft_Tissue_Coverage_for.8 .

February 20, 2010

PREVENTION OF ACUTE AND CHRONIC OSTEOMYELITIS USING WOUND VAC (NPWT) PROTOCOLS: George Cierny, MD

Review Article:  Warner M et al; Comparison of Vacuum-assisted Closure to the Antibiotic Bead Pouch for the Treatment of Blast Injury of the Extremity. ORTHOPEDICS, 2010; 33: pp77-87.

A retrospective study of 24 patients suffering blast injuries to the lower extremities.  Prior to closure, half were initially treated with VAC (vacuum assisted closure) and half with an antibiotic bead pouch. The same surgeons performed all surgeries. Findings: VAC-therapies produced more late Methicillin-resistant Staphylococcus aureus (MRSA) infections (30% vs 0%), more unanticipated returns to the operating room (4:12 vs 0:12), required more surgeries to affect closure (at ~12days vs ~8days)and cost ~$1,000 more /patient once a $23,000 investment was made to purchase a single, VAC machine (KCI; SanAntonio, TX).

 Dr. Cierny comments: Although several studies have suggested that VAC will decrease the need for free tissue transfer in like/like wounds following trauma1,2, others found no significant difference in time to closure3, an increase the amount of S aureus in the wound bed,4 a statistically significant increase in colony count during use,5 and infection /nonunion rates similar to historical controls (suggesting no benefit to the use of VAC over conventional dressings.6   Hallock7 contended that VAC does not prolong the time allowed for successful definitive wound closure and Stewart and Keating8 found VAC not as good as early soft tissue coverage (for acute wounds).  Although Morris9 found weak evidence to suggest that negative pressure therapy is superior to saline dressings when healing chronic wounds, Stannard et al10 , in a prospective, randomized study of 62 open fractures, found patients treated with NPWT one-fifth as likely to develop an infection compared with patients randomized to controls treated with wet-to-dry dressings until closure.

The consensus:  NPWT is more comfortable /convenient for the patient and healthcare team, effectively decompressing (displacing)  the inevitable need (energy) for complex and sequential reconstructions.  Despite its controversies, the use of external fixation and NPWT in the treatment of blast injuries and gunshot wounds resulting in open fractures with severe soft tissue injuries has become the mainstay of damage control orthopaedics.    In our experience, however,  15%-20% of patients with refractory infections following long-term  NPWT protocols have had retained sponge-fragments (gossypiboma) discovered in their wounds at the time of debridement and all of these fragements grew ‘culture positive’ for the primary, wound pathogen(s).   For us, NPWT is extremely helpful in managing acute /peri-operative wounds.   However, we find it of limited value in the chronic-wound scenario unless the wound has first been rendered 100% live and is no longer in need of any further reconstruction (ie; bone grafts, tendon repairs, etc.).   GC  02/20/10 .

Bibliography (1-10): -1- Herscovici D Jr, Sanders RW, Scaduto JM, Infante A, DiPasquale T. Vacuum-assisted wound closure (VAC therapy) for the management of patients with high-energy soft tissue injuries. J Orthop Trauma. 2003; 17(10):683-688. -2- Dedmond BT, Kortesis B, Punger K, et al. Sub-atmospheric pressure dressings in the temporary treatment of soft tissue injuries associated with type III open tibial shaft fractures in children. J Pediatr Orthop. 2006; 26(6):728-732. -3- Song DH, Wu LC, Lohman RF, Gottleib LJ, Franczyk MPT. Vacuum assisted closure for the treatment of sternal wounds: the bridge between débridement and definitive closure. Plast Reconstr Surg. 2003; 111(1):92-97. -4- Mouës CM, van den Bemd GJ, Heule F, Hovius SE. Comparing conventional gauze therapy to vacuum-assisted closure wound therapy: a prospective randomized trial. J Plast Reconstr Aesthet Surg. 2007; 60(6):672-681. -5- Weed T, Ratliff C, Drake DB. Quantifying bacterial bioburden during negative pressure wound therapy: does the wound VAC enhance bacterial clearance? Ann Plast Surg. 2004; 52(3):276-279.  -6-Dedmond BT, Kortesis B, Punger K, et al. The use of negative-pressure wound therapy (NPWT) in the temporary treatment of soft-tissue injuries associated with high-energy open tibial shaft fractures. J Orthop Trauma. 2007; 21(1):11-17.  -7- Hallock GG. To VAC or not to VAC? Ann Plast Surg. 2007; 59(4):473-474. -8- Stewart KJ, Wilson Y, Keating JF. Suction dressings are no substitute for flap cover in acute open fractures. Br J Plast Surg. 2001; 54(7):652-653. -9- Morris GS, Brueilly KE, Hanzelka H. Negative pressure wound therapy achieved by vacuum-assisted closure: Evaluating the assumptions. Ostomy Wound Manage. 2007; 53(1):52-57. -10- Stannard JP, Wolgas DA, Stewart R, et al; Negative Pressure wound therapy after severe open fractures: a rospecive randomized study.  J. Orthop. Trauma, 2009; 23(8): 552-557.

