Infection

Multiple steps are involved in reducing the risk of postoperative infection. All of these are important for avoiding infection after fracture surgery.

• Aseptic technique
• Perioperative antibiotics
• Soft-tissue care
  • preservation of blood supply
  • hemostasis
  • debridement
  • stabilization of fractures
  • tension-free wound closure
• Nutritional support
• Temperature control

Read the full chapter on prevention of infection.

A fracture wound that becomes infected almost always results in prolonged treatment and compromised outcome. A surgeon who treats fractures must be aware of factors which affect the risk of infection. Every effort should be made to reduce the risk of infection by following basic principles of fracture care, rather than the illustrated treatment.
Should infection develop, it is important that this complication be promptly recognized and effectively treated according to basic principles of patient care, surgery, and microbiology.
Basically, the factors which reduce a patient’s ability to resist infection should be corrected to the extent possible. Necrotic, or severely injured tissue, and foreign materials should be removed surgically. Wounds should be closed as soon as their condition permits. Fractures should be stabilized surgically. Internal fixation devices compromise host resistance, and need to be removed unless they provide absolute stability, and infection responds promptly to treatment. Infecting microorganisms should be identified, their antibiotic sensitivities defined, and appropriate specific antibiotics administered as an adjunct to surgical treatment.
Fracture wounds essentially always include some damaged tissue, thus increasing the risk of infection beyond that seen with early acute hematogenous osteomyelitis (which often responds to antibiotics without surgery).

A variety of factors influence the prognosis of fracture wound infections. Unlike hematogenous osteomyelitis, a fracture wound begins with damaged soft tissue and bone, and thus locally reduced resistance to infection. There may also be necrotic bone, and perhaps foreign material, where bacteria are protected from host defenses and blood-borne antibiotics, often sheltering in biofilms.

Factors to consider in classifying infections are:

• Duration of infection
• Anatomical area of bony involvement
• Host resistance (systemic and/or local)
• Status of fixation
• Fracture healing status
• Bacteriology

Onset of fracture-site infection can be related to the time elapsed since the fracture occurred. However, the actual onset of infection may be delayed, beginning some time after the injury. This is relevant since progressive infection leads to additional tissue damage, and spread of infection outward from the original infected site. It is sometimes difficult to know exactly when an infection begins. When it is first diagnosed sometime after the original injury, a careful history from the patient and/or review of laboratory data may suggest a shorter duration of active infection.
Remembering the above, it may still be helpful to consider the major features of infection classified according to time after injury.

Early infections generally occur less than 2 weeks after surgery. Their clinical signs are:

• increasing local pain
• redness
• swelling
• wound drainage
• disturbed wound healing
• fever

Typically, infecting organisms are highly virulent (staphylococcus aureus, Gram negative bacilli). Clostridial infections (gas gangrene, or tetanus) are other significant early infections.

Early infections need prompt surgical treatment for debridement as well as appropriate adjunctive antibiotics.
Such infections are not “superficial”, as the entire fracture wound is almost always involved. Only surgical exploration allows comprehensive assessment and care.

In addition, tissue samples taken at this time offer the chance to culture organisms hidden in biofilms.

Surgeon neglect allows the infection to progress to a point where relatively simple debridement may not succeed.

When symptoms have been present for less than 2 weeks, and internal fixation implants still provide absolute stability, it may be possible, after thorough debridement and with appropriate antibiotics, to retain them until the fracture is healed. Should the infection fail to resolve rapidly, repeated debridement, including implant removal with alternative fixation will be necessary.

• Infection may not be seen until several weeks after surgery.
• More aggressive treatment is usually necessary.

Click here to read more about delayed presentation of infection.

An infection which has been present in a fracture wound for more than several weeks is a serious and challenging problem. Typically, such wounds have failed previous treatment attempts, or have been neglected.
If internal fixation devices are present, they almost definitively have microorganisms within a layer of adherent slime. These chronic fracture site infections also include dead bone and soft tissue. The necrotic tissue may be localized, or diffuse. Without its complete removal, there is essentially no hope of controlling the infection. Furthermore, fracture healing will not occur until the infection is controlled and tissue viability restored.
Treatment requires radical debridement, often requiring several operations, and fracture stabilization, almost always with external fixation. Extensive bone removal may result in a segmental defect, or loss of an involved joint. So much tissue may have to be removed that reconstruction becomes less successful than amputation. Failure to control infection may also lead to loss of limb.

• Posttraumatic osteomyelitis may recur, sometimes years after the original infection appears to have resolved.
• Treatment depends upon:
  • fracture healing
  • implants
  • sequestra

Click here to read more about recurrent osteomyelitis.

The anatomical classification of osteomyelitis (see diagram) is important for understanding and localizing the infection.

• Type I (medullary osteomyelitis) diffusely involves the intramedullary cavity, essentially always after medullary nailing. The entire medullary canal is involved, and will require debridement (nail removal and reaming).
• Type II osteomyelitis is superficial, may be present under a plate, but is rarely, if ever, seen with fracture-site infection.
• Type III osteomyelitis (localized full-thickness cortical involvement), will require debridement of all necrotic bone. During debridement, the full extent of the necrotic area becomes evident. This may weaken the bone, or produce significant dead space. Soft-tissue coverage may be inadequate and require reconstruction. Fracture healing may be a problem that requires identification and treatment.
• Type IV osteomyelitis diffusely involves the entire circumference of at least a segment of the bone. Usually the entire bone segment must be removed to eliminate necrotic tissue and persistent bacteria.

