1. Nonunions—A nonunion represents an arrest of the bone healing process. Classically, nonunion of a long bone is defined by the US Food and Drug Administration as a fracture that has failed to show progressive evidence of healing over a 4- to 6-month period. In reality, once a fracture has lost the potential to progress with healing, it is a nonunion.
2. Delayed unions—Delayed union has been defined as a fracture that has failed to achieve full bony union by 6 months after the injury. This definition generally applies to long bones, however, and is therefore incomplete. To include fractures that would generally heal much more quickly (eg, distal radial fractures), the definition of a delayed union is now a fracture taking longer to show progression toward healing than would normally be expected.
3. Fractures with large segmental defects—These fractures clearly are functionally nonunions from the time of the injury and should be treated as such.
1. Common factors—Often the cause of nonunions is multifactorial; however, there are usually a host of common denominators that contribute to the development of a nonunion (
Table 1). Of all potential causes, inadequate fracture stabilization and lack of adequate blood supply are the most common.
2. Infection—Infection in and of itself does not preclude a fracture from healing; however, it can certainly be a contributing factor to a fracture failing to progress to union. Clearly, even if the fracture does heal, the osteomyelitis must be treated. Hence, eradicating infection should be a concomitant goal along with achieving bony union.
*David W. Lowenberg, MD, is a consultant for or an employee of Stryker and Biotech.
3. Fracture location—Location of the fracture can be an important contributing factor, as certain areas of the skeleton (eg, carpal navicular, distal tibal diaphyseal-metaphyseal junction, proximal diaphysis of the fifth metatarsal) are more prone to the development of nonunion.
4. Fracture pattern—Fracture pattern can influence the development of nonunion, especially when the fracture occurs in the diaphysis of a long bone. Segmental fractures and fractures with large butterfly fragments are more prone to nonunion, probably because of devascularization of the intermediary segment.
[Table 1. Causes of Nonunion]
Table 2. Forces Involved in Four Common Mechanisms of Injury*]
a. The mechanism of injury (Table 2), prior surgical as well as nonsurgical interventions, host quality (ie, underlying metabolic, nutritional, or immunologic disease), and use of nonsteroidal anti-inflammatory drugs (NSAIDs) or tobacco are vital factors in determining proper treatment of the patient.
b. Additional important factors are pain at the fracture site with axial loading of the involved extremity, as well as motion at the fracture site perceived by the patient.
2. Physical examination
a. The examination should include a detailed evaluation of distal pulses and patency of vessels as well as motor and sensory function in the limb.
b. Actual mobility of the nonunion, or lack thereof, is another important factor in deciding on treatment.
c. The limb should be evaluated for deformity, including rotational deformity and any resultant limb-length discrepancy, as this might affect treatment decisions.
3. Imaging studies
a. High-quality radiographs are the gold standard in evaluating fracture healing. To assess for a nonunion, four views of the limb segment in question are the first essential study.
b. If these radiographs fail to clearly determine union, then a CT scan with reformations reconstruction can be quite helpful. The value of CT can be diminished, however, if there is significant hardware at the fracture site.
c. If limb-length discrepancy or deformity is a potential issue in the lower limb, a 51-in, full-length, weight-bearing view of both lower extremities is required.
d. Bone scanning can be a helpful adjuvant; however, it is rarely used as a sole determinant of whether a nonunion exists.
Figure 1. Algorithm for classification of nonunions.]
4. Laboratory studies—If deep infection or chronic osteomyelitis is suspected, then screening laboratory studies (complete blood cell count [CBC], erythrocyte sedimentation rate [ESR], and C-reactive protein [CRP]) are warranted.
D. Classification—An algorithm for basic classification of nonunions is provided in Figure 1.
E. General treatment issues—Nontreatment is a viable option in a small percentage of patients because some nonunions can be asymptomatic (eg, hypertrophic clavicular shaft nonunions). Also, in some instances, the treatment can cause greater morbidity than the consequences of leaving the nonunion untreated.