 

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.

October 30, 2009

EARLY INFECTION FOLLOWING TRAUMA

INFECTED NON-UNION ,TIBIA:  George Cierny III, MD    REOrthopaedics, CA.

Dear Dr. Cierny,

I just wanted to let you know that I finally ran my marathon!  At age 49, getting back in shape was a struggle but, I ran and finished the Atlanta ING in 2007 clocking in a total of 26 miles. 

   Thank you so much for your hard work and perfectionist attitude.  My leg NEVER hurt me throughout my training.  It truly was a miracle.   Everyone who knew be during the early stages of my recovery from the accident was amazed I could walk, never mind run.  I’m so grateful my husband perused finding the best doctor for me and,  that some how, we found you. 

    I just wanted to let you know how much of an impact you make in the lives of your patients.  You cured my osteomyelitis and restored the lifestyle that I so need and enjoy.    I am truly grateful that you, Dr. Cierny, were my doctor.  To thank you does not begin to express my gratitude.         Sincerely and best wishes,    Joanne Marcone / Atlanta, GA

September 4, 2009

BONE INFECTION FOLLOWING OPEN FRACTURE

TREATMENT OF OSTEOMYELITS; RIGHT FEMUR

Thanks,Doc.                                                                                                                           After the accident, my life was shattered by the reality of how what you think is important can always be replaced by your need to survive.   It seemed foolish to reflect on “why me”, when what was important was really “what’s next?”    You treated my  infection and healed me,  in the process (Featured Case #4).   Because of what you were able to accomplish, “what’s next” now includes building  my world, not saving it.                                                                                                            I am now able to plan for the future without worrying when my next flare-up (infection) will show or how I might be an amputee before the year was out.   My original doctors told me I would never run again.  Others told me I would have to fight the infection (osteomyelitis)  forever.  My life was put on hold ……. until I met you.   In one visit, you told me what it would take to get rid of the infection and how we would do it (the treatment protocol).  Then, we put that plan into action.                                                                                                     Today, I am able to live my life without limitation, moving beyond the pain and the uncertain-ty, the surgeries and the medicated means of life I lived for so very long.   Please, never forget the good you do for all your patients by helping them become people again.  I know I never will.

In appreciation,  Steven C. Berry /Asheville, NC                                                           ————

August 26, 2009

TREATMENT OF BONE INFECTION FOLLOWING OPEN FRACTURE INJURIES

Posted under: OPEN FRACTURES, OSTEOMYELITIS TREATMENT, TREATMENT OF BONE INFECTION— George Cierny @ 3:02 pm

 

Bone Infection Following Treatment for Open Fracture Injuries

            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 (bacteria); surgical implants (plates, screws and rods) 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, crush-injury and pre-existing health conditions compromise the host response.    As a result, osteomyelitis (bone infection) and fracture non-union are the most common complications following treatment for open fractures.  Once a bone infection is diagnosed, the goals of treatment are three-fold:  timely intervention; creation and maintenance of a live, clean, manageable wound; adequate and durable fracture fixation.   

Strategies to Minimize Complications:

1) After treatment for an open fracture, follow patients closely: culture all wound drainage; serially check CBC, ESR and CRP values; manage wound-healing disturbances aggressively, especially in compromised hosts (B-hosts).  

2) Treat the bone infection as either an ‘early’ or a ‘late’ process, based on the time lapsed since index-contamination (early < 4weeks).   http://www.osteomyelitis.com/pdf/treatment_protocol.pdf

3) Base antimicrobial therapy on multiple tissue specimens and pathogen sensitivities and use bactericidal antibiotics whenever possible.

4) Reverse all amenable, host co-morbidities and optimize the host response throughout treatment. http://www.osteomyelitis.com/pdf/staging-paper.pdf

5)  Select ‘low-risk’ methods when treating ‘high-risk’ patients ( see  Cierny III, G., DiPasquale, D. Treatment of Chronic Infection. in the Symposium: Extremity War Injuries: state of the art and future directions. JAAOS , Vol 14, No. 10, 105-110, October 2006. 

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