Patients vary in their ability to resist infection. In some cases, a patient’s response to infection is so impaired that all efforts at treatment fail. To understand the problem of posttraumatic infection, it is important to assess each patient’s immunocompetence.
Local factors are limited to the site of infection and include focal arterial insuffiency, venous stasis, previous radiation therapy, etc.
Systemic factors that impair host resistance include tobacco smoking, malnutrition, diabetes mellitus, renal failure, chronic steroid use, HIV/Aids, etc.

Cierny has provided a classification scheme for host resistance in addition to that presented above for anatomical classification. Both local and systemic factors are involved. Cierny’s classification simplistically identifies the uncompromised patient as Class A. If significant compromise is identified, the patient is class B, either based on local factors (B ^L), systemic factors (B ^S), or both (B ^L,S).
Class C patients are either so compromised that the risks of treatment outweigh the benefits, or the symptoms of their infection are sufficiently limited that surgical treatment is not indicated.

Class A host
A class A host is a healthy patient. Their infection was not the result of impaired systemic host resistance. It must be remembered that a very severe injury can result in a focal defect of host resistance, because of locally impaired vascularity and tissue damage. An otherwise healthy patient with this degree of persisting local damage actually belongs in class B (B ^L).
Class A hosts are usually able to tolerate any appropriate surgical procedure. Tissue response to infection is strong, soft-tissue viability is excellent, and healthy tissue is available for transfer, if needed. With or without long-term antibiotics, the host is able to recover from a completely resected infection.

Class B ^L host – local disease
A class B ^L host has locally compromised soft tissue, or bone. The patient’s injury, or previous surgery, or both, may compromise tissue healing. For example, the patient may have had radiation, or previous injury to this region. Other potential local impairments are vascular disease or lymphedema, which impair wound healing and response to infection.

This particular patient’s localized ischemia may be correctable with arterial reconstruction, with improvement of his host resistance classification.

B ^S host – systemic disease
Many systemic diseases can affect a host, reducing ability to fight infection. Extremes of age, malnutrition and obesity are three very common causes of systemic host problems. Smoking, alcohol, steroids, etc. also compromise host resistance. Systemic diseases such as diabetes, renal or liver failure impair tissue response to infection.
With such patients, every effort must be made to identify and treat the systemic problems, but it is not always possible to restore normal host resistance. In practice, when dealing with an active infection, it is appropriate to begin treatment involving drainage, debridement and appropriate antibiotics, with minimally invasive fracture stabilization (external fixation). Preferably, impaired host resistance can be improved before definitive surgical reconstruction. If this is not possible, treatment failure, and/or amputation become likely.

Class C host – poor surgical candidate
Class C patients are either so compromised that the risks of treatment outweigh the benefits, or the symptoms of their infection are sufficiently limited that surgical treatment is not indicated.

Bacteriology of fracture wound infection

• One, or more, bacterial species may be present
• Source: patient’s skin, scene of injury, hospital contamination
• If signs of infection, get multiple surgical (deep wound) specimens for culture and sensitivity

Click here to read more about bacteriology.

Fracture infections are influenced by factors involving the fracture and its prior treatment. Infections interfere with fracture healing. Infections are harder to eradicate from nonunited fractures. Treatment plans must address a nonunion, if it exists, with decision about bone resection, stabilization, bone grafting, etc.
Fracture fixation devices impair host resistance. If they provide absolute stability, this benefit may overcome their detrimental effects. Thus, in carefully selected cases (low-virulent organisms and healthy tissues), internal fixation may be retained, if stability is adequate.
If there is instability, or the infection fails to resolve promptly, plates, or intramedullary nails should be removed, and replaced with external fixation.

Fracture wound severity may be the most important factor influencing risk of infection. An additional influence is the ability of the host to resist infection, based on both systemic and local factors. This has been discussed above in reference to classification of fracture infections.

Most research shows that infection rate increases with severity of soft-tissue injury. Less important is the bony injury, providing that the bone that has been injured has a blood supply.
The AO classification of fracture wound severity separately addresses Fracture, Integument (skin), Muscle, Nerve and Vascular injuries. A full understanding of wound severity requires consideration of each of these elements. Particularly important is a separation of closed from open fracture wounds. This is done in the integumentary (skin) classification. Open fractures have a notoriously higher risk of infection.
The AO classification provides strength to the statement “a fracture is a soft-tissue injury that happens to have a broken bone inside”.

The commonly-employed Gustilo-Anderson open-fracture classification separately identifies open fractures with arterial injuries that require repair to restore limb viability. Gustilo and others demonstrated a 50% risk of osteomyelitis after such injuries, with amputation a frequent outcome.