F. Nonsurgical treatment
1. Fracture brace immobilization with axial loading of the limb is a viable treatment option for certain rigid/stable nonunions.
2. Bone growth stimulators (inductive or capacitive coupling devices) are an option in some patients. Published controlled clinical studies remain scarce, however, and the use of these devices is essentially limited to the United States. Clear contraindications to electrical stimulation include synovial pseudarthroses, mobile nonunions, and a fracture gap >1 cm.
G. Surgical treatment—The basic goal of surgery for nonunions is to create a favorable environment for fracture healing. This includes stable fixation with preservation of blood supply to the bone and soft-tissue envelope, the minimization of shear forces, especially in nonunions with a high degree of fracture obliquity, and good bony apposition.
1. Hypertrophic nonunions
a. The defining factor in hypertrophic nonunions is that they have viable bone ends; these are usually stiff in nature.
b. Generally, these fractures "want to heal" and have the proper biology to heal, but they lack stable fixation.
c. Treatment is therefore generally aimed at providing appropriate stabilization and is most easily achieved with internal fixation (plates and screws, locked intramedullary rods, etc).
d. The nonunion itself does not generally need to be taken down, unless required for proper fracture reduction.
2. Oligotrophic nonunions
a. Oligotrophic nonunions are generally lacking in callus. They often resemble atrophic nonunions radiographically but in fact have viable bone ends.
b. Oligotrophic nonunions occasionally require further biologic stimulus and can behave like atrophic nonunions.
3. Atrophic nonunions
a. The defining factor in atrophic nonunions is often the presence of avascular or hypovascular bone ends. These are usually mobile, and so atrophic nonunions are often called mobile nonunions.
b. Occasionally, oligotrophic fractures that go on to nonunion because of muscle interposition can look and behave like atrophic nonunions despite having viable bone ends.
c. Treatment objectives for atrophic nonunions
i. The apposition of well-vascularized bone ends
ii. Stable fixation with the use of hardware, be it internal or multiplanar external fixation if the need exists
iii. Grafting to fill bony defects and provide osteoinductive agents to the local environment. Autogenous iliac crest bone grafting is the gold standard for osteoinductive agents. The recombinant bone morphogenetic proteins (BMPs) are promising alternatives. Other graft materials (eg, crushed cancellous allograft, demineralized allogenic bone matrix) are, for all practical purposes, osteoconductive only.
iv. Preservation or creation of a healthy, well-vascularized local soft-tissue envelope
a. A pseudarthrosis, which is in effect a "false joint," is often present if infection exists, and the bone ends are always atrophic with impaired vasculature.
b. When a pseudarthrosis is exposed surgically, an actual joint capsule with enclosed synovial fluid is found.
c. To heal a pseudarthrosis requires complete surgical takedown with excision of the atrophic bone ends, followed by proper surgical stabilization with preservation of the remaining bone and soft-tissue vascularity.
5. Infected nonunions
a. Although infection does not prevent a fracture from healing, if a fracture goes on to a nonunion and becomes infected, the chance of healing is low if the infection is not eradicated.
b. Infected nonunions are often pseudarthroses and should be treated as such.
c. Treatment goals
i. Remove all infected and devitalized bone and soft tissue.
ii. Sterilize the local wound environment with the use of local wound management techniques (antibiotic bead pouch, vacuum-assisted closure [VAC] sponge, etc).
iii. Create healthy, bleeding bone ends with a well-vascularized soft-tissue envelope.
iv. Provide fracture stability.
d. Achieving the treatment goals most often requires a staged approach, with multiple surgeries.
e. Because the treatment often results in a significant amount of bone loss, bone transport or later limb lengthening using the Ilizarov method is often beneficial.
f. Placement of a free muscle flap can be crucial in the management of the local soft-tissue environment if the soft-tissue envelope becomes deficient after treatment or the soft-tissue envelope is overly scarred and dysvascular.
g. The surgeon must be well versed in the use of free tissue transfers to successfully treat difficult nonunions.