Early identification of a wound infection is the first step towards prompt treatment, which itself is a requirement for optimal results. Any fracture wound, whether due to the injury, or created by the surgeon, is at risk of becoming infected. Recognition of those factors which predispose to infection may increase the surgeon’s alertness to the possibility of infection. Early signs of infection are not specific and may easily be misinterpreted. Inflammation is normally present in the region of a fracture, even without infection. Often, the first sign of wound infection is that the inflammation fails to resolve normally. Certainly, increasing signs of inflammation (wound drainage, redness, swelling, pain and tenderness, fever) must be regarded as a strong indication of possible infection.
Should the surgeon be concerned about infection, efforts to diagnose, or exclude this possibility, must be undertaken without delay.

Presence of bacteria within an inflammatory wound exudate is definitive proof of infection. Often this is most readily obtained by sterile aspiration of the wound, or by exploring it surgically. Microscopic examination (Gram’s stain) of the exudate, and appropriate bacteriologic cultures provide evidence of bacterial presence. Most fracture infections are due to readily evident bacteria, although previous antibiotic treatment may interfere with microbiology studies. It has to be borne in mind, additionally, that there may be few planktonic bacteria in the wound and that most bacteria may be trapped in biofilms. Occasionally, increasing inflammation is evident without recoverable bacteria. While occult infection may be the cause, the surgeon should remember that a non-infectious cause of increasing inflammation is mechanical failure of fracture fixation. This may also co-exist with infection.
Systemic signs of inflammation, often associated with infection, are provided by several laboratory studies (see below). By themselves, none of these prove nor exclude infection.

• Serial wound examinations
• Maximal daily temperature
• Complete blood count (CBC) with differential white cell count
• Erythrocyte sedimentation rate (ESR)
• C-reactive protein (CRP)
• Imaging
  • Plain x-rays
  • CT scan
  • MRI
  • Bone scan
• Bacteriology (Gram’s stain, culture and sensitivity)

An important guide to treatment is provided by classifying an infection according to several parameters:

• Duration of infection
• Anatomical location
• Status of fixation
• Infecting organism(s)
• Viability of bone and soft tissue
• Host resistance to infection

Optimal management of an infected fracture requires consideration of each of these factors. Thus, each must be evaluated.

Clinical symptoms and signs are most important for identifying the presence of infection. Increasing pain, drainage (either purulent or sero-sanguinous), swelling, redness, warmth and tenderness all suggest the possibility of a wound infection. Progressive worsening of one or more of these findings is confirmatory. Thus, serial examinations may be required. While some inflammation is caused by a fracture, its severity should progressively decrease. Local infection must not be mistaken for normal postoperative inflammatory signs.

In early infections, x-ray imaging procedures typically play a minor role. Radiographic findings of infection are usually not evident until at least 2 weeks after the onset of infection, even though bone involvement has already occurred.
Imaging becomes important in the later stages of infection. It is helpful to examine serial x-rays for progressive changes that suggest infection.
Radiographic signs are neither sensitive nor specific for infection. E.g., radiographic evidence of implant loosening may be present with instability, infection, or both.
Ultrasound is useful to identify accumulation of fluid (hidden abscess). The method is non-invasive, and may reach deeper layers, especially in the thigh. Ultrasound can be helpful for guiding diagnostic needle aspiration.

CT
Computed tomography better demonstrates differences in bone density, such as the dense white necrotic sequestrum illustrated here. It also offers a cross-sectional guide for exploration and debridement, particularly for bone fragments.
As with plain radiographs, CT scans offer no specific diagnostic sign for, or against, infection.

MRI
MRI presents an improved resolution of soft-tissue abnormalities and shows greater anatomic detail than other imaging studies. Once again, MRI signs of infection are non-specific. An additional disadvantage of MRI is the artifacts related to metal implants.

Bone scan
Uptake of technetium-labelled phosphate compounds (TCN-MDP) is increased in areas of high vascularity, including infections and bone healing. With infection, a 3-phase bone scan shows increased uptake of labelling in all 3 scan phases.
Absence of uptake suggests impaired vascularity, or bone necrosis. Bone scanning detects increased bone remodeling which is present around all fractures for 12-24 months. Bone scanning can not differentiate aseptic hardware loosening from infection. Bone scans have little value in the early postoperative period of acute fractures.
Indium-labelled white blood cell scans are more specific for inflammation and infection. The illustration shows a larger area of labelling (surrounding hyperemia and inflammation with TCM-MDP than with indium white blood cell technique). However, false positives and false negatives still occur, and such scans can be positive in un-united fractures.

Fluid can be aspirated sterily preoperatively and sent for culture and Gram’s stain. Tissue specimens should be sampled from 3 or more suspicious sites, with two pieces of tissue from each site (one for microbiology and one for histopathology). Both aerobic and anaerobic cultures should be undertaken.

PCR bacterial identification, if available, is a more rapid and reliable technique than standard cultures.

Histological investigation can reveal a bacteriological etiology even if the bacteriological tests are negative. Superficial wound swabs should be avoided because of low sensitivity and frequent contamination by bacteria not responsible for the infection. Prior to tissue-sampling for culture, it is important to discontinue any antibiotic therapy for at least a week, or two.