H. Pearls and pitfalls
1. It is best to achieve as stable a fixation as possible to allow for joint mobilization above and below the nonunion. Because these limbs have already been through much trauma, the periarticular regions are prone to stiffness.
2. A healthy, well-vascularized soft-tissue envelope is necessary for healing of tenuously vascularized diaphyseal bone ends. The generous use of free or rotational muscle transfers enhances the healing environment by providing more vascular access.
3. If union fails despite optimal treatment, metabolic or other endogenous problems that can inhibit fracture healing should be sought.
a. NSAIDs—One of the most common culprits is a patient's use of NSAIDs. These medications can inhibit fracture healing by preventing calcification of the osteoid matrix.
b. Tobacco use—Smoking has been shown to play a role in the inhibition of bone healing, with an increased risk of nonunion in those who smoke or use tobacco-based products. Nicotine causes arteriolar vasoconstriction, thereby further inhibiting blood flow to bone and the already compromised area about an injury. This, in effect, acts as a secondary insult to the already compromised site of bone and soft-tissue injury.
1. Classically, osteomyelitis occurs via hematogenous seeding or direct inoculation, most typically secondary to trauma.
2. Hematogenous osteomyelitis (see chapter 28, Osteoarticular Infection) is most commonly seen in the pediatric population. It occurs with seeding of the bacteria at metaphyseal end arterioles.
3. Possible pathogens include not only bacteria but also fungi and yeasts, but Staphylococcus, Streptococcus, Enterococcus, and Pseudomonas represent the preponderance of cases.
B. Types of osteomyelitis—Osteomyelitis is further subcategorized as acute or chronic.
1. Acute osteomyelitis
a. Acute osteomyelitis generally represents the first episode of infection of the bone.
b. It is characterized by a rapid presentation and a rapidly evident purulent infection.
c. Acute osteomyelitis can become chronic over time.
2. Chronic osteomyelitis
a. Chronic osteomyelitis can be present for decades.
b. It can convert from a dormant to an active state without a known antecedent event or as a result of a local or systemic change in the host.
C. Biofilm-bacteria complex
1. The biofilm-bacteria complex that develops in orthopaedic infections, whether osteomyelitis or hardware infections, makes these infections difficult to treat.
2. The biofilm-bacteria complex is the entity comprising the bacteria in an extracellular matrix with a glycocalyx.
3. This matrix is avascular, making it difficult for bacteria to penetrate.
a. A draining sinus tract with abscess formation is the classic presentation of osteomyelitis. Often, the sinus tracts are multifocal in nature.
b. In acute osteomyelitis secondary to trauma, the clinical manifestation of the disease is exposed bone or a nonhealing, soupy, soft-tissue envelope over the bone.
c. Indolent infections might present with only chronic swelling and induration; occasionally, recurrent bouts of cellulitis accompany this.
a. Radiographic evaluation with four views of the affected extremity is necessary to initially evaluate for osteomyelitis.
b. Osteomyelitis can present acutely as areas of osteolysis, then chronically with areas of dense sclerotic bone because of the avascular, necrotic nature of osteomyelitic bone.
c. When a necrotic segment of free, devascularized, infected bone is left in a limb over time, it becomes radiodense on radiographs and is called a sequestrum (
Figure 2). Occasionally, this will be engulfed and surrounded or walled off by healthy bone; it is then called an involucrum.
3. Laboratory studies
a. Hematologic profiles can be useful in the workup for osteomyelitis. In chronic osteomyelitis, however, it is not uncommon for all laboratory indices to be normal.
b. The common blood tests that should be ordered include a CBC with differential, an ESR, and a CRP.
c. In acute osteomyelitis, an elevated white blood cell count (WBC) along with elevated platelet count, ESR, and CRP level may be present; a "left shift" of the differential is often present as well.
d. In chronic osteomyelitis, the WBC and platelet count are usually normal. Often the ESR is normal as well, and occasionally the CRP level is also normal.
e. Surgery or trauma can also elevate the platelet count, ESR, and CRP level. In this setting, the platelet count generally returns to normal once the hemoglobin level has stabilized to a more normal range; however, the CRP value normalizes within 3 weeks, and the ESR returns to normal within 3 to 4 months.