If the infection possibly involves a joint cavity, the need for draining and debriding that space must be appreciated. At the slightest suspicion of septic arthritis, joint aspiration should be performed to evaluate the affected joint. If there is presence of infected fibrinous deposits, arthroscopic, or open synovectomy must be performed. Arthroscopic irrigation should be performed repeatedly, every 2-3 days, until inflammation resolves. If arthroscopic debridement is unsuccessful, consider open synovectomy. If there is cartilage degradation, arthrodesis may be unavoidable. Infected joint wounds are different from hematogenous septic arthritis, and usually require surgical treatment.

Initial treatment
Before starting antibiotics, it is important to obtain adequate cultures. Several samples should be obtained in the operating room from different locations within the wound. Only if the patient is systemically septic should one consider antibiotics prior to wound exploration.
Selection of antibiotics for initial treatment is based upon the antibiotics sensitivities of likely infecting organisms, including a history of previously positive cultures, for recurrent infections.
Generally, broad-spectrum, intravenous antibiotics are advisable as soon as cultures have been obtained. Initial antibiotics are selected, based on institutional frequency statistics ( see table on left, Trampuz, Zimmerli 2006) and results of Gram’s stain.
Methicillin-sensitive S. aureus is still the most likely infecting organism in most areas. Institutionalized patients have a higher risk of MRSA so that Vancomycin may be advisable.
Gram negative coverage is wise for hospital-acquired infections. Ask about allergy history and modify antibiotic selection as necessary.
All of the above should be considered provisional treatment until culture results are returned. Consultation with an infectious disease specialist can be very helpful in selecting appropriate antibiotics, their doses, and interpreting cultures.

Definitive antibiotic treatment
Once culture results and sensitivities are known, it is possible to choose the optimal antibiotic for management of a fracture wound infection. Remember that antibiotics are adjunctive to adequate debridement, and recognize that an infection that does not respond may need repeat surgical exploration and debridement. Once again, antibiotic selection is aided by consultation with an infectious-disease specialist or internist with interest and experience in antibiotic management. This is particularly true when dealing with resistant organisms and patients with drug allergies, or sensitivities.
Prolonged intravenous antibiotics (e.g. six weeks), use of combinations of drugs, and continued oral medication after initial intravenous therapy all need to be considered.

Locally administered antibiotics may have a supplementary role in the management of musculoskeletal infections. Particularly when the infected wound has poorly perfused areas, or “dead space”, antibiotic-laden cement is frequently used, both to fill the space and to deliver high doses of local antibiotic with low risk of systemic toxicity. A common technique is the use of antibiotic-laden polymethylmethacrylate (PMMA) beads.
Antibiotic-impregnated beads may be purchased in some countries (at some expense), or made by the surgeon more cheaply. One gram of cefazolin (a first generation cephalosporin) is cheap and accessible. It is mixed with 1 standard package of PMMA and, as it hardens, beads of 5 mm are carefully wrapped around a non-absorbable heavy nylon stitch (see intraoperative photograph).
Tobramycin powder (1.2 grams) may also be mixed with PMMA for broader-spectrum coverage.

If an infection is strongly suspected, the surgeon should proceed with exploration of the wound, obtaining tissue for culture, and removing all non-viable tissue and exudates.
Debridement (see below) is the surgical excision of necrotic and/or infected tissue from the wound.

Tissues to be removed include

1. Exudate (hematoma and pus)
2. Abscess membrane
3. Sinus tracts
4. Granulation tissue
5. Unhealthy wound margins
6. Dead bone, including sequestra.

Look carefully for dead bone and any remaining foreign material. Preserve nerves and blood vessels and viable tendons. With acute wound infections, internal fixation devices may be retained, if they provide absolute mechanical stability and are unlikely to have a significant volume of adherent bacteria. With more-established infections it may be wisest to remove all local hardware and provide stability with an external fixator.

The surgical excision must be complete and thorough.
Adequate, timely débridement is the most important element of the treatment of a fracture-site infection.
With well-established infections, there may not be a clear demarcation between viable and non-viable tissue. Radical excision may be necessary to eliminate infection, even though it may increase the complexity of reconstruction.

After débridement, the surgical site should be thoroughly irrigated with Ringer-lactate solution to reduce the bacterial population. In cases with large amounts of dead tissue, or grossly purulent wounds, repeated surgical clearances are indicated. Deciding what tissue to remove and what tissue to retain is the essential challenge of débridement . Such decision-making is learned from experienced surgeons and by practice. Common errors are failure to remove enough compromised tissue, and/or to do so in a way that injures the retained tissue. An organized approach that proceeds in orderly steps through tissue levels is required. Any non-viable skin is excised. The incision should be extended, as necessary, for adequate exposure of the whole infected zone. The depths of the wound are then exposed, and must include all of the previous surgical exposure. Any extension of hematoma, pus, or necrotic tissue, should be explored fully.

With acute wound infections, internal fixation devices may be retained, if they continue to provide absolute mechanical stability. If the implants are loose, and in more established infections, it is advisable to remove all hardware and to restabilize with an external fixator.

Excise the surface of the exposed tissue to leave clearly viable margins of subcutaneous tissue, fascia and muscle. Non-viable bone also must be excised.
In areas where dead bone exists, removal with a high-speed burr, or osteotomes, until bone bleeding is encountered. Small bleeding osseous vessels (“Paprika sign”) indicate viable bone.
Abundant irrigation helps to remove bacteria, bits of dead tissue and blood clot, and improves the surgeon’s ability to examine the wound.