[Figure 2. Radiograph of a 24-year-old male 2 years after an open tibia fracture. The dense, necrotic cortical bone at the medial border of his tibia represents a sequestrum.]
4. Tissue culture
a. The diagnosis of osteomyelitis is dependent on obtaining appropriate culture specimens.
b. The gold standard for proper diagnosis is obtaining good tissue samples for culture. If an abscess cavity exists, this can sometimes be performed adequately with needle aspiration.
c. Appropriate bacterial and fungal plating of the specimen is of paramount importance.
1. The most widely accepted clinical staging system for osteomyelitis is the Cierny-Mader system (
2. This system first considers the anatomy of the bone involvement (see
Figure 3), then subclassifies the disease according to the physiologic status of the host (
3. This staging method helps define the lesion being treated as well as the host's ability to deal with the process.
4. Prognosis has been well correlated with the physiologic host subclassification.
F. General treatment principles
1. Once the osteomyelitis has been staged and the host's condition has been defined and optimized, a treatment plan individualized to the patient's condition and goals can be determined.
2. Ideally, the goal of treatment is complete eradication of the osteomyelitis with a preserved soft-tissue envelope, a healed bone segment, and preserved limb length and function.
[Table 3. Cierny-Mader Staging System for Osteomyelitis]
[Figure 3. Schematic illustration of the Cierny-Mader anatomic classification of osteomyelitis. Type I is intramedullary osteomyelitis; type II is superficial osteomyelitis with no intramedullary involvement; type III is invasive localized osteomyelitis with intramedullary extension, but with a maintained, stable, uninvolved segment of bone at the same axial level; and type IV is invasive diffuse osteomyelitis, with involvement of an entire axial segment of bone, such that excision of the involved segment leaves a segmental defect of the limb.]
[Table 4. Physiologic Host Classification Used with the Cierny-Mader Osteomyelitis Classification System]
G. Surgical treatment
1. Surgical debridement
a. Surgical debridement is the cornerstone of osteomyelitis treatment.
b. Aggressive debridement is often required to remove all infected and devitalized bone and tissue.
c. The single most common mistake in treatment is inadequate debridement with residual devitalized tissue remaining in the wound bed.
d. Debridement of any dense fibrotic scar is also necessary because this is often quite avascular and represents a poor soft-tissue bed for healing.
e. Atrophic skin that has become adherent to the bone (eg, the medial border of the tibia) also requires debridement because of its impaired blood supply and compliance.
2. Skeletal stabilization
a. Skeletal stabilization of the affected limb is necessary for all type 4 lesions as well as some type 3 lesions where a large amount of bone has been removed.
b. Stabilization is most often accomplished with external fixation or a short course of external fixation followed by internal fixation. It also can be accomplished with antibiotic bone cement-impregnated nails.
c. If a segmental defect is created with the debridement, then proper planning in skeletal stabilization must occur from the start, with a clear and comprehensive plan established to gain bony stability of the limb.
d. For small defects (<2 cm), acute shortening remains a reasonable option for treatment; defects can also be stabilized with rods or plates once infection is eradicated, then the defect eliminated with bone grafting or osteomyocutaneous free tissue transfer.
e. For some large osseous defects, the best option remains bone transport.
3. Dead space management
a. Debridement creates a dead space; this space requires appropriate management while the infection is being eradicated.
b. The dead space can be filled by means of local muscle mobilization, a rotational muscle flap, or a free muscle flap.
c. The VAC sponge is a useful short-term adjunct to assist in dead-space management until definitive soft-tissue coverage is achieved; however, its long-term use is questionable, and if placed directly over cortical bone for an extended period, it can lead to desiccation and resultant death of the cortical bone in contact with it.
d. Antibiotic-impregnated polymethylmethacrylate (PMMA) beads are a time-honored method of dead-space management; they also provide an effective means of local, high-dose antibiotic delivery. Most surgeons make their own beads by mixing PMMA with tobramycin and vancomycin powder. Other antibiotics used include gentamycin, erythromycin, tetracycline, and colistin. Resorbable materials including calcium sulfate, calcium phosphate, and hydroxyapatite ceramic beads with antibiotic impregnation have recently been introduced, but their clinical efficacy has not yet been well established.
i. Antibiotic-impregnated PMMA beads can be used effectively with or without a closed soft-tissue envelope.
ii. With an open soft-tissue envelope, the beads can be placed, then the limb and wound can be wrapped with an adhesive-coated plastic film laminate. This provides a biologic barrier with high-dose local antibiotic delivery and classically does well for 4 to 6 days before requiring changing because of leakage.
iii. With a closed soft-tissue envelope, the beads can be left in for an extended period to further ensure that infection has been controlled.
4. Soft-tissue coverage
a. A close working relationship with a microsurgeon experienced in soft-tissue mobilization and free-tissue transfer is imperative in managing these complex problems.
b. Microvascular free muscle transfer is the gold standard for restoration of a well-vascularized soft-tissue envelope after infection, trauma, or osteomyelitis.
c. Rotational muscle flaps are a good adjuvant for certain soft-tissue defects or when access to a microsurgeon is not possible. Rotational muscle flaps are particularly useful about the pelvis, thigh, and shoulder girdle.
d. Flap coverage combined with bone transport to fill large bone and soft-tissue defects can be performed safely and effectively with good long-term results.
5. Antibiotic coverage
a. An infectious disease consult and parenteral antibiotics are mainstays of the treatment of osteomyelitis.
b. Classic treatment protocols involve a 6-week course of an intravenous antibiotic regimen; however, no empiric data have shown that this is necessary. Recent data suggest that with proper and meticulous debridement, dead-space management, and soft-tissue management, a shorter duration of intravenous antibiotic delivery is as efficacious as a longer course of treatment.
c. With the sharp increase in organisms developing resistance to standard antibiotic protocols, such as methicillin-resistant Staphylococcus aureus and vancomycin-resistant Enterococcus, care must be taken in choosing an appropriate antibiotic regimen. Newer antibiotics such as daptomycin have been incorporated into the antibiotic armamentarium for the treatment of such pathogens.
d. In certain instances (C hosts), long-term antibiotic suppression can be the treatment of choice. The choice between a single and a multidrug regimen should be made carefully, with consultation with an infectious disease specialist, to minimize the chances of further development of pathogen resistance.
III. Limb Deformity Analysis
A. General principles
1. To understand whether a deformity exists, the parameters of a normal limb must be known.
2. Generally, the contralateral limb can be used as a control; however, with certain conditions (eg, metabolic bone disorders), the contralateral limb is usually abnormal.
3. Many nonunions develop a resultant deformity, and malunions, by definition, have a deformity.
4. Limb deformity is more of an issue in the lower extremity than the upper extremity.
5. Normal lower extremity alignment values have been established and are provided in
Figure 4. The mechanical axis of the lower extremity passes from the center of the hip to the center of the talar dome. Ideal limb alignment is defined as when this mechanical axis line passes through the center of the knee.