A “second look” and possibly further debridement should be considered until the wound surface is completely viable. Staged debridement is illustrated to the left.

After the first debridement of an infected fracture wound, it is usually wisest to defer suture closure. Closure may be considered when final debridement has been completed.
Empty space (“dead space”) under tissue flaps, or within bony cavities, within the debrided wound allows reaccumulation of exudate and may become a reservoir of bacteria. Antibiotic levels may be low in this poorly perfused fluid accumulation. Filling this dead space in some way is an important part of wound management.

Alternative treatment strategies for filling dead space include antibiotic beads or other temporary space fillers (calcium sulphate, bone cement, etc). The wound itself should be covered to avoid dessication or contamination. This can be done with an impermeable dressing (adherent plastic), or vacuum-assisted closure, as illustrated. The latter, by applying sub-atmospheric pressure reduces dead space volume in pliable tissues.

A significant bone defect may be filled with antibiotic beads, or other space filler. Recently, the technique of Masquelet ( http://www.ncbi.nlm.nih.gov/pubmed/19931050) is proving attractive. This involves insertion of a solid antibiotic-containing cement spacer which is left in place for 6 weeks while a membrane develops around it. Then the spacer is removed and the surrounding osteogenic membrane is filled with autologous bone graft. This often consolidates to fill small to medium-size defects. This membrane does not form satisfactorily around cement beads, and is destroyed during their removal.

As long as a plate and screws provide absolute stability, fracture healing usually can take place despite the presence of treated infection, in spite of the presence of a metallic foreign body. It appears that stability is more important than the negative effects of the foreign body upon host defense.

Typically, fixation remains stable in early infections (up to 6 weeks or so). No matter when, if the implants are loose, they must be removed. External fixation stabilizes the fracture while avoiding a metallic foreign body in the infected wound, and is often the best choice for early fixation after infection.

If an infection is identified and treated early, and its fixation remains stable, with appropriate debridement and antibiotics, the infection typically responds and remains suppressed during fracture healing. In spite of successful fracture healing, recurrent infection often results in ultimate hardware removal.
After the “infected hardware” is removed from the united fracture, and the wound debrided, the infection usually resolves satisfactorily with a low risk of recurrence.

If a fracture site infection develops after intramedullary nailing, it is likely that the infection has spread along the medullary cavity. The infection may be early, or late, before or after union. Adequate debridement requires removal of the nail and reaming of the medullary canal.

During initial clearance, a distal opening is created at the lower end of the nail track, in order to allow debris from reaming to escape, and to drain the “sump”. The canal is then reamed to a diameter 1.5 mm larger than the removed nail, and is thoroughly and copiously washed out with Ringer-lactate solution.
If there are obvious cortical sequestra, these need removal by open procedure.

An external fixator should be applied for stability, if the fracture is not healed.

If the infection is early and due to a less virulent bacterium, then renailing might be considered.

If the infection is early and due to a less virulent bacterium, then renailing might be considered. If the infection is late, or due to resistant organisms, external fixation may be preferable. An alternative is to place temporarily a reinforced, antibiotic-containing polymethylmethacrylate (PMMA) “nail” into the medullary canal, after reaming out the infective membrane and thorough lavage of the IM canal, also excising any sinus track and any sequestra.
An antibiotic-loaded PMMA nail is prepared by injecting liquid bone cement, pre-mixed with antibiotics (e.g. tobramycin 1 g per cement batch) into both ends of an appropriately sized chest tube which is vented in the middle to allow complete filling. A small-diameter flexible rod (e.g., nailing guide wire) is inserted before the cement hardens. The chest tube is then cut off.
The “nail” can be left in situ until the fracture has healed, or until the infection is under control, and then replaced with a solid metallic nail – a solid nail is used in order to avoid the hollow nail’s becoming a hiding place for bacteria.

Since external fixators are usually distant from the fracture wound, their removal is rarely required, but adjustment, or reinforcement, may be required to ensure alignment and stability.
Should an external fixator pin track become infected, it should be removed, the pin site debrided, and a new fixation pin placed through clean tissue. A common mistake is that such pin tracks are not thoroughly debrided. This may be done most easily with a hand drill and a bit slightly larger than the residual pin hole. Inadequate pin-site care may result in persistence of infection.

If a fracture has become infected, it requires debridement and external fixation. The diagram at the left demonstrates proper external fixation placement.
The details of external fixation must include planning for wound care and preserving access for flap coverage. Additionally, fixator configuration should provide for excellent stability.
An external fixator can be used as a temporary, or as a definitive stabilizer. Even if external fixation will be used definitively, a temporary fixator may be best after initial debridement. This aids repeated debridement and wound care. Once further wound access is unnecessary, apply a new fixator that provides optimal stability.

Consequences of incorrect/correct insertion of pins/screws for external fixation.

a) Complex fracture caused by direct trauma.

1. Devitalized margins of the main fragments.
2. Devitalized intermediate fragments.
3. Partially vital intermediate fragments still attached to the periosteum.

b) Drilling at excessively high speeds or with blunt drill bits produces heat necrosis in cortical bone.

c) Insertion of the Schanz screws or Steinmann pins with no or inadequate predrilling produces considerable heat and small, necrotic fragments, or ring sequestra.

d) Correct predrilling, correct placement of the Schanz screw. This minimizes the risk of pin-track osteomyelitis.

After debridement has been satisfactorily completed, in one or several procedures, consideration must be given to choosing the best means of wound closure. A tight suture closure risks wound healing problems. If possible, a delayed primary suture closure may expedite management. If this is chosen, the surgeon must watch for wound breakdown, or recurrent infection. Another alternative is to leave the wound open and allow it to heal by second intention. This is more appropriate for a narrow wound without exposed hardware, bone, or other sensitive tissues.

If the wound is widely open, or tissue protection is necessary, some form of flap coverage will probably be necessary. Vacuum-assisted wound closure can be used to reduce the size of an open wound and promote granulation tissue which may accept a split-thickness skin graft. An alternative temporary dressing for an open wound is an impermeable adhesive drape to create a space (bead pouch) for antibiotic beads. A clean granulating wound with a healthy viable base may be closed with a split-thickness skin graft.

Closure with local or free flaps is typically appropriate for larger and more complicated wounds, once they have been adequately debrided.
It is important to close a complex wound promptly rather than leave it open and risk superinfection.

The following example shows a soft-tissue and bony defect in the anterolateral aspect of the leg. A locked intramedullary tibial nail is visible in the depths of the defect.

The pedicle must be surrounded by an adequate soft-tissue cuff, in order to ensure good venous drainage. This also helps to prevent kinking of the vessels. The gastrocnemius is preserved in the bed of the donor defect.

Flap in the defect.

Debridement of soft tissue or bone may leave dead space between bone ends, or under flaps. If present, this should be filled, usually with a material that delivers high levels of antibiotics. This illustration shows antibiotic beads placed within potential dead space under a muscle flap. If this is done, plans should be made for later exposure and removal of beads with probable replacement by bone graft.

The anatomical classification of adult osteomyelitis helps determine definitive stabilization.

Medullary osteomyelitis (type I) is associated with an intramedullary nail which may or may not have been removed during initial surgery for infection. If the tissue is healthy, the bacteria are sensitive, and the patient is systemically healthy, it may be appropriate to stabilize the fracture with another nail.

Superficial osteomyelitis (type II) is typical of a healed fracture with superficial bone involvement, often under a plate. After removal of the plate, this superficial necrotic bone is removed with a burr, or hand instruments, until bleeding bone is seen. Replace fixation only if fracture healing is tenuous. Wound closure may often follow soon after such superficial debridement.

Localized, full-thickness osteomyelitis (type III) may be associated with a non-united fracture. Debridement back to bleeding bone may remove so much cortex that the structural integrity of the bone is compromised and pathological fracture might result. Mechanical protection will be necessary, typically with an external fixator. More complex options for soft-tissue closure (local or free flaps) may be required. In some cases plates, or nails, will be chosen for fixation. They should not be applied until wound coverage can be carried out. Similarly, bone grafting is often necessary, and this should be delayed until coverage is healed.

Diffuse osteomyelitis (type IV) has widespread areas of infected and/or necrotic bone, so that extensive debridement may be necessary. This may result in a segmental defect. Such defects will require bone grafting, bone transport, or fixing in a shortened position if loss of length is acceptable. Wounds associated with type IV posttraumatic osteomyelitis often need complex flaps for closure. Such widespread infection may require amputation for successful treatment.

Elements of infection control:

1. Identification of the infecting organism/s
2. Eradication of infection by surgery combined with appropriate antibiotics and systemic support
3. Creation of viable and stable soft-tissue environment
4. Actual skeletal reconstruction comes next
   • Concern about reconstruction may limit debridement
   • Consider likely reconstructive options (bone graft, transport, even amputation, etc.)
   • Preserve options (e.g. by incision placement and/or external fixator pin locations, etc.) if doing so does not compromise infection control

Skeletal stability provides:

1. Fracture healing
2. Functional aftercare
3. Enhanced wound care
4. Eradication of infection
5. Final reconstructive surgery (soft tissue and bony)

External fixation

External fixation is a time-honored means of stabilization in infected fractures and nonunions. It provides stability without the need for implants inside the infected wounds.

In septic surgery, external fixation may need to remain for up to a year, or more. It may be necessary to replace one or more pins during the course of treatment. There are 3 basic systems:

1. External fixation with Schanz pins and tubular frames
2. The Ilizarov ring fixator anchored with tensioned wires
3. Hybrid ring fixators (anchored with both tensioned wires and Schanz pins)

All three systems have advantages and disadvantages. The Ilizarov frame is much more difficult but can be used for compression and lengthening. Hybrid frames are simpler and tension wires may have fewer pin-related problems while external fixation with Schanz pins is the simplest and is very adaptable.
These frames must provide stability as in any other fracture fixation situation. If there is a question of stability (loosening or infection) then they must be replaced.