B. Mechanical parameters (Figure 4, A)—Essential mechanical parameters that must be compared between limbs are the absolute limb segment lengths as well as comparative limb segment and total limb rotation. Limb lengths and deformity parameters are independent of each other, as are rotational deformities, and all must be measured separately. The nonrotational deformity parameters that must be measured and compared with the contralateral limb on appropriate radiographic views include the following:
1. Lateral proximal femoral angle (LPFA)
2. Mechanical lateral distal femoral angle (mLDFA)
3. Joint line convergence angle (JLCA)
4. Medial proximal tibial angle (MPTA)
5. Lateral distal tibial angle (LDTA)
C. Anatomic parameters (Figure 4, B)—Anatomic limb measurement parameters define the alignment of the bones themselves and do not have to mirror the mechanical axis. In the normal limb, however, the mechanical and anatomic parameters should yield the same measurements at a level from the knee distally. The unique anatomic parameters of the lower extremity are the following:
1. Medial neck-shaft angle (MNSA)
2. Medial proximal femoral angle (MPFA)
3. Anatomic lateral distal femoral angle (aLDFA)
D. Evaluating lower limb alignment
1. The gold standard for evaluating lower limb alignment is a weight-bearing radiograph of both lower extremities from the hips to the ankles on a 51-inch cassette, as well as true AP and lateral views of the affected limb segment(s) (
a. The mechanical and anatomic axis angles described above are measured on the radiographs. This allows determination of the segment level of deformity (whether it is at the level of the femur, tibia, or joint line due to soft-tissue laxity), degree of deformity, and type of deformity.
b. To locate the exact site of the deformity, the mechanical and often the anatomic axis of each limb segment must be plotted.
[Figure 4. Standard mean values (with ranges) for normal lower extremity limb alignment. A, Mechanical alignment values. B, Anatomic alignment values. MNSA = medial neck-shaft angle; MPFA = medial proximal femoral angle; aLDFA = anatomic lateral distal femoral angle; JLCA = joint line convergence angle; LDTA = lateral distal tibial angle; MPTA = medial proximal tibial angle; LPFA = lateral proximal femoral angle; mLDFA = mechanical lateral distal tibial angle.]
2. Mechanical axis deviation (MAD)
a. The MAD is defined as a distance that the mechanical axis has deviated from the normal position through the center of the knee (
Figure 6, A).
b. This measurement is particularly helpful when treating the common ailments of genu varum and genu valgus.
[Figure 5. A, Illustration showing method for correctly obtaining weight-bearing AP radiograph of both lower extremities. B, Correct technique for obtaining consistent, true orthogonal views of the leg.]
[Figure 6. A, Mechanical axis deviation (MAD) is measured at the level of the knee joint and represents the distance that the mechanical axis is displaced from the normal for that limb. The "normal for the limb" is defined as the point that the mechanical axis passes in the contralateral, unaffected limb or a point in a range of 0 to 6 mm medial to the center of the knee, depending on what information is available. B, Illustrative examples of the effect of femoral and tibial translation on the mechanical axis of the limb.]
Figure 7. Translation of a limb segment can have a compensatory or an additive effect on an angulatory deformity depending on the directional plane of the translation.]
c. The measurement of the MAD combined with the measurement of the accompanying joint orientation angles is particularly useful in the treatment of any juxta-articular deformity about the knee.
3. Diaphyseal deformities
a. These deformities, especially those that are posttraumatic, are often not simply just an angulatory problem. More often than not, there is an accompanying translational or rotatory deformity.
b. Translational deformities can contribute at least as much to mechanical axis deformity as do angulatory deformities (Figure 6, B).
c. Translational deformities with accompanying angulatory deformities can either be compensatory, whereby the translation is away from the concavity of the deformity, or additive, whereby the translated distal segment is toward the side of concavity. Hence, a limb with an angulatory deformity with an accompanying compensatory translational component can in effect have no or negligible mechanical axis deviation of the overall limb (Figure 7).
4. Center of rotation and angulation (CORA)
a. To determine the true site of deformity, and not just the limb segment involved, the CORA must be plotted.
b. The CORA represents the point in space where the axis of mechanical deformity exists and the virtual point in space where the virtual apex of correction should occur.
c. The CORA is plotted out by drawing the mechanical axes for the limb segments (
d. When the affected limb has no translational deformity and no other accompanying juxta-articular deformity or additional site of deformity, then the CORA is at the site of apparent deformity.
e. If a deformity exists secondary to angulation and translation (eg, malunion), then the CORA will be at a site other than that of the apparent angulatory deformity. This is the result of the contributory effect (regardless of whether it is a compensatory or additive translational compononent) of the translated limb segment.