Internal fixation with plates or nails

Plates and nails involve metallic implants in the site of infection. They may compromise successful treatment of infection. They should be used with caution in an infected wound. In some cases with early, or mild, infection, these internal fixation devices may be retained, or, perhaps more safely, be removed and temporarily replaced with external fixation. Then, once infection is completely resolved, plates or nails might be considered for reconstruction of the now-uninfected fracture site. As with external fixation, any retained plates, or nails, must provide stability. If there is any question of instability because of loosening, or poor bone contact, then the fixation must be revised.

Control of infection, and restoration of stability should be achieved before definitive wound closure. Once inflamation and suppuration have ceased, and fixation is stable, the next step, especially if there is a defect or impaired healing is considered likely, is wound closure with local or free flaps, according to the “reconstructive ladder” model advocated by plastic surgeons. Definitive bone reconstruction may be more successful under a healthy, closed wound. Alternatively, traction histogenesis and papineau grafting (see below) may be carried out with an open wound.

As a rule, soft-tissue coverage without complete debridement of underlying infected tissue is useless.
A second rule denotes that wound closure under tension will usually fail. The wound edges necrose, the wound opens, and infection is unavoidable.

These two rules emphasize the importance of

• complete debridements
• soft-tissue coverage without tension.

These rules apply to initial treatment as well as the management of infected fractures.
If direct suture closure is not possible, consider rotational muscle flaps, fascio-cutaneus flaps, or free vascularized flaps. Negative pressure dressings (vacuum-assisted closure) are very useful in some open wounds, or open soft-tissue defects. Open bone-grafting is an alternative approach.

If an open wound involves loss of skin and subcutaneous tissue, but has a base of healthy muscle, fascia, or tendon sheath, granulation tissue will form on the base and a split-thickness skin graft (STSG) can be applied, or the wound can be allowed to heal in from its sides (second intention).
A moist environment promotes granulation tissue formation. Muscles provide the best tissue for granulation.
Bare bone (without periosteum), exposed blood vessels, nerves and tendons (without paratenon) all are harmed by dessication and do not support granulation tissues and STSG. Alternative coverage techniques should be used. These tissues should not be left exposed, and should be kept moist with appropriate dressings. Definitive coverage should be done as soon as possible.
The “reconstructive ladder” shown on the left presents in increasing order of complexity the options available for wound closure, and is helpful for treatment planning.

Reconstruction of an infected fracture site should almost always be done with autogenous bone graft or traction histogenesis (Ilizarov technique).
Autogenous cancellous bone graft from any standard site is of well-recognized value for promoting union and filling smaller defects. It revascularizes quickly, with minimal risk of sequestration. For treating tibial fractures, posterolateral, or central placement, adjacent to healthy muscle, may avoid the infected focus. For the humerus, femur, or forearm, the best position of the graft depends upon the defect, the soft-tissue envelope and the fixation.
Bone defects remaining after resection of dead or infected bone are challenging to treat. The longer the defect, the more difficult the treatment. Circumferential defects of 1-6 cm in long bones usually heal if filled with autogenous bone graft, and stabilized appropriately. Defects greater than this usually need traction histogenesis or free vascularized bone transfer.

Open cancellous bone grafting (Papineau technique), leaving the graft exposed beneath a nonadherent dressing, is a well-tried technique for reconstructing defects. It is best used for strengthening partial segmental defects. It can achieve bony bridging and secondary soft-tissue coverage concurrently, since granulation tissue should form over the graft and under the moist dressing. A split-thickness skin graft can then be applied.

Some of the superficial bone graft is inevitably lost and will have to be removed before granulation occurs. This technique has a fairly high reported success rate.
A more modern adaptation is to use a vacuum-assisted closure system over cancellous bone graft.

This case shows an infected subtalar fusion treated by Papineau technique, using vacuum closure.
The case illustrations are taken from Archdeacon MT, Messerschmitt P (2006) Modern Papineau technique with vacuum-assisted closure. J Orthop Trauma; 20(2):134-7.

Slow distraction of an osteotomy with stable (usually external) fixation creates new bone. Distraction usually is limited to 1 mm per day.

When matured, this resembles the original bone in shape and strength. This technique, while slow, is particularly suitable for defects of more than 6 cm. This technique can be applied to a fresh osteotomy, distant from the site of the infected fracture, and also to a healing fracture site. Similar fixation can be used to compress a fracture, or osteotomy, to promote healing. Angular deformities can be corrected as well.
The techniques of traction histogenesis can be applied with any stable form of external, or even internal, fixation.
Diaphyseal bone can be transported over an intramedullary nail, which helps support the new (regenerating) bone. This allows earlier removal of external fixation, but introduces a foreign body with risk of recurrent infection.

Rarely does systemic infection flare out of control in patients with chronic osteomyelitis. Thus, for these patients, amputation is almost never an urgent, life-or-death decision. However, should repeated attempts to control infection, gain bone healing and restore function be unsuccessful, amputation may prove to be the most appropriate way of restoring function and allowing the patient to resume a more normal life.
The decision to amputate should be considered carefully and individually, including patient and family. One should compare the best predicted outcome with limb salvage with what is expected from amputation. The length of time required for treatment, and the complications that might occur on the way are also important factors. Prosthetic function with a lower extremity amputation, particularly below the knee, is much more successful than what can be achieved with upper-extremity amputations. The availability and cost of prosthetics must also be considered, and they vary among different health systems.
Different cultures, countries and religions provide different perspectives to this controversy. The individual patient’s preferences within his or her social setting must never be forgotten.
The surgeon’s job is to educate the patient about realistic expectations.

If after due consideration, the patient decides that continued efforts at limb salvage are not desirable, the surgeon should recognize that amputation offers an opportunity for rehabilitation and restoration of function and plan the most functional level of amputation proximal to the diseased tissue. Using Cierny’s physiologic host classification, type A hosts are generally better candidates for limb salvage, while type B hosts, with impaired resistance to infection may be better served by amputation. Type C hosts, for whom treatment is worse than their disease, are not surgical candidates unless their condition can be improved enough to tolerate surgery (either reconstruction, or amputation), or unless the infection flares out of control.
Consultation with a prosthetist may be helpful for the surgeon. The patient may wish to discuss amputation with another person who has undergone this procedure at a similar level. Once all of the infected tissue has been amputated, further infection treatment, beyond brief perioperative antibiotics is no longer required. Just as with elective limb salvage surgery, efforts should be made preoperatively to help the patient attain the best possible nutritional and physiologic condition with suppression of active infection, or preliminary debridement, perhaps even a preliminary amputation just above the infected wound.

In this Class A host with an infection developing only 2 weeks after fracture surgery, prompt operative treatment is necessary. This includes aggressive debridement, microbial cultures and appropriate antibiotic treatment.
Fixation hardware should be checked for stability and left in place unless it is loose or prevents adequate debridement.
Antibiotics are begun as soon as cultures are obtained, and adjusted as necessary based on sensitivity results. Conventionally, they are continued for 6 weeks. Wound and fracture healing can be anticipated to proceed uneventfully.

This class A host had ORIF of her lateral plateau fracture. Healing was slow, and she returned with an open wound 24 days later. She immediately had aggressive debridement and antibiotics for 2 months. Wound and fracture then healed uneventfully.
The hardware was retained, but may have needed removal, or complete revision, if instability had been evident, or the infection failed to resolve.
Once the fracture was securely healed, the hardware was removed.
Infections often occur if hardware is left after initially successful treatment.

This class B host needs to have careful diabetic control as the infection will make the patient’s diabetes less responsive. Furthermore, diabetes mellitus, especially if poorly controlled, reduces host resistance to infection.
Once medical condition is stabilized, surgical debridement can be performed. This involves debriding the sinus tract, removal of all hardware, irrigating the medullary canal after re-reaming to a larger size. After obtaining cultures, appropriate antibiotics are started and continued for at least 6 weeks. If the fracture is healed, no further interventions are required, unless infection recurs.
If the fracture has not healed, refixation will be necessary. Replacement of an IM nail may be considered after a few days if the infecting organism is of low virulence and sensitive to the chosen antibiotics. Alternative (external) fixation may be more advisable, particularly in this diabetic patient.

This man, having presented at 4 weeks postoperatively, with a delayed, or hidden infection, had instability because of hardware failure and infection. Surgery with debridement and refixation, microbial cultures, appropriate antibiotics was necessary.

Standard follow-up was performed, but this patient presented at 6 months after the fracture had healed, requiring complete debridement and removal of all hardware and another course of appropriate antibiotics (after culture).
This patient remains at risk of another infection recurrence.

The image on the left shows a case of a young man, a class B host, who required smoking cessation education. He had a hypertrophic nonunion. Biology was present, but stability was impaired. The nail was removed. A short segment of fibula was excised. The tibia was re-nailed after reaming to a larger diameter. A culture of the reamings was positive and appropriately treated with antibiotics.
The tibia quickly healed. Given the fracture’s excellent blood supply and callus formation, providing adequate fracture stability plus adjunctive antibiotics addressed both fracture healing and infection.

This class B host had a delayed onset wound infection, with a healing fracture according to x-rays and symptoms.
She was advised to stop smoking and then underwent debridement and removal of hardware, with microbial cultures. The fracture was ununited. Antibiotics were started and, 10 days later, she had placement of an IM nail. Antibiotics were continued intravenously for 6 weeks.
This patient had posterolateral tibial callus present. This area was healing but required additional mechanical support.
The second image shows satisfactory healing after nail removal.
The fibular ostectomy offloads the fibula and loads the tibia, enhancing biomechanics for healing.

This patient had an acute fracture, necessitating internal fixation. However, a late infection occurred. X-rays and subsequent debridement revealed an ununited fracture with minimal callus formation. Intercalary necrotic bone was debrided. The fracture was stabilized with an external fixator.

Appropriate antibiotics were administered. Bone graft was placed in the fracture defect and between the tibia and fibula above and below the fracture. This combination of treatments improved both biology and stability of the atrophic nonunion. Delayed healing occurred with satisfactory outcome.

This 40-year old motorcyclist had had acute fixation of an open pilon fracture. The picture on the left shows the wound 10 days after ORIF. It was smelly and the patient was acutely septic.

This intraoperative image shows loss of soft tissue and bone. Extensive debridement was undertaken to control the infection. Systemic antibiotics were administered. This patient turned out to have clostridial gas gangrene. To save his life, the limb was amputated.