5. Evaluation in the sagittal plane—All the measurements and plotting of limb axes done in the coronal (AP) plane can also be done in the sagittal (lateral) plane, although sagittal plane deformities are better tolerated in the lower extremity.
6. Upper extremity deformities—These same methods of deformity analysis also can be applied to the upper extremity. Common sites of posttraumatic deformity are at the elbow, secondary to malreduction of supracondylar fractures, and at the wrist, due to shortening and deformity secondary to malreduction of distal radial fractures.
1. General principles
a. Order of correction—Alignment deformities should be corrected in the following order: angulation, translation, length, then rotation. In correcting the rotation, especially if an external fixator is used, a resultant residual translation can be encountered. If this is the case, then this residual translation must now be corrected. Utilizing this progression of correction of deformity parameters leads to the most predictable proper restoration of limb alignment.
b. Rotational malalignment is the most common posttraumatic deformity encountered; however, it is the least precise of the variables that can be measured. It is most often assessed clinically by comparing the affected limb with the contralateral limb.
[Figure 8. Determination of the center of rotation of angulation (CORA). A, The mechanical axis of the limb is drawn, and the MAD determined. B, The mLDFA, JLCA, and MPTA for the limb are determined. Because the mLDFA is in the range of normal, and the JLCA is parallel, then the deformity exists in the tibia, as the MPTA is abnormal at 74°. C, Because the mechanical axis of the femur is normal, the mechanical axis line of the femur can then be extended down the limb to represent the mechanical axis of the tibia. D, The distal mechanical axis is defined as a line from the center of the ankle and parallel to the shaft of the tibia. The LDTA is found to be normal. E, The CORA is now defined as the intersection of the proximal mechanical axis line with the distal mechanical axis line. Imagine translating the distal segment at this level and see how the point of the CORA changes. Mag = magnitude of deformity.]
c. Various values of acceptable lower extremity malalignment have been published, but there is no definitive value as to the maximum acceptable rotatory deformity tolerated in the lower limb. Most experts do concede, however, that any rotatory deformity of the leg >10° is poorly tolerated in most individuals.
2. Surgical technique
a. Order of correction—Alignment deformites should be corrected in the following order: angulation, translation, length, and then rotation.
b. Newer versions of external fixation allow simultaneous correction of all deformity parameters without the need for the residual translation correction. However, the need to follow the classic order of correction remains.
c. Simple deformities without clinically significant limb-length inequality can usually successfully be corrected with the use of locked rodding or plate and screw osteosynthesis.
d. Regardless of the method of fixation used, the need for proper preoperative planning and templating remains.
Top Testing Facts
1. Stable fixation is of extreme importance in treating all nonunions. Particular attention should be paid to the elimination of shear in nonunions with a large degree of fracture obliquity.
2. It is best to achieve as stable a fixation as possible to allow for joint mobilization above and below a nonunion. These limbs have already been through much trauma, and hence the periarticular regions are prone to stiffness.
3. A healthy, well-vascularized soft-tissue envelope is necessary for healing of tenuously vascularized diaphyseal bone ends. The generous use of free or rotational muscle transfers enhances the healing environment by bringing in more vascular access.
4. If union fails despite optimal treatment, one should look for metabolic or other endogenous problems that are inhibiting fracture healing.
1. For a successful cure, all necrotic bone and soft tissue must be meticulously debrided.
2. Proper dead-space management and soft-tissue coverage are equally important to achieve a satisfactory outcome.
3. Properly stage the host and the bone involvement at the beginning of treatment so that an appropriate treatment plan can be established.
Limb Deformity Analysis
1. The types of deformity that can exist in a limb are angulation, translation, length, and rotation. Rotation is generally measured clinically, whereas the other parameters are measured on appropriate radiographs.
2. Translation deformities can be as deleterious to limb alignment as angulatory deformities. Translation deformities can be either compensatory or additive to an angulatory deformity, and it is important to recognize this.
3. Because angulation is a phenomenon independent of translation, an apparent site of deformity might not actually be the true CORA. Therefore, this site must be precisely determined by making the measurements on long radiographs.